Differential Diagnosis in Conventional Radiology Francis A. Burgener, MD
Martti Kormano. MD
Tom1 Pudas. MD
Professor of Rad1ology Umvers1ty of Rochester Medical Center Rochester. NY
Formerly Professor and Cha1rman Department of Radiology University of Turku Turku Finland
Department of Radiology Umvers1ty of Turku Turku hnland
USA 3rd cd1tion
2190 illustrations
Thieme Stuttgart · New York
IV Ubrary of Congre!>s Cataloging- in-Publication Data
is available from the publisher.
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1 2 3 4 56
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v
Preface
Convt>nllonal r.ldtography remains the backbone of our ~pe cialry desptre the advent of newer and posstbly more exCiting tmagmg techmques such as computed tomography, magnetic resonance imaging, and, most recemly, posttron emtsston tomography. In contrast to many of these newer methods. conventional radiography ts pract1ced not only by rad10log1sts but also by a large number of climcians and sur geons. Wtth each examination. one IS confronted with radiologic findmgs that require interpretation in order to arrive at a general dtagnosttc tmpresston and a reasonable dtffcrenttal diagnosis. To assist the film mterpreter m .Jttammg thts goal. this book i~ b.l!>ed upon radiographic findings. unlike most other textbook~ m radiology that are disease oriented. Since many disec1ses present radiographtcally m a v.Jnety of mantfestations. some overlap in the text •s unavoidable. To minimize repetttton, the d ifferential diagno~is of a radio graphtc findmg is presented in tabular form whenever fe.Jsible. Most tables hst not only the various d1~a~es that may present radiologically m a specific pattern, but also de scribe in succinct form other characteristi(ally cJSsoctated radiographic findings c1nd pertinent clinKal data. Rcldtographic illlustration~ and drawings are included to demonstrate visually the radiographic features under dtscusston. The transition from film to digital radiography hcls had a great impact on conventional radiology smce the publication of the ld~t edit ton. Th1s ch.1nge, however. did not .1ffecr the w.1y radtologtc dtagnoses are ascertained. Sinn~ the publication of the last edition the n.1mes of a few diSOrders have ch.1nged (e. g., hl\tiotytosts X is now known as l.angNhans tell hi~tiotytost\) and a few new diseases have been recognized (e. g., femoroacetabular impmgement and severe .!Cute rt>sptratory distress syndrome or SARS). These facts were taken mto con~iderarion in thts new edttton. The chap ters "locali1ed Rone Lesions" and "jmnt Dtsease~> have been completely r<'wntten and newly Illustrated since I rook them over from Dr Kormano. The chapter "Trauma and Fractures" has also undergone a maJOr overhaul with the mdus1on of specific fracture mes Several chapters m the abdommal sec-
tton constdered to be of lt'sc,er tmportance in the age or computed tomography have been ehmmated to comply wtth the publisher's request not to alter the overall volume of text. fhe chapter on mammography has been deleted because the subJect could no longer be covered with the reqUired dPplh to be useful 10 the framework of thts text. In rhe rpma10mg chapters. text ha~ been updated. many illusrratlons replan•d, and a large number of new 1llu~trations added A "changmg of the guard" has also taken place Smce Dr. Martti Kormano's professiOnal endeavors no lonrt"r mclude clinical radtology, he was not able to take on the task of up dating his 011ginal contributions to the text. Fortunately for all concerned, he was able to find in Dr. rom• Pudas a vt>ry talented young radtologist to take ovt>r the revtsion of his original chapters. I hope this new r<'vtsed thtrd edition will IX' as well received as the previous ed1t1ons. The concept of an imag10g pattern approach m tabular form rather than a dtseaseoriented text was Introduced 10 1985 with the first edmon of Differential D10gnosrs in Conventional Radzology and has s10ce been adopted by many authors. I take this as a compliment: after all, tmllatton is the smcerest form of flattery. This book ts meant for physicians with some experience in convt>ntional radiology who wish to st rengthen their diag· nostic .1cumen. It is d wmprehensive outline of radiographic findings and will be particularly useful to radiology residents preparing for their SJX'Cidlist examination. espec•ally sim:e the exposure to tonvemional radiogr.1phy during their train ing continuously decreased in the past in favor of newer imaging modahlles. Any physitian involved in the mterpretdtton of conventtondl radtographs should find tills book helpful in dtre([ proponton to his or her curiosity. lr is my hope that the third edition of Differeurial Diagnosts in Comentronol Radrology will prove as intrr~stmg as Its predecessor'> to medical students. residents. tddiologists, and physicians involvt>d m the Interpretation of conventional radtographs. Francis A. Rurgener. MD
VI
Acknowledgements
It IS impossible to thank individually all those who helped to prepare the t hird edition of this textbook. I wish to acknowledge the staff of our publisher Th1eme. m particular Dr. Clif ford Bergman and Mr. Gcrt A. Kruger. I also appreciate the willingness of Ms. Annu.• Hollins and Ms. Stefame Langner, both of whom were r<'Cently as~igned by Thieme to this project to deal with my old -fashioned style relying mainly on pdper, pencils, hard copy, and the telephone. I am deeply mdebted to Dr. Gertrud Collman, Stemach am Attersee, Austna, who translated the last ed1tion of th1s text into German and suggested many alterations and corrections which have been incorporated into this new edition. My gratitude goe!> to all the radiologists whose cooperation made available Illustrative cases to complement the ongmal collection or to replace older illustrations. I am indebted to Drs. Stl•ven P. Meyers, johnny U.V. Monu, and Gwy Suk Seo, all staff members of the University of Rochester Radiology Department, and to the former residents Drs. john M. Fitzgerald dnd Wael E.A. Saad for providing selected cases. I greatly appreciate the invaluable contributions to this project by two former faculty members of our department.
Dr. jovitas Skucas, professor ementus, has provided me with a substantial number of gastrointe~tinal cases from his exquisite collection to replace or complement the illustrations in this text. Following his retirement, Dr. Robert F. Spataro donated his enure urogeOIIal teaching file to me. from which I have selected a few outstanding cases for this new ed1tion. I also wish to express many thanks to jill Derby, lona Mackey, and Marcella Ma1er for the1r assistance in preparing the references and ro Sh•rley Cappiello for her general asSistance. Last, but not least. I am most grateful to Alyce Norder who left the Umversity and me after 30 years for the richness of the mdustry. She is the only person capable of deciphering my longhand dOd, .1s 10 the past, did a superb JOb 10 typing, editmg, and proofreading the manuscript of the new edition of this text. Despirl' her heavy workload as executivl' assistant in her new endeavor, Alyce was kind enough to perform this task m her spare 11me, for which 1am deeply grateful. Fmally I apprcoate the support of my w1fe Therese, who has generously given her prec1ous family t1me for the preparation of th1s book. francis A. Burgener. MD
I would hke to express my deepest gratitude to honorary professor Marttl Kormano who mvlfed me to carry on his work in th1s new edition. I continue to admm~ the massive amount of work th.lt he and 01. Burgener originally put into the project m the early mneteen e1ghties. rhe hundred~ of hours wh1ch Dr. Kormano and I have spent together editing this edition have been a great pleasure It was a fasc1natmg time in my life. I espcc1ally want to thank Drs. Kimmo Matt1la and Seppo Koskinen for mtroducing me to musculoskeletal rad•ology, dnd for their extraordinary teachmg and support. Many thanks also belong to Drs. l:rkki Svedstrom, Risro Elo. and Pt>ter B. Dean for encouraging me on my way m the field of
radiology. The many fa~cinatiOg discu~~•ons I havl' had with Drs. Seppo Kortelainen and Tel'mu Paav1lainen brought me much delight. on non-radiological copies dS much as on professional subjects. I also express sincere thanks to the ~taff of the publishers. Th1eme. especially to D1. Chlford Bergman and Mr. Gert Kruger. f-Inally, much granrude 1s due to Mr. Markku Livanaien for his valuable asmtance with technical ques tions. and to Ms. Pirjo llcl.mko for all her help with general matters. Many othe• individual~ helped in various ways w1th th1s project. and though I cannot name them all.l am grateful for rhe•r conrnbut1ons. Tomi Pudas. MD
VII
Contents Bone .. . . ... .... ... .. . . ..... .. ... . .... .. . 1 Osteopenia • . • • . . . . . . . • . • • • • • . . . . . . . . . . Francis A Burgener 2
3
4
3
9 Orbits franm A. Burgener •
••••••
0
•••••••••••••••••
•
••
•
•
0
'
233
10 Nasal F-ossa and Paranasal Sinuses . • .... . .. 239
Osteosclerosis • • • . . . . . . • • • . . . . . . . . . • . • . Francis A. Burgener
15
Periosteal Reactions Francrs A Burgener
41
11
Trauma and r ractures . . . . . . . . • • . . . . . . . . .
53
12 Spine and Pelvis . ..... •... . .. .. . .• .. .• .. 257 Marter Kormano and lomr Pudos
75
13 Clavicles. Ribs. and Sterman . . . ........... 307 Martti Kormano and Tomi Pudas
Franrrs A. Burgener
Franos A Burgener
5 localized Bone lesions fronds A Burgener
6 Joint Diseases . . . . . . . . . . . • • . . . • . . . . . . . . . 129 Francis A. Burgener 7 Joint and Soft-l1ssue Calcification . . . . . . . . . 189 Martti Kormano and Tomi Pudas
Jaws and Teeth ....... . .......... .. .. . Francis A Burgener
247
.. ......... 315
14 Extremities . ...
Francis A. BurJ{ener Marter Konnano. and Tomi Pudus
355
15
Hands and Feet Martti Kormano and rorm Pudas
16 Cardiac E:nlargement . . . . . . . . . • • • . . . . . . . 397 Martti Kormano and Tomr Puda$
21
Interstitial lung 01sease • . • . . . . . . . . . . . . . . 513 Francis A. Burgener
Mediastinal or Hilar Enlargement .•. • ...... 437 Martti Kormano and lomi Pudas
22
Pulmonary fdema and Symml•tncal Bilateral Infiltrates . . . . . . . . . . . . . . . . . Francis A. Burgener
8
•••••••••
•
•••••
•
0
•••
••••
Skull .. . .. ••. •• . • .. .... .. • . •... .. . ... 203 Francis A Burgener
Chest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 395
17
18 Pleura and Diaphragm ..... . ...... • ...... 465 Martti Kormano and Tomi Pudas
23
Pulmonary Nod 1les and Mass lesions f"rancis A Burgener
537 551
19 Intrathoracic Calcifications . . . • • . . . . . . . . . . 477 Martti Kormano and lbmi Pudas
24
Pulmonary Cav1tary and Cy!>tlc les1ons . . . . . 569 Franos A Burgener
20 Alveolar Infiltrates and Atelectasis . . . . • . . . . 489 Francis A Burgener
25
Hyperlucent lung . . . . . . . . . . . . . . . . . . . . . . 583 Martti Kormano and Jorni Pudas
Abdomen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 597 26 Abnormal Abdominal Gas Patterns and Dilatation and Motility Disorders in the Gastrointestinal Tract ....... . . . • . . • .... . 599 Francis A Burgener and Martti Kormano 27 Abdominal Calcifications . . . . . • . . . . • • . . . . . 631 Manti Kormano and francis A. Burgener 28 Abnormal Mucosal Pattern in the Gastrointestinal Tract .•• . . . . . .. . ....... . 653 Martei Kormano and Tomi Pudas
29 Narrowmg in thC' Gastromtec;tinallract ..... 683 Francis A. Burgener 30 Filling Defects in the Ge~strointestinal Tract .. 713 Francis A. BuQ.:eller
31
Ulcers, DivertiCula, and fistulas in the Gastrointe'>tinal Tract .•..........• ... . .. 747 Martli Kormano and Tomr Pudas
VIII
Contents
32 Gallbladder and Bile Duct Abnormaliltes .... 767 FranCIS A Burgener
33 Abnormal Renal Papillae and Caltees .... . .. 781 francil A Burgener
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 839 Index .................................. 841
34 ftlltng Def£>cts in the Urinary Tratt . .... . ... 789 franns A. Burgener
35 Urinary Tract Obstruction and Dilatation .... 811 Fruncis A. Burgener
IX
Abbreviations
ABC AC ACTH AIDS All AML ANCA ANT AP APVR ARDS ATN AV AVF AVM AVN BOOP BPOP
.tncurysmal bone cyst duomiocl.tvicular Uoint) adrenocorticotropic hormone acquired immune deficiency syndrome dcute lymphoblastic leukemia acute myeloblastic leukemia antmcutrophil cytoplasmouc auto.mtibodres ant error anteropostenor .tnomalous pulmon.try venous return dtute respiratory distress syndrome acute tubular neaosis drteriovenous arteriovenous fistula .trtenovenous malformatron .w.1scular necrosis hronchiohus obliterans organrzing pneumonra brzarre parosteal osteochondromatous proliferation Bx biopsy caluum Ca CAD coronary artery disease CAM cysuc adenomatoid malfonnation CHF congestive heart failure cytomegalic rnclusion dise.tse OD chronic lymphatic leukemia Cll CMV t ytomegalovi rus CNS <.entral nervous system uyptogcnrc organizing pneumonia COP COPD thronic obstruccive pulmonary drsea\e CPP <..Jkium pyrophosphate drhydrate nystals CPPD <.akrum pyrophosphate drhydrate deposrtron disease CRr-.10 chronic recurrent multrfocal osteomyelitis (1 computed tomography drsea~e D drrterential dragnosis uu UDH development dysplasia of the hrp DIC drs~emrnatron mtravascular coagulauon DIP desquamative interstitial pneumonitis drstalmterphalangeal (joint) DIP DISH drffuse idiopathiC skeletal hyperostosis DIS I dorsc1l intercalated segmental instability EAC external auditory canal eosmophrhc granuloma EG F female FAI femoro.tcetabular impingement ga\troesoph.Jgeal GE Gl gJ\lrointesunal GIP grant cell interstitial pneumonitis GIST ~:astrointestin.JI stromal tumor HAD cdlnum hydroxyapatite crystals HADD c.Jinum hydroxyapatite crystal depo\IUOn disease Hb hemoglobin HD Hodgkm drsec1se HIV human rmmunodeficrency vrrus HRCT high-resolution CT hrstory Hx lAC rnternal c1udrtory canal IM mtramuscular
IP IV IVC L
LA lCH lE LIP ll lll llQ lUl lUQ LV M MAl MCP MFH Ml MPS MR MRJ MS MTP NHL NUC PA PAI'VR PATH PAVM PCP PDA PE PET PFFD PIP PNET PO
mterph.tlangeal {jomt) rntrdVtllOU~
inferior vend c.tva left left atrium Langer hdn\ u•ll hrsuocyrosrs lupus erythemdtosus lymphorclrnter~trrial pneumonrtis lower lobe left lower lobt' left lower quadrant left upper lobe lett upper qu.1drant left ventnclc male Mycobacterium avium rntracellulare
metacarpophalangeal Uomt) mahgnant fibrous hisuo<.ytoma middle lobe mucopoi)'Sdccharidosis magnetic n.·sonance magnetic resonance rmaging multipll' sdl•ro~r~ met.H.trsophalo~ngeal {joint) non ·Hodgkrn lymphoma nudear mt>dicine po\tt'IOalltl•rror partial anomalous pulmonary venous return pathology pulmonary artenovenous malforn1.1tron Pneumocy\tis carinii pneumonia patent ductus artenosus pulmonary embolism positron emr~sron tomography proximal femoral focal deficiency proxrmal interphalc1ngeal {jomt) primitive ncuroectodennal tumor per orc1l PTlD post tran~plantc1tion lymphoproliferative disorder PVNS pigmentt'd villonodulc1r synovitis rrght c111 ium RA RA rhcumatord arthritis RBC red blood cc•ll rewuatory di\tre\s \}'ndrome RDS RES ret it uloendothelial system Rll right lower lobe RSD rent•x '-YillPc1thetic dystrophy RUl rrght upper lobe RV rrght ventncle SARS '>t'vere c1c ute re<>prratory distress \yndromc ~ternoc lavrwlc1r {jomt) sc sacroiliac {joint) Sl SLAC scapholunare .1dvanced collapse SLE systemrc lupus erythematosus sc .1 pholl .1 pe11otrapezordal sn lAI>VR total anomalous pulmonary venous retm n tubertulosis TB tnangular fibrocartilage TfC TFCC trrangular fibrocartilage complex
X TMJ TNM
UIP UPJ
Abbrev•ations tl'mporomand•bular JOint turn or· nodl'-ml'tastasis u~ual intl'rstitial pnl'umonitis ur<'tt·ropelvic junction
us ultrasound ureterovesical junction UVJ VCUG voiding ~tourethrogram VIS I volar intcrcalatl'd spgml'ntal instability
1
Bone
3
1
Osteopenia
Osteopema is defined as a decrease in bone dens1ty caused by reduced bone formatiOn and/or increased bone resorp tion. Reduction m bone formation may result from either inadequalt: matlix formation (e.g.. disuse osteopo1osis and protein defitiency of any etiology) or inadequate matnx calofication (e.g~ o~teomalatia). Primary hyperparathyroidism i~ an ex.unpl!.• or too much resorption or both bone matrix and mineral. A combination of these cause~ result
rmmeralizatlon present m the maJority of o marrow d1<;ease (e.g. metastase~. mfections and storage diseases) may aho result in osteopenia Approximately 30;o of the bone mineral must be lost before a d1fference in the bone density can be detected by conventional radiography. More sensitive techmques useful for earhr1 dctrction and quantification of ostropcmamcludr axial wmputed tomography and photon or x ray absorptiometry. II ~hould ai!>O be borne in mind that thr normal bone density changt>s with age, increasing from mfancy to age 3'5-40 and then progressively decreasing at the rate of 8 % per decade in women and 3% in men. The rc1diogr.1ph1c findmgs of o"teopenia are loss or hone dens1ty and cort1cal thmnmg. Osteopema may either be generalized or localized. and 1ts differenrral diagnos1s 1s d1s cussed ~eparatcly m Tables 1.1 and 1.2 . In osteoporosis, a combmat1on of loss of bone density and cortical thmmng may result man apparent mcrease m den· sity of the cortex and vertebral endplates, that appear as
thin, sharp lines (Figs 1.1 and 12). Bone resorption occurs preferentially in the transverse trabeculae, while the trabeculae along stress lines are accentuated. Resorption of all trabeculae in a vertebral body produces the •empty box" sign. As a result of compression fractures the vertebral body may depict a dep•eso,ed endplate or become wedge-shaped. biconcave (fish Vt'rtebra) or umformly compressed (pancake vertebral body). Cartilaginous (Schmorl's) nodes are causc·d by displacement of a portion of the intervertebral di~c into the vertebral body W1th the exception of osteogrnem lmperfecta, bones do not bend m osteoporosis. A pred1spos1t10n towards fractures. however. exists in the brittle bonrs. especially in the vertebral bodies. ribs, hips and wri\tS. fracture healing is delayed and the callus formation poor. Abundant callus forma tion 1n osteopenic bones may occur, however. with exogrnou~ (iatrogenic) or endogenous (Cushmg·s syn· drome) hypercortisolism and osteogenesiS 1mperfecta. In osteoporosis. sl.'rum calciUm, phosphorus and all and i' more characteristic TI1h h oftt>n mo\t obv1ous mrhe vrnrbral bocl1es. In the skull, a blunrd mottled appearance s1milar to hyperparathyroidism is charactt>nstlc Bones are softened and have a tendency to bend resultmg in deformities commonly found in the thorax. vertt>bral column, pelv1s and rxtremities. Pseudofrartures (Looser's zones or Milkman's syndrome) occur frequrnrly and represent tnfractions with incomplete healing. They are found in
L .-· r ~ l~--J
)- 1b f1q. 1 1 OSteopenla. a Osteoporosis: Oeoss1f1ed. blcon<<~ve vertebral bod1r~ (f1sh vertebrae) w1th thin but dens.c-appearing e-nd· plate~ and pror.,intnt wrticdl trabeculae. The supenor cndpldtes typically are afft'Ctt'd more severely. b Osroomolooo: Un1fonn dt'CX\IIicahon with loss of trabecular detail ("ground·glass .1ppear· anct.>") and wrnpr~sion fractures. fish vertebrae tend to be
c smoother them 111 mlt'OpOrC,\r\ "' >d II'!Volve '>uJX'IIOr and mfenor endplatt'\ with equal S.C\1\'IIly. c Hyperparothyroidi~m: A "ruqqer jersey spine" is uwally only lou 1d in secondary hyper parathyroid· ism (renal osteod}'lotrophy), wnereas primal') hyperpdra1hyro1di\m depicts a bony tel
4
Bone
a rig. 1.2
b Osteoporo~is (a), osteomalacia (b) and hyperparathy(c and d). 05teoporo~i~ (a)· Thin ~harply defined end
roidism platP5 v.ith accentl•at10n of the "1?rt1c al trabffulae are seen. Osteomalacia (b): Unoformly boconcave "ertebral bodies v.ith poorly definl-d <:ndplate~ and blurred tralx-culae are seen. Primary
the scapul.l (latt•ral marg~n), nbs. clav1cle, ischial and pubic rami, femur (especially medial aspect of the neck), and other long bones. Characteristic laboratory findings in osteomalacia include a shghtly low to normal serum calcium, a low serum phosphorus and an elevated alkahne phosphatase. Bony tes1ons are found in less than half of the patients with hyperparathyroidism. Subperiosteal resorption along
c d hyperporathyr01d1sm (c) Thin poorly defined endplates With blur· ring of the trabecular pattern 111 the Vl'rtPbral bod1es are ~een . Secondary hyperporathyrO/dtsm (d): Blumng of the trabewlar pattern
in the vertebral bod1es IS .uwciated v.1th thi<.kening and sderosis of the superior and 111ferior endplatcs ("ruqger je~ spine").
the radial margin of the phalanges 1s VIrtually pathognomonic. rhese erosions occur mo\t often in the prox1mal and m1ddle phalanges of the tndex and middle finger (Fig. t.1 ). Absorption of the term mal tufts .md cortical striations ("tunneling of the cortex") are commonly assoc1ated w1th this condit1on. Endosteal resorption occurs in long bones. Resorption may also be ev1dent 10 the acromial ends of the
Fig. 1.3 Hyperparathyroidism of the h.tnd. Subperiosteal resorption and cortilal51rMtton•., u\ually lx•\t 5eell on the radial mar· gins of proximal and middle phalanges of ~ond and third finger. A magnified vocw of the5e lond1ngs IS demonstrated in insert a, whereas 1nsert b shows a normal cortex for comparison. Additional findings include resorption of the tufb. penartitular soft-tissue calcifications, brov.n tumor~ (third metacarpal and capitatum), and roint cart1laqe calcificatiOn (often 1n the triangular fibrocartilage between ulna and corresponding part of the proximal tarpal row) .
1 Ostcopenia
clavicles. the sacroiliac jomts. the symphysis. m the calcaneu~ .lt the insertion of the plantar fascia and in the ribs (usually in their upper borders). The bone is softened re~ult mg m secondary deformities such as basilar impression in the ~kull and kyphoscoliosis. Cyst-like Jes1ons and ~o-called brown tumo.-.; occur in tubular and flat bones. While b1own tumors heal after removal of the parathyroid adenoma and may evPntually even become sclerotic. cysts remam unchanged after treatment. Granular deo~s1ficauon of thP skull results m a "salt and pepper" appearance ResorptiOn of the lamina dura around the teeth is commonly present. Soft tissue c.Jicifications (especially arterial and para-articular). JOint cartilage calcifications (especially mem~ci and the Inangular fibrocartilage in the wrist). nephrocalciOOSIS, and nephrourcterohthiasis are common fl'aturt>S of hyper-
5
parathyroldt~m. Pancreatitis. peptic ulcer disease and gallstones may also be associated. Classic laboratory find10gs in primary hyperparathyroidism mclude a high serum t.alcium. a low serum phosphorus. and an elevated alkdline phosphatase in the presence of bone disease. An increased boor drnsity is often associated with secondary hyperparathyroidism (renal osteodystrophy). In these case~ th1rkrnmg of the superior and infer101 end plates of the vertebrallxxl1es ran result in a "rugger jersey spine·. ThP skeiPtal changes 10 d1rferem forms of hyperpcJrathyroidism are 1dennral. although brown tumors are more com moo 10 primary hyperparathyrOidism. wherec1s osteo~clero sis and extensive soft-tissue calcifications are more often found in secondary hyperparathyroidism
6
Bone
Table 1.1
Olffer~ntlal
Oiagncxiol of Generalized Osteopenia
Etiology
Comments
Osteoporosts
laboratoo-y findrngs: serum calcium. phosphorus and alkalinc pho$phatase all norm.ll.
Senile Of' postme~us.l
Most common form of osteoporosrs. Fem.Jit.os o~ffected more often and more sevt't't'ly than males. Compression fractures typKally spare the less weight beanng C('nlkal and upper thoracic 'iptne.
Dmlse iltrophy
Prolonged irnmobilintaon from any cause (e.g., neuroi'Tl1JSC\Jiar disordCfs. cast).
Protein deficiency (e.g .• mMnutrl· bon, Mphrosis) (Ftg. 1.4)
PlJre dietary protem defkiency is rolre. In undCfdl'\lcloped countri~. extensive osteopcnia is .Jssociated with kwoshiorlcor. a marasmic protein-calorie malnutrition affecting mostly children. Protein deficiency secondary to malalxorptiOn is more common (s«> under osteomalacia). Abnormal protein metabolrsm is the underf'trng cause of ostPoporosrs in scu111)' (vrtamin C deficrency) and different rodocrinologK di\orders.
Juvenile (idiopathk)
Between ages 8 and 14. characterized by .Jbrupl on~
Osteogenesis lmperfecta (Ag. 1.5)
Osteogenesis imperfecta congenita (fractures prc.'scnt at birth) and tarda (fractures absent at birth). Deformities resulting from returrent fractures in later life and bone bendrng characteristic. Both disorders inherited.
Homocystlnurla
Inherited drsorder that presents radiographrcally as combrnation of osteoporosis. Marianlike changes (e.g .. arachnodactyly). and meto~phystoal and toprphyseal widening.
Anemia (fig. 1.6)
Bone marrow hyperpldsia causes widenrng of the medulldry ~pi!Ce. <:ortlc.i!l thinninq. and trabecular resorption by pressure atrophy. Occurs in severl' ~ron de{icimcy and ~ckle cell anemia. but is more pronounced in thalas~ia. where.! generalized cy~tic appear.mce. particularly of the flat bones, is char acterhtic. Deossification is caused by diffuse infrltration and prolrferauon of tumor ctolls in the bone marrow resulting in endosteal erosions. cortical thinning and trabc:-cular resorpll
Bone marrow infiltriltlon (e.g. mul· tiple myeloma, carcinomatosis) (Ftg. 1.7)
Other more characteristic radiographiC findings are often associatc.'d v.ith the d•sease suggesting the correct diagOOSts (S@'e Chapter 6).
Connective tissue di~ (especially rheurniltold ilrthritis)
(continues on page 8)
,:--· ........
·-....
.'
. C>
2 ~4
-3 - 5
6
b a
Fig 1 4a, b 5curvy. C.hn\t', rrng-hkt' takificatron dround the epiphysis (Wnnbe•qe,·s line). (3) dense. linear calcifications in the distal metaphysis ("v.hte line of frankel"). (4) a small bone spur immediately adjorning the "white line of Frankel" (Pelkan's spur). (5) il rildrolucf'nt band proximal to the "whrte line of Frankel" (Trummt>rfeld lOll<') ••md (6) subperiosteal hemorrhage (calcifies only after LhCiolpy is lnstrtutt-d). fplphyseal separation and/or fragmentation In the reqion of the metaphysis may also be associdted.
1 Ostcopema
7
a
a
b
Ftg. 1 Sa. b Osteogenes•s lmperfecta. Olffuse osteopenia with bt--v 9 dt'b mtltt'~ of thE narro ... '
b Ftg. 1.6 Thalassemia major. Chest (a) and p<'lvt\ (b). General· i7l'OpP11t 1 <d by rt'd bone m.1rrow hy· perplasia, w1th matn Involvement of the central or flat bones characteristic. Note .Jiso the bulbous widenmg of the anterior ends of the ribs.
t'nt1rg dS gcncro~liLed osteopenia rn the spme In th1s c.:tst' hov. .t>r, edcmlllt' destruction of ll and the destr<>yc>d left p<'d1ciL oft 5 suggest the mahgnant process.
8
Bone
Table 1.1
(Cont. ) Differential Diaqnosis of Generalized Osteopenla
Etiology
( . mm.:nh
Endocrine disorders
Hypogonodtsm: osteoporos~s assoceatcd \Mth delayed ep1phy<;eal fusion (e.g .. Turner's syndrorTH', eunuchoidism). Cushmg·~ syndrome; chronic excess of glucocOJticOtds. Addiwn's dis· rose: insufficiency of the adrenal cortex. Dtolx>tes mellitus: ostcopenia present m about 50% of Jlolllroh Hyperthyroidism: often associated w1th cort~eal striations best seen 1n metacarpal bones. S('C also under hyperparathyro1d1sm m this table.
Drug-Induced (e.g.• stl!rolds, heparin) (ftg. 1.8) OsttomOioclo (ftg. 1.9)
\teroids: large dosages o~~er \t-veral month\, Heparin· 15.000 to 30.000 unih for six rnonth\ or longer. laboratory findongs in osteom.:~lacia: serum calcium slightly low to normal: serum phos· low; alkaline phosphatase elevated.
phoru~
Deficient absorption of calcium and/or phosphorus; 1. vitamin D defkiency
Dietary causes. or lack of sunst ine Adult: cxteomclocio. loss of bone demity woth blurring of both cort1cal margon~ and trabeculae characteristic. Bov-.ing dt>lormot1es .1nd pseudofractures occur frequt'ntly. Children: rickets (Fog. 1.10) Most commonly found in premature infants. D<wlops mort commonly between 6 and 12 months of .:~gc. RadiographiC features mclude: mdi\tonct, fr.1yed and c-onca11e metaphyses ("cuppong") with perpendicular trabeculile PxtE'nding towards the epiphyseal areas. Q('la~d apj>('arancE' of epiphyseal OS~If1cat10n centers w1th blurred margins (DO: Scurvy: sharply outlint'd ep1phy<;es). Bulky growth pl.!tl'\ on IOf\9 bones result in swelling around the joints ilnd a "rachiti< rosary· at the costochondral junction~ of the m1ddle nbs.
2. Malabsorption
Drseases of the gastrointest1n<1l tract, hcpatobiliary ~ystem .1nd pancreas associated with malabsorption are the most common cause of Vitamtn D def1ceency in developed countries. RKkets and osteomalacia i~ commonly .u~odted with sprut'. celiac di\OOSI?, Crohn's d~tose, ~krodermo. small bowel f•~tulos. blind loop syndromes. srroo/1 intestmol bypass surgery. and gastric or smo/1 bowel resection.
3. Dietary calcium dl!fidl!ncy
bttemely rare.
Defects in renal tubular or intestinal caldum phosphate transport system;
t. Vetamen 0-resistant rickets (x·linked hypophosphatemia) and pwudo-vitamin D deficiency rkkets (Ags. 1.11 and 1.12)
Proxomal tubular resorption of phosphoru\ deueaSftl. Inherited (X-1 'l~ed dominant and autosomal reces,ive) disorders woth \lmolar dinKai features (sho \tature. multiple fractur~. varu~ Of valgus deformities of the knees. bowing ddormiti~ of the long bonE'S in the lower extrem1ties and musculcsr weakness), but only the latter condotion es commonly iiSsooatt'd with convulsions. fnthesop.1thy in the spine may resemble ankylosing ~ndylith but Without crosoons In the ~r01hac JOtnh.
(contmws on po~ 10) Fig. 1.8 Steroid-Induced osteoporosis. Osteoporosis with thicken1nq .1nd !>
Osteopenia Fig. 1.9 Osteomalada. Marked demineralization with blurring of the innt•r cortteal margins and loss of trabeculalions are charactPml•<. Several pseudofracture~ .m~ seen. prt>senting as sderot•c tranwerse lines in the t1bia.
Fig. 1.11 Vrtamin [).resistent rickets (x-linked hypo phosphatemia). o~teopenl.l Wlth multiple fracturPs/pseudofractures and antenor bowing deformity of the t1b1a IS seen.
Fig. 1.10
9
Rickets. Ch.Jr.JC·
teristic changes 1nclude: (1) ~teopema. (l) poorl) cakif1ed and defmed ep1ph)~. (3) widentng of the epiphyseal cartilage pl.lte. (4) Wld<-rung, cupping. and fra}'lng of the meto~physes. (5) pt>IIO\teal reactions. o~nd (6) bowmg deformitie\. Grl>cnsttck fractures arp ai\O com monly o!SSOCiated, but not present in this c a\!'.
Fig
12 Vitamin
0 -resistent rickets (x-lilnked hypophosphatemia). Mild osteopnia w1th bowing dcform1ty and pseudofracture '" the distal femur and genu vo~rum is
seen.
10
Bone
Table 1.1 (Cont.) Different ial Diagnosis of Generalized ~l•o~ nl• Etiology
Comnwnts
2. Renal tubular acidosis (Fig. 1.13)
M- raboh acidosis attributed to renal loss of alkali. Pathogenesis of osteom<~lacia in this cond1tton is unclear. Commonly a~\ociatt-d w1th nephrocalcinosis and nephrourolrthiasis.
3. Fanconl's !iyndrome (De Toni· Debr~Fanconl syndrome)
ldropathic or acqwed d1sorder characteriLed by hypophosphatemia, glucosuna and ammoa< klurid. The idrop.Jthic form rs often ci\SO<.Iclted with cystinmis (widespread tls~ue dcposi· lion of cystine crystals). The a<:qwred form may be secondc1ry to Wilson's disease (rarE. fa· milic1l disorder with impaired hcpatit excretion of copper and characteristic pigmentation of the cornea (Kayser neischer ring(, multtple myeloma and lead or cadmium poisoning.
Chronic anticonvulsant drug
AntKonvul\ants (e.g Phenytoin) .md many tr;mquihze~ 1nduce tx>patlc t>nrymes that ac<eiNate degradation of biologically active v1tam1n 0 metabolites.
therapy
Flbrogenesb lmperfKt.a ossium and axial osteomalacia
Hypophosphatasla (Fig. 1.14)
~porathyroidism
(Ftgs. 1.15
htxog~is imperfecta ossium {axial and o~ppendicular bone involved) <1nd axial osteom
AutO'>omal rec.~sive disordt>r With a wide spectrum of chnkal severity. Generalized deflclerlt bony mineralization is found radloqraph~tdlly. The most severe sl<elctal mvolvement rs obserllt'd 1n neonates. in whom the d1seo~se is often fatal. In childhood the disorder resembles ri< keh, but a ssociated Irregular lucent extensions into the rnetaphyst.-s representing uncalcif1ed bone matrix are characteristic The adult form is chdradcriLed by radi· oh.K.cnt bones, pseudofractures, and fractures occurring after minor trauma that show delo~yed healing with minimal callus formation. Biochemrcal hallm.Jrk: low allwline phosphatase. Labordtory findings of p11mary hyperparathyroidism: serum calcium high: serum phosp~atase clcvatt'd In the presence of bone disease.
and 1.16)
phorus low; alk.aline
Pnmary hyperparathyroidism
Found with parathyroid adenoma. pnmary chief cell or clear cell hyperplasia of all parathyroid gi.mds. and parathyroid carcmoma.
Secondary hyperparathyroidism
Compensatory mechanism in dll)' state of true hypoco~lcemicl. Usually due to chronic renal faiiUil', lx.rt may also be caused by hypovitaminosis 0 and malabSQrptlon of calcium. In chronic renal disea!>e, the sl<eletal changes a1e u\ually d combination of hypcrparathyroid· 1sm, ostE'omalacia and osteosciNosls. Th1s complex IS best referred to as · reno/ osteody-
Tertiary hyperparathyroidism
Dt-vek,pment of an autonomous p.uathyroid adenoma In chromcall)· overstimulated hyper· pla\tlc parathyroid glands (e.g., following ren.JI trc1nsplantation).
strophy:
fig 1 13 Renal tubular a cidosis. Increased bone density secondary to renal ostcodystroph). is seen. Note also the extensive bi· latet al n..·phrocalcinosis.
fig 1 14 Hypophosphatasla. Ostropenia and a rad1olucent le~ton (c1rrows) extcndmg from the growth plate 1nto the distal femm mctdp~ls rf'prt'Wnting uncalcllied bone matnx are seen.
1 Osteopenia
11
I tg. I 15
Hyperparathyroidism. '>ubperithe rc!didl margin of the proxuNI phc~lc111ges of both index finge~. Brown tumor\ involving the diilal phalanx of the It-It tndex ftnger and the entire right thtrd metit<arpcJI boot>. Resorption of the tuft\, ~PE'odlly tn tile thum~ . The cocte• tn the metacarpals and phalanges depscts ftne stnatlons. o~tecll r~rplton be~t ~n c~long
Ftg 1 16 Hyperparathyroidism. Subperiosteal r~'orpttMS \PPn along thP radtal marg clS of tht> pro..un<~l cltxl middle phaldnges of the se<.ond ft~'f dnd the middft• ph.Jianx of the third ftng<'f art' vir· tually diagnostic. ( ortical nriations are also evidPnt.
12
Bone
Tabl 1.2 Diff"r"ntial Diagnosis of localized Osteopenia Etioloq-~
Comments
Disuse atrophy (local immobilization): 1. fracture (more pronounced dis tal to the fracture site) 2. cast l . neural paratysls 4. muscular paratys1s
~•des 1dent1cal radiographic featur~ as in gener.JII.Ied ostl"Openia, the kxahLed form m.Jy .Jbo have a patchy appear,mce due to spotty cortical thi11ning (e.g., reflex sympa· thetic d~trophy).
Reflex sympathetic dystrophy (RSD, Sudeck's atrophy) (Ag. 1.11)
R.Jpid development Of Oftffi patchy OSit.'OJ>OfO~tS ciSSOCidted with painful SOft-tiSSue Sv.eing follov.1ng trivial trauma. CerebrO\Iascui.Jr disorders, cervical spondylosis, discal hemiatiOO, poslinfectious stat~. cak1f1C tendimlls, vasculitis, and nl'Oplasm are other ill'phcated conditions. Probably of neurovascular origin.
Regional transitory osteoporosis
A pamful self limited osteoporosiS in m1ddle aged or elderly patients. Most often found in thl' hop ("transitory demmerali1ation of the femoral head") • but may also •nvolve any other major joint. Associated with disabihty lasting 2 to 4 months
Shoulder-hand syndrome (Fig. 1.18)
Pain and stiffness in the shoulder combined w•th pain, swelhng and v.lsomotor phenomena 1n the hand following an acute illness (e.g. myocardic1l infarction, in which condition it is usually located on the left side). Radiographic.!lly, it resembles refl<•x sympathetic ¥trophy.
Bums and frostbites
R.ldiographic findings consist of osteoporosis, bone resorption, osteonecrOSIS, and ¥trophic soft tissue calcifications (burns}.
Inflammatory: 1. rheumatoid arthritis 2. osteomyelitis l . tuberculo~s
localized osteoporosis is uSU<JIIy the first, .Jithough nonspecific, rc~diogr.Jphic manifestation of .Jny inflammatory disease.
Bone Infarct and hemorrhage
In their early stages, both bone infarcts and hemorrhages produce locali7E'd demineralizatKlfl. With he.Jiing. les•ons become c~lcil•('d and evt'ntually osteosclerotiC.
Radiation osteonec:rosls (Fig. 1.19)
Roldio1tion changes are dose-related, with a thrt!~hold k·vel of 30 Gy clnd cell death occurnng .Jt 50 Gy. Radiographic changes occur one year alter radiotherapy at the earliest. They ¥e initially often predominantly lytic, and progr~s 1/'orth tune to a miXI'd lybc olnd Klerotic stage
Tumor (Feg 1 20)
Chteol~'t c metastases and multo pie myeloma mu~t pnm.!nly
bE' con\idered. Pnmary bone tumors (bemgn or malognant) rncl)l prPSerlt clS tocah1ed deo\SifKatiOn. but only rarely. (contmUPS on page 14)
f•g. 1 17 Reflex sympathetic d ystrophy. Patchy dE'rnlllt'ldlllatlon mo~t '>t'Vere near the joints is quite cholractcristic.
1 Osteopenia
13
Ftg. I 18a b Shoulder-hand syndrome D.oo\stfK.lt on hmtted to the lt>ft ~•ldt>r (• ) and hand (b) SE>veral weeks followmg myocardial infarction is characteri~tic.
a
b
rt t>nd
1 19 Radiation osteoneuosis. Ot:os~iftc.atoon of the di~tal
h d.avtclf' v.tth endostt>al bont. resorption ts seen 4 years alter •rr.Jdklttun for bre.a\t carcinoma.
Ftg 120
Multtple myeloma. Oem•neralt7Jlton 1S most pro1• 'Is eflt'x symp.JthetiC dystrophy 1n
nounced n.... Fig. 1 17
14
Bone
Table 1.2 (Cont.) Differential Diagnosis of Localized
Osteo~nl:
Etiology
Comments
Paget's disease (lytk phase) (Fig. 1.21)
Skull: osteoporosis circumscripta. Long bones: usually a well-defined and V- or wedge!>haped area of deossificatiOn origlnat1ng In the subchondral bone of an epiphysis.
Fibrous dysplasia (F1g. 1.22)
Both purely lytic lesions and a homogeneous, "ground glass" appearance occur. besides prPdominantly sclerotic manifestations. Cortical thinning and bony expansion is commonly associated with lytic IE.'sions in tubular bones.
a
b Fig. 1.21 a, b Paget's disease. The lytic phase in two different patients. RE.'Iativety well-defined V-or flame-shaped areas of deossi· fication containing strands of increased bony densities in a slightly expanded shaft are characteristic (a: proximal tibia, b: distal tibia and fibula).
Fig. 1.22 Fibrous dysplasia. Widening of the humerus. with a ·ground glass· appearance and a tew scanPrE.'d patchy sclerotic arE.'as. is evident.
15
2
Osteosclerosis
Osteosclerosis is defined as an mcrease in bone density caused by mcreased act1v1ty of osteoblasts or by osteogenic or chondrogemc tumor cells formmg bone-hke tissue. Calcification of tissue other than osreo1d w1thm bone is usually dystrophiC m nature and may also increase the bone density radiographically. Oss1ficauons w1thm the medullary cavity commonly present as homogeneous. fluffy. cotton-like or cloud-hke densities. They most often are caused by bone islands or osteoblastic metastases (Figs. 2.1 and 2.2). Calc1ficauons w1thm the medullary cavity typically present as punctate. annular, comma shaped or shell hke densities and are commonly as soc1ated w1th chondro1d matrix tumors and bone infarcts (Figs. 2.3 and 2.4 ). The increase in bone dcns1ty may be scattered or d1ffuse. This distinction appears useful in the differential diagnosis of osteoblastiC reactions. since certam diseases may excluSively present as scattered (solitary or multiple) sclerosis. Accordingly. the differential d1agnos1s of these entities will be discussed separately in Tc1blcs 2.1 and 2.2. Table 2.3 lists sites and commonly used eponyms for idiopathic c1vascular necrOSIS.
Ftg. 2 2 Osteoblasbc metastasis (breast carcinoma) All 0\t('()bla\tlc I~ on 1\ ~ -.•n 1n the 1tert. .h<mteroc clled
Fig. 2 1 Bone is land A -clerotte focu~ ts set>n 1n the mtertrochan· tenc area. The ~tOn depocts both t1ny rad1atmg bont> ~pocul~ m 1t\ periphery and a Cffitral rcldiolucency. both radrographic featues that help to d1fferentrate rt from an o~teoblastic metastasis.
Fig. 2.3 Enchondroma. An oblor19 esP
h
lo o
74 P
Bone infilrct An ob><'
oE-
~ion
wrth
\hell-like- Ca •lfKdtiOnS IS ~Pen m the distal femur shalt.
16
Bone
Table 2.1 Solitary or Multiple Scattered Osteosclerotic Lesions Comments
Disease
Radiogr.tphic Findings
Bone Island (e nostosis) (Fig. 2 .5)
Rad.onuc.odc bone imaging Is not"mal. \Ill I crrcumscnb ·d isolated area of increased den\rty r.trt>l} l'XCetc>dmg 1 em in diametet". A vety slow (DO: (ht(:oblastK metastases arc rnvarldbly associated wrth a mart...edly increased radronudide growth in sile is occasionally observed. Margins demonstrate characteristically tiny spiculations or a uptake.) "brush" border. A ct-ntral radiolucency is occasion- A large. verv dense and structureless bone rsland >Mthon tht> m. dul ar)' cavity rs often called enosall) observed. Occur at any location but pelvis an trofl1o (frg. 6) \1 'rthoul proper drnKal hrstory upper femora appear to be most common loca>LL a lc '"' i• •ten lnd~inguishable from a sur· tions. greatly exnSCthocrylo!t' ct>mmtt'd boTH! lesiOn (F19 2 7 ). Rare famrlial do'>Ordt:r 10t c1ssodc1t~d With clinical Multople rOUfld or ovoid bone densities ranging m sire from 2 mm to 2 em. May demonstrate a radi· symptoms and therefore incidentally discovered at arJY age. No rncrt'ased radionudide uptakE> is found olucl'nt centl't'. Can be found in all bones, but in bone scans. skull, mandrble. nbs. sternum. and vertebrae are only rarely ifl\IOived. In long bones they are charactemtrtally located rn rnetaphyses and epipf¥t's, whereas in the scapula and pelvis they are typically found around the glenoid fossa and acetabulum.
Os~ldlosts
(Fig. 2.8)
re~pt>ctively.
Osteopathla striata (Fig. 2.9)
Chondrodysplasia punctata (congenital stippled epiphyses) (Fig. 2.10)
Multiple epiphyseal dysplasia (Fllirbank's disease)
Dense longitudonal striations that involve the rnetaphyses and may extend into the epip~e~ and draphyses. In the ilium. the hnear densities r E'ptpiJY~al ossrfrcation ct-nters. 00: Zellweger's cerebrohepatorenol syndrome. where the stippling is limited to the patella.
Irregular mottled calcifications of the cpiphyws diagl'lOS('d in children and adolescents. Sequelae in the adult consist of epipf¥t'al rrregulanttB, degeneratiVe joont changes. and rarely. asymmetncal shortl'l'ling of tubular bones.
Rare and usually awmptomatic bone di~order. Oc· casionally associated with focal dermal hypoplasia (Colo's syndromf')
Rare gffietoc.ally hett>rogeneous eprp~eal dys· plasia associatE' on sire and coal~e to form a normal appearing single ossific.Jtron centet" Can be considered to be the tarda form of chondrodysplasia punctata. Crrtmrsm wrth ddayed app<'.lrance of noppled and fr<19rnented Ppiphyseal ouofKatron cpntf'rs and sclerotic rnet.Jphyseal bands must be differentiated.
(continues on page 18)
Frg. 2.5 Bone rsland y.., •11-!ly with tiny spiculations rn ots p<'nphery ("br~h· border) rs seen rn tht• ihum.
Fig. 2.6 Large bone island (enostoma). A larye. "" 1 dense and structureless lf".oron IS o;een on thP proxrmal humerus.
F 2 7 Methylrnethacrytate bone cem~t. Sequelae of ex Cl "'•th s Jbsequent u'lllt nlilkJ of a grant cell tumor arc )t:Cn in ti'c distal femur.
2 Osteosclerosis
17
a
fig. 2.8 Osteopoikllosls. Multiple round to ovoid sclerotic le· stOns me rsuring a few millimeters m drameter .ne seen. In the tubular boo..\ they are charactenstrcally located rn the metaphyses and f'plphy\e\
b Fo.,.. 2 9 Osteopathla striat a l 91tudmal striations rnwlllrn<J the pelllr~ a) .:.'ld rno •ly tht ddphyses of the femur dnd tib~ (b ) are ..een.
Ftg. z 10 Chondroc:lyspbsia punctata F Uflctate calcrhcat•ons are seen rn the Nutt: al·.o tho. w•deoed and irregular rm:t~physes
ep•phy~
18
Bone
Tabk 2.1
(Cont.) Sollt.ary or Multiple Scattered Osteosclerotic lesions
Disease
Radlo.,a,Jnc Rndings
Comments
Melomeostosis
Presents in £ ly ~tntore cortex. The le\ion may ~imu late wax flowing down the side of a candle. Osteoma-like protrusoon~ and !>Oft tissue os~ofKa tions may be a~~ociatt!d.
Often omoted to a srngle lomb, tn whkh one or more bones may be affected. At an advanced stil
Protruding mass lesion composed of abnorm~lly dense bone woth strlKtlJreless appearance. It rarely exceeds 2 em on doameter. and os usually confollt'd to bone that I~ produced by the periosteal membrdlle. It aro~os from the outer or onner t
Benogn hamartomatous lesoon consostong exdu· sovely of osseous tisslJe. GnrdrM'I''s syndi'OITJe: Multople OHE'omas associated v.oth soft tissue tun'Ors and prl!-mdiKJnant pol\lpo~s. mamly of the colon.
Predomonantly sclerotic lesoons, either as a soht ary focus (enchondroma, osteochondroma, chondrosarcoma. osteood osteoma. osteoblastoma. osteosarcoma, and Fwong·~ sarcoma) or as Multi· pie loco (enls, and osteo!>
Dofferential diagnosos of bone tumors 1!. doscussed on detail In Chapter 5.
(Ag. 2 .11)
Ost~
(Ag. 2 .12)
Benign and malignant bone tumors (figs. 2 .13, 2 .14 and 2 .15)
(continues on page 20)
Fig 2 11 Melorf1eostosis. Sclerosis of \t'Vt'ral metacarpals and phalaf"gE's cau\ed by cortocaltho<.kef"oi)(J, oftm wtth onvolwont'nt of only one stde of a bone. The presentation of the di!>OrdE'r has ~en compdred with the "flowing of wax down a burning cdndle.· Note also tht> mvolvemt>nt of the small osteoma-lokt> protrusions from the proximal phtllanll of the third fingPr (ulnar sodt>) and the moddle phalanx of the folJrth finger (radial side).
2
Fig. 2.12 Osteoma All abnormally dcn~e lc~ion with ~tructure- lt>ss appt>aranct> is characteristiC In this rase. thE' mtt>oma originated from the outN tablt> and could f'a~ily be palpated.
F1g 2 14 Parosteal sarcoma Th s ~terlor cortiCal tumor of the distal fl'mu d1c1~ ~ s pre-..:nt• cl' c1n lneqularly defined sclerotic les1on tn thi ••mt .o~terio. projection (vit>Wed fact'-on) . The lateral prOJt'Cllon of th1s sarcoma l'i shown 10 F19 4 49
O~trm< lrrosis
19
Fig. 2.13 Osteosarcoma. A rc1ther homogeneous sclerosis of the d1stal ft>mur spanng only a sn1.1ll port1on of thf' subchondral bone in the latercJI femur condyle IS seen.
Ftg 2.15 Ewing's sarcoma A rel.lt111ely poorly def111E'd sclerotiC IS ~en n L3 '1\1{)1· j • posterKJf two-thtrds of the lt('rte· bral bocly c1nd J".'Ciocl.,s.
lesion
20
Bone
Table 2.1
(Cont.) Solitary or Multiple Scattered Osteosclerotic Lesions
Disease
Radlographk Flndir.gs
Ost~
Poor!) dl fmcd .m·~ of oncrt>awd density WJth ondi!>- In childr.-n, l._;_.kemta, nl'tlroblastoma, and EWing's hnrt or kist trabe< ular ~tructu rE'. With increase tn sarcoma ml'tastascs must be considered. although suE'. adjacent mE'ta~ta'>es may coalesce, r~ulting fi- thf>~e le\ion\ are more commcnly lytic l.lfofore ncolly tn mo\t doffuse sclerosis. Wtth the exceptton of trNt fJ1Cflt ts lnstttuted. renal and most thyroid r arconomas whiomyf!ittrs (CRMO) or SAPHO (synO\Iitts, acne, pustulosis, hyperostosis. osteotis), respecttv('ly Solitary or multiple osteosclerotic lesions and fluffy POEMS is the acronym for polyneuropathy, or· spkulated hyperostotic. areas preferentially at sttes ganomegaly, endocrinopathy, M protein, and skin of ligamentous attachment in axial and para-axial changes. locations. M. all caust>" duonK Stlerostng-type 0\teomyelitis. Sc.lffosinq osteotn)'f!irti) of Gorrlos a lov.-grade chrOflk ioff!( tion not associ.Jtt..'riosteal and cortical t hickening or even broad-ba~ed excrescences resE'mhling o~teomas. Commonly in ribs or metatarso~ls following a Healed fractures result in a localized increase on bone den'>lty. fatigue fradure. finclo ng~ eX-pendent on both location and time A Prest>nts clinically with Jctivity-related pain that is fracture lint> (wrtic.al or complete) is not always relieVE'viIOO\ \uch a~ fobfou~ rOfticdl dP. healt'gre!>\ and pnsist o~s !><:k>totic foco. lytle mcta~tascs (e.g .. from bronchogenic carcinomi!, btt'cl\l larcinoma, lymphoma) and multiple my· eloma rNnik'Stations may respond to local irradia· tiort, chemotherapy. andfor loormone therapy by bc.·loming o~tcosderotic. 8fown tumors in ptimary hyperparathyroid ism belomc Stlerotic after removal of the p;~rathyroid adenoma.
meustBft (r19. 2.16)
Multiple rnyelofN ~a
cell granuloma
(Ag, 2 .17)
POEMS syndrome
Chronic or hNied
osteomyelitis (Fig. 2.18)
Brodie's abscess (fig. 2 .19)
Tropical ulcer
Callus formation (Fig. 2.20)
Stress fracture (Fig. 2.21)
HNied bone lesion (F.g. 2 .22)
2 O!>teosclerosis
21
Fig. 2.16 Osteoblastic metastases from prostatic car· cmoma (a) involvmg the spine and pelvi\ and from Hodgkin'~ disease (b) involving only the left fourth and fifth rib. The in· volvement of different vertebral bodies vane~ from barely visible, poorly defintd areas of inueased densities rn some vertebrae to almost complete sclerosis ("ivory vertebra") in l4.
b
a
Fig. 2.18 Sclerosing osteo· myelitis of Garre. A homogeneous sclerosis of the proximal spindle-shaped tibia shaft is seen.
Fig. 2. 17 Plasma cell granuloma. Scattered osteoblastic lesions and a larger osteoblastic area in the left ilium adjacent to the '>i!croiliac JOint are seen.
22
Bone
Fig. 2.19 Brodie's abscess. Radiolucent lesion with surrounding reactive sclerosis in the distal tibia metaphysis is characteristic
Fig. 2.21 Insufficiency fracture. A poorly defined osteos derotic zone is seen in the lateral aspect of the proximal tibia.
Fig 2.20 Healed fracture. Irregular widening of the shaft. cortical thickening and sclerosis is seen in this healed comminuted fracture of the prox1mal femur.
Fig. 2.22 Brown tumor In primary hyperparathyroidism, a before and b five years after removal of a parathyroid adenoma. Healing of the brown tumor resulted in a persistent sclerotic focus.
a
b
2 Osteosclerosis ;~bl
23
2. I {Cont.) Solitary or Multiple Scattered Osteosclerotic Lesions
Bone Infarcts (old)
(Ftgs. 2.23 and 2.24)
Rad10gr.,tMc Ftndmgs
Comments
often lot ld in the prmumal ()( distal ends of long tubular bones. HE'aiPd mfarcts present as ir-
Infarcts an• oftt>n assoctatl'd wtth other diseases such as occlus~ va5eular dt~ase. s.tckle cell anemta, pancreatttis, connectiw tissue dtsease. catsson dtsease. Gaucher's dtsease. and radiation ther-
Mo\t
regularly calcified areas tn the medullary cav•ty. demarcated from the normal booE' by a dense serptg•nou:. contour ()( trregulcJr streaks. The calciIK.atlons "'dY ev-entually progress to ossification.
apy. A \itnildr c.tlc tfkallon 111 tilt! medulla of long bones can occa~onall~ be seen aftet removal of an intra
{conllnues on poqe 24)
a b
a
Fig. 2.23a. b Bone Infarcts. Irregular pcnpl1eral nm calcifications are seen in the distal femu (a) and morl' l'xtensive in both the d1stal femur and proximal tibia (b ) ·n tht'SE' p.1til'nts WJth sickle cell anem1a.
I ig. 2 25 Enchondroma. An 1rregular calclfiC<~tton tS seen tltcJt t\ most dense in tts
ct>nter.
b ftg. 2 24a b Bone infarcts In an attempt to heal th.. OI'Qin.. I ale .,., r'l rt bo comes osstftl.'d from 1ts J>t;rtpht.-. ~ .o..o u•.. c~ .. too and t'llefllually presents as c1n urcqular sclerotic le!>!OO a:. ~een tn the proxim.~l femur shalt tn a and about the knee ., b.
24
BonE:'
Table 2.1
(Cont.) Solitary or Multiple Scattered Osteosclerotic Lesions
Disease
Radiographic Rndlngs
Comments
Radiation osteonecro-
M")) pt, ""' 1t ~ar $ after therapy as a mixture of sclerotiC and lytic lcs100s even when no infarcts helve occurred.
lhi~ ~ond1hon can be dJffNentiated from a local tumor re
Scquei.Je of cJva~cular necrosis in epip~ conl.lst of ~lerotk and cyst1c areas of flattened and ir· regular joint \Urfaces. which lead to early second· .ary degcneratM' changes. particularly in the weight-bearing joints. Most idiopathic ava\Clllar necroses occur during ch1ldhood and adolescence. Idiopathic avascular necroses occurring in adult· hood are found 1n the medial femur condyle (Ahl· bOck's dr~eose. also reffered to as spontaneous osteorn>cro~\ about the knee or SONC) and 1n the lunate (Kienb&k's drseow). Ahlback's disease typi· cally occurs 1n the elderly with female predomr· nann• and occasionally affect the lateral femoral ar the trbr.ll condyles. New evidence suggest it rt'J)fe-.enh a stress (insufficiency) fracture rather than a \pontant'Ous ostt'Onecros1s. Kienb&k's di~ease is usudlly found in young adults In an advanced stage. the lundte ~h~ increa~ bone density, f1 agmentation, and compression.
May be found in c1ny disorder associated \Wh medullary bone infJrcts. Avascular necros1s is caust.'
C.an cause umform areas of increased bone den\ity in the sderotic phaw. In the reparative (m1xed l}trc and sclerotic) stage. the disease is characteris· tl(ally a\..ociated w1th cortical thtekening rest,lting in enlargement of the affected bone. Any bonE' can be affected; "cotton \111001" appearance of the skull and "illory vertebral body" are representJtive examples of the scI erotic phase of the di\ease.
Purely sclerotic phase IS ic\\ common than the combined destructrve and reparative stage vir· tually pathognomoniC for the d1sease.
Fibrous dysplas~
Besides havrng a cyst-like or "ground glass" ap· pear.mee. it can also present as purely sclerotic le· loiOns. Manih~\tat1ons are u~ually associated v.ith bone e l(pamion. partiwlarly in tubular bones. With more extcns1vc mvolvcment. bone deformitie~ al· most 111variably occur.
Occur\ in mollO\totlc. and ~totrc forms. An C»)rfying fibroma of the slia. and can be considered radrographkally as a locah1ed manifestation of this disease. Ossifying frbromas occunng 1n long bones. especi.llly in the tibia and to a lesser extend frbula are referred to as ostf'O/rbrom dysplasia (fig. 2.29)
M.Jstocytosls
Can pre\ent w1th focal or diffuse bone mvofve.. mt·nt. fOred. wcll-dt>fined \Cicrot1c foci often alternating with drea~ of bone rc~refd<.tion. Skull. spine. ribs. peiV1~. humenu\, and femur are preferred sites of illllolllement.
Majonty of patu~nts df.'Vt'lop skin les1ons containing lllcl\t cell\ dur111g the frr\t year of lift>. Hepatos· plenomeqaly. lymphadenopathy. and pancytoperia may ~ a\sociat<.'
sis (Rg. 2.26) Avascu~r
(epiphysul) necrosis (AVN)
(Fig. 2 .27)
Pilget's disuse (F"eg. 2.28)
(Rg. 2.30)
(continues on page 26)
2 Osteosclerosis
25
Fig. 2.26 Radiation osteonecrosis. Mixed osteolytic and osteoblastic lesions are seen in both pubic bones with several pathologic fractures 7 years after irradiation for bladder carcinoma. fig. 2 27 AvaS
Fig. 2 29 Osteo fibrous dysplasia. Anterior bowing of the sclerotic and slightly widened t1bia shaft with a thickened Irregular posterior cortex and several lytic lesions in the anterior cortex are seen. Similar but less severe changes are also present in the fibula. Fig. 2.28 ~clrrotic
Paget's disease. A slightly thtekened and umformly clav1cle ~~ ~een.
Fig. 2.30 Mastocytosis. Multiple sclerotic foci are evident.
26
Bone
Table 2.1 (Cont.) Solitary or Multiple Scattered Osteosclerotic lesions Di~ase
Radiographic Andings
Comments
Tuberous sclerosis (F19. 2.31)
Oft. ~ p t. ·nting ~~>1th scattered intracerebral calc' ftCat10ns. renal hamartomas. and bone lesions. Charaoons may be seen 10 the hands and feet.
Ra t familial disorder v.ith defect in developing ectodermal structuoes. Present clinically woth ad~ noma seha
Sarcoidosls (flg. 2 .32)
rocal or gcnercdized osteosclerosis is a rare
A more charac:tf'rlstlc pn!sPntatJon that is found espec1ally in the bones of the hand conSists of ostt'Opt•nicJ with d codrsent:d, retiwi.Jted or lacework trabecular pattt'rn and loc.:~hzcd cystic ("punched out") lesions.
manifestcJtion involving spine. pelvis. skull. ribs. proximcJIIong bones c1nd terminal phalanges (acroosteosclerosos).
Fig. 2.31 Tuberous sclerosis. lr· regular sclerotic areas are inter· sperwd with small cyst-like le sions.
Fig. 2.32 Sarcoidosis. Poorly defoned patchy sclerotic areas are noted Lhroughout t 1e spine.
2 Osteosclerosis Table 2.2
27
Gen eralized Diffuse Osteosclerosis
. on •
Radiographk Findings
Comments
PhysiologK osteosclerosis of newborn
Cortical tl Kkening and .Jbundant spongiosa for· mation can rt>Sult 10 considerable osteosclerosis. mamly affecting the long tubular bones.
Sdt.'I"OtK changes disappear gradually during the first weeks of life and have no pathologac signif•· c.1nce. Can be found In more than he! II of all pre· mature 10fants.
SyrnlllE'tn~clllfliiOivement
Ch.lngt'\ an congenrtal syphalts caused b)' a combi-
Congenital syphilis (Fig. 2 .33)
of metaphy~ and di·
aphy\cs, With the epi~al ossification centers
being Sp
Erythfoblastosis fetalis
natiOn of luetiC osteomyelitiS and nonspecific trophK disturbances an enchondral bone forma· tion. Rad•ographiC changes may bt present at borth or develop subsequently.
Predilection for dastal femoral and proxamal tibial metaphyses and adjdtent diaphyses where irregu· lar longitudinal lytic and sclerotic densities are found, giving a "cclcry-stilk" appearance. M£>t.aphyse
Caused by matl'lnal rubella anfectlon 10 the first trimester of pregno~nose may re~ult on so malar bony changes.
Transvt>r~
Congenotal ht>molytK an£>moa caused by Rh factor lncompatibahty. Clinically, severe prolonged jaun· dicl" (icteru~ grcl\lls neonatorum) and generah1£>d edema (hydrops fetahs) are associated.
of tt
metaph)'seal bands and diffuse sclerosis may be present.
~ daap~
(corllmtJt>s on pag£> 28)
Fag. 2 33 Conge nita l syphilis. ScleroSIS of the daap~iS iS CdUSed by COrti· cdl thockenang and penosteal reac· tooos. Destructrvc lcsaons are no longtor recogmzable tn thas healing phase.
Fig. 2.34 Rubella embryopathy rrC9ular longatudonal lytoc and sciE'fotic densot1 ~ 111 th 1\!dl fr r and pro.. mal tabaa ("cl"il"ry· stick" appedodlltt') re c · ttn,r.c. Melc'!ph~\1'\ dre \hghtly tr· regular. but not cupped.
28
Bone
Table 2.2 (Cont.) Generalized Diffuse Osteosclerosis Disuse
RMiiographic Rndi' 9
Cornnwnts
lnf.mile cortical hy(Caffey' s diseotSe) (fig. 2.35)
Cortil.al tl..ck.:ring, sometimes with asymmctriul distribution. M.mdibie cl.wides, long bones (especi<~lly ulni!e). ub~. skull. scapula and pelvis ,ue in· volved, 1n th.1t ord<'r of frequency. lubuli!r bones may have a spmdl~>-~hape appe<1rance srnce only the diapll)"CS .ue involved. A laminated perio~teal reaction is only associated in the healing phase. Solitary or multiple, often asymmetric invoii/Cmcnt of the di.lphyses of long bones (especii!lly femur and tibia) with sdt·rosh and hyperostO'>is.
l • • •.tmnun dise.1se of unknown etiology with onset 1n the frrst 5 months. Climeally. the affooed bones arc associated with tender soft tinue swellings and fever. Recovery occurs over a period of a ftw weeks to several months. R()('ntg£'n changes rE>gress within a year.
pero5tcnn
Ribbing's disease
Progressive ~al ~(Engelmann
Camuratl disease) (Fig. 2.36) Generalized cortical hyperostosis (van Buchem's disease) (F'eg. 2.17)
Hereditary hyperphosphatasla (Juwnile Paget's diseotSe)
Cranlometaphyseal dysplasia
Hypoparathyroidism
Usually asymptomatic and often considered as forme fruste of Engelmann C.1murali disease. When a solitary bone IS invoii/Cd the drfferential do· agnosis 1ncfudes chron1c sclerosJng ostf'O(TI)'ditis of Carre. Cortical thickeninq of the long bones begrnninq rn Thrs autosomal dominant tr.Jom~illed neu· the mkhhaft and progressHag peripherally. resultr001uscul.u disease is usually diaqnosed between 4 ing in a spindle-shape appearance with relatively and 12 years of age. ChdrdCtcrhtit clinrcal featurE's abrupt tran~tion to normal bone. Involvement of in< lude a peculiar wide-bas<.'d, waddling gail, muscular weakness, .1nd malnutnt1on. other bones wrth sdcrosrs is less common. Diffuse symmrtric ill sclerosis and cortical thicken- R.1re .1utosomal recess111C disorder occurnng in rng. predominantly of the diaphyses of all tubular adulthood with male predomrnance. bones. Sclerosrs dnd thickening occurs also 111 th£> Worth's syndrome: Autosomal dominant form. with vault and b.1se of the skull. m<1ndible, clavicles. ribs sim1lar but less severe radiogrdphit frndir~. is often detected incidentally on radiographs oband spine (par liculo~rly affecting the spinous processes). tained for unrel.1ted reasons. Marked cortrcal thickening c<1n be found 1n .111 Rare autosom<~l recessive disease developing usubones. In the long tubular ~s the process inally in the second or third year of hfe With stnking, volws the entire hone rather than only the dtpred~ection for t~ of Puerto ! of the skull (calvarium and and cranir1~rty of the ihac crest. and marginal moval of the parathyrOid glands during thyroid sclerosis of vertebral bodies can also be found. surgery. Ossofrcation of musck> 1nsl'rtion and hgamenb and ~rudohypoporathyroidism d11fers from the primary subcutaneous calc1ficatrons occur. lnthE'sopathy in form by thE' presence of short ml'tM:arpal and the spine re-.ernbles drffuse idiopathic skeletal hymetatar~al bones and the lack of rE'Spon~e to parol· pero~tosis (DISH). In the skull cal\arialthickenrng, thyroid hormone substitution therapy. basal g.1nglion calafiCation and defective dent1t1on ~dopsrudohypoporotflorrordism has sinular radioare characteristic. graphic features. but no blood chemical changes. (continuE's on page JO}
2 O!>teosclerosis
29
~rg.
2.35 Infantile cortica l hyperostosis (Caffey·s disease) Pt>uostf'ill re.1c ttons wrth subsequent corlitdl thickcnrnq result in widened i!nd reliltively dense di <~physe\ of tht• long boot"i rn the upper extrermty.
Fig. 2 36 Progressive diaphyseal dysplasicJ (Engelmannumurati d isease) to tKi!l thr• lu r rnq of drffer nt sewrity 1n both femurs of the ...Jmc p;~tient p;odu...ed spindk •. klpl'
Fig. 2.37 A Craniodlaphyseal dysplasia. Mc1rked cortrcal thickening of the ~hort tubul., 1:..10 of th t-.1M in seen
Generalized cortlal hyperostosis (van Buchem's disease) Syrr metf'I<JI vk- 0<. nd c rhcal thr kE>nrn<J pr -dominantly of the doaphy:.c-. of tht: ft:mur (a , <~• od the trb1.. o~nd f,.., ria (b).
< hg. 2. 37
is seen.
b
30
Bone
Table 2.2 (Cont.) Generalized Diffuse Osteosclerosis Disease
Radiographk Rndlngs
Comments
Osteopetrosis (marble bones. AlbenSchonberg disease) (Fig. 2.38)
Symrnctncal ncrea~e m bone denSity rangtng from minim.JI to extreme rna-, be found. All bone~ may be lnvolvro With no predilectton for a specif~<: lot.1· tron \OAth in one bone. Tubular bones lack modelmg. often cau~mg flaring of the ends (Erlenmeyt: fia~k deformity). longitudinal and transllefse stria· liOns a~ \WII as "bone-within-bone" appeara••ce occur.
Rare hered•tary bone disorder With usually normal !>erum calcoum, phosphorus. ,md 4lkaline pho\phatase levels. At least four different types are differentiated. one of which ts associated with tubular acidosis.
Pyknodysostosls
Dtffu\C Osteoo;clerosts occurs but difft>f'> from o~teopetrost~ by the alxt>nce of both Erlenmeyer fla\lo: deformitiE-s and "bone-wtthin-bone" appeardn<e. Hypoplasta of the mandible and ~hort bones of the hands and feet wtth osteolysis of the distal phc1lange~ c1re chcJrciCteristic.
Rare cJuto~mal rP< ewve dtsorder conshttng of osteo:.< leros•s. short stature, frontal and occipital Msing. \IT1dll f.1ce with tt'
Dysosteosclerosls
Sclero~ts
of skull. nbs, clavicles and tubular bones \llnil.lr to osteopetr·osis. However, platyspondylia and lucent areas in the expanded diametap~f'S allow differentiatiOn
Autosomal recessrve dtsordN manifested m early choldhood with small stature. dental anomalies, abnormal bonE> fragility. and occastonally neurologtc symptom\.
Melorheostosls (Fig. 2.39)
Causes asymmetrical or uniform cortical thickening. ll\ually limited to one extremity. with a predilection for tubular bones where it presents as continuous or tnterrupted streaks of sclerotic areas.
When fl.'atures of mclorheostosis o~re ptesent together with fmdtngs of osteopoikilosis and osteopathia striata. then the dt\Ordt>r i~ often referred to as mixed sdcrosing bone dystrophy (Ftg. 2.40).
(contmues on page 32)
b Fig. 2.38 Osteopetro sis . Otrfuse and symmetrical osteosclerotic involvement of the entire sl<eleton ~ charactenstJC. Note "bonewithin-boo<' appearance in the p<'M~ .:~nd tarsal bones (ill) pelvis; (b ) hand; (<) foot
2 Osteosclerosis
31
a
Ftg. 2 40 Mixed sclerosing bone dystrophy poikilo~i~ o~teopathia ~triatcJ
Feature~
of
cJnd llelorheostosts are seen.
~teo
b Melorheostosls hn\tVt' predomtnclntly band· like ossificatt IS ~r< \ter in r •an~ bone~ of the nght ~ode of the patient shown here in th.o nqht hemithoro~J< (a) and right humerus (b). The left stde was normal.
Fig. 2.39a, b
32
Bone
Table 2.2
(Cont.) Generalized Diffuse Osteosclerosis
Disease
Radlogrilpfllc Find111gs
Comm nb
Metastiltic diseilse (extensive) (Ag. 2 .41)
Gt
Most commonly from carctnoma of prostate and breast.
Myelofibt"osis (myelos clerosis, myeloid metaplaslil) (Ag. 2.42)
Approxtmately h.;lf of the patients develop a dif· fuse (rarely patchy) osteosclerosis. Ribs. spme, pel· VIS, humeri, and femur are most often inwlved. M.mive splenomeg.1ly is usually apparent radiograph~eo~lly. Extramedullary hematopoiesis. evident as d p.nasptnal mass. may be present. Both find lngs may help to dtfferentiate myelofibrosis from osteoblastiC metastases, fluorosis, osteopetrosis. and renal ostrodystrophy.
Clin1cally characterl1ed b)' hepatosplenOO'egaly. anemia. thrombocytopenia.
Anemias and leukemias (Ftgs 2.43 and 2.44)
Present radJOgro~ph1cally more commonly With a lo<.s of bone den'>ity and coarsening of the trabecular pattern. Generalized sclerosis may occur, particularly in sickk cell anemia.
fxtramedullary h~matopoiesis can be associated with all blood di!.<>fd~rs. Splenomegaly IS usually present e.ICcept en the adult sickle cell patient (presumably be
Multiple myelomil
Uniform sclerosis is a very rare manifestation.
Charactenstlc bone marrow and laboratory find· ings
Gaucher's disease (Fig. 2.45)
M.JY present in the reparative stage with diffuse osteosclerosis. CharcJcteristic for Gaucher's disease in the femur is the combination of avascular neuo'>is of the femoral head, Erlenmeyer's flask deform1ty of the d1stal end. and multiple osteolytk and/or sclerotic lesions in the shaft.
The radiographic. f1ndings described are seen tn the
'll'r.>
11l"d diffuse osteosclerosis.
chronic form of Gaucher's d1sease, whereas the .xute infantile form is characterized by pathology in the resptratory and central nervous system and is usually fatal in the first year of hfe.
(continues on page 34)
rig. 2.41 Osteoblastic metastases from prO$· tatic carcinoma. Generahzed diffuse osteos· clcrosis i5 seen.
2 O!>teosclerosis
33
frQ. 2 42 Myelofibrosis. Urlfuse symmetuc and somewhdt patchy oskopcnia rs seen involving the lumbosatrdl area, pclvls dnd proxrmal femora.
b
a fig. 2.43 Si ckle cell anemia A nonumform cuplike depression of only the centrdl portions of the upp
frg 1 45 Gaucher's disease Al:.lsculdr neuo~s of the femordl £> head and sderotit thdr Q ~ 111 the proximdl femur c~re wident.
Fig. 2.44 Leukemia A CQdr\l"nPd trabecular pattern and "cortical tunneling" (longitudinal stri.Jtion~ in the cortex) with an overall increased bone density Jre seen in this child wrth acute leukemia.
34
Bone
Table 2.2 (Cont.) Generalized Diffuse Ost eosclerosis Disease
Radlographk Andlngs
Comments
Erdheim-Chester dis-
Sym ,etri<. patchy or diffuse osteosclerosis and cortical thickening of the diaphyses and metaphyses of the major long bones. with relatrve spc~ring of the epiphyses and axial skeleton, are characteri\tic.
Affects r~ o ld women rn thE' f1fth through SC\Icnth decade. X-1nthomatous pc~tches in the eyelids and mild skeletal pain can be present. but patients may also be asymptomatic.
The .1dvanc!'d ~tage of the polyostotic form may eventually result m a deformed and drffusely \clerottC \kelt'ton. Enlar~t of all involvfod bones~ cortkal thickening r.. a radiographic hall· mark of the disease.
Common cause of ostt>osdl.'fosis obsefwd in an asymptomatiC p.atrE'nt agl'd OVE'r 40. 1he radiographic d1c1gnosls 1s supported by marl<edly elevated lot'I\Jm alkal1ne phosphatase and normal serum cakium and pllosphorus levels.
Fibrous dysplasia (pol· yostotic: form) (F.g. 2.48)
Similar to Paget's disease. Can present as diffuse sclt•rosl~ of the 1nvolved bone associated wrth wrdE'nrng and cortical thickening. The manifestations Clre prE'dom1nantly unilateral, and bone d£'formlties are common.
Clinically, "cafe -au-lait" pigmentations v.ith irregular outlinE' ("coast of Marne" appearance) are found 1n approxlm.1tcly ont' third of pc~tients with thE' polyostOtiC form. Alkaline phosphatase is normal c only m1ldly elevatf'd.
Mastocytosis
Can prc!.Cnt throughout the skeleton as diffuse sclerosi~ that is not sharply demarcated from nor· mal bone and often intermingled with osteolytk areas.
See also Table 2.1
Tuberous sclerosis
Can prpsent as diffuse osteosclerosis similar to mastocytosrs.
See also rabiE' 2.1
Sarcoidosis
Diffuse ostrosclerosis is a rare manifestation.
Sec also Tab~ 2.1
Renal osteodystrophy (F.g. 2.49)
FE'atures of osteomalacia. hypefpclrathyro1d1sm, and sc!Pro\i\. ThE' lattE'r might be the dom1nant frnd1ng and is often combined w1th soft tissue cal· cificatl(lll\. A "rugger jersey" spine (dense endpiJtes with relatively lucE'flt centers resultmq in a stnped appearance of the spine) is most charac· teristlc.
Represents t he ~kE'I •tal rE'sponse to chronic renal disease of any origin. In primory hyperparathyroidism, sderosis IS vrrtually hmit!'d to cases that are healing.
Oxalosis (Fig. 2 .50)
SciE'rohc, rnetaphy\eal bands and "woolly" or "Petget l1ke" sclcrosis are combined v.ith features of rt>nal osteodystrophy, 1ndud1ng a more generalb-ed form of osteosclerom.
Oepositron of calcium oxalate c~tals as a pnmary hercd1tary (autosomal -recl'Ssive) disorder, or more commonly associ.1tt'd With chrome r('nal d1sease. Extensrw nt>phrocakrno~l\, nepllrollthic~sis. and extrarenal soft -t1ssue ck>posrtion of cak1um oxalate occur.
Hypervitaminosis D,
Pr~nt with dense transverse metaph~'Seal bands and genN alizcd sclerosis.
In childrc:-n.
FluoroSIS progre~ses from coarsening of the trabecular ~tructures to a dense uniform sclerosis. CharoKtcristically, the findings are most pronounced in the axial skeleton. although all bones may be involved. Periosteal reaction may be preSt'nt. btcnsivc ligamentous calcifications are characteristrc. particularly in the sacrospinous and s~crotuberous ligaments.
C.m be found at any Jge. Clinitc~liy. the most characteristic feature is mottling of the enamel of the teeth. Chronic fluorine rntoxication occurs. when the drinking water contains excessive fluoride concentratiOns (endemic in cl'rtain regrons of India) or with chronrc fluoride thNapy in too hiqh dosages (e. g .• for ostroporosls).
sse (lipid granuloma tosis) (Fig. 2 .46)
Pitget's disease (Fig. 2 .47)
Idiopathic hypercalcemia of Infancy (Wil li.sms syndrome), In· toxlcation with lead, bismuth, or phosphorus (Fig. 2.51) Fluorosis (Fig. 2 .52)
2 Osteosclerosis
35
Fig. 2.47 Paget's disease. Prroominantly sclerotic involvement of the right hemtpelvis. left iltum (inferior half) and left proximal femur is seen.
Fig. 2.46 Erdheim-Chester disease Inhomogeneous sclerosis with cortical thickening and relative sparing of the epiphysis is seen in the distal tibia.
Ftg 2.48 Fibrous dysplasia (polyostotic form). Mtxed osteolytte (some with ground glass appearance) and osteosclerotic involvement of the right hemipelvis .md proximal femur is seen.
fig. 2 49 Renal osteodystrophy. xlerOStS IS particularly dense at the endplates of the vertebral bodies, resulting in a characteristic "rugger jersey" spine appearance.
36
Bone Fig. 2.50 Oxalosis. Diffuse "woolly" sclerosis of the axial skeleton and proximal femora is associated with bilateral dense and small kidneys.
Fig. 2.51 Hypervitaminosis D. Generalized sclerosis and transverse bands in slightly widened metaphyses are seen.
Fig. 2.52 Fluorosis. Increased bone density varyang from a markedly thickened and coarsened trabetular pattern to uniform sclerosis.
2 Osteosclerosis
37
Table 2.3 Avascular Nec:rosis of the Bone Eponym or Name of Disease
Etiology
Time of Occurrence
Cai11~Kummel-Vemeuil
Childhood
S
Idiopathic. posttraui'Tl.'lttC. eosinophilic granuloma Idiopathic
Buchman
Idiopathic
Adolescence
Ischial apophysis Ischiopubic: synchondrosis
M1kh
IdiopathiC
AdoleS<enc e
Van Neck
Idiopathic
Childhood
Symphysis pubis
Pil'!son
Idiopathic
Adolesct>nce
Fnedrich
IdiopathiC
Adulthood
He!\~
ldiop.sthic Post fracture and other causes similar to a11ascular necro'IIS of femoral head (see under this subject in this table)
Childhood Adulthood
dissecans
ldiopdthic. posttr aumati<. Idiopathic. posttraumatiC
Adolesct'nce. adulthood Childhood, adol~ence
Osteochondritis dissecans Bra1l'lford
Idiopathic. posttraumatiC
Adolescence. adulthood
Head of radius
Idiopathic
Childhood
Diml ulna (epiphysis)
Burns
IdiopathiC
Childhood
locatiOfl Spine
Vertebral body (~ebra ~na)
Vertebr•l epiphysis
Adol~ence
~Ms
Uiac aest
I.Jppff extremity
CJavk:le (lower half of sternal end) Head of humerus Head of humerus (Fig. 2.53)
Head of humerus capitulum of humerus (F"tg. 2.54) Capitulum of humerus
A11ascular necrosis
O~teochondnti~
Panner
Hond ChUdhood.ado~ence
Scaphoid
Preher
Scaphoid (proximal part)
Avascular necrOSis
Idiopathic Posttraui'Tl.'ltK
Adulthood
Lunate
K~enbOc:k
Idiopathic. posttraumatic
Adulthood
Entire urpus
Cafft>y
Idiopathic (bilatC'fal), posttraumatiC
Childhood. adolescffice
Heads of metacarpals Bases of phtllanges
01etnch Thiemann
Idiopathic Idiopathic, po'lttraum.ltic
Adole~cerx.e
AdolcJ.cence (continues on page 38)
b
a F19. 2 53 Avascular necrosis of the humeral head Sclerotic and lyt1c ch.mgrs 1n tho hum 1al 1>- •d IMtl"> lragm•-ntat1on of the JOint su1face (<~rr~) .ut sc.;n.
Fig. 2.54 A11ascular necrosis of the cap1tulum of the humerus (Panner) (2 ca~<''~J a: f <~Q TIE' 1 •or (If I'll' \ •ghtly SClerotiC capttulum oumt>11 ~~ \t:._.,, (clr;w l b: ') lt•roltc R">IOf• m the capttulum humcn •s s.ccn IMth he. "9·
38
Bone
Table 2.3 (Cont.) Avascular Necrosis of the Bone Eponym or Name of Disease
Etiology
Teme of OccurTence
FefTIOI'ill hod epiphysis (Ftg. 2.55)
legg Calve-Perthes
Idiopathic
Childhood
Femoral head epiphpis
Slipped capital femoral
ldiopathc. pmtlraumatic
Adolescence Adolescence. adulthood Adolescenc.e. adulthood
Location Lower eKfremiry
epipl¥i~ ~·he~
ChtrochondritiS dissecans
ldiopathtc, posttraumatic
Femoral hod
AvClsciJiar necrosis
Creater trochanter Medial femur condyle (less commonly lateral femur con-
Mandl Ostrochondritis dissecans
Idiopathic. degenerative and associated with d ~tarecty of dis· eases (e.g .• congenital dis· orders. hematologic and reti· culoendothelidl diseases. post· lraumatic (especially subcapital hip fracture). post-lnflam· matory disea~es. endocrino· logic and metabolic d1wrder~. collagen diseases. pancreatic diseases. alcoholism. steroid therapy. post-irradiation. and ca1sson disease. Idiopathic
Adole~ccnce
Idiopathic. posttraumatic
Adolescence, adulthood
Adulthood (usually cJftcr c~ge 60 with female predominance)
dyle) Medial femur condyle (leu commonly lateral femur condyle. rarefy tibial condyles) (F'tg. 2 .5 5 a)
Ahlbd
IdiopathiC, stre~s (insuffi· dency) frcJCtures
Medial or lateral femur con· dyle
Avascular necrosis
Patella Patella (secondary ossification center at lnmtor aspect of patella)
KOhll'f Sindlng·Larsen·Johansson
Posttraumatic and other causes ~m•lar to avasctJiar necrOSis of femoral ht>ad. Idiopathic
Childhood
Idiopathic. posttraumatic
Adolescence
Patella Intercondylar spines of tibia
Chteochondritis dissecans Caffry
Adoii.'Kence. adulthood
Medial tibia condyle
Blount
Idiopathic. pmtlraumatic Posttraumatic Idiopathic. posttraumatic
Tibial tuberosity Distal tibia (epiphysis)
Osgood·Schlatter I iffert -Arkin
Idiopathic. posttraumatic Idiopathic. posttraumatic
Diaz
IdiOpathiC Idiopathic. posttraumatic Posttraumatic and other causes similar to avascular necrO'il~ of femoral head (see under this subject in thi~ table) Idiopathic IdiopathiC Idiopathic. posttraumatic Idiopathic. po)ttraumatic
Adolescence Infancy. childhood. adoles· cence Childhood. Adolescence Ch1ldhood
Foot
Talus (Trochlea) Talus (Trochlea) (Rg. 2 .56) Talus (Trochlea)
O~teochondritis dissecans Avascular necrosis
Ch1ldhood Adole!><.mce. adulthood Adl•lthood
Base of fifth metaUrsal
Iselin
He~
Osteochondritis dissecans
Idiopathic Idiopathic. pmttraumatic
Adolescence Ch1klhood Adulthood Ch1ldhood. adoiPSCt>fl(e. adult· hood Adolt>scence Adolescence. adulthood
Freiberg
Idiopathic. posttraumatic
Adolescence. adulthood
Th1emann
ldiOpathK:
Adoles<.cnce. adulthood
Epiphysis of cakaneus N~ular
Navicular (Rg. 2 .57) Os tlbiale extemum
of metatarsals (most
commonly first) Heild of metatMSMs (most commonly second) (F'Ig. 2.58) Base of phalanges
Se\ler Kohler Mueller Weiss Haglund
2 Osteoscleroc,ic, fig 1.55 legg-Calve-Perthes dist!ase A flatH>nl'd. fragmented c11ld latcrcJII}' diSplaced capitcJI epi~S is cU· soc1ated v.ith c1 ""1dencd and shortened femoral nP<"k .
39
flg. 2.55a Ahlback's disease (spontaneous osteonecrosis about the knee or SONC) A O\teochondral deff>< ""•th m ld surround1ng '>
~Kj 1. 56 OsteochondritiS dlssecans of the t alus. A small, ovdl· shaped bony fragment is seen 1n an art1cular defect located 111 the me· dial a~pe< t of the tc1lar dome (c~rrovv).
Hg. 2 57 Avascular necrosis of the navicular bone (MuellerWeiss). A wlldp\ed \clerot1c navicular bone w1th secondary degenerative lhcJnge\ in the talonavicular jo1nt is seen.
f1g. 2.58 Avascular necrosis of the head of the second metatarsal (Freiberg). Sckro\1\ "''d flclttt'o r of the head of tt vnd metdld•sal is seen.
41
3
Periosteal Reactions
attention lhe~e perrostedl reactions ran be lammated (·onion skm·). perpendicular ( ·:.unbursr-), or amorphous
A p<>nosteal react1on 1s a common response to a van<'ty of Into the bone. lmportant d1rterential diagnostic clues may be obtarned from both p.Jtterns dnd locations of penostt'al reactions. After an acute inndence. it usually takes three weeks before a periosteal react1on can be diagnosE'd radiOgraphically. Penosteal reactions should be class1fied as e1ther solrd or mteiTUpted. f.ach of these two has1c forms of pen osteal rt>act1on consi~t of several subtypes. furthermore. 11 appears useful for the d1ffl'rential diagnosis to discriminate betweE.'n conditions wuh localized or generalized periosteal react1ons. .l,ohd periosteal reactions can be thin (I mm or less in thickness) or thick (2 mm or more). A thin periosteal reaction might repre~nt an early stage of a high ly aggressive bone lesion or a chrome. benign process (f1g. 3.1 ). On the other hand a thick periosteal reaction usually suggests a benign condition. Thick periosteal reacuons may be further subdivided rnto stra1~ht. elliptical, and undulatmg, each subtype suggesting somewhat different diagnostic possibilities ( Fig. 3.2 ). An inteiTUpted periosteal reaction, in general, signals an acute and rapidly progressmg process requiring 1mmedia te sult~
(fig. 33 ) A d(•\tnl(tive bone le\lon a~'iOts acute osteomyehtrs or a m.Jhgnancy. A local elevation of the penostcum that is calcrfied dt the site of lis l>onc msertion 1s known as "Codman's triangle" ( Fig. 3.3b). Onginally considered a~ a s1gn of a malignant bone neoplasm. it has been recognized thdt it can also occur with ben1gn processes such as osteomyelitis, subperiosteal hemorrhage, and fracture. When the periosteal rt'action eventually blends with the adjJcent cortex. cortical thickening occurs. However, cortical thickcnrng may also dcv<'lop by excessive endoste.ll or perioste.JI new bone formation without stripping the periosteum away from the cortex The differential d1agnoses of vanous bone les1ons w1th penosteal reactions art d 1scussed rn Table 3 1 Under a variety of degeneratrvt. tr.Jumatrc and mnammatory cond1t1ons, a periostitiS IS found at the insertions of many tendons and ligaments causing the appearance of -whiskering" ( F1g. 3.4 ). The most common location is the pel
Fig. 3.1 Thin p mm or smaller) periosteal rea<.· tlon Thrs •s an rndett>rmr·
nate frndrng. since tt mc~y indicate a chronic benign process that progre~\es slowly, 1f evt'f, to a sohd thick periostedl reaction: or it rndy represent the earli est stage of an aggressive bone lesion that progresses rdptdly to an interrupted periosteal re&tion.
a
b
Fig. l 2 Solid periosteal reactions rnd1C.1tlng a ben19n bone le-I> sron. ~ rh~-~ (7 mm or larger) P' •riOSte rl reaction b Undulating perro~tN• r~a ... >11.
c Periosteal c.oJkmg d Flhptical periosteal re-
dctton.
c
d
42
Bone
v1s. where the ihac crests. the ischtal tubero~1ties and the 1schiopuhic rami are affected. Other s ites of extrapelvic involvement mclude the femoral trochanters. the patella. the calcaneus. the dorsum of the foot. the mfenor clav1cular margm at the attachment of the coracoclavicular ligament. the humeral tuberosities, and the olecranon. As the pen ostitls progresses the "whiskers" become more prominent, and may transform into spurs or other bony excrescences re· ferred to as ertthesophytes. They tend to rl'main relatively illdefined or fluffy in ankylosing spondylitis (Fig. 3.5), Reiter's syndrome and psoriasis. In these inflammatory conditions. erosions or ~lerosis of the adjacent bone may be associated. Tl1e enthesophytes in diffuse idiopathic skeletalllyperostosis 1IJISH) (Ftg. 3.6 ) are bilateral and symmetrical. but wnhout adJacent eros1ons or reactive bone sclerosis. These
spurs ate well demarcated and often urcgular in outline, especially m the calcaneus. Degenerative di~case oftendons and ligaments 10 the elderly may produce s1mtlar enthesophytes. but they tt>nd to be lt>ss prom10ent and less Symmetric. I ocahzt>d spumng at the inst>rtions of tendons and hgaments occurs m conJunction wtth chronic stress or as sequelae of an old injury. Spur formations are commonly found in the calcaneus. patella and trochanters with acromegaly. Lig.1mentous and tendinous calcifications rest>mbhng DISH and predominantly involving the axtal skeleton are encountered in fluorosis, hypoparathyroidism, and vitamm D resistant rickets (adults). but m.1y be associated 10 these conditions with osteosclerosis, which is parttcularly striking in fluorosis. rig. 3.3 Interrupted periosteal reaction s md1catlrtg an .1ggress1vt or malignant bone le\IOn. a ldm1nated ("onion sk1n") periosteal rec~c tion. b Perpendicular ("sunburst") perio~teal rec~ction and Codman'\ tric~rtgles clt both ends (arrOW1). c Amorphous penO\tl'al reaction.
a
b
c Fig. 3.5 Ankylosing spondylitis Fluffy cnthcsopathy along the iliac crest\ and ischid woth sclerosis of thl' adJacent bones IS associated woth fusion of the sacroiliac JOints and the visualiZed part of the lumbar spine. Not!! the dehcate bridgirtg syn~mophytes in the lumbc~r ~p1ne. ArthritiC changes with circumferential (axial) joint space narrowing and early erosions arc also seen 1n both h1ps.
Ftg. 3.4 Whlskering. Penostito\ dt tho- n\> •rt1on of tendons and ltg.JmPnts found woth a vclrlt'ty of degeneratll•e. tr clUrndtiC .!I'd inllc!mmdtOfy conditions. Pretgrcssion to formation of spurs or bony P~crP,ct>nces (enthesophytt'\) PQ\\Ible.
DISH. Wtll dcf~ned 1th bony excres..encd ...at can be d1fferenhiltl'd Ill cortKal c~nd cancellou~ bo11e are as~ociated w1th nonndl sauollld< JCIIlh dOd fused lower lumtxtr spine by huge Fig 3 6
ent~>Opathy ~
paravertl'brc~l o~sifications.
3 Periosteal Reactions
43
Table 3.1 Diseases with Periosteal Reactions Preferred locations
Distribution
f>Hiosteal llr ... f
Phystologlc periosl.ltls In Infants
Comments
>5
long bo~
Gent>rahzed and symmetrical
Solid thin or thick
[)ev(·lops in second or third montl1 of bfe. e\peci.llly 1n prematures.
long bones
Generalized and symmetrical
Sol1d ttvck or !armnated
A~soctatcd wtth tran~ve~e ~tnptng of metaphy1es and destructive leSions, inati.111y involving the corners of the metaphyses adJacent to the c art1lage plate.
Mand1ble. clavode. scdpula, rib\, tubular bon~ (limited to d1·
Solitary or mult1ple
Solid thick or lamt· nated
ClinK ally t ender solt-t1ssue swellongs are associatl.'d with the affi.'Cted bone. OllSI.'t occurs 1n the first fwe months of hie.
Generalized
Solid, undulating or occasionally laminated
A~sociatcd
(Fig. 3.7) Congentt~l
syphilis
(Ftg. 3.8)
Infantile cort!UI hy-
perostosis (uffey's disease) (Ag. 3 .9)
aphy\e~)
Hypervitaminosis A
Tubul. r bone~ (espe· cidlly uln.1), metatarsals, clavicle, tibia, fibula (limited to di· aphyses)
wtth tender soft in lhildren u~u.1lly between 1 .md 3 years old. Prostaglondm tnfusions in neonates (to maint.1on pat<'ncy of the due· tus-d<'pendent congt>nital heart d1sea\e) may re~ult in similar bony ma~~t>s
ch~ng<'s.
In older children and adole\cent~. pt>nosteal react•ons and hyperos· tos1s 10 the axial and appE>ndKular ~iwlcton \lmtlar to DISH may bay be found w1th chronic .adminl\trattoo of rtt1noid ckug~.
(contmue<> on page 44)
Fig. 3. 7 Physiologic periostitis in infants A ~c-hd. th1n P"f'O' t ·al r actiOn .~ fvund ..10..g the I'T'It'doal a'pe
Fiq 3.8
Congenital syphilis. Solid thick peno
r 9 lnfant1le cortical hypel"ostosis (uf· fey's disease). A am• r l!t'd pt'I'IO\Il'cll rei!CIIOO •~ s.:..·n along the femur
didph}'\1\.
44
Bone
Table 3.1 (Cont.) Diseases wtlh
•W~,
t " otl w.. actium PenostNI ReKtions
Scurvy (hHiing) (Fig. 3.10)
long bones
Generalized
Solrd thick
Caused by calcrficat•on of the sub· periosteal hemonhagc.
Rickets (healing) (Fig. 3 .11 )
Long bones
Generalized
Solid thin, thrcker laminated
Caused by co~kifitatlora of the subperiosteal osteoid. Associated with mineraliLation of the Lone of provisional calcification thcJt appears as an irregular dense area In the epiphyseal cartilage. separated by a thin radiolucent lrne from the metaphysis.
Tubular bones, mandible
Generalized and sym- Solid thin or thiclr.. metncal or laminated
In children with bone pain and often v.rth fever. HyperphosphdtE'rn~ may also be present.
Pachydennclperio5tosls long tubular bones. (primary hypertrophic: especially radius. ulna. osteoarthropathy) tibia and fibula. less (Fig. 3.12) common in metacarpals, mct.Jtarsals. and phalanges, pelvrs. ribs and clavidcs.
Generalized and sym· metncal. May extend from the diaphyses into the metaphyses and epiphyses (DO: Secondary hyper· trophic osteoarthropathy. where it does not extend into
Solid thick. often with sh.Jggy. ir· regular excrcs· cences
Familial condrtion Wlth skin thicken· ing and cortical thickening. Periosteal new bone form.Jbon tends to blend with thickened cortex. Almost exclusively found in males with prediiE'ct10n for blacks. Onset in adolescE'Oce.
Secol"ldMy ~
Cffieralized and sym-
trophk osteoar-
rnetrK<~I
Solid thin or thid. (often undulating and cloaking) or lcJmincllt.'
In patiE'nts with bronchoqcnk carcinoma. and occasionally v.ith <.hroni<. dtseascs of lung. ga~troin testinal tracL or cardio\ia)cular system.
!>olid thm. lami· n.1ted. perpendicular (thin SpiCUIC'S) or amorphous. Cadman's triangle occur\
Periosteol sarcoma· limtted to the cortE'x of long bon!' draphySC'S (especially femur and trb4a). PE>rpendrcular perio~lE'dl rPactron and Cod· man's tnangle are ch.Jra< tl!rt~trc.
theep•~).
thro~
(Fig. 3.13)
Osteosarcoma (Figs. 3 .14 and 3 .15)
Femur, tibia, humerus, c1nd mandible
localized
Porosteo/ sarcoma: a l.nge radiodense k>\lon with smof:d to the el
Fig. 3.10 Scurvy (healing). This characteristiC p<'riostecJI reaction is caused by calcification of the subperiosteal hemorrhage.
Fig. 3.11 Ricke ts (ht>dhng). Thrs periosteal rE>action ~~ c.Jused by c.Jicifrcation of the subperiosteal osteoid.
3 Periosteal Reactions
45
f1g. J 12 Pachydermopertostosls {primary hypertrophic osteoarthropathy. A solid. thick. and ~haggy perio~teal reaction i~ seen
b
a fig. 3.13a. b Secondary hypertrophic osteoarthropathy Solid thin and laminated. occasionally undulating peno)teal re.JCttOns are seen m the radius and ulna (a ) and tubular bones of the hoJ. 1d (b)
Fig. 3 14 Osteosarcoma (osteolytic). A poorly dt:fmcd osteolytiC k•sion is sren in the distal femur c1ssociated with c1 large amorphous periosteal reaction posteriorly.
<J Fig. 3.15a, b Osteosarcoma (2 cases). A permeatiW dt-structiVt; lesion v..ith osteoblclstiC areas and amorphou) pc· riosteal reaction, inter spersed with thin per· pend1cular ~pteuiE'~. ~~ seen m a (ortlc.al th1clo.· ening v..it laminated pc riostcal react1on 1s seen in b.
b
F1q. 3.16 Parosteal osteosarcoma. A cngc, rad•odenst> lesion With irregular margins IS at· tached postenoliy to the d1stal femur en char acteristic location.
[>
46
Bone
Table 3.1 (Cont.) Diseases with Periosteal Reactions Disease
Prfterr.cl Locations
Distribution
Pwiosteal
Comments
ReactiOns
Ewing's sarcoma (Figs. 3.17 and 3.18)
Under .20 yr. tubular bones CM.>r 20 yr: flat bone<>
local17ed
Solid thin, laminated or perperr dicular (thm spocui!!S). Cod· IT1c1n·~ tnangle occurs.
Other sarcomas (e.g. chondrosan:oma, fl. brosarcoma) and pri-
1oog bone\, nat
LocaliZed
(Including reticulum
Solod thin, thick or amorphou~. RarPiy solid thKk, lclmonated, perpendicu· lar or alllCll"phou\.
cell sarcoma)
Cod1T1c1n·~ tric~ngle
1104''1'\
mary bone lymphofN
Penosteal reac.tion~ are rare in these coriditions. CortiCal thKkenong in a chondroid matrix t umor suggesh low-grade chondr~rcorna rather than enchondroma.
i~ unu~wl
Solid thon or lam i natPd. Perpendicu lar in skull Rarely solid thick.
Interrupted perio~t('al reactions are common in children (e.g., l<'ukcrnia and metastases from neuroblastomas). Solid periosteal reactoon or locali1ed cortical thick· ening h associated with meta~tases from prostatic and
leukemia and metastases (Figs. 3.19 and 3.20)
long bones, ribs
Multiple
Osteoid osteoma (F.g. 3.21)
Femur, tibia, fobula, humerus. vertebral
localized
Elliptical and dense. Rarely solid thm .
RadoolucPnt ontracortical nodus woth or without central calcifi<:atoon 1\ cla<>sical, but not alway~ demonstratPd.
Other benign tumors and cysts
Loc.cJ ii.zed
Solid thin or thick.
Pl!Jiostec~l reactoOII'> usually c!S· sociated with bone expansions arid/or pathologic fra(.tures.
Acute hematogenous osteornyelms (Fig.3.22)
Solitc!ry, rarely multi· pie
Solid thon or thick, laminated or per· pendicular (short and ~quat sptcules). Cod· man's tnangle oc·
E.ilrio~t rad109raphoc fmdings: bone destruction after 1 Y.Pek. periosteal reactions after 2 Y.Peks. and sequestn1m formation aftl'f 3 w<'eks. Orgamsms: staph).iococci, \treptococci , salmonella (especially in sickle cell anemia). pscudomona~. klebsiella (often with intr.JV('nous drug abuse), less common: pneumococci, meningococci, brucdla, fungi. viruses. and para sit~.
br~st
•uch
tur~.
carcrnomos.
(continu<'S on page 48) hg. 3.17 Ewing's sarcoma. A poorly d efin<'d permeatove osteolytic lesoon os seen in the proxomal lemur with beginning laminated periosteal reaction on it\ outt>r cortex.
3 Periosteal Reactions F.g 3.18
47
r IQ l 19 Neuroblastoma
Ewi ng '~ ~rcoma .
metastasis A permeative IE'\ion 111<1th a Codman's tnanqle (ill row) and a faint pet pcndic.ular peuosteal re· action is seen. A solitary neuroblastoma metastasis IS radiOgr.aphrcally often md1\· t1ngU1shable from a twir.g's
A barely perceptive permea-
tive osteolytiC IP~1on in the femur ~haft ~~ a\~iated ~~~
S<~rcoma.
f.g. 3.20 OSteoblastk metastases (breast card noma) &.~ides a laryc osk bla~tK mt tastases 1n the lt.>tiKlf"i!lllE'<"k and mtertrochdntPric arPa loc.Jh/Pd thickenir.g of thP cortPx 10 the femur shaft is aho t·vidl"r't (arrOY'IS).
fig. 1 21 OSteoid osteoma A dense. ellipti· cal pe imtcal reaction With a nidus (arrow) is diagrros· trc.
Acute osteomyeli•ctr" ~e I• ·sror· I >lHJdt:u b; cl od,. ,lni!ted pcrrosteal rcac tron is seen. 22
t is
c1
t
48
Bone
Table 3. 1 (Cont.) Oise~
Oi\~ase\
with Periosteal Reactions
PrefftTed Locations
Distribution
Periosteal
Comments
R....~tu.n
Chronic osteomyelitis (Fig.3.23)
Osteomyelitis from contiguous Infective source (rig. 3.24)
Hands. feet or adja· cent to decubitu\ ul· cers
Tuberculous osteomy· elitis (Fig. 3.25)
Solitary. rarely mult1· pie
Sol1d thtck. often undul
Thick perio~teal reaction a\· sociated With sderosh. c1r1d ~attered radJOiu((·nt clrt.'cl~ which may contain a dPn\P bone \f'<JUPstrum.
localized
Solid thin or thick.
Periosteal reaction associated with bone destruction and ~lcro\h. Commonly found in dlo~bctcs mel· titus, quadriplpgia and va~ular insufficiency.
Solitary, rarely multi· pie
Sol•d thin or thick.
S1milar to hcmittogel"lOUS 0\tromy· elit1s, but osteopenia 1s morE' pt"onounced. where~ prrimt£'al reactions and o\tP~Iero~s are le\s. S1milar hnd1ngs a~ in tuberculosis are seen in otyp•co/ tuberculosis bacilli and BCG ostf'OITlye/•t•s.
Syphilis
long bone. ~kull
LocahLed or generall7f'd
Solid thin or thick. often undulo~ting and with squat spr
In early acquired syphilis, an extensive gent'rclliled pe110\tcal rec~ction and cortical th1tke11111q is the most common osseous man1fe\tcttion. The radiologic hallmark of the ter· tiary ~tage of the disea~e co~isb of dense bony ~lcro~s with areas of destruction (gumma formation).
Y.ws
Long and \hort tubular bone-.. shrll
localized or general· iLed
Solod thin or thick, often undulating and with ~quat spicules. or lami· lloJted.
Occurs in tropcal chmate, and is usually a<.quired before puberty. Radiographic features srmdar to syphilis and bejel (prevalent in the Middle East). The c.1usati\C or· ganisms of these three spirochetal diseases arc morphologic.JIIy indis· tinguish.lble.
Tropical uker
Tibia (anterior aspect of middle and distill third)
localized
Solid thick, rlliptiral or undulating.
Common In Cf'ntral and Africa.
Leprosy
Hands, feet
Solitary or mulhpiP
Solid th10 or thrck. or laminated.
May be aSIDOo!tcd with bone dt>struction. Nrorop;!thrc bone mamfestatiOO\ are, howewr. much more common and rharactenstic.
Rheumatoid arthritis Ouvenlle)
Peripheral .:md aJ<.icll skeleton: Pf'rldrli
localized or generalized
Solid thin or thiCk or lo~rnindtcd.
Common UIJUvt'nne ri"K:umaloid arthritis: very rare in i!dults, and never a dominant feo~turc.
Psoriatic: arthntis (Fig. 3.26)
A~
above, preferen· tially in hands
localized or Geroeralized
Sohd thrn or th1ck or lamrnated.
Periosteal reactions not uncommon. Irregular bony e)(Cre\Cence-. characteristic.
ReiUr's syndrome (Fig. 3.27)
Calcaneus. short tubulo~r bones of foot. tibiol, and fobtlld
localized. seldom qeneralized
~hd thon or thick (ultPn "fluffy") or lamrnated.
Perio~teal
Polyarteritis nodosa
Long tubular bones (pt"eferentially lower limbs) a11d metatarsals
Generalized o1nd sym· metrical
Solid thm or thick. ch,lfa<.teristically undulatong.
Radiographically somilar to hyper· trophic 0\terurthropathy Pain and swelling of the ~r extremity may be a5sociated.
fa~t
reaCtions common.
(continu~
on poge 50)
3 Periost eal Reaction<,
Fig. 3 23 Chronic osteomyelitis. A poorly defmed. r 1,.1'<1 lytoc and SCietO(Il IC\IOu I~ cl~·
soc: iatcd woth a riostt~c~l
~hd
pe-
reaction (serratla
marcescens osteomyehlls in an mtr.JVCnous drug abust'r).
Fog 3.24 Osteomyelitis in di;~betes mellitus A dest ructrve le \oo'l around the thud lllt'tatarwphalangeal JOII'I woth pe~rostealre atiiOn rs seen.
a
49
fig. 3.25 Tuberculous osteomyelitis. A poorly de foned lytic IE'510n IS assOCiated w1th a thon sohd peooste
b hg 3 27 Reiter's syndrome a Ill-defined periosteal reilCtions around the .mkle and b Ourfy "whrskering" rn the po~tt>roor and Inferior aspect of the ldltar,eus c1re quite charatteri\tic.
F1g. 3.26 Psoriatic arthritis. Besides erosive ilrthritoc changes ex ten~ ·rro .t tr nd Ylerosis is seen producing an ·,vory hand·.
50
Bone
Table 3.1 (Cont.) Diseases with Periosteal Reactions DISease
Preferred Loations
FrKtures and stress fractures (Fig. 3.28) long tubular
Electrical and thennal Injuries
bon~
Uppe1 extremity
Vascular and lymphatic lower extremity dlwase (F".g. 1.29)
Bone Infarct
long tubular bone~
Eosinophilic granuloma
Distribution
Periosteal Reactions
Comments
'>olitary or multipll'
Solid thin or thick or laminated. Cod· man's trianglt> oc· curs.
Pt'riosteal reactions drt' similar in traumatiC and patholog1c fractures.
Solitary or multiple
Solid thin or thick or laminated. Cod· man's triangle occurs.
Traumatic (including bott~ed child syndrome) and hemophilia.
localized
Solid thin.
Ostt•olys1s, osteosclerOSIS. p£'nartic· ulc1r ccJinfic at ions and heterotopic bone formation ar£' frequently as· sociatPd.
localized or gt'neral ized
Solid thin or thick, often undulating.
Arry disease associ.ltcd with venous and/or lymphiltic stasis. Vascular calcifl(ations and phlcboliths may be associated.
Solitary or mult1pl£'
<;ohd thin or thick
E~pecially in sickle c£'11 disease, where the periosteal reatlion may ai'>O be caused by osteomyelitis. Hond·(oot syndrome: inf.mt [) 1s of the shor tubular bones cau\lng per1osteal reactions tho1t are indis· tinguishable from osteomyelitis. Ouurs in young children (alief' age aq£' 18 months) with sitkle·cell dis· £'ase.
Solitary or multiple
Solid thin or thick. Rarf'ly lam1nated.
Destructive bone le~lom may con· t<11n bone sequestrum.
localiLcd or general iLed
Solid thin or thKk. often undulating .:md cloaking.
Combination of <~vascular necrosis of the femoral head, Erlenmeyer flask deformity of the dtstal femur, circumscribed osteolytic lesions, and bone infarcts are charilcteristic for Gaucher's di'ifase.
(Langerhans ceU his-
tiocytosisI Gaucher's and other storage diseases
long tubular bones, spine, and pelvis
Thyroid acropachy (F"!g. 3 .30)
~;larly
Tubular bones, p.!ltlc· Bllat£'ral and rf'latively Solid thin or thick, occasionally v.ith hands and feet symmetrical sholt and squat sp1cules.
Usually one yedr and latt ilft r treatment with thyroided• .m or radio.lctive iodine.
Renal osteodystrophy (Fig. 3.31)
long tubular bones. metatarsal. pubic rami
Generalized and sym· metrical
Solid thin or thick, occasionally laminated.
Tuberous sclerosis
Tubular~~
Sohtary or mult1ple
Solid thon or thick, often undulating.
Neurofibromatosis
long bones of lower extremity
Solitilry or multiple
Solid thKk, often undulating.
is not clear.
Fluorosis
Tubular bones
GeneraliLed and sym· metrical
~olid thick, often undulating and cloaking.
Osteosclerosis and ossifiGitiOn of hqaments and t£'ndons at their in sertion.
Gardner's syndrome
Tubular bones
Multiple
Solid th1n or thick, often undulating.
Osteomas and int£'st1nal polyposis ar£' associated.
Solid thiCk .
Part1cularly at tendon and hgdrnent 1n~ions Into bone ("wh1skering").
DISH (diffuse idtopathc \p1nt>, pE'Ivis. lower t.'ultiplt> and often skeletal hyperostosis) extremity (commonly symmetrical (Fig. 3.32) patella and calc<~neus)
Associated with findings of hyper· palathyroidism and ostros< lcros1s. Very rare in primary hyperporothy· rord1sm.
Pathoge~s
of thh mantfestation
3 Periosteal Reactions
51
seen in the
Fig. 3.29 Venous stasis. A thi<.k, undulatinq periosteal reaction in t he proximal tibia, and particularly fibula is iiSSodated with ex· tcnsive varicosis.
fig. 3 30 Thyroid acropachy A thllk , .w;mmctric. 9laggy periostitis ·~ sa'fl n tht. fonqt. ·th prl.'dolc
Fig. 3.31 Renal osteodystrophy (lolfll1c )(lcro~o\ o\ d\'>()(lated Yiith a sohd thock p.. iosteal " ' the later.Jl femur wrtex and lamonated on the m..-doal fer. - · .~r ~ •
Fig. 3.28 Stress fracture. A hcdling ~toe~~ fractUic is fibula shaft woth exuberant callus formiltoon.
52
Bone fig. 3.32 DISH. "WhtskNing" along tilt> iliac crest. ischiopubic ramus and femor.JI trochanter~ associated with hypertrophic spur~ at the superior and inferior m.uqins of the acetabulum.
53
4
Trauma and Fractures
resorption along the frctcture margins become~ evident and in undisplaced flclctUieS may allow at th1~ stage (several days after the inJUI y mddence ) an unequivocalrad1ographic diagnosis. Perio~teal and endosteal callus formauon usually becomes visible two to three weeks after injury ctnd is first evident as a thin periostl'al reaction and irregular mottled calCIfications about the hal1ure. mcreasing wlfh ume in density, and finally developmg bone texture. 1he healing process of a noncomphcated frc1cture from injury to consohdauon takes one to several months. fracture heahng progresses more rap1d ly in oblique or c;piral fractures. in a smgle fracture. and m younger patients. The healing process IS slower m larger bones. m transverse fractures. in t he presence of mult1ple fractures, ctnd w1th mcrea~mg age of the patient. A delayed umon I'> found with poor reduction, inwmplete immob1h2at1on, in the presence of infectiOn. in vitamin C and(or 0 deficienCil'S, and in areas of preexisting bone disease (pathologic fractures). Infections are particularly common in compound fracrureos. where extenSIVE.' soft-tissue damage i\ cc1used by either a fracture frc1gment pll'lung through the s!.;m or by an object (e.g., a projectile) penetratmg from the out~ld(', Malumon fl'fers to a fracture that is healed w1th ~1rnif1cant fracture fragment dl\placemeont and(or a ngulat1on. A nonun-
The rad1ologic diagnosis and differential diagnosiS of an acute fracture ~~ usually not associated with any problems. A sharply demarcated fracture line is the hallmark of an acute fracture Dependmg on their radiographiC appearances. fractures are classified into different types (Fig 4 1 ). Occasionally, however, a frank fracture line cannot be demon~trc1ted in undisplaced fracture~ Immediately after mJuryewn when films in several prOJt'ltlon~ are taken. Demon\trauon of either a con.cal break that has to be differentiated from a nutrient artery or disruption of the normal spong1osa pattern may be the only clue in the-se instances to d1agnosl' a fracture-. Magnetic re~onance imaging or a nuclear med1cme scan IS othl'rWise required to arnve at the correct d1agnos1s. In the presence of clinical evidence of a fracture. a zone of mcreasl'd bone de-nsity or an abnormal .mgulat1on may sugge~t radiographically an acute fracture. although these find mgs can .Jiso be encountered in healing fractures and other bone diseases. At least some degree of soft-t1ssue swelling can be seen radiOgraphically in virtually all acute fractures. but th1s findmg IS of little use to different iate a fracture from a d1stort1on or other soft-tissue injuries. Fracture healing begins with an acute mnammatory response resulting in the organization of the fracture hema toma by invasion of fibrovascular tissue. At this stage. bone
)
/
L I
( b
c
d
Fig. 4.1 dusificatlon of fracture according to their radiographic appearance. a Avulsion fracture (secondary to forcible tearing of hqament or tendon attachment). A chip fracture has the \.tme ro~d•<>graphic appearance, but is caused by direct rmpact b TranWt'r\e fr<~cture (secondary to sheanng force to opposite sides of a bom· or to Impact force along tr.msl.1!rsc a>.rs). An obliqu.. fractuu. (not shown) occurs secondary to impa<.t along an obhque a s• c '>piral fracture (secondary to rotcJry·typc injury).
e
g
h
d longrtudincJI lrcJchJrt• (\l•tondary to rrnpc1ct force c1long lonqitudinal axis). e T, V·, os Y-shcJped lractUJc in proximity of 1oinh (secondary to impact force along longitudinc1l axis) f lmpung effect of a pro)€'< tile). h fra ture IMth butterfly fragsncot. I Segmental fratture.
54 10n
Bone
characrenzed by failure of fracture healing 6 to 9 well delineated and oftE'n sclerotic and a frank art>a of mtervenmg t ranslucency is present. Nonunion may result from the same complications assoc1ated with delayed union or by interposition of soft tissue between the fracture fragments. Hypertrophic nonunion 1s commonly caused by contmued mot1on at the fracture s1te. ln these cases the fracture line persists or exces· IS
month~ after mjury. The fracture margin~ are
sive and prolonged bone resorption c1t the frauure margins occurs. Eventually the bone ends become sclerotiC. and there is a varymg degree of non-bridging external callus formation. Atrophic nonunion is thought to result from extensave bone de.lth. The radaographiC appearance is t hat or a persistent fracture hne wathout demonstrable callus formauon (Fags. 4.2 and 4.3). Nonunion may eventually progress to pseudarthrosis formataon (Hg. 4.4 ).
hg. 4.2 Nonunion. a HypertrophK (elephant foot) b Hypertrophic [hor\e feet c Oltqotrophlc d Atroph1~.
a
b
c
Fig 4.3 Hypertrophic nonunion. The d1~t.al t1b1a shaft fracture sh~ rclatM!Iy smooth. sclerotiC borders without endosteal or pcnosteal bony bndging of the fracture lim•. A hea led fibula fracture Is also ev1dent.
Ftg. 4 4 Pseudarthrosis hc1d ckveloped 2 yec1r~ c~fter c1 frcKture of I> the hur ·ru~ th.tt ~tlows clc!ssical tha~ of Pagers di~a~.
d
4 Truwnu and Fractures hocturc healing m osi£'(JRC'I C'.l/.1 impe~:fi:cla is complicated b) pscud:u1hrosis fonnalton wiUt a lughe1 incidence than in nonual bone. P:.cuc.lurthw~is ll> abo a conunon fcatLue in nw·(Jjihromalo.\i.l. "lle..-re 1! i;, mol-t ofic..11 found in the lower l\\o-Utinl~ of the ltl••·• (l1g ·1 5). P~uo:larthro~is occ~ abo infibmz,.\ ttv.1p/a.1ia, 1111ich olkn dcnK•nstmh.:.-. lx>ne change. rndJOgmph•call} ~umlar to neurohhromato~•s The two dL'r orders carL ho11e\c.."r, dk11 he ) their >km manilt:slat10ns The t:~tfc-ml-latt 'l)(lh in ti!>mtL' d).spla-.ia arc trrcgularly outlined ("coll't ol Maine" appcarnncc), \\bere<Js the~ arc s11100thl\ outlin..xt 111 tlc..'llrnhbromato~ls ("coa_. of <.:uhl(>ml8" llpJ~muu.:e). l·urthc..11nore, the presence ol cutaneous liiTomas i." ch.mtct.:ri.st•c tor the latter conditio1L "( O#l~('flilr./ p.~<'l,rmthro.\1.\" is u rure condition that ma\or ma\ not lx; rdutcd to neurofibromatosis or fibrous dy~;pbbia (fonne fnbte'~). r mcture:; of Ute prot/mal l!llti!<'I'Lo.\ t>U;Ur lx.1 w~.:en one or all four maj01 scgmellls, \\ hid1 intlud~ the articular ~'gluent (:matomit: ned. frudure), the Jllu,unal humc1LL' shall (surgical n<..-cl. frm:ture). the g•eatc• tuhcr<>MIY and the lcs....:r tul-,.:rosit) 'llle modili<..xl N<..'Cr.fot.r-.I<'Y,mt!lll clm.\({ictllion is based on the number ot' drsphitL'C.I SL'gtnents Any fracture that is not or only mmimally (h..-s..., thmt I em) displaced and not or only mimmall} angulatcxl (kss titan 45°) is disregarded 1\ one-part lrncture may inmh e an) or all lour anatomic segments but there 1s no drsplacement or angulation between fracture frug.m<.."fll •. 1\ two-part fr.1cturc indicat~ that onh one ~'glllc.."ftt rs displac<..xl in !elation to the Um.:c that n..maiu wtdi.-.lll.tc~-d tn me mtad. 1\ three-part trdcturc commouh c01tsil>!s of a di~platcd greUr-pi"lrt rr.tclur~ nw~ be a,..-,ocbt.xl "1th ciUtc.:r anto.:rior tlt ()(l~l.:nor dislocation '11-,.: nwohc"ftll.."flt of the articular surli•ce Ill an mttc:nor fmcturc-di.-.location IS referred tc as "hc1d sphllmg" and 111 a J'O"l.:nor lracture-dislocatron trs "imprc...,.,Klll".
55
fmctur~s oflhe c/bmr may mwhe the distal lnunerus, and proximal mdius rutd ulna I 'lm-urt•wlar lradurcs ofUte di.stalllwncm-. it vohe tt..: q>ic;tmdvlc:- wtd supwwnc.lylar l!Tca. Intra-articular fwdtl!CS of the dist.1l humellL' ma) im oh e either Ulc trochlea or tl1e C<tpitclltun alt•t1e (ltatl.';(Ond~ l.1r fracture.) or l>uth l l'lt<•IKhl:n <>I int.:u:ondvlar tmcturt:S \\ith or \ltthont strpr.te:ond\1 tr cummmullou) I wdure. or Ulc radial head arc.: l'<>mmon 111 adults, but wlll..'ll nondisplaccd or nunimnl~ dL"I">Iaccc.l may h.: dilhcult to demonstrate 1\lth routme rndiograpluc pn>.Jc..'dJOn~ /\n f ssex-1 oprestifrnctl.Jl' cons1't ~ ot a comminut~xt dtl'pla,:c..-<1 lmcture of the r..tdKtl head fLw•dutc..xl 11 1th poskrit>r sublll'<~hon of the distal ulna. r rnctllf<.'S of Ute pro:..unal uhta may im oh e the coronoid PTOC'-"'" t>l the oli..'Cntllt>ll, but the fbrmer mrdy occurs a:; an isolakxl injul) A Mont<.-ggia fraclurl is the H:O.."lll:iHtion olu pto\.imal ulnar shan fmdurc 11 ith dishlU•li<>n ol the radiul head. noth the ape' ot'angulation ot'thc ulnw fmdure wld the dislocallon of Ule radial head ar~ ant<."fiOI lilt\ llC I (60" o) JX>sterlm in l}llC 2 ( 15%), latcral m type l (2m'l>) and ~nmlur to tVJl<: I hut as. sociated with a md•u~ shall lracturc at the le\el olthe ulllllr fracmre m type 4 (5 ·~ .) Ftg 4.6). /\( iafenzz((raclure con~tsts of a fracture ofthe distal third olthc mdius wtth ungulati011 apex dorsal and medial (ulnar) aswcl3tcd \\1Ul doNal and medial dislocation of Ute ulna m the dislHI mdioulnar JOint (Fig 4.7). Fractures of Ule distal mtlizc1 mdude I Coll<•s JrnctwC' (C."\.1ra-articular, tLsuullv o~cun ing alxllil 2 to 3 em from the articular surface 1\ith t\T•IUJIIy radial mxl dorsal dil.placemc"ftl and angulation ape.:' 1ol.u of the distal radill' fratture fmg.ment and fr.x1ucnt ll"-"l>Ciallon ol an ulnar styloid ft,Jclure). 2. Smitl frt:ltru·l! (e,lrll- or intm~utx.ulm froctutc 11iili \ olar di~rlateJtll..'llt t>f the ll <>r cl mgi'lv\ frac/ IVI' ( lntdure t>f Ute r-.xlial styloid pnx:css) (l•g 4 k ) Ihe ~<tphoid 1s the most COIIlJll()Jt)) fmcturcc.l cmpul l)(>llC 'Ilk! liucture may be located m the di.quJ pole ( 5 % ), tubc..'n;k (5 %), waist (75 % )or proximal pole (IS 'X) (I ig.4 9 ). Ct•mmon ct>mplicatiOtL., of a
ltg 4 5 Nomuoon and llM!udlutluosi:, totmation in ncllfolib10matosis. a A truelure 1s ~'CII in Ule tibia that shows unlc.:rior bo\\1ng. h Si,lllOilths trlkr H. f>eriostc.:al callus limno.ttion and ()()IIC I CSOI ptillll OC.:Cllll"cd around Ute ft.ltlurc liagm~.;nts, but Ute tractllle has not heakxl (nonuruon). c live years an....,. a I )c.;pltC variow; cOn'L-rvall\ e and surgiCal hcsis l~•s f(•nncd. 1\ot.: abo the rowing and namming (oii..TConstriction) <>I' the hhula (chamcteristic of III:UWiilllllllato,is) in\\ hich a IJC
a
b
c
56
Bone
I 1"
')
I
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/
I
I(
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M<,nt.:ggia fradurc (I~ p: I) l 'uk.lurc 1>f the pw\imal ulnar 'h:11l \\llh anteri<>r angulnhon at the IIIII!\ nnd anterior disk,_ t1tl u>n of the raJml head •~ -een.
T1!!.4.6
I fig.4 7 Gallcau.i fracJurc. fmcturc of th.: distal radttC> \\ith angulation IIIII!\ mcd~al and dorsal and postcrnmcdtal d1slocat10n of the ulna 111 the di,tal mdioulnar joint 1s dmgnosllt The radiu& frudurc frup.mcnl>. mav ali>tl O\'Crl11p.
J~
...
~
\t !
)<
'tt
!
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'-->..-., ,......,
I b
a
\\'! \'(\~}.. ~I ?<J •
( (
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fig.4.8 Distal mdiul. fracturc&. a Colh · .fnl(/lllt Dor~ displacement nnd nngulahon apex ,·olar of distal fnt(!ncnt b Srmth fracturc V<~lar dt'lllan:mcnt of di,wl lragmclll c t/(Jton fi'(J(tiUl · lntraartiwlar imdurc l.'lthc dor>al dil>t.al r.u.hu' d limdunwr. l.'r thm!JIcur'~ Jm:tun : I raclurl: of fhc radial styl01d l'lf'<'CC'-'
Fig.4.9 Scapl101d fintturcs may imohe di!'tal pole (a) tuh.:rde (b~ wai!.l (c) <•r pro\inutl pt>h: (d).
4 Trauma and Fractures scaphoid waist fr.:ICture mclude nonunaon and avascular necrosas of the proxamal fracture fragment. The most frequent ligamentous mjuril's of the carpdl bones arc centered around the lunare .1nd mclude scapholunate das'iocaataon. penlunate daslocataon. midcarpal dislocation and lunate dislocation. Scapholunate diSsociation (rotary subluxation of the scaphoid) (fig.4.10) is assocaated with an injury to the scapholunate ligament.lhe condition IS diagnosed on the dorsovolar view of the wrist by either widening of the ~pace between the ~c:aphoid and lunate measuring more than 2 mm in the midline between the!>e lO carpal bones or more than 4 mm at their proxamal border. respectively. (ferry thomas sign) and/or a volar tall of scaphoid producmg a foreshortened scaphoid with characteri!>tic: ring shadow (sagnet ring sign). ln perilunate dtslocataon the lunate is volarly rotated. but remams in articulation wath the radaus and the capatctte is dorsally dislocated with regard to the lunate. In lunate dislocation the volarly rotated lunate is also
57
completely volarly daslocated with regard to both the radius and capatate whac h remam ahgned (Fig. 4 11 ). l'ericarpal dislocation can be consadt>red a stage betwet>n penlunate and lunate dislocation wuh antenor subluxatron of the volarly tilted lunette with regard to the radius and compiNe do~l dislocation in the lunocapitate JOint. Pt>rilunate d1slocatrons may be associated With carpal bone fractures. I he prefix ~trans ~ind icates which carpal bone(s) rsfare fractured (e.g., trans-scaphoid p<'nlunate drslocation). Intra-articular fractures of the base of the first metacarpal may be simple (Bennett fracture) (Fig. 4.12) or comminuted (Rolando fracture). In these conditions the fi rst metacarpal is frequently dor~lly and radially dislocated or dasplaced. respectively. cctuscd by the pull of the abductor polhm longus. A boxer's Jracwre mvolves tht' neck of a metacarpal (most commonly the fifth) with characteristic dorsal angulation at the apex. A gamekeeper's thumb (skier's thumb) (F1g. 4 13) results from rupture of th£' ulnar collateral hgam£>nt of the first
fig. 4.10 a , b Scapholunate dissociation .md rotary ~u!). luXdtion of the ~caphOtd. An injury to the scapholunate ligament is dio19noscd by e.ther widenrng of the drslance between ~c.-tphOtd and lunate (Terry Thoma~ ~1gn) {a) or by rotary subluxatron of the stdphoid producmg the ~rgnct ring sign (b).
a
b
frg. 4. 11 Perilunate and lunate dislocation. a Norrndllater dl wrist. b perilundtc drslocdtion. c lur1dte dislocdlion. C cdpitatc. L. lunate. M )"1 mctacarp.JI. R: radius. S: scaphOid.
M
c
(
c
s
s
R
R
\
b
I
R
c
58
Bone
metacarpophalangeal JOint that may be? accompamed by the fracture of the base of the proximal phalanx. In the pelvis stable and unstable fractures must be differentiated (F1gs. 4.14 and 4.15). In unstable fractures t he pelvic ring formed by the sacrum and pelVIS 1~ totally d1srupted m two or more places. Stable pelvic fractures include avulsion mjuries (anterosuperior and anteroinferior ihac spines and ischial tuberosity) and/or complete d1uupt1on of the pelv1c ring hm1ted to a smgle locat1on. Pelv1c fractures may extend into the acetabulum where involvement of the dome (acetabular roof), anterior (iliopubic) wall or column and posterior (1h01SCh1al) wall or column mu~t be differentiated. Fractures of the proxrmal femur may be cla~~11ied as capital, ~ubcap1tal, m1dcervical, bastcervJCal, mtertrochantenc and subtrochanteric (F1g. 4.16). Cap1tal fractures are uncommon and usually assoc•ated w1th postenor h1p diSlocation.
After healing they may be Impossible to differentiate from avascular necrosis of the femoral head. Frequent complications of displaced femoral neck fr.1ctur~ are av.1~cular necrosis of the femoral head and nonumon. Fractures about the knee may involve the d1stal femur or the proximal tibia. Distal femur fracture~ may bt' t'Xtra-artirular (supracondylar) or intra-articular (rondylar or intercondylar). Fractures of the prox1m.1l tlbta may involve. besides the intercondylar eminence, the lateral or, less frequently, the medial t1bia plateau or both. The articular surfact of the tibia plateau may bC? split, depressed or both. Crur1ate hgament injuries are frequently associated with fractures extend tog into the intercondylar emmence of the tibia. A Segond fracture is an avuls1on fracture of the lateral proximal ub1a JUSt distal to the JOint line at the insertion of the reinforct>d capsule. This fracture has to be differentiate-d from an avuls1on of Gerdy's
Fig. 4.13 Gamekeeper's (skier's) thumb. A tiny avuls1on fracture (arrow) of the ulnar aspt•ct of the proximal phalanx of the thumb is
ftg. 4.12 Bennett fracture. A simple intra-articui.Jr fracture (<~rrow) of the base of the fu·st metdC.Jrpdl with radial subluxation of the latter is seen.
seen.
4
5
6
Fig. 4.14 Stable pelvic fractures. 1 Avulsion of .Jntcrosuperior iliac spine. 2 Avulsion of anteroinferior iliac spine 3 Avulsion of ischial tuberOSity. 4 Iliac wing fracture 5 !.acral fracturE' 6 Un · lat('ral superior and mfenor pubic rami h ach.r('S (u addition a fracture of the contralateral superior or inferiOf r, 1b;c r 1mus may also be .tSs<xiatt'd). DO: Straddle fracture 10 fig 4 15.
4 Trauma and f ractures
59
(~ I
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b
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rig. 4. 15 Unstable pelvic fractures. a Strc1ddle frc~<1ure (both superior and inferior puboc ramt (or •~h•al rami) are fractured. b Magaigne frc~
s.Kroiliac joint may be frilcturt:d). c Bu l
2 3 4 5
6
ftq. 4 .16 PrOXImal femur fTactures. 1. t.Jpttal. 2 s 1lxapt 1l 3 Ml(] e!VKal 4 basiCervtcal, 5 ntertroch~ 2 . 3 and 4 art> femur neck fractures
60
Bone
tubercle (insert1on of the 1h0t1b1~1 tract) that 1s located anterior to the Scgond fracture and u~ually only visualized on an external oblique but not on a frontal radiograph. Fractures of the ankle can be classified as unimalleolar. himalleolar. tnmalleolar or complex (comminu ted fracture of the d1stc1l t1b1a c1nd fibula). A fracture of the distal tibia caused by axiaiiOcld i~ called pilonfraccure when the frc1cture line extends mto the articular ~urface of the distal tib1a. the tibia pia fond. lnJunes of the ankle are commonly caused by mvers1on ( supmat1on. adduction) or eversion (pronation. abduction} of the foot and may be associated with external (lateral) rotation of tht.> foot. 01ese injuries may be ligamentous. osseous. or both. Depending on their radiographic presentation (Fig. 4.17) bot h mechanism and severity of the in jury can be asses~. Osteochondral fractures of the lateral or less commonly the med1al talar dome may be associated
j
/ I
/ a
-
resulting from impingement of the talus on the fibula or tib1a. respectively. Fibular shaft fractures may be assoc1ated with ankle injuries. A Dupuytren fracture consists of a distal fibular fracture 2 to 7 em above the ankle JOint hne associated with disruption of the distal tibiofibular syndesmosis and the med1al collateral (deltoid ) ligament. The s.:~me inJury without disrup tion of the di~tal tibiOfibular syndesmosis 1s termed Pott fracture. A l\loisonneuw fracture ( fi~. 4 18 IS an eversionlateral rotatiOn type injury similar to the DuPuytren fracture and consists of a proximal fibula fracture, d1sruption of the tibiofibular syndesmosis and a medial malleolar fracture or tom medial colla tera l (deltoid) ligament. Fractures ofthe talus tend to be vertical. typically involving the neck of the ta.lus. or comminuted and occur most often from forced dorsiflexion of the fooL Osteochondral fractures
j b
Inversion
EversiOn
~) ( c
d
lnverston lat rotation
Eversion-lat. rotation
Ftg 4 17 Ankle fractures a lnver\ion injury (20\.). Hori,ontdl (dvul~ion) lrac.tu1e of the lateral malleolu~ and oblique (talar impaction) fracturE' of the medi.JI malleolus, both originating at or bt>low the JOint line. b Eve~ion 111Jury ( 10%). Horuonti!l (i!vul~lon) fracture of the mediC! I mdllcolu~ and oblique (talar Impaction) frac· turc of the lateral malleolus. both originating at or below the joint line. c lnvc~ion- lateral rotation Injury {60:1:). Oblique (spiral) fracture of the d1stal fibula origindtinq anteromed1.JI at or up to 1.5 em above the joint line and extend1ng in do~l and prox1mal d~rectton. FractLJrE's of the medial and ~terior mdlleolus and anterior tibial tubertle may be as~ociated . 0 EversiOnlateral rotation inJury. Fracture of the medial malleolus assoc1ated w.th a homontal supramalleolar (2 em or htgher above the JOint line) frc!C· ture of the dtstc~l ftbula . Fractures of the po~te rior mc~lleolu~ and i!Ot(-rior tibial tubercle may be aS\OCtatE'd. Note thclt instead of a malleolar fracture the correspond1ng ligament may be torn . Widt'r•ing of the mort1~ (InJury to the tibiofibuli!r syndesmoSIS consist•ng of the anterior o~nd posterior tibiofibular ligaments, infenor tranwerw ligament (immcdiatPiy d1stal the latter( and interOS\eous membrane) can be diagno~ed when the di~tc1l tibia and fibula no longer overli!p on the mort1se view. Avulsion fractures of the ilnterior tibial tubercle and ~terior maiiE'oius inditdll' injulit'S of the anterior and posterior tibioftbular ligamcnh rc~pcctively. and are or1ly found with rotational injuries (modified I dnge-Hamen classification).
Fig 4 18a. b Maisonneuve fracture A fracture of the medial malleolus wtth shghtly w.dened morti~ ev•dent by the loss of the normal ttbiOfibuldr OV\!IIi!p is ~ecn in (a). Frcl
a
b
4 Traurnd and Fractures
61
Cervical spine injuries arc caused by hyperflex1on (e.g. ante-
of the medial or lateral t.llar dome may be associated with inversion or evers1on injuries of the ankle. Tatar dislocations may be pentalar involvmg the tdlocalcaneal and talonavicular joints or total mvolvmg besides the aforement ioned joints also the tlb1otalar joint (~float~ng talus"). Seventy-five percent of calcaneal fractures extend Into the subtalar (talocalcaneal) JOint. Depression of the subtalar JOint IS d1agnosed by the BOhler's angl<.' (angl<.' betw<.'Cn lin<.'S drawn on lateral radiograph from the highest point of the subtalar joint to the antenor process of the calcaneus and posterosuperior aspect of the calcaneus respectively) measuring less than 28 d~rC<.'S. Chopar1 fracture-dislocation Involves both the talonavicular and calcaneocubo1dal JOints and abutting bones. Lisfranc fracture-dislocation Fig. 4.19 mvolvcs the tarsometatarsal JOints. In the homolateral form all metatarsals are dislocated laterally. whereas in the d1vcrgent form the first metatarsal is dislocated dorso-mcd1ally and remam~ng metcltarsallclter ally. Associated fractures most often occur at the base of the second metatarsc1l, followed by the base of the third rnetatar· sal and the first and second cunei forms. A first ray separation is diagnosed when the JOint space between the medial and Intermediate cune1form IS widened. An intra articular avulsion fracture of the base of the fifth metatarsal has to be diff<.'rentiated from a )ones fracture referring to an extra articular transverse fracture of the proximal fifth metatarsal shaft. jones frattures have a high incidence of non union.
rior wedge fracture. anterior subluxation. and bilateral locked facets with anterior ~ubluxation of the superior vertebra). hyperextension (e.g. avulsion of anteromferior comer of a vertebral body. typiCally at C2). hyperrotat1on (e.g. rotary atlanto ax1al di~loutaon). hyperflex1on and rota · t ion (e.g. unilatt>ral lockcd f.Jctt). I.Jtcrat hyperflexion (e.g. unilateral uncmate process or pillar fracturt) and vert1cal compression (e.g. burst fracture). A jefferson fracture is a burst fracture of C1 pre~l.'nting cla~sically with bilateral dis ruption of both antenor and pnstenor arches and with lateral displacement of both lat•·ral mas~cs. Dens (odontoid) fractures (Fig. 4.20 ) are classified based on their location: Type I fractures occur cephalad to the base of the dens. and are usually obhqucly onented. They are stable and must be differentiated from an oss1culum terminate ( ossicle of Bergmann) at the t1p of the dens Type II fractures are unstable transverse fractures at the base of the dens and must be differentiated from an os odontoideum. Type Ill fractures extend from the base of the dens 1nto the body of C2 and are usually Mable injunes. I hey can be differentiated from type II fractures on the lateral radiograph by disruption of the 1101mal Mnng shadow" of the ax1s cc~used by the pedicles. A hangman's fraaure (fig 4.21 IS il hype1exten~ion injury of the axis presentmg with bllilteral peditle fractures and varying degrees of anterior subluxcltlon or frank d1slocauon of the body of C2. Thb fralture cc1n be cOJmdered as trau-
fig 4.19 lisfranc fracture-dislocation (homolateral form). lateral dislocation of all metatarsals i\ \{'('11. Fracture~ of the ba~s of the second and third metiltill \ills are assodated.
Fig. 4.21 Hangman's fracturP. f• iltturt> of tht pcdicles of C2 (arrow) wath only minamal drll'IIO ~ubluxat10n of the body of C2 is seen.
\ a
lype 1
b
Type3 c the base ofthe de s. c WI' 3 fractur •xtP >dang from the base of tht dens into tht body f C2
Type 2
fig.4.20 Dens fractures. a Ty~ Fracture 'u\ually oblique) cephalad to the base of the den\ b Type 2: Tran\1/l'rse fracture at
62
Bone
matte spondylolistheSIS of C2 and IS nowadays most commonly found in automobile accidents when the face strikes the windshteld. A clay-shoveler's fracture (Fig. 4.22) is a n oblique or vertical avulsion frc1cture of the spinous process of C6 or C7 (occastonally T1 to TJ) caused by a sudden load on the flexed spme. Teardrop fractures (Fig. 4 23) 10 the cervtcal spine may be assoc1ated with both hyperextension and hyperflexion injurIes. In thl' extension teardrop fracture the avulston arises from the anteromfenor corner of a vertebral body usually at the level of C2 or 0. lhts injury is in contrast to the flexion teardrop frc1cture stable c1nd the t riangular frc1c ture frc1gment produced by hyperextension is small and does not exceed 10 size one quarter of the !>
graphiC fi ndings mclude mcreased saginal diameter of the vertebral body, mcreased interpediculate distance, retropulsion of the posterosuperior portion of the vertebral body and moderate to marked antenor wedging. 3. Seat- belt injuries (Chance fractures) are caused by hyperflex1on of the spme resulting in distraction injuries of both the middle and poste· rior columns associated at times with antenor compression of the vertebral body. The radiographic findings depend on whether the injury IS predommantly osseous or ligamentous. A horizontal sphumg of the vertebra beginning m the spmous process or lamma and extendmg through the pedicles into the vertebral body wit hout anteroposterior subluxation is characteristic. Ligamentous injuries can be diagnosed by widening of the interspmous dtstance, increased height of t he intervertebral foramma. a nd perching or locking of the facet JOints. 4. Fracture dislocation inJuries refer to the complete dtsruption of all three spmal columns. The hallmark of these severe. mually mtxed osseous-ligamentous mjuries is the presence of intervertebral subluxation or dislocation. while the loss of hetght of the mvolved vertebral bodies characteristically is commonly relattvely small. Traumatic fractures of the spine havl' to be differentiated from subacute or chronic compression fractures associated with osteopenia. These fractures are frequently located in the mid thoracic spine, whereas traumatic fractures are preferentially located in the thor<Jcolumbdr region. A narrow zone of increased dens tty below the fractured end plate. produced by impacted t rabt>culae and/or allempted fracture healing. is commonly prt>sent 10 compression fractures associated with osteoporosis. Fractures in cllildren may present w1th spcoal features. Greenstick fractures (Fig. 4.25 are incomplete fractures of the relatively soft growing bone perforating only one cortex and ramifying within the medullary cav1ty. Bowing fractures (Fig. 4.26) present as antero postenor or lateral bending of the radtus. ulnar or fibula Without evidence of a bony break. Companson radtographs of the oppos1te side are often reQUired for correct dtagnos1s. Torus (buckling) fractures Fig. 4 27) produce a buckling of the metaphyseal cortex in children and osteopenic adults. Trauma to the bone 10 children and adolescents often 10volves the cartilage (growt h plate. as long as the epiphyses are not closed. These injuries can be classified into different types us10g the Salter· Harris method (F1g. 4.28 ). A SalterHarris type Ill fracture 10 t he lateral dtstal tibia t>piphysis is referred to as juvenile flllaux fracture (..1g. 4.29). A trip/one
Fig. 4.22 Oay-shoveler' s fracture . Oblique fracture of the spinous proc~s (arrow) of C7 is s<>cn.
Fig 4.23 Flexion teardrop fracture A fracture at CS IS seen con· sisting or tht: s ,.;ller anteroinfenor teardrop fragment (arrow) and a larger posterior fragment tho1t 1s postenorly d1splaced into the spinal canal.
4 Trauma and rractures
-
0
re
v
•
~
~
-~
F
I 2
•
4a
•
p
I
~ /~
•
\
63
•
J -.
~
• 3
-J -i Sf
.... ....
4b
Fig. 4.24 Thoracolumbar spine fractures 1 Normal 2 (om· prE"i~•on fro~cture. 3 B .rst fracture. 4 (hance fracture (4a onelevel, 4b . tvvo-lcvd). S fracture-dislocat•on. D. ntervertebral disc. 1: lnterspmous l•qamcnt. F: Facet (apophyseal) joint. P: Pt.>di
1
5
S: Spn10us prOCe\~ T: Tranwl'r~e process. V: Vertebral body. SF In 5: Superior f.lct't CJf the middle \ertebra. Note that a torn •nter· spinous ligament may .11~ imply tears in the anterior and posterior longitudillcll ligarner •h dnd hgamcntl.Wll na\lJffi. f~ 1• 4.26
Bowing fracture. A fracture of the adius shaft is associated \lllth a m.ukcd bending dcform1ty (bowing frac· ture) of the ulna without evidence of a cortical break.
64
Bone
fracture of the drstal libra m adolescents represents a variation of a Harris-Salter type IV InJury (Fig. 4.30). Two, three or four fragments (parts) may result with two fragments bemg most common. A traumatic tpiphysiOiysis of the femur head is particularly common in boys between 10 and 15 years of age. although a hrstory of acute trauma IS oftt>n not avarlable. In these cast'S
of slipped capital femoral epiphyses (SCfF), repeated lowgrade trauma is believed to be the triggering mechanism. The displacement of the femoral head in relation to the metaphysiS is almost always m a posterior, inferior and medial direction (Fig. 4 .31 ). Multiple fractures and dislocations man mfant should raise the suspicion of an ··abu'>ed child syndrome.- More subtle find-
! fn
I
zJ
rig. 4.27 Torus (buckling) fracture Buckling of the metaphyseal cortt>x of lht> destal ri!dius (arrow) is seen.
"'
II
VI
VN
Fig. 4.28 Salter·Hmains att.-.ched to the epiphysis. Prognosis is good. Type Ill Incomplete trclnwer~e lclceratron of the cartilage plate associated with lonqitudlnal fratture through the epip~is.
\
/
a b Fig. 4.29 Juvenile Tillaux fracture es a Harris· Salter type Ill fracture rnvolvrng the postt>nolatN al (shown here) or anterolateral aspect of the distdl tibia epephyses (a . anteropostenor, b· lateral).
IV
v
VIII tx Prognosis is b.ld if the fracturl' h not reduced With smooth joint surface. Type IV· Oblique longetudinal fracture through epiphyses. cartilage plate. and meta~i,. Prognmi~ i~ bad ef the fracture is not pt>rfPCtly reduced. Type V Crll\hing of the cartilage plate With intact bone. Prematun dosurl of the platl.' and stoppage of growth es relatively common. Type VI Trc1uma to the peri· chondrium weth tethering of growth plate Typ€.' VII: fractur€.' of the epip~i~. Type VIII: fracture of the metclph~is. Type IX. Avulsion injury or the pcriostt>um.
41raumaandfractures ings in this condition include injuries to the cart1lage plate, metaphyseal fragmemauon and avuls1ons. the latter producing a charactenstic "bucket -handle" deform1ty. posttraumatiC metaphyseal cupping and cortical thickening I fig. 4.32). The evaluation of dislocations requ1res rad10log1c examination~ in at least two proJeCtiOns ( F1g 4 .33 W1th a single projection. a dislocation a~ well a~ a potentially associated
65
avulsion or compresSIOn fracture is ea~ily m1ssed. 'I raumat1c, hab1tual. pathologic (secondary to JOint d1sease), paralytic, .1nd congenital dislocations are differentiated. fhere is no longer any contact hl'tween the two JOint surfaces in a complete dislocation (luxation), whereas in subluxations (incomplete dislocation~). a parual contact between the JOint surfaces 1~ sull m.lint
J
b
\
Fig. 4.30 Triplanar (triplane) fracture (two-part) of the d1~tal tibia in children consists of a VL'ftical fracture of the cpiph~s in the sagittal plane, a horizontal fracture in the .1xial plane through the lateral and anterior aspect of the growth pl~te and an obhque fracture of the metaphysis tn the coronal plane cxtl'nd•ng from the grov.1h plate to the postenor cortex of the t1bia (a: Mllt'ropo~te rior, b. lateral).
Ftg. 4.31 Traumatic epiphysiolysis (slipped capital femoral epiphysis). lht nght ft:<nordl h. Jd •·· d1\placed medially, downward and backward. Nuk also the WJdemng of the physis, the irregularities of the met~phy\1\, and thc blurnrtg of the JUnction between the metaphy\•s and the eptphyseal carttlage plate. all of which are e.nly \lgn\ of .m •mm•nent sltp. The\e findings are best appreciated when compar(·d '"''h the nQfmal k:ft h1p.
f , 4 l2a, b Abused child syndrome. a H< ·a tng fractures are •er ., th , .u.uerus, rad•us. and u ''d b More rec:cnt avuls•ons of the m('tapiJY'eal Comt'rs (arrows) produce the charatteristi< "buc.ket·handlc" deform•ty 1n infants.
b
a
66
Bone
OsteochondritiS diSS(.'<"ans appears to be caused in a great maJonty, 1f not all ca\es. by stress. usually of chronic nature. The medial femur condyle i\ the most common site of involvement. but the d1sease has also been observed in the lateral femur condyle. the d1stc1l tib1a, the talar dome, the capi tulum of humerus ( fig.4.34). the pcttella. and the heads
of the femur. humerus. and metatarsctls. especially the first. The bony fragment may still bE' located in the corresponding defect of the c11 ticular surface or may have become completely separated from the latter and form a loose imraarticular body. The differenllctl dragno~1'> of loo'>e imra-articular bod1e\ IS shown in T.tble 4.1.
Table4.1 Differential Oiacjnosls of Loose Intra-Articular Bodies Oise-
Preferred Location
Osteoc:hondritis disse· cans
Number of l oose Bodie$
Othet' Radiographic Flnclin,.s
Comments
One
Defl•ct (ptt) 1n articular surface at the \lte of origin.
Preponderant in young males.
Osteochondromatosis (syllOIMI) (Fig. 4.35)
large JOints, bursae
Multiple (often more than 10). relattvely unt· form in size, one-third not calcified
joint effusion common.
Preponderant in young to middle-aged males. llypertrophk c
Trauma (chondral and osteodlonclral frac· tures)
None
One or more. not al· ways calciFied
Evidcrxe of old tr
Secondary to avulsion of bone and/or cartilage (artiCular surface, memscus).
Septk or tuberculous
None
One or more
EVIdence of jo1nt de\trucllon and deformity.
Rare. Chclracteristi< dini(al history.
DegenBatfw joint dls· e-
V.eight·bearing jomts
One or more detached spurs
Osteophytosis, sclerosis, subchondral cysts, and joint space naffOVoiing.
~ually
1n elderly patients. Synovial chondrometoplos10 m.1y also occur \lmlJI~tmg osteochondromatos1s.
CPPD arthropathy (F.g.4.36)
Large joints of upper and lower extremitie~
One or more
Similar to dcgeneratrve joint disea\c, but more de~tructive and progrcs· sive. Cllondrocakrnosis and subchondral cyst formation arE' common and often prominent.
Elderly patients.
Avascular necrosis
Hip, knee. shoulder
One or more
Advanced stage with flattened or colla~ed articular surface
Bone infarcts may also be present. May simulate osteochondritis dis~cans tn the knee, but is often bicondylar or
Neuropathic ar· thropathy (hyper· trophic fonn) (F.g. 4.37)
V\(;t(jht·bcaring jotnt~
Multiple, varying size
Marl-.ed sderosis, dhintegratlon of articuldr \urfaces and subluxa· tion.
loss of pain sensation (didbetes, syphilis (Char· cot jointJ and other neurologic di">Ordt>~)-
arthritis
bilatero~l.
4 Trauma and Fractures
67
Hg 4.33a, b Posterior dislocation of the shoulder- with impaction fracture of the humeral head . a In the obliQUl anteroposterior projection. the ~teri01 d1slocation is diffinrlt to apprt>ciatt> (nor mally tht'fE' •s a slight overlap bt>twE'en humeral head and glenoid fos~ In th1s projrttion). b The axillary proje glenOid fossa is now e\lident.
fir 4.34 Osteochondritis dissec:ans. A small bony frag mt>nt (arrow) i\ locatE-d in a subchondral dt>fffl of thE' cap•tulum of the humeru~.
a
b
b Fiq. 4.35a, b
jors
Osteochondromatosis (1 pat1ents). a
~lbo\
b knee. Multiple loose bod•es are scrn 1n both
68
Bone
Stre~;s fractures can be subdivided into fatigue fractures and insufficiency fractures. Fatigue fractures occur m normal bones with the application of an abnormal !>tress or torque cau<;ed by a new strenuous or repea ted activity. lnsuffidency fractures occur when normal stress is placed on an abnormal (ost<-openic) bone. Stress fractures ar~ usually symptomatic. Th~y bcgm as small cortical cracks, and may p10gress to subcortical mfraction and eventually a fra<.t ure running tra nsvers~ly across the bone (Fig. 4.38). If the fracture line cannot be d~monstrated radiographically. magnt'tic resonance im aging (MRI) or a radionuclide examination ar<' always posi
tivc and may provide an early dragnosrs. MRI, however. has comparable sensitivity and superior specifiCity to bone scmtigraphy in the assessment of stress fractures. Osteomyelitis and bone tumors such as osteosarcoma and osteord osteoma can be d1fferent1ated from a stress fract uf<' on th<' basis of both characteristic locauon and the typical history of st ress fractures (Table 4.2 and Fig. 4.39). At a later stage, periosteal reactions w1th subsequent localized callus formation and cortical thickening obscuring the fracture line. are found in the diaphyses of tubular bones (Fig. 4.40). In an epiphyseal and metaphyseal location (e.g., tibia plat~au) and cancellous
Fig. 4.36 CPPD arthropathy. Advanced arthntiC changes with numl'rfll \ akrhc and osseou\ bodtes rn the Joint space and suprapat~IIM uurY (arrow) are wen.
fig. 4.37 Neuropathic arthropathy. FragmPntahon of the 101nt surfaces With ~ever al irregular loose bodre\. \clero\r\ and subluxatron\ are ~ rn the mt'latarsophalangeal joint\.
r g. 4 38 a. b
Stress fractures (2 p.~tients). (a) A trans~~erse linear radrolu<.ency (arrow) is a\socrated with mrld localilffi cortical thickcnmg m the femur shaft. (b) The \tre~\ fracture presenting initially as poorly defined sclerotic band (arrow) in the medial <~~tx'<.t of the femoral neck progressed to a complete subcapital fracture.
a
b
4 Trauma and fractures
69
Table 4.2 Strt'Ss Fntctur ..\ (Fig. 4.39) locabon 1. Lower cervical Of' upper thoracic spinous prouss
Acttlllty Shovclinq
2. Clavicle
~toperatrve
3. CorKotd process of scapula
Trap shoottng
4. Ribs
Carr)'lf'9 heavy pack (first rib), golf. cough•09
(radical neck d•ssectiOn)
5. Humerus: distal shaft
rhri1Wif'9 a ball
6. Ulna: cOf'onoid process shaft 7. Hook of hamate
Pitch•nq a ball. throwi09 a ja~elin, pitchfork work. propelling wheeld1air
8. Lumbar vertebra: pars In terartkularis (spondyloly·
B.JIIct. lifting heavy objects. scrubbing flOOf'S
Holdang golf club. tennis racket. baseball bat
sis)
9. Femur. neck shaft
BcJIIet. running Ballet. marthing. running, gymnastin
10. Pelvis: obturator ring
Stooping, bowling. gymnastics
11. PateUa
l lurdling
12. Tibia
Runnang (proxamal shaft an children. mid- and di\tal \haft in adult$)
13. Fibula: proximal or distal
jumpinq. parachuting running
shaft 14. Calcaneus
jumpmg. parachutang. prolonged standing. recent tmmobth · ld!IOn
15. Navicular
~tamptng
16. Metatarsals
Mar<.hing. stamping on ground. prolonged standing. ballt>t. postoperative bunionectomy
17. 5esamolds of ,.re01t toe
Prolongecl stand•ng
on ground. marchang. runmng
r .q
4 39 Locations of stress fractures. The num bo <\ 1n thE' feg .. onespond t.> thE: numlx'f~ in Table 4 2.
Fag. 4 40a, b Stress fractures. (a) A heahnq stress fractur "'1th Clltensive periosteal callus formatron i~ sren in ttl<> \econd metatarsal No other streu fracture wa\ daaqnosed at this time. sequelae of ,Jrthroplasty andudinq resection of the base of the proximal phalanx of the great toe arl' incidentally also evident. (b) Thr~ months later the \tress frtJcturl' in the second metattJrstll has proqressed in healing. A second heahng stress fracture is now seen in the thard metatar~al \h.Jft and a new nrcss fracture v.•th 011ly rnanamal \dt>ros•s an the nt'ck of the fourth mctc~tar~l (c~rrow)
a
b
70
Bone
bone, a band-like focal sclerosis usually Without appreCiable penosteal reaction is more charactenst1c fig 4 41 ~ Osteoporosis and rheumatoid arthntls are t he two most common conditions in which msuffioency fractures are encountt>red Remforcement lines (bont bors) presentmg as well-defmed, usually t hm sclerotic lines extendmg partia lly or completely across the marrow cav1ty m patients with ostcopema have to be differentiated from poorly defined, band like msu ffioency fractures (Fig. 4 .42). Rcmforcement lines can be considered as unmaskmg of growth arrest lines occurring in childhood. although their pathogenesis is unclear. fhey are modental findmgs without cli nica l relevance. Pathologic fracrures occur at sites of pre ex1st mg abnorma lities and are often caused by a mmor trauma t hat wou ld not fracture healthy bone (Figs. 4.43 and 4.44). The rad•ograph•c d1fft>renrial diagnosis between pathologiC and nonpathologiC fracture can at times be d1fficult, partJrularty w hen the injury occurred days to weeks pnor to t he first radiologic examination. In these cases. bone resorpti on oc-
cumng at the site of a nonpathologic fracture may simulate an underlymg pathologiC lesion. On the other hand. a smaller underlymg lytic or sclerotic bont> lt>sion ca n be m1ssed radJognphically, particularly m the presence of displacement at the fracture Site In rhese cases. the demonstration of orher lyt ic or sclerotic les10ns as Wt'll as the absence of a history of trau ma or the lack of fracture pain should suggest the possibility of a pathologic fracturt. PathologiC fractures can also occur as early as five months after radiatiOn t herapy· that is. at a time when the bone does not revea l any radiation -induced changes. AvuL~ion fracrures (Fig. 4.45) at the Site of ligament and tendon att.lchments can be differentiated from accessory osSJcles by the lack of a clearly defined cortical margm characteristic of the latter condition (Figs 4 .46 and 4 471. The diagnosis can be further supported by tht' d tmonstrauon of a cortical defect or irregulanty m the adJaCt>nt bone. Avuls1on injunes are caused by e1ther a single VIOlent traumatic event or repetitive injuries. They are partiCularly common m ch1ld-
Fig. 4 41 Stress fracture . An 1rrpgular sclerotic band i~ SE'Pn paralleling the posterior bordt>r of the calcaneus (arrows).
F1g. 4 42 a. b lnsuWKiency fractures versus elnforcement lines (bone bars). (a) O~tropenia and a poorly defined sclerotic b.lnd (arrows) as· sociated with a small sclerotic focus (arrowhead) are characteristic manifestations of insuffiCiency fractures. (b) Thin, well-defined sclerotic lines extending partially or completely across the di~· tdl femur and proximal tibia 1n ostropen1a are VIrtually diagnostic for remforcement lines (bone bars) In contrast to insuffiCit>ny have no clinical implication~.
b
4 Trauma and fractures
71
ren. smce the physe.ll (artilage of an apophysts IS constderably weaker than tendmous or ligamentous t1ssue Several avulsion inJuries about the pelv1s and hips occur m young ath letes mcluding the antenor superior or mferior ihac spme. ihac crest. isclual tubero~lly, pubic ~ymphysis (adductor muscle insenton sites). and greater or lesser trochanter. Calcifications and oss•ficat•ons developing m a ligament after acute or repeated low -grade trauma can be tmposstble to differentiate from an o~stcle. ~•nee both may be well corticaten t£>rmed myositis ossthcans. smce u occurs most commonly m muscle but •~ also found in tendons. hgaments. periosteum. and other conn£>ctlve tissues. It fr£>quently develops after m~ruon of a JOint prosthesis. par ticularly m the htp, and m parapleg•c patients. OccasiOnally. myosttls osstficans can m1m1c a parosteal sarcoma (F1g. 4.49). It can be d1stmgu1shed from the latter by the fact that the periphery ts both more dense and smoothly outlined (•eggshell calctfication·) and by the demonstratiOn of a fine radtolucent lme separatmg the lesion in tts entire length from the adjacent bone (fig. 4.50) A central amorphous calCification associated wtth a soft ussue mass is not found m myositis ossificans and suggests rather a synovial or extraossrous osteogenic ~rcorna. whert> it is present in 30'!: and 50% of the cases. respectively. ExceSSive callus fonnatron followmg a fracture may occastonally have a wmor- hk<.> appearance. It ts found in frac· tures that have not been properly tmmobtli7ed. These fractures may not have been dtagnosed because of a decreased sensttlvtty to pam secondary to a neurologic disorder. Smce fracrures are nor immobth7ed m the battered chtld syndrome, excessive callus formauon IS common m that condition too. It ts also a~sociated wtth elevated sterotd blood concentrations (e. g .. Cushing's syndrome and stero1d therapy).
fig. 4.43 Pathologic fract ure . A hip frcKture through a large osteolytic metastasis from a renal cell carcinoma involving the femur neck is ~n.
hg. 4.45 Avulsion fracture . A fracture of the posterosupe· rior aspect of the cal cancus at the Achilles tendon tnsertton with ~upcrlor displacement of the avulsed fracture fragment is ~een.
a
b Pathologrc fracture a 1¥ rn•ttc al brt"ak (arrow) t~ bare~ 'lli~ible in th( r 1d1u t c t , 1>db nt Wtth mtJittple myeloma in the ante>upu>tl-..o. P•OJC:..!ton b '' thl' lateral projl-ction, the pathologiC fracture (arrow) can bt· bt:tt r appreciated bc
72
Bone
12. 13. 14. 15. 16.
Fig. 4.46 CharacteristiC locations of accessory bones (numbered) and sesamolds (shaded) In the wrist and hand. a Anteroposterior projection of the wrist b lateral projection of the wrist. c Anteroposterior projection of the hand: 1 epitrapezium 2. calcification (bursa. flexor carpi radialis) 3. paratrapezium 4. trapeLrum ~ecundarium 5. trapezoides secundanum 6. O\ \tylor~um (carpal bone or carpe bossu) 7. O)~rtulurn Gruben 8. capitalum secundanum 9. 0) hamuli propnum 10. O) llt'\ilhanum 11. os ulnare extl'mum (calnfrratrons rn bursa or tendon)
17
18. 19. 20. 21. 22. 23. 24. 25. 26.
Fig. 4.47 Characteristk locations of accessory bones (numbered) and sesamoids (shaded) In the ankle and foot. a An· teroposterior projedron of the cmkle b lateral projection of the ankle c Anteroposterior projection of the foot. 1. acce~~ory bone (or sesamoid) between the medial malleolus .md the talu\ 2. o\ \ubtibic~lc 3. tdlus atteSSOIIUS 4. os sustentaculr S. os trbiale externum 6. os retinaculi 7. accessory ossicle (or sesamoid) between the lateral malleolus and the talus 8. os subfibul,ne 14. os supranaviculare 9. tdlus ~nmdarius IS. os rnfranavicularE' 10. os trocllledrl' tcllcanei 16. os intercuneiforme ~ 11. os tngonum I)~ 17. os cunE'OITietata~le 12. O\ talotrbiale 18. os rnterml'tata~le 13. os supratalare 19 . os unci 20. secondary cuboid 21 . calcal'l('us sccundanus 22. os acces~um supracalcaneum 23. os subcalcis 24. os perona!!I.Jm (peroneal cxsrdE>) If 19 25. os ve'>dlrclnum (....._ 26. os wneonavrtulare medrc!le 27. ses<~mum tibiale anterius .28. os cunrometat.Jr\c~le 1 plantar!' 29. os 1ntercunciforme.
os radrale externum avulsion of thl' scaphoid, not an acct·ssory bone persisting center of ossification of the radial styloid process a((essory bone between SCdphold .Jnd rad1us (paranaviculare) os centrale carp1 hypolunatum epilunatum accessory bone bl'lwcen lunatum .Jnd triqut-trum epipyramk avulsion of the \tyloid procf'Ci\ of thl' ulna ("trrangulare") persi\tent nutleus of the ~t)IIOid prcxes~ of the ulna \mall osseous element in the radroulnar joint cdl
l
~111)
~ !'
I \I
I
b
10 I
II
m'
I
•
il
)l
•... tt l I
I l
1i
'•~~
t
1'')I ;,·,,t,,/~ ~J
4 Trauma and fractures Finally. fractures occurnng m osteogenesis imperfecta may to heal with excess1ve callus formation. Fractures extending to the articular surface result m a joint effusion (hemarthrosis). In fractures of the rad1al hecJd, c1 JOint effusion displacmg the anterior cJnd/or posterior felt pad mc1y be the only radiograph ic finding (Fig. 451 The demonstration of a fat-fluid level in the shoulder or knee is presumptive evidence of an mtra cJrtlcular fracture but can only be demonstra ted when the exposure is made with a horizontal beam Fig. 452). Pseudofractures (Looser's zones, Milkman's syndrome) c1re assumed to be mcomplete stress 1nsuffi ciency) fractures. presenting radiographically as narrow (2 to 3 mm) radiolucent bands lying perpendicularly to the cortex (Fig. 453). At a later stage. sclerosis develops around these lesions. making them more readily detectable. Pseudo fractures are present in v1tamm D deficiency (osteomalacia. fig. 4 49 Parosteal osteosarcoma. The densely sclerotic lesion is solidly at tached to the poste nor cortex of the diStal femur
73
PellegrtniStleda lesion A shelllike oss1ftcat1on (ar row~) along the medial femur condyle dl'vt'lopcd w1thm one month o~fter an acute msury to the mecllal collateral ligament of the knee. Fig. 4.48
fig 4.50 Myosltls osslflcans (post-traumatic). Trn.- o~~ific.a tion along the m<'dial femw ~haft Is scpa rated 1n its ent1re length from the adJacent bone.
fig. 4.51 Joint effusion (hemarthro~is) secondary to radial head fracture. The JOint effusion is ev~dcnt from the positive pos· tenor and anterior fat pad sign, evident as sail like radiolucencies along the d1stal humerus (arrows). Demonstration of <my rad•olucent area postenet1y alway\ md1catt'\ a joint cffus1on (positl\1! posterior fat pad s1gn). v.hereas a small oblong radiOlucent area along the anterior aspt>ct of tht> d1stal humNus can be normal. The anterior fat pad sogn IS only onchca!lve of a JOint t>ffuSion when 1t assumes a tnangular or sa1l-loke \hape, a\ m th1s Col\1.'. Note also tne fracture in the radidl head, whoch not uncommonly cscdpes radiographic detection even when radiographs on multiple projectiOn are taken.
74
Bone
rickets). renal osteodystrophy, Paget'<> d1sease. fibrous dysplasia, a nd hered1tc1ry hyperphosphatas1a nuvenile Paget's disease" or are rarely 1d1opath1c. They are located in the femur (neck and shaft). pubrc .1nd rschial ramus, scapula. clavicle. nbs. ulna (prox1mal shaft), radius (distal shaft), metacarpals, metatarsals. and phalanges. f'wutnent artenes p1erce the diaphyses of tubular bones obliquely. Their site of entry and angulation are fa1rly constant and, characteristically, the vessels point away from t he dom inant growing end of the bone (the end w1th the epiphyseal center m short tubular bones. or the end with the later fusing epiphysi~ in long bones). In the long tubular bones of the upper extremity they run towards the elbow. whereas m the lower extremity they run away from the knee ("to the elbow/ go, from the knee/Oee"). Nutnent arteries may be evident rad1ograph1cally as oblique lctdiolucent cortical channels thclt ~hould not be confu!oed with f1auure lines (Fig. 4.54 ).
Fig. 4.53 Pseudofractures (Looser' s zones) in Paget's disease. Multiple pseudofractures are seen presenting as small radiolucent lines with adjacent sclerosis lying perpendicularly to the outer cortex of thl' femur shaft. Note also the bowing deformty, thickened tortlces. and coar!>efled trabecular p.1ttem of the femur charactt>nstic of Paget's d1sease.
Fig. 4.52 Fat-fluid blood level sec:ondary to tibia plateau fracture. A folt Ouid It-vel, pilthoqnomomc of an intra·olrticular fracture. IS seen in the suprapatellcn bursa. It IS caused by the lighter and more radiolucent fat (arrows) layering on top of the heavier blood in the joint (l1pohemarthros1s). Th1s finding can only be seen when the rad1ogro~ph i~ takl'n w1th honrontdl beam.
Fig. 4.54 Nutrient arteries. Oblique radiolucent cortical channels are seen in charactt'nstic location (arrows).
75
5
localized Bone lesions
Convent1on.1l radiography remams the pnmary 1rn.1gmg modahty for the evaluation of skeletal lesions. The combinatiOn of conventional radiography, which has a high specificity but only an intermediate sensitiVIty, With radionuclide bone scanning. wh1ch has a h1gh c;ens1t1vity but only a low specificity is still the most efrooM• method for detectmg and diagnosing bon<' ll'SIOns and d1fferentiatmg between benign and malignant conditions. Conventional rad•ography. is. howevt>r.limited m delineating the intramedullary extent of a bone lesion and even mo1e so in demonstrating soft tissue involvement. Although magnetic resonance imaging frequently contri butes to the characterization of a bone lesion. its greatest value lies in the ability to accurately assess the intramedullary and extraosseous extent of a skeletal lesion. A solitary bone lesion is often a tumo1 or a tumur-hke abnormality. but congenital. infectiou~. •~chemiC and traumatic disorders can present in similar fashion. Differentiation between a benign or malignant bone les1on 1s not always possible. Signs of an aggre~~•ve or mahgn.:mt osseous lesion mclude rapid growth. large \17e, poor demarcation. cortical v1olat1on. mterrupted penosteal reaction and soft tissue extension. S1gns of a nonaggress1ve or ben1gn os'>l'Ous lesion mclude slow growth. small 511e. ~harp margmatlon. cortical expansion without corneal v1olat1on. sohd penosteal reaction and no soft ussue extens1on. However these radiologic features are noc mfalhble and many exceptions occur indicating the need for h1stolo~IC confirmation in the appropriate semng. In osteolytic lesions a geographiC, moth-eaten and permeative pattern of bone destruction are commonly diS· cerned A geographic l£>sion (l'lfS. 5. 1 and 5 2) has a well-de· fined margm separatmg 11 clearly tram the surroundmg nor mal bone. The zone of trans1t1on of normal to abnormal bone IS short and a sclerotic border of various thickness may surround the lesion. GeographiC lesions are usually benign. espeCially when they are marginated by a sclerotic rim. Multiple myeloma and metastases. however. frequently pre sent as geographiC I<"SIOns Without sclerotic borders (Table 5 1). A moth eaten /es1on ( f 1g. 5.3 ) 1s a poorly demarcated focus of bone destruction with a long zone of transition from normal to abnorrn.1l bone md1catmg its aggressive nature and rapid growth potential. Malignant bone tumors. osteomyelitis and eosinophilic granulomas frequently present w1th th1s pattern of bone destruction (Table 5.2 A permeative lesion (f1g. 5.4 ) represents the most aggressive bone destruction pattern With rapid growth. The lesion merges Imperceptibly With the normal bone. H1ghly malignant tumors infiltrating the bone marrow such as round cell sarcomas (e.g. Ewmg's s.ucomas and lymphomc1s) typically are associated with this partern of bone destruction. It is, however. also found m acute osteomyelitis c1nd rap1dly developmg osteoporoSIS such clS reflex sympathetic dystrophy. Infiltration of the cortex may abo be as!>oCJated with these conditions. presenting as cortiCal stliation or tunnelmg.
f 19 5 1
Geographic lesion A wel l-do no.ar• at '
Geographic lesions. Mult1ple wt:ll demarcated (punched-out) purely lyti<. lesiom arc .een in the vault of the cranium (multiple myeloma).
rig. 5.2
F1g 5.3 Moth-eaten lesion. A poorly demarc.Jted osteolytic ll'\ion (arrows) is seen in the distal femur (nonHodglun lymphoma).
76
Bone
Table 5.1 Solitary well defined osteolytic lesion ')ubchondral C) st tassociatt>d v.ath Jr:t uta~. trauma)
-.>t~:n'leCros•s.
or
Gout (1ntraosseous tophus) Amyloido\i\ lntraos\eou~
g;mglion
Simple (unicdmeral) bone cyst Aneury\mal bon£' CY\t ~pide1rn01d
inclusion cyst
The cortex reprt'st'nts a barrier to nonaggrt'~~ tve lesions. Benign medullary proct'sses may leavt' the endosteal surface in tact or product' endosteal scalloping ( Ftf. 5.5 Tht' latter findmg •~. however. also frequently st>en w1th mult1ple myeloma and metastases. Progressive endostt'al erosion associated w1th sohd new pen osteal bone depos1tion crt>ates an expanded osseous contour indicative of a nonaggressive bemgn skeletal lesion Aggressive skeletal les1ons may penetrate the ent1rc th ickness o f t he cortex (1'1g. 5.6 ) and ~orne times mduct' a v.uiety of interrupt<>d periostea l react1ons mcluding onion pt>el, sunburst a nd ha1r-on end patterns or a
Glomus tumor
Table 5.2 Solitary poorly defined osteolytic lesion
lntraosscous lapoma lnchondroma Chondroblastoma
Ho-I ; .mgMTlil
Chondromyxoid hbroma
ChondroblastomcJ
Nonossilytng fibromd
Osteobla~tomd
Ocsmoplastic lll>forna
Giant tell tumor
Ostffibldstoma
Fibro,arcoma
Gi.mt cell tumor
,ldlign.Jnt f•b1ou~
~lbro\arcoma
Chondnr,.~rcoma
Clear cellthondro\c'!rcoma
Osteosarcoma
Angaosarcoma
Ewang's sarcoma
Plasmatytoma/multlple myeloma
AngiO\c'!rcoma
MetastasiS
Multrple myelomc1
l:.osanophahc granuloma
Metastasis
Brown tumor (hyperparathyroidism)
Lymphom.J
hi~tiocytoma
Hemophilic pseudotumor
Langcrhans cell histaocytosis (eosanophili<. granuloma)
Osteonecrosis (bone infarct)
Hcmoph•hc pscudotumor
Brodie's absccss(cY\tic osteomyelitis
Ost('Oflecr0\1\ (bone anfarct)
lahrous dysplasaa
Osteomyelitis Brod1P's abSCPSS
Sarcoidosis
Sarco1~s
fig. 5.4 Penneative lesion. A poorly def1ncd osteolytic lesaon mcrgang Imperceptibly with the normc1l bone is seen in thl! proximcJI femur. Note also the begannang laminated periostE>al reaction an the subtrochanteric area (Ewing \c'!rtomd).
Fig. 5 5
Endosteal sc:alloplng
Sharply demarccJted eros o11s of the inner cortex of the rcJdaus and ulna caused by multiple osteolyt1c lesions is seen (mu ltiple myeloma).
5 Localized Bone Lesions Codman's tri a ng le. They art> m ost comm only associated w ith osteosarcoma. Ewmg's ~arcoma. and osteomyeli tis a nd a re d1scussed m greater de tai l m chapter 3. The matn x of .:1 skelet.:~lle~1on m ay be mho mogent>ous because it con tam s a reas of calcification or OSSljication. CaiCt ficattons a ppea r as n ng-hke. nocculent or neck h ke rad iodense areas F1gs. 5.7 a nd 5 8 ) Intramedu llary matn x calcificatiOn 1s pn ma nly assooated With cartilaginous tumors and bone mfarcts Ta ble 5.3 ). f OCI of mtramed ullary ossificat ions are more homogeneous and often 1vory- like a nd a re most often caused by bone ISlands. osteoblastiC meta'ifaq>s and pnmary bone forming neoplasms (Fig. 5.9 ). They are di s· cussed m detail m c hapter 2.
77
Table 5.3 Bone lesions with calcification lntraosscou~
ipc.• !l.J
Os teo< hondrorTlcl
Enchondroma Pemxteal (juxta<.ortiCal) chondroma Bizarre p.Jrosteal osteochondrormtous prohfcrat1on (BPOP) Chondl-oblastoma ~pid!>la epip~ahs
herr11meltca (Trevor's d1scase)
Fibrocart
Fig. 5.6 Cortical penetration. A poorly defined, mixed osteolytiC and osteoblastic l~lon Is set'n 1n the d1stal femur penetrating through the medial cortex. The late ral cortex is expanded and thinned but still intact (osteosarcoma).
Osteoblastoma (mdus) Ossify1ng f1broma Gnathic tumors (see chapter 11) Chordoma Chondrosarcoma (all variants) Metastasis (espt•wtlly thyroid carcmoma) Gout (intraosseous tophu\) Osteonecrosis (bone infarct) lntraosseous hematoma Osteogenesis imperfect.! (popcorn co~lcoflcdtlons 1n enlarged epimeta~es)
Fig. 5.7 Matrix cak lflcation. A floccUlent, ring lt' dust• r of calcif1cat1011 1\ ~n in the d1stal ff'mur (enchondrorTlcl)
Matrix cakiflcation. An irregular. shell-1 (..e
f1g. 5.8
c.alcof1c.a lion is seen in the di~· tal femur (bone infarct).
fig 5 9 Intramedullary ossification . An t
rt'g liar. I\!Ory-ltlcl' r J Of sderOSIS IS
set>n in the proxomal humerus (enostosis or g1ant bont> 1sland).
78
Bone fig 5 10 Septation. A lytic l5ion wtth extenstve delicate trctbeculdtion 1nduced by the tumor i.s seen in the iliac wing. Note also the locahzt'd corttcal violation (arrow) 1n the superolateral aspect of the lesion (aneurysmal booe cr.;t).
Septa lion of the matrix represents another mechamsm of new bone formation evoked by a neoplasm (fig. 5.10 ). In other instances int ratumora l septatlons represent t he remnants of the ongmal bone matrix largely destroyed by the neoplasm ( F1g. 5. 11 ~- Septatton is associated w1th both bt>nign and malignant les1ons. Delicate thm trabeculae typically a re found m giant cell tumors and aneurysma l bone cysts, lobulatt'd trabeculae in nonossifymg fi bromas. spiCUlated or rad iating trabeculae in hemang1omas and Irregular coarse trabecula in a vanety of benign and ma lig nant lesions. often of fi brous connect ive t issue o ngin (Table 5.4 ). A um form ha1y tncrease m radiodens•ty m an osteolytiC les1on IS termed ground gloss appearance. It is most charactenstic for fibrous dysplas1a (Fig. 5.12). but is occas1on.1lly also found in simple (umcameral) bone cysts in t he adult. The demonstration of a sequestrum ( rig. 5.13) representing a segment of
Table 5.4 Osteolytic lesions with trabeculation/ septation
fiq. 5.11 Septation. A large expansile lytic lesion v.ith remaining remllclnts of the ongtnal bone matrix produc tng a \eptated appearance, 1s scE'n in the ilium (plasmacytoma).
Fig. 5.12 Ground glass appearance . A slightly expansilc osteolytic lesion with a hazy increase in df'n~ity is seE'n in the proximal tibia (fibrou~ dysplas1a).
~imph: (lli.IC..tmeral) bont> cr.;t Ancurysm
Fig. 5.13 Bone SNJuestrum. A lytic les•on containrng a small sderotic sequestrum in its cer1ter is surrounded by dense sclerosi\ and corticdl thilkentng in the tibta (chronic ostcornyelitts). A healed fibula fracturt IS incidt>ntally also seen.
5 localitcd Bone lesions &t~
nccruti~
(Tabk
5.5).
Baze expansion malignant
k.,.it•lt,.
itldicHlih~
L.,
bone
~·rn lx
~t~Om) dit~
of chronil:'
as.-.~ i~ttcd
\lith
1!1 a slo" l} j;r<>\\ int;
both
tumor
bmig•t
and
the bone cr<>-
• ion on tl..: Ud,..:r .:urt.:" • ~uoup..•"·'''d b) bon~ app<>i>ition on tit.: out..:r .:trto:" ( rig. 5. 14). In the in, tancc the wrto:" r.:-
79
hf 5. 14 I 'J"~Il'ilc lc•ion \\ith intact co11c". \ n t:\J"ut' ilc, mullilwu-' laltd k ,ion '' 11 h m ta,·t. thmn~ or tlnd.. ,·ncd c·<>rtc" '" >ecn in the do,lllt: <)>I)
mau\S int".:t at aU time•. but tho: thi<.J.. nc"' t•f tlti• '"'" t.:odi· .:al •lt.:U ttta) 1x: diu,,.,, \\hcn "'lllJ"lf•d to t~ miginal 0:011<"- TI1~ lllh:tfa.:c Jx:l\,c'<.ll tiQnllal and C\l)alld.!d Cort~" rua) be Hlkd on \ltlb d, ,...., luk 1111d ofi, n ;, 1\:f,rrcd to "' bullre.\ \llli( (I tl} 5.15). It " li>tuld. anw11g <4ocl:<. "ith c...,iJ..,.. phi!i<; {:l''llllUIOllloll>, ltiiUJf'\Sill:tl bt>IIO: t.\''b and a-tooblaJ.-
In rap1dl~ ~~twmg ltmll>n. II><: "'"' "'"'" ft•rmatioo 1....-p up \ltlh Ill<: bv1 ~<: hr.:al..d<.•\\11 r.-,.ultmg in t.:ortiCO riofr.t:m or .frllllii dcstmllion (I ll' 5.16) ( I able:• S.6 and Ioma.•. catmot
5.7)
Table 5.5 Osteolytic lesions containing a sequestrum or bone fragment S1mplc (unicamcml) l><>nc q>l \\ith patholoric lracturc (tnllen tragmcnt ~ign) l~ibr~arl!OJna
Mcta'lill>l'
hutu.: frarnu.:t1t)
{M.:tlth... !-..h:lt.:c.l
(s.:qu~>'-1•<1
h<•IIC ltarmcnl)
Bone k-.ion \\ith P.'llwlt•t;" I '"ilk'f'htli, granult~l
Commmuto:d
.1
lrndur~
(l'ru,1urc frngn1.:nt)
('-~111-'htnn)
lra.:tur, (mlr.un,
dlSpb.:e
111.:111) O>k<·tn~ditis
('«j<~~lnl!ll)
Hnld~e', ~~·,.,.,~
lnfc~t.-d 1~11
Blllll>fl
(•«lll~tnnn)
trocl (rmg ~"I''Nrut11)
"-"<JUe-tnml
m.:Usta.«..,.,
Ill -~til (C:O.tfl<'(~llhC
t:l~d•"flllt'ld,
t-..t~c.Jola.
tJt:tl lh.:c.ro~L'. lll•lh.: lkifl undt.~gmng
crnnuknna ,.,,~<'m)diti>,
a\~tlhtr :th.:":tt~l
r&lia-
r II]..~ 15 BuUrt"'smg. I t'<.'al1/cd «•rtMtl thk~<11111& (ar1<•\\!o) "s.-.;:n m th.: pro.Jmal liht•l:l at th.: inlo:h h:<-n ll(•mlal '-''(lf1~x and cxP.'~td,'(! t.'Ort:" <•I th<:· O>UC\1\11.: k'""' (M<'"~'mal hone <\1<1)
hurr
huk and normal \ariants)
Table 5.6 cortex
Expansile osteolytic lesion with intact
Simple (llnK'3tllcml)
hc>n" <')'I
.\nctuysmul hone <)>I (e
lihrom;o (-.:.,nhl<')
Chuntln>lll}"''id r-.;e,mc.:~Mf\·u.g
flhnmiJ (-.:~4..-.:Uin\.:")
l>e•mopla,tu: lit>nma
I it:-~ I(•
()!.t.:obht.-tonta
tu.m_ •\n ~~i,.:\:lltrk, ''PaJl~ilc. u.kol~ti, J..,oon in lh" di>t.tl
roMrt< ma Cll<~lc.ln'r"an.ltfltt.l.
h"inorluli< {;ramol,una Drmm tumur (h\p<tparnlh\'midi."n)
lluntopluli, l'""d<.(LUJu 1 llcaliogl!l,alcd
lrJ.:turc
Osktlllt\dltts (• g. >pma H111tllill IJiulang•'l> 1•1 mdacarpal>l n tulx.,.,ul•"")
hhrous d) spla
( or1 1cal ds'>lruc-
kmu r mdJ~l)>i> and cplph) ""' J,n>l..e thn>ugh the "N1..:x '' llh t'lfll) a I""'\' u•rtl.:al 1\.ltlO.ull , lcmaming (giant
<ell
IUlllN)
80
Bone
·n... '"'"
•> >I
le-.oon '"thin a lx•nc pro• id~ an diacn<"'i' In tul>t•lar hones the lQcatK'Il for dll·ndrt>l>lastoma.'. dear
loca/1011 ol a ;.()ltt3r)
nn!'(>rtant epiph) '''
duo: to the correct
'' a •'('oOlfll<'tl
d•<•ldl'()!.aJ'~l"lla>,
mlra<'"·COl"
nk!tas~. hj'(·ma.~. ~ubdx>ndral aold l~ldu.'' ahM;,-..,.,,. Giant cell
gangba
tum<'"' <>nt•mat~ on the metaph)'" hut <1111c~l) penetrate IlK: dt,..cd l~R"'1h plat~ and cxt.,nd inl<• the " '"'';hondral hone <>-tcood <"'teomas (intra-art•c·ular prc-.~llation). enchondronHh ;md eosinophilic emnulomn.• <>cc:os oooutlly are nl'o lound in the cp•physe~. but the di:unctnpll)>i' is a more characlcriq•c locntion for these Inmon. ('l'nhlc 5.~). I ~•ions comm<>nly lt.....-at~ on the cp•pll)loC. nrc nbo 1<1u nd about the JOont~ o l llat boflC", patella and carpal and tarsal hc:>nes. T) pical metaphy!iea/ l~ioot' mdtld.: tK•Jtol'-tnncc from the ST0"1h plat.:. chondromp.oid lihr<'tna \\ ht I ('Oolc'(Xhondroma. HrodJc's nhscc.,.,., nlC',ii~'"S fibromas, s imple (unicnmcwl) bone C) Sis in nduJt,, c nt;hondronuL,., osteoid o-t~omn.'. Q.'tO fociliw.tcd b) the idcntilicatiou of it.> c.;ntcr \\ilh ••~;md to 11,., medullar) lanai and ""'rt""· T)pical centro/ k-,.i<.•n indudc >implc ( uniumual) bu'k! ~)~ ..:u...bondromll.'>. lihoou:. d)•pl...,.ia and hone inlarcb. Eccmtric lesions induoc ruk.un,mal bone
''"'" giant <:ell tumors
and d iQildrom\'Wid fi bromas. T)pi<:al cortical k'!>iNt.' are n('lll()&,if\'ing fihn"'u.' and <'l'teQid '"' ''(lmas Cl •g. 5. 17). Surface leMons llfl'c lrt•m the cout~r surlace t>f the <:oJ1~>. (e.g. stufacc hi!Ut-gnuk t"-tcoo,;.ucoma). j uxlacof/tcal/esiolls (l'ig.•. 5. 18 and 5.19) ciln he divickd mto (l>etht•'c <>ngmatmg from the deep layer t>f the p.rio!.leum m,..tcall •.,.ions) and thow de rhcd lrt>ln the tlUI~r la)Cr ol the !'(!fit"lcum and gr~ming in an exoph~1il pattern (paro>teal 'I} P•"al c>.ampl"' of .tuxla<'(>riJcal 1..'!-Jt•ll> indu& k.,.wr" I th• JMi< teal <"'lrol'llrcoma and part"kal <'<'lrol'llrcoma (lahh: ~ .9)
Table 5.8 lesions
Common location of tubular bone
Eptphyses cyFI (a.,..'
Suhdtmldral trauma)
(1111 r4u~M.·t~tl.'
11 itb
arlhntO.. '"""""''""'~
lnphlL')
. \m}l•·•tl•·'" l nt mn1-"'CC 1 ll~
g.lllt.:llnn
Intta l)S..'-'.:tlLL'
hrx~ma
<.lwJKin•Narl:u.ia q·iph)~calos hcmimchcn (I rc"'•'• t1J-.'.l-
m
llld.>.J•Il)~J')
Clear ce U chontlro&'IK()fll3 ~ldastasJS
llrt'tl"''
allKl.~
Metaphyses S1mplc (uni
bone cy"l
bt.li MJ C)~t
( ~,._,""-·ltondroJ Jla
<.1lC>ndrNn) ~o•d l\:rit~..:zt1
hl>rl'nl3
d""'IIWid
1\
IA.-..m<·rlm.uc
lll>rom,,
T'tlluo.:tf<'OIIIll
l\laltgn.lllt libwl'' ht,ll<..:) toma <. hondn"'3fcmna (~kut•HI~o.~ltlla
f\lcttt..,lii'IS
(J!;tcomycl• t.-
BJodi.", "'"~C"" I ihn~w~ t.l~~pJ.a,ia Dlametaphysls Si•·•rl• (unicztMnl) hone C)-.t (in rulull•) lntraus..-cous
hi'<Xtlll
f J'k.'il•ulnltn:t
Table 5.7 Expansile osteolytic lesion with cortical violation .\no.;u";m a l h<>JJC C)'l (cccclllric)
1\..'Tit»o.t'-.tl dtuudn•tna l\t•ru,~if\·u1)'
():...tL.'tltd
IJ 'idu nu•itl indu,ion c:y ' ' ( ihnnus htnwr
llcJnangJ<•IIllt
t.lSI..,'t.'ma
<>-k•~'""lt>ma <~"'P•=<·iall)
1\dam.mi iiK'lJlla
('l ull)
Chtmdront)'X<•id I )..""Jnopl....atc
fihttlrrta
ll<•JM.' ,, )anti
ankriN
tUn~)
IJhrt>s.~r«>tl~t
libruma (<'nuJIJi<)
t.lalttnant lii'INL' histi<X)10
libR•nta
( ),,.:
\nt,'lO!iateoma
Multipk OJ)doma t.lda.U.~L'
1\t.•li~;nant
hl>rl>tl' hi.,tioc)toma
(.' h( ·ndtt)~an.·(\llle:t
I ~n1rhorn"
I ang.. rhans ..:dl lush<'14.~10~i!' (co~in<-~phil i ..· gntrull<~tno.t)
Brown """'" (h} pcqmmthyrotlli>m) I kmt•ph•h•• t"Cthl<'lumor
• \nt;H~:\ri,.'Clf1H1
l'ln.-Joa.:} lom3/rnullipk l'.ld" ln.
<>-kt•llOis m~d<•JO:t
(In 111 l.rdnc). th~n••d. hm!J)
I k11101~"""' P'<'\ldotumor
(hone inf.,.'CI)
(),t,~·ltl\ditis
bbmus
hl..•l!
d ) "J'Ia•ta (C"JX'Ci.tll) :UlknN 1•1'1")
.,
5 localized Bone le!>ions The knowledge ot the age ofa porienr rs fundamental to the correct mterpretatlon of any bone lesron. Moq bemgn symptomatic bone tumors are d iagnosed m patients below the age of 30 yea rs. Asymptomatic benign bonE' lesrons are however a frequent mcidental fi nding at .my age. Primary malignant bone t umors m children and adole~cents usually consrst of osteosarcomas and Ewing's sarcomas. Neoplasms typrcally dragnoscd between the age of 20 and 40 years include grant cell t umors. parosteal sarcomas and adamantlmomas. Symptomat ic bone tumors d iagnosed a t the age of 40 years and older must be conside red malignant untrl pro ven otherwrse with the vast ma)onty bemg erther metastases. lymphoma or multiple myeloma. The d rflerentral d iagnosrs of localized bone lesions rs drscussed m Table S. l O
Tabl•
~
81
Fig. 5. 17 Cortical lesions. Multiple osteolytic le .rom are seen within the cortex of the tibia. The largest k>sron has e~ended from the corte~ into the medullary Sp.lle .md o~djacent soft tis~ue (metastases from bronchogenic carcrnoma).
9 C. rtical lesions
Localized elliptical cortical thickening Osteord o•.tt>oma o~tcornychti~ Stre<~
(lhromc)
fractvre
loahzt'd dt>fKt of •xtemal cortl'x
r '
.te'
<'
• •'
I'
'!t.rvmedial a•peet of dr~taf femur)
f rbrorn.Jtosrs Ado~mar
unoma
(~pt.'Crdlly
antcnor trbla)
Osteofrbrous clysplasia (t>specially antenor tihra) Ewmg'\ ~rcoma Metastasis (especially from bronchogenic carcinoma) Hyperpo~rathyroldi~m
lndudrng brown tUITlOf'
Gouty tophus
Fig. 5. 18 Juxtacortlcal le· slon. A defect (arrow) wrth
minimal punctate matrix cal· cifications i~ ~ren 1n the outf'r cortex of the proxim.JI humerus surrounded by penosteal new bone formation (periosteal Uuxtacortrcal) chondroma).
Adjact>nl soft trssue nE'Oplasm or a~e~~ Subperio~teal
osteomyelitis
'>ubpenoste.al hl?mdtoma AvtJision fra
Juxtacortical tumors and tumor-Ilk• lesions Parost""'' lipon sis
.1 (mo~y
rnduce cortical thic kt>nrng or hyperosto-
PdrU)lt'.JI hcmangrorna (may induce cortical thrckening or hy· perostosis Osteoma Osteochondroma Pt>nostcal ou~tacortrcal) chondroma Bizdrre parmtl'al osteochondromatous prolrfcratron (BPOP) Pcnosteal u~tO!cortlcal) de
Parosteal myos1tls os~lflcans Spurs (congenrtal, post traumatic) Enthewpathy OsteophytOSIS
Fig. 5.19 Juxtacortl· cal lesion. An ossifoed mass With adja(t>nt cortical tht< kt>ning i~ seen in the po~terior aspect of the drstdl femur (paro~tt>al mt~rcoma).
82
Bone
Table 5.10 Localized bone lesions Dlseas.-
ll~phit
Subchonclf-al cyst (Fig. 5.20)
Solit 1r1 CJ mt.lbple deft'Ch rnea~uring up to 3 em in di- As~1ated with osteoarthnt•s. cakium pyrophosphate aml.'ter with sclerotic border located in the subchondral dihydrate crystal depcxitK>n disease (CPPD). bone (pressure segment) of a jomt. Communication osteollt'Crosis (ilVaSCIJiar necrosis) and rheumatoid arwith JOint may be prC$Cnt occasionally allowing gas to thritis). pa~s mto the cyst (pneumatocyst). Traumatic C)"its are the sequela of a bone InJury, but may be larger and not necessarily associated with an arthritic proce-.s.
lntraosseous
Unilocular or mult,loct.lar. well-defnwd lytic epiphyseal lesion. oftm With sclerotic margin. The lesion does not communiCate with the adjacent joint. Preferred loca· tions are the med•al O'ldlleolus of the tibia, femoral head, acetabulum and carpal bones.
A hernlotKJn p.t (fi
Ctf'ltrdlly l<>
Asymptomatic uniP\\ fro~cturE'd. Usually d•agnosed before the age of 10 years wrth a 3:1 O'ldle predomi· nance. After that age bone cysts tend to appear rr10re often in flat bones such as pelvis or calc.meus. Echinococcol (hydatid) cyst\ o~re found in 1% of ~nfected patients presenting with single or multiple el(pansile cystic lesions ("bunch of grapes") preferentially located in the pelvis and sacrum.
ganglion (F"tg. 5.21)
Simple (unlc.lmet""al) bone
cyst (Figs. 5.23. 5.24 and 5.25)
finclngs
Comments
Aneurysmal
Presents most commonly as an t'Ccentric, expansile o.teolytk lesron With mt.Jct or d1srupted cortex 1n the (Figs. 5.26 and netcJphysls of " long tubular bone. Extensive sclerosis t the interface between normal and expanded cortex 5.27) ("buttressing") may be present. Delicate thin trabeculatiOn is ch.aractenstic and an e)pansde ballooning lesion may produce a ·soap-bubble" appearance. Other com· mon locat1ons rnclude the pcxterior elements ot the ~ne and the peMs. v.tlere a large soft t~sue compooPnt 0'\dy s•mulate a malignancy.
bone cyst
Pnmary le~•ons are usually dragnosed Ill the first. St'C· ond or less frequently third decades of lrfe with slight female predominance. St'Condary aneurysmal bone cysts (20%) are found in grant cell tumors and less frequently in osteoblastomas, Simple bone cysts, non· ossifying fibromas. teleangrectOJtK osteosarcomas, metastases. ftbrous dysplasra. Paget's disease. and others.
(continuet on pof)f! 84)
Fig. 5.20 Subchondral cyst. Oegeneratrve changes with a large subchondral cystiC lesiOn with sclerotic margin is seen in the medial tibia plateau
flq. 5.21 lntraosseou s ganglion. A smdll cystic lesion (arrows) With slightly sclerotic margin is seen in the medial malleolus In the absence of arthrit•s in the ankle.
5 I ocali7ed Bone lesions
83
Fig 5.22 Herniation pit. A cystiC lesion (arrow) with sclerotic margin os seen in the anterolateral aspect of the femoral neck.
I ig. 5.23 Simple (unicameral) bone cyst. A sep· tated osteolytic lesoon with cortocal thonnong os seen on the calcaneus
Fig. 5.24 Simple (unicameral) bone cyst. A multiloculated cystoc lesion with expanded cortex is seen on the humerus.
I ig 5.25 Simple (unicameral) bone cyst with fallen fragment sign. A cystic lesion with pathologoc fracture and a linE-ar dense frJgment at the bottom of the cyst is seen in the proximal humerus
Fig. 5.26 Aneurysmal bone cyst. An eccentric osteolytoc lesoon is seen in the pmxirndl tibia abutting the open physis.
Aneurysmal bone cyst An E>xp.m~oiE> trdbeculated oppE>arance 1\ ~l't'n origonatosteolytoc lesoon woth roap.tx. bl ing rrom the gredter trO<.hdllteo.
Fig. 5.27
84
Bone
Tablt'
5 10 (Cont.) loollzed bone lEsions
Disease
Radfoo¥aptuc Fmdlngs
Comments
Epid«moid (lndusion cyst) Rgs. 5.28 and 5.29)
h l•oJO :..~ul It: iun prL'Senh a~ welt-defined o~teol)•tic defect. often Wtth ~!erotic margin. occurring in the lf'rminal phalanx of th£> hand or rn the ~kult. Tht> lesion may be expam1le With thinning or destruction of the cortell. Sk~olllc\lon~ u~u<1lly mc.,~ure 1 to 5 em in drameter and m.1y be limrted to the diploic space or t>xlf'nd thro11gh ont> or both tab~ . All 1m'9ularly shap«:t button sequestrum 1s usually present in larger skull lesions.
lliuLIIy dld<JilO «! in the second to foorth decades of life with slight mal(' prl•dominanle. A h•story of trauma is often present suggest1ng 1ntraosseous implantation of ectodermal trssue w1th ~u~N'quent clevelopment of an epidcllll04d. The lt.~10n ~lined with c1 stratrfled squamous ep1thdtum shedding keratin clebris th.Jt breJks clov.n and forms cho~terol.
Glomus tumor
lntraosseous glomus tumor presents as a well-defined >\teolytrc lesron rn the term1nal phalanges of the hand lndistinguishJble from an epidermoid on plain film radiography. Drfferentiat1on rs however possible with MR im.191ng, whert> the glomus tumor depicts marked contrast enhancement. often with characteristic "salt and pepper" -'Pflt'clrance.
Glomus tumors occur in patents of any age, typtcally arc netther palpable nor v1slble and present 1n f1nger· t1ps with ach1ng pain and point tenderness. Secondary bone Involvement from a soft tissue glomus tumor is much more common (e.g. temporal bone). In th«.> hand such a le~ton presents as shallow. well-marg1· nated erosion 1n the .ldJ.tcent bone, usually 1n the tuft of a terminal phaldnx..
lipoma (Fig. 5.30)
Wl'll·circumc;crib«.>d osteolytk lesion. often surrounded by a sclerotic border. Irregular thrck bony ridges are fre(juenlly found rn larger lesions. May conta1n a cen· tral cakificd nidus (especially in the calcaneus). De· monstration of fc1tty tissue within the lesion by either CT or MR imaqing is virtually d1agnostic
Besides the calcaneus rntr.tosscous ltpoma occur most commonly in the metaphyses of lof19 tubular bones. especially the fl'mur, t1b1d dnd frbuld. A relatively typi· cal location of larger lipomas is the femoral neck abut· ting the intertrochanteric: line. In this loco~tion they resemblt> f1brou\ dy\plasla Lrposorcomos rdrl·ly o~me 1n bone.
Liposcl«osing myxofibroma (Uposcleroslng myxofibrous tumor. L5FMT) Fig. 5 .31
Well clefincd lytrc or "ground glass· lesion, often with markedly sclerotic-border occumng typically (80%) in .he pretroch.mterrc and intertrochc!nteric rpgion of the prox1mal femur. Fat is not always demonstrated with either CT or MRI
Rare benrgn lesion commonly d1agnos«< as Incidental f•nding 01' presenting With patn 1n patrents between 20 and 70 years of age. Malignant transformation occurs in less than 10lt of ca~. May be a vanant of fibrous ~plasia or rf'present a bumed oot or infarcted in· traosseous hporna (continues on page 86)
a
b Epidermoid (indu~on cyst) All t>xpano;rle osteo\ion ~~ v ·n the: d1~tcll ph IMIX of the thumb.
Fig. 5.28a. b lyt~ ~
Fig. 5.29 Epidermoid (inclusion cyst) All Irregular osteolytic lesioo v.ith sltghtly bt.~ led margin 1s ~n 1 the vault of the skull.
5 localized Bone Lesions
85
a b
Fig S.JOa. b Upoma (2 cases). An osteolyti<. lesion in the c.alcaneus contaming a small central calc1f1ed n1dus (representing fat necrosis) is virtually diagnostic (.a). Awell-circumscribed osteolytic lesion with sclerotic border dnd irrt'gulctr thick trabeculation in the
femoral neck abutting th!! intcrtrod1d11tenc line IS quite charac teristic (b). The demonstr.Jlion of f.Jtty content by either CT or MRI differentiates this le~ion from hbrous dysplasia.
Fig 5 31 liposderosing myxofribroma round les1on w1th sclerotiC marq1n seen m the pretrochanteric. reg1on of tilt' prox1mallema~r (arrow)
IS
86
Bone
Table 5.10 (Cont.) localized bone lesions Disease
R~lographlc
Hemang•o~
'ipm,. ( c ~ llt'rtinl trabecular pattern ("corduroy" appearance) m the vertebral 00. die\ 1\ ch.aracten\IIC. Diameter of thickened vertiCal trabewlac i~ rather umform (00: Mul· t1plc myeloma. meta~ta~s and Paget's d•sea~. whiCh mcl}' prPsent With irrPgular coarse trabecular thlckeolng). Extension into the postt'IK>r elemt'nb. p.1ra~r\CII tis~~. and~ nal canal i~ rare. Skull. 5hghtly expansde o~teolytic lesion with rad•atlng ( 'sunbu1st") pattern. Tubulor bont><": Poorly defined osteolytic lesion With •atti e hkc trabecular pattern.
Usuall) fOl.nd en pat tents over 40 ~ars of age with female pre· dominance. OccasiOnally non Hodgkin's lymphoma (espcciaUy the hi~tincytec type) and mo•a,ta~s (e.g. brt>ast caronoma) may SIIT'Uiate a hcrflCir- orr m the spine. Cystic onqlomatom (I eq. 35 ts haractertzed by Widespread cystiC ~1oos often ~um -1 y a nm of sclt>ro~1s. They IT'ay progress to osteosclerotiC tC)ton) simulating metastases. The cond1tioo is freque1 tly associated With widespread vtsceral in\'Oivernent. Cystic lymphongiomotosis pr~nts en a simtlar fashion. Accumulation of contrast material in bions during lymphography IS di· agnostic.
Bony protuberance demonstratmg cortical and 1 1t>dull.11y wllhi1Uity v.1th parent bone IS diagnostic in the tubular bones. The lesion may be pedunculatt.-d (with na11ow stalk and bulbous tip) or sessile (with a broad, flat base). Osteothondromas characteristi<:ally originate from the met.1phy~s and point away from the nearby articulation. The tip of the osteochondroma is coverE'd by a hyalene cartilage cap that may contain regular ~tippled cakificallon\. A lc1rge CcJrtil<~ginous cap containing Ifregular cak•firat1oos i~ suspicious of malignant trc1nsformation. Osteochondromas In the pelvis frequently are l.nge .md diffiCult to differentiate from lesions th.lt have undcrgooc malignant transformatiOn. In the ribs osteochondromas frequently occur at the costochondral junction. MahgMnt transformation may be best assessed with MR imaging A cartilage cap of 1 em or less 1n thiCkness ondicates a bffiign lesion. wherPas a cap thiCker thffi 2 em IS suspicious for malignant transformatloo.
Osteochondromas occur In children and adolescents as a sk>wiy grO\ving painless m.m. They .ue entnnately lt'lated to the physis and ct'ase to enlarge with fus1on of the adjacent growth plates. Rarely osteochondromas may develop in the adult after trauma. 00: 1. Subungual exostosis (rig. 5.38) projcch from the dor· somcdial aspect of the tuft, usually of the great toe (80%) or other distal phalanges of the foot 01 hand. 2. Reactive bony excrescence in mcd•al portion of base of distal phalanx of great toe (normal variant). 3. Turret exostosis arises on dorsal surface of proximal or middle phalanx 1n a f1nger (post-traumat1c). 4. Svprocondylor process of humerus (f1g. 5.39): Spur orig•nating from the dnteromt'd•dl dSJM'C t ()f tiM' d1\t"l hun rus pointing towards the elbov.r (ptl)'logenctK vestige) 5. Pes ansermus spur may mmliC a small osteochondroma in the medial aspect of the proxim.JI tibia (enthcsophyte. occasionally associated v.tth an~rinus b~itis). 6. Ptnt-troumotic spurs secondary to healed avulsion fractur~. 7. "Tug" lesions at tcndtnous attil"h"""n' "tes 1n the lower extremity. Hereditary multtple exostoses (fig ' 40) Pf•~nt wlth mult1ple, usually bilateral and symmetric ostPCton awv"'tt-d W1th bone modeling deformities. In metochondromotoSis (ftc; ; 41 ) r 1ultiple osteochondromas and eochoodrorllCIS COCXISt Spt. ily Ill the hand• and feet.
(Figs. 5.32. 5 .33
Osteochondroma (Figs. 5.36 and 5.37)
Findings
Comments
(continues on page 88) Fig. 5.32 Heman· qloma. A rather uniform coar~ llt'rtical striation pattern ("corduroy" appearance) seen in the vertebral body of L4 is virtually diagnostic
Fig. 5.33 Hemangioma A slightly expansile lesion w1th margiMI sclerosis and charactenstiC radiatang bony spicules within the lesion is seen in the vault of the skull.
5 Locali7ed Bone lesions
87
Fog. 5.34 a , b Hemangioma (2 ldW\). A poorly ddined osteolytoc lesion (•!rrOW'i) woth loJtticc like troJbecular pattt>m is seen in the o•.chiatoc ramto\ (a ) ;tnd prmumal tibia (b )
a
b
fig. 5 36 Osteochondroma (pedunculated). A bony pro tubcrance demonstratong cortkdl and medullary continuity with the tibia and pointing away from the knee i\ charactf'fl\tJC.
Hg. 5.35 Cystic angiomatosis Multiple well demo~rcated osteolytoc lt>soons surrounded by ~clt'fosos are seen in the pelvis and lJpper ft>mur.
Hg. 5.37 Osteochondroma (sessile). A broad based bony outgrowth from the lt>\ser trochanter with calc1f1ed cartilage cap 1~ wen. Th1s lesion cannot be differentiated from a lowgrade penpheral chondrosarcoma.
Fig. 5 38 Subungual exostosis. An lrregul.n bone protubeli!I1CP onglndtcs from the dor~omcdii!l as pet t of the tuft of the grci!t toe.
88
Bone
lable 5 10 (Cont.) L.JC h1rif
~ ~'flt
1, sk m
Disease
Radio.,r~k
Dysplasia epiphysealis hemlmelica (Trevor's dis· ease) (fig. 5.42)
lobulated ~~ecx , .nass (artiCular chondroma) protrudmg from an epiphysis. carpal Of tar~al bone. Prewnts il'lltially in infants as Irregular oss1fice~tl0fls adjacent to the involwd bont>. Preferential involvement of the medial side of a lower extremity (e.g distal femur. prox1· mal and distal t1hia and talu\). Multiple bones in a single extremity are aflt'cted 10 two-thirds of cases.
f tndln._s
Enchondroma Well-circumscribed. oftl'n lobulatE-d. osteolytic le'>ion (figs. 5.43 and with e~teal scalloping composed of hyaline· type 5.44) cartilage With varymg degrees of cakif1cations. Preferred locations are the metdphy~!> of the long tubulcJr bones and the dl.lphyses in the short tubular bones of the hands and feet. CortiCal expan~ion and patholoq1c fractures are frequent f1nd1ngs 1n the hands and feet. but malignant tr andormat1on IS very rare in tht>\C locations. Transformation to chondrosarcoma in the long tubular and flat bol'e\ should be suspected w1th an en· larging radiolucent area, the disappearance of pre-existing calcifications or pat! ologic fracture.
Comments
------------------
Prt-\t'l ts 1n tholdren and young adulh w1th swell1ng. pain and deformity localized to one s1de of the body.
Fnd01ninantly involvmg one side of the body. The affected bones often are shortened and deformed. After ce~~ation of growth the ll.'sion no longer increases in size unle~s malignant transformation has taken place. t-stimated lo occur in 5 to 30% of pat1ents. Moffuccn syndrome (fig. 5 47) con\l)ts of mull1ple enchondlomas dnd soft tissue hemangiomas containing mult1plt> phleboliths. (contilltJt'S
fig. 5 39 Supracondylar process A spur IS seen originating from the anteromedial aspect of the d1stal humerus and pointing towards the
elbow
on page 90)
F~g. 5 40 Hereditary multiple exostoses 8f'Sides mult1plt> osteochondromas modt'llng deformities In both the proxomal and distal radiu~ c1nd ulna are also evident .
5 Locali1ed Bone Lesions
89
Ftg. 5.42 Dysplasia epiphysealis hemimefiu (Trevor's disease). An enla1ged medial malk"OIU\ with an irreqular. lobulated and parttalty calofted mass in tl~ ttp ~~ \een. Calofted les~ons are alw present m the medtal aspect of the talu\ and navtcular bone.
Ftg 5.41 Metachondromatosis Multtple enc:hondromas are seen in the hand.
~teochondromas
ftg. 5 43
and
Enchon-
droma A lesion contatntng nocculent. punctate and c1rcular cakifiCations is seen in the proximal humerus. An old avulSIOn fracture of the grt:>atcr tuberostty IS 1ncidentalty also present.
r.g
5.44 Enchondr-oma An Pxpansile I 1()0 wtth sl,ghtty \Cieroti<. margin and fatnt matnx calctftcation is st>en tn the middlt> phc1Llnx of the thrrd frnger. ~teolyt <.
90
Bone
Table 5.10 (Cont.) Localized bone lesions Racllographk Findings Cak,,f, ~(50 , soft tim.e m.ass with erosion of the ad· Periosteal Ouxtacortlcal) JdCent cortex al'd val)ing d~rt>e cl periostitis. Meta[lt¥es of long bones .and h.ands are most comchondr~ (Figs. 5.48 Mld rronly affec.ted. 5.49) Bizarre
parosteill osteochondroma taus pro-
Comments
AJ .ag< o~re affec.ted but the tumor is usu.ally diagnosed under age 30. Slight male predomltl
Well-margonatfsde or pedunculated mass or heter>toplc ossofoCdtoon aoslng from the cortical surface wothout medullary continuity between the lesion and the adjacent bone is characteristic.
Occu•s usudlly on tl•e hanch and ft>et (occasiono~lly on long tubulo~r boocs) Without age and sex predtlec.tion. A history of trauma is t:\lldent in some pdtocnts.
Well-defined, often lobulated lytic lesion ill\/Oiving the
Benign cartilaginous lesion occurring between the ages of 5 and 25 years w1th slight male predomonance.
liferation (BPOP) (Fig. 5.50) Chondroblas
~physis or apophysis of a long tubular bone with or toma (Figs. 5 .51 and without thin sclerotic border and matrix calcification ( • 50%) Is characteristic. A sohd periosteal react1on in 5.52) the adJacent metaphyseal shaft can be induced by
bone m.arrow edema sunounclinq the lesion. Appro:~~!· mately 10% or chondroblc1stomas occur in the hands and feet with predilection for the talus and calcaneus.
(continues on page 92}
Fog. 5.46 E11chondro matosls (Oilier' s disease) Multiple en· chondromas art associated with severe modchng deformities in the dtstal fem ur. tibia and fibula.
Fog S 45 Enchondromatosls (Oilier' s diwase) Mu ltiple ench "d '"s .are \~r r tl ~ hand spa 1ng the thumb a nd distal ph.a•o. -9'<:>·
5 Localized Bone Le~ions
91
F1g. 5.48 Periosteal ijuxtacortlcal) chondroma A corti< i!l df feet with surrounding sdt>r~•s and adjacent soft lls!>U! tcllcific.ations (c~rrow) is seen in the first mc·tacarpal bone.
Fig. 5.47 Maffuctrs syndrome. Multiple en
F.g 5 49 Periosteal (Julltacortical) chondroma An PC<E'ntrK osteolytiC lesion v.1tl sclerotic:. margin. buttresso11g (arrow), and faint matnx cale~focoJtions is set=n in the proximal fibula.
Fiq. 5.50 Bizarre parosteal osteochondromatous proliferation (BPOP) A · mushroom c.c~p· like ossified mc~ss (<mow) ari\ing from the dinar aspect of the first metatarsal bone is seen.
Fig. 5.51 Chondro· blastoma. A slightly lobulated osteolytiC les100 Wlth famt matrix cak1f1cation is seen in the humeral hc.td. A wlid peri· osteal rcJction (arrow) and shght dol· fuse 'iCIPfO\IS of thE' metcJpi'}'SIS adJiKffit to the luion is also evident.
F.g. 5.52 Chondroblastoma A lytrc lesoon v.1th sclcrotrc margin and matnx cakrf1Cat10n s... •n 10 tl < trp of tht> grt>ateo tubt'rosrty.
IS
92
Bone
Table 5.10 (Cont.) Localized bone lesions Radiographic n ndings
Comments
[ccentric met<J~ .yscal osteolytic les100 wrth cortical e · pansion, coarse tralx!culation, endosteal scalloping and scalloped sclerotic medullary border is commonly wen. Destruction of the cortex re lowt>r eKtrernity. but occasiooally also found in pt'lvi~ and foot.
Lnt. .. unon benign cartilaginous lesion occurring between the ages of 5 and 25 years v.1th sltght malt' predomrnance and presenting wrth ~lowly proqressrve pdtn, tenderness, swelling and re~tnttion of mot10n is typicdl FibrocortilogenotJs mt>Senchymomo is a very rare )Olttary cxpdn~ile osteolytic lesion wrth spotty or ring like calci fications, cortical destruction and roft tissue invasron ongoNtrng most oftpn in the metaphysis of long tubu· tar bones. Age distribution is similar to chondromyxoid fibroma.
Saucer-like defect rn the posteromedral cortt'K of tho d"tal femur often a\soci.'lted with adjacent sclero periostrtt\ and roft·tiSsue swrlltng.
O
Nonossifylng fibroma (Figs. 5.55, 5.56 and 5.57)
Sm.llllesions prt>scnt as round or oblong, well delineated, radiolucent areas on the cortex with normal or sclt>rotic adjacent bone. They typically arise in the metaphysis at a ~hort distance from tht' physis. larger lesions presPnt as a wPII delint>ated. eccentric. ovoid osteolytiC area rn the diametaphyses. They frpquently have a multiloculated ap~arance and both cortiCal expansion and thnmng may be evident. The long tul>1.1lar bones, ~peci.Jify the trbia and lemur. art' most frequently affected. Wtth ltmt' tht' lesion\ md}' spontaneously dt~dppt>ar or become sclerotrc
Usually di.:~gnoscd in patients under the age of 20. Smellier IC'siOOs are referred to as benign fibrous cortical dcfrcts. They are asymptomatic and doo~gno~d as rn· cidE'ntal finding on routine radiography and occasionally are multifocal. They usually r('()rt'\~ spontaneously or IP\\ commonly t>nlarge and migrate wrth growth into the diaphyses eventually berng r£>fened to a~ rtOnossrfying frbromas. Pathologic frc1ctur~ 10 larger lesions arE' 1101 uncommon. Joffe-Componocci synd~ consists of multiple nonossrfying fibromas associated with c fC.o~u.lcJit spots. mental rt:tardation and hypogonadis'l Benign fibrous histiocytomas (Fig. 5.58 e histologically identical to nor10ssifying fibrom..,, but present as shghtly more .aggressive lesions in patients over age 20 without srte predilection.
Desmoplastic fibromil (F"tg. 5 .59)
Ct>ntral osteolytic lesion with trabeculatt'd, soap bubblt' Rclre benrgn neoplasm occurnng 111 the ~cwrld or third or honeycomb pattern in the metaphyses of long tubu- dC'Cades of life. Pain and swelling are tilt' leading cllni· cal symptoms or a pathologo<. lr.Jxpansion with t'ndostPal t'rosion and ltmrted periosteal bone for- \l.'flting feature. matiOn may be assocrclted.
Chondromy xold filwoma (ftg. 5 .53)
....
~
(juxtac:ortical) d.smotd (Fig. 5 .54)
(contmun on page 94)
fig. 5. 54 Periosteal (jux· tacortkal) desmoid. A saucer-like defect in the postE'romedial cortex of the distal femur wrth ad1acent sclero~s rn a child vo.ith unfu!>Cd physis is virtually dtJgnostic.
Fig. 5.53 Chondromyxold fibroma. Atl expansile eccentric osteolytic lesion with irrt'C)ular trabt'culation. drswlved cortex. and scalloped ~lt'rotrc medullary border is seen in the disto~i femur metaphysis.
5 Localized Bone Lesions r.g. 5 55 Nononifylng fibroma A sl.ghtly oblong ec centrir l(";iofl With multdoculated appearance cmd Klerotk mdrgtn ~~ ~t'n tn the di\tal femur metapl,~i~.
fig. 5.57 Nonosslfylng fibroma (he.~led) An oblong eccentric sclcrotrc focus ts seen m the dtstal ttbta.
a F.g. 5 59 a , b Desmoplastic fibroma (2 cases) A central. relat"' ly poorly dt>fti'V'd. slightly expansrle o~teolyt1c lt>\ton with
93
Fig. 5.56 Nonosslfylng fl broma. A large oblong t":Ct'n
tnc ostrolyttC l(";ion v.rth S<.o.,-roti< margin and pc!thologk frc~<.ture 1~ ~~~ rn the distal tibia.
ftg. 5.58 Benign fibrous histiocytoma A central in tramedullary les1on woth Klerotic marg1n and trabecu latroo 1s seen 1n the prox1~l humerus \haft.
b honeycombrng and surroundrng ne"" bone formatron Is see11 in thl' superior pubrc ramu\ ,,nd body of both patients.
94
Bone
Table 5.10 (Cont.) Localized bon.> I luns Disease
Radiogr.,hk Findings
Comments
Bone Island (enostosis) (figs. 5.60 and 5.61)
Single or mult1ple intraosseou~ foci of homogeneously bone most often found in the pl'lvis. proximal femurs and spllle. They may be round, ovoid or oblong ~nd arl.' aligned with thl.' long axas of the trabecular ar· chitecture. I any bone spKuk>s rad1at10g from the pe· nphery of the lt>Ston are QUite characten\tK A somewhat radiolucl.'r't center may occas•onally be enCetlntered. Range on ~11e from a few millimeter~ to d few .ent•meters.
Incidental find1ng in all age groups. Lesion~ mc~y ,lowly increasE' or dt>crPdSE' In si/E' over years. BonE' scint()9raphy 1s usually ncgatt~. (DO: osteoblastic metcl\tdst><.). A rurettogpd and mt'lhylmethocrylatt' ct'mf.'ntt'd bone leSIOfl may re<;emble a large enostos1s. Ostropo;lalos1s: Numerous small sclerotic foc1 With sym· metric d1Stribut100 m penart•culaf locations.
Osteoma (Fig. 5.62)
Mau of either uniformly dense compact bone or less deose cancellous bone protruding from the skull and rac1al bones (t>Specially the paranasal ~nuses). RarE>Iy osteomas .mse from the cortKal surface of the clavicle, pelvis .md tubular bones.
Gordner's syndromf.': Autosomal dominant disease consisting of multiple osteomas. colonic polyposh and ~oft tissue tumors (especially desmoids). Tuberous sckrosrs: Mult1ple osteoma-like I~ ions may be associJted, espec•ally 10 the mE>tacarpals and metatar-
Osteoid
Cortical radio!• "'!fll k>sion (mdus) measuring less t han 1 em in diameter \UI· rounded by a zone of unifo•m bone sclerosis (elhptic.al th1t kt'ning of the cortex) is virtually diagnostic Tht: nidus Is not alwd}'S Identified With plain film radiogra· phy and occasionally has a cakoficd center. lntra-ortKulor location: A nonconsp1cuous small radiolucent focus often without significant reactive sclerosis may be nr"Sent inducing a synovial inflammatory response tl1.1t may result in secondary artlvitic changes. Carpal ond tarsol bones. A p.Jrti<~lly or completely cal· cified les1on without or only mild reactive sclerosis is charilt tt.-ristic. Spine: Art osteosclerotic focus in the posterior elements is the most common presentat•on. A scoliotic deform· ity is usually associated with the leSIOn and •s located near •ts .lpel< on the concave s•dE.' of the curve.
Occurs in patienh betw~en 7 and 25 years of age w1th a male predomin. Ke of 3 to 1. Pain i~ the hallmark of the disease, usually more d 1amatic at night and .Jmel· iorated by aspirin. Bone scintigraphy shows .Jn unusual intense uptake in the center of the IE.'Sion (nidus) differ· cntiating ol from chron•c. cortKal osteom)-chtis w1th small abscess formation. Localized cortical thicl<ening uuSf'd by a stress fracturE' typically is assoctated With a transverse linear radiolucency In the lumbar spine a unilateral osteosderotK focus about a pedicle IS frequently caused by a hypertro phied intra-articular pars caused by uniloterol spondy/y· sis of the contralateral side.
den~e
sal~.
osteoma (Figs. 5.63, 5.64, 5 .65, 5.66 and 5.67)
Diop/¥1~
of long tubular
~:
(continu~
on poge 96)
Fig. 5.60 Enostosis (large bone Island) An osteoblastic lesiOn with tiny bone spicules radiating from ih pt.-nphery is seen in the proximal humerus metaphys•s.
fig. 5.61 Enostosis (large bone is land ). An trrt.-gular shaped large o~teoblastic le~ion with rT'inlmally spiculated bordef is ~n in the tlium.
5 localized Bone lesions Fig. 5.62 Osteoma A slight!}' lohulatf'd dense .e mdSS ~~ seen protrud1ng 1nto the frontdl sinus.
oo
95
Fi'j ~ 63 Osteoid osteoma ll· l1pt1c ,,I cortecal thlckenmg s se- '11 m tht· l<'mur shaft. The nidus is not idt>nt1hed 1n this case w1th convt:ntloncll film radiography.
Osteoid osteoma. An expan· sile cortical lesion (arrow) with only min· imal surrounding sclerosis is seen in the prov1mal phalanx of the index flng<'r.
Fig. 5.64
f1q. 5.66 Osteoid osteoma. An ost('()S· clcrotic focus (clrrows) IS ~n in the left postcoor clements of L1 located at the apex on the concave side of the assoceated mild scoliosis.
fig. 5 65 Osteoid osteoma. An osteolytic lesion (arrows) weth calc1hed center (tcJrget lesion) 1s seen in tht: lateral cune1form that depiCts an OYerall slight incr~ase in dl'n\ity w1th the exceptiOn of its laterell clnd d1st.!l cl)pt:lt
96
Bone
Table 5.10 (Cont.) localized bone lesions Fi~
Disease
Radeographk
Osteoblastoma Figs. 5.68 and
l.onq tubular bones:
5.69)
Giant cell tumor (Figs. 5.70 and 5.71)
Comments
Usuo~ll).- diagnosed in the second and third decades o f life with a malt! predomrnance of 2 to 1 and similar rn Prther the medullary or cortrcal bone of the diaphy· ~~~ and Pfe~nt as expan~ile osteolytic lesions oltl'n clinical presentatron as in osteoid ostromas. with areas of calcification or ossifrcation. surrounding The size of the n1du\ (actual si7e of the ost('olyt1c lebone sclerosis and frequently l'xuberant ~lid periosteal s.ion) may be used to diff('rentiate bet....een rll.teobldsreactiOn. tornas (>2 em) .Jnd ~tro1d ~tromas (; A well·delined exparnrle ~tedytK les~on that Is Aggressive (mo/ignont} osteoblostomos .Jre d1Ht>rentlc!ted p.1rtially or extensively cakrhl'd and surrounded by from the t)pical (COfli!PntioooJI) osteoblastOfnas by a mrld \clerosis at best. 1s commonly found rn the poste- more aggressive pnts. much greater likelihood to recur. The radioloyK feel Hands, feet and pelvis: Shghtly expansile lytic lesions tures of both typt.'S ;nc similclr, but cortical violation with 11arying degrees of m.1tnx calcificationfossificatron with t omor extl'nston into the neighbonng soft tissues and surrounding reassrve osteoblastomas. mon presentation
In thP long tobtJlar bones (85 %) a giant cell tumor prPPnts as an eccentric expc~nsile ostcolytK. lesion, oftt.'fl with a deh'-dte trabecular pattern ("soap bubble" ap· pcar.Jnce) extending from the mt'taphysis into the sub· chondr.1l bone. The margins of the lesion may be w(•ll or poorl) defined, but sclerosis and periosteal reactions art> typtcally absent. Cortical breakthroogh with spread into the adJacent soft tissues occurs. Occasionally the tumor rs found '" pel111s, ~crum. nbs. vertebral bodies. h
Occurs usually in the third and fourth deudes of life wrth equal sex drstubution. Tumor recurrence is about 50% rn excised and grctftcd lesions, but matkedly re duccd when cemented wrth methylmethacrylate m stead of bone grafts. Malignant giant cell tumors (including maltgnant transformation of a benign g1ant cell tumor) account for about 5%. The giant cell (reparative) granuloma (FIQ. 5. n ) t as a
more benign course ctnd s1milar hrstologic '"'d rddiOIogk features as the grant cell tumor, although cortical 11iolation with spread into neighboring soft timrcs does not occur and a prcdilectron for facial bones and short tubular bones of the hands and feet exists. (continues on
Osteoid osteoma (intra-articular) A nonconspicuoos radro4ucent focus (arrow) w1thout pPriosteal reactron IS seen medially dt the JUnction bet...,t>t:n femoral head and neck.
poge 98)
fiQ 5.67
Fig. 5.68 Osteoblastoma. An osteolytic lesion with exuberant solid periosteal reactions (arrows) and buttressing (arrowhectds) is seen in the proximal fibular diaphysis. A second cortical lesiOn (curl!('d ctrrows) with faint matrix c<~lcification near the fibulc1r head was cauM!d by a periosteal Ouxtacortkal) chondroma
5 Localized Bone lesions
97
Ftg. 69 Osteoblastoma. All expan!Hie osteolytic lesion w1th en· largemcnt of the pedide (arrow) and faint surrounding sdero\1~ is s('E'n 1n tht> lt>ft posterior elements of U at the apex on the concave side of the associdted '< ol1o~•s.
Fig. 5.70 Giant cell tumor. A poorly demarrated osteolyti<" le sian with faint trabeculation .Jnd cortical violation is S('E'n 1n the distal femur.
~IC). 5.71 Giant cell tumor. An expanslle. W(•ll-dcmarcated ostl'O· lytK le .ion with ·soap bubble" appear ante is seen in the distal r.!dous.
fig. 5.72 Giant cell reparative granuloma A slightly expansilc osteolytiC l<'sion is seen in tht' base of the l1fth metatarsal
98
Bone
Table 5.10 (Cont.) localized bone lesions ~dio._r~
Flndmgs
Chor-doma t1 ucti\I'C exp...1s•Je oo..to:OiytiC lesiOn with large soh (F'~gs. 5.73 .net tl~suc rna~' and lntro~tulll()(.tl c.tkifitations in about half 5.74) the cases Is charactcrbtlc. Originates from the sacrum and coccyx (60%), cbws (30%) and spillt' e\pec~ally C2 (10%). Sacrall5ion~ chdrat.temtiC.tlly grow ante< orly. In the spne vertebral collapse. sclero!>ts (ovory vt'rtebfa) ard enl.!rged neural foramma are additiOnal manifest.r tJons.
Comments
S-..;c ve..... cygeal chordorNs occur •n 40- to 60-year-old patients v.ith male predom•nance. Spheno-occipital chordomas are usually diagnosed In 20- to 40-year-old patients Wlthoot st"x predllectJOn. The chondrOid chordoma 1\ a vctrlant compmtng onethud of all clivus dlordomas Wlth better progi"'ISK and partl(uf.Jrly prom1nent caklfrcatiOfls. Hematogeneous meta~>tases m.1y eventually de\elop in .about one-third of all chordomas.
Adam.Jnti· noma ( <~ngM> blutoma) (F~g. 5.75)
Su19le or multiple, central or eccentric, mult•locular, shghtly l'xp.lnsilc, sharply or poorly delineated oste<"lytic le!>lons w•th or w thout reactiVe sclerosis m the d aphy\1s of the t1bia (85 %) with preferential involvement of 1ts antenor corteKor other long tubular bones. Oc casJOnally wrtital de~truction, exuberant periostitis and a soft tissue mass are associated.
Ameloblas·
Pre~ent.Jtton rdnges from unilocular cyst to multilocu lar. often trabeculated lcs1on with cortical expansion or de\tructlon and occas1onally large soft tissue mass in the n1.1ndible or. much less commonly, the maxilla.
u~ lly diagnosed in the fourth and fifth decades of life v.ithout gendN predilt>cllon. See chapter 11 for differentiatiOn from other gnathic lesions.
W• I or poorly marginated osteolytic lesiOn with Qt•r ,ral lack of both periOsteal reactM 11 and osteos.c:leroses 1s typical. Irregular thin thiCk Intra-tumoral W'ptatron, cortlc.al \iolatJOn and solt t•ssue mass are frequently •ssoc 1ated. Oy\trophic cak•fications and ~uestered bone fragments are occasronally seen v.•th•n the tumor. Pl'elerenteal involvement of the rr etaphyses of the long tubular bones (70%) with frequent exten~ rnto the d1c1physes and eptphyses.
Rare malignsions 1s reflected 1n the greatly variable radi01og1c presentatiOn. May complicate Pag('t'~ disease, honP infarcts. radiatiOn necrosrs and chroniC osteomyelitiS.
toma (Fig. 5.76) Frbrosarcoma (Figs. 5.77, 5.78 and 5.79)
Uwally diagnosed in the th~rd and fourth decades of hfe IMth sl19ht m.1lc predomrnance. Hrstory of trauma 1• fr ~ "'t Locar ,wei 1ng ts the maJor cllmcal finding. DO: Ostto{lbrom dy5plasio. See under fibrous dyspl.uia at the end of tl- tabl !.
(conlrnun on page 100}
n
5.74 c hordoma. A h..rnisp rical e Kpa. l!.lle csteolytic leSIOn (arrows) v.ith slightly sclerotic mar· gin originating in the posteriOr aspect of the vertebral bocly of ( 4 led to the infiltra· t•on of the remaimng vertebral bocly with subsequent pathologiC compress•on fracture.
F1 S 73 Chordoma .n osteolyt iC le~>•on (arrows) wtth slightly \( ~eerl •n the sacrum.
5 loc.dliLcd Bone lesions
99
hg. 5.75 Adamantinoma. A shghtly expan~'le, well to poorly demarcated, multilocular k>ston wtth reat t1ve surrounding sclerosis 1\ ~n 1n the tibia.
Fig. 5.76 Ameloblastoma. An expclnsilc. multiloculated, osteolytic lesion with both endmt<>al ~rallop1ng (arrows) and cortical violation (arrowhead) is ~een 10 the right mdnd1ble.
fig. 5.78 Fibrosarcoma. An expansile trabeculated leSIOn IS
S~
In
tht' 1nnommate bone of the acetabulum (ar· rows).
rlq. 5.79 Fibrosarcoma. A poorly defmed osteolytic lesion 1s \f't'n 1n the ihac bone d bovc the acetabulum.
Fig. 5. n ~>ndosteal
Fibrosarcoma. A poorly ckmcu<:ated lyti<: scallopmg 's ~en 10 the femur d1aphysis.
l.:~ion
with
100
Bone
Table 5.10
(Cont.) Localized bone lesions
Disease
Radiogrilphic Findings
Comm..1\U
Millignant fibrous histiOcytomil I Figs. 5.80 and 5.81)
A pooriy defaned onE'Oiyt1c les100 v.ith cortical destf\K· t10n, large soft tiSSUE' mass c1nd a~t>nce of both peri· osteal recJCtlon and nf!W bone formcJt1on is the most common pr~nlcJtion. The (•nds of long tubular bones from diaphysis to cpip~ls arc affected in 75 percent of cases with strong prcdik><.tion for the lower extrem ily. Osseous expansion is unusual but may be observed in flat bones such as JX'Ivl\, nbs. ~aptJia. and stemum.
Occurs ~t any age. but the mcJjority of Cil~es .Jre doagnosed in the frfth. sixth and seventh decade~ or life w1th \hght n c1le predommance. The lt·\ron (clnnot be radiographically differentiated from a highly malignant fibrosarcoma May develop in abnormal bone such as Pagefs disease .tnd bone infarcts or secondary to radiation therapy.
Chondrosar-
A slightly expans1le. mlllt1lobulated osteolytic lesion with cortical thicl<enang. cndost('al erosion and scat· tNed stippled or 1rrt>gular calcifiCations IS charactemtic. Matrix calcihc01tion r!'~('nt1ng the most specific hndang is only present in about two-thirds of the cases. Les•ons Without m.Jtll .. calohcatiOils are virtually lmposstble to dofferentiate from f1brosa•com.Js. Demonstr.Jtion of a poorly defined ostcolysi~. cortical violcltion .Jnd large soft tissue mass indicate a highly aggressive lesion. but an int('rrupted p('riost('al reaction typically is absent. H()\11/('ver more often a geographic destruction pattern is prest>nt sugg••sting a less malignant process. The tumor has a predolect1on for the metaphyses of the long tubular bones (especially femur and hu~) c1nd flat bon~ (C!>peCicllly pelvis) dnd the 1/ertebrae.
CX.curs u~ually between 30 and 60 years of age with male pr('dominance. The tumor arrs('S f'ithcr de nO\IO 10 the mE-dullary CiMiy or rs c<JusE'd by mcJlignant transformatK>O of an cnchoodrOmcJ. Low-grade chondrosarcoma~ .JIE' extremely diffocult to dofferentlate from enchondromo~s. lrregulclr mcJtrix cakolocdtlons (as opposed to JXJn< tdte, ring and ar<.-lil<e calcificatiOns). large c1reas of noncalcihE'd tumor matrix, poorly defined osteo~s and cortic,!l thickening (even solid) suggest all malignancy.
~alignant transformation of c1 bemgn osteochondromc1 is suqgested by demor1stratoon of scattered .md irreguI.Jr cakific.Jtions in the co~rtilaginous Cc1p of the tumor, associated soft tissue mass (non-c.o~kified cartilag(' cap) and destruction or pressure erosion of the adjacent bone. Differentiation of an ostE'Ochondroma from a pe· npheral chondrosc~rcoma rs not reliably possible on the basis of co1M'nt1onal rildrogrc1phy an
local pain and growth of an osteochondrOmcJ m adulthood suggests clinically malignant transformation. The nsk of m.Jiignant transformation is much higher in patients with hereditary multiple exo~toses (estimated to be up to 25 %) than in a solitary osteochondroma (about 1 %) Ro~r('ly a J"IE'ripheral chondrosarcoma d('velop~ de novo from the p('riost (periost('o/ or JWctOCortiCol chondrosorcomo).
central lflgs. 5.82, 5.83 and 5.84) Comil,
Chondrosarperipheral IF•gs. 5.85 and Comil,
5.86)
(continues on poge 102)
f 19 r, 80 Ma lignant fibrous histiocytoma A high~)' aggressive p •rrr ·at" e les• rnvolving the femoral hi-ad. oe<.k, and rntertrodoo~ntt rot rt-<Jion without periosteal reaction is seen.
fig . 81 Mahgnant fibrous h istiocytoma . A h1ghly destructive les10 or q nc1ting in the distal radius and extend1ng mto the drstal uln.J and c dl p.ol bones is seen
5 Localized Bone Les1ons Fig 5.82 Central chondrosarcoma (low grade). A slightly expanstle lesion Wtlh extensive sbppled calcifications. and endosteal scallopmg IS seen 1n the prox1mal t1bla diaphySIS Th1s leston cannot be d1fferenbated radrographecally from an enchondroma
Frg 5.84 Cortical chondrosarcoma (low grade) A small expansde cortical lesion (arrow) w~h fatnt matnx calcification and sclerotic marg1n ong1nates from the posterior asped or the distal femur metaphySIS.
101
Fig 5 83 Central chondrosarcoma. A well to poorty demarcated osteolytic leston wrth Irregular matnx calaficat1on and new cortical bone formation is seen 1n the proximal femur.
Ftg 5 85 Peripheral chondrosarcoma. A broad-based bony protuberance wrth extenSIVe 1rregular calcifications or the cart1tagmous cap 1s seen ong.nat1ng from the postenor bbia metaphysis.
Fig .5 86 Ma ltgnant transformation or osteochondroma 1n hereditary munipte exostoses. Mult1ple exostoses w1th modeling deform1t1es or the pelvis and both proximal remora 1s seen. The large exostosis ong1naltng beneath the nght lesser trochanter with cartilage cap calcrficattons is assoaated with a son mass (arrows) IndiCating malignant transformation
102
Bone
Table 5.10
(Cont.) LocaliZed bone lesions
Disease
Radiographic F indir~ga
Comments
Clear cell c:hondrosar-
Poorly or well defined (sclerotic borders), slightly expanSIIe epiphyseal lesion with central calcifications in abo~ one-third of the cases is characteristic. Most frequent locations are the prox1mal ends of the femur, humerus and tlblil
Rarecarblag1nous bone tumor occurring between 25 and 50 years of age wrth slight male predominance. Radrographic features are virtually 'Identical to a chondroblastorna
Dedifferenbated chondrosarcoma (FIQ. 5.88 and 5.89)
Featuresof tow-grade chondrosarcoma (nonexpanSIIe O&teoi}'1Jc lesion v.1th 1ntact cortex and matrix calcilicatioo::o) and of highly anaplastic sarcoma (expansile. poor1y defined osteolytic lesion with cortical destruction and large soft tissue mass, but usualy without caiCificabon) are characteristic. The transition between these two tumor components is usually abrupt Distribution of the tumor is s1mllar to convenltonal chondrosarcoma wrth femur humerus and pelv1s be1ng the most frequent srtes of Involvement
Occurs in patl8f'lts over 50 years of age v.1thout gender pred~ect1on. Presentswrth pa1n, soft tissue swelling or pathologrc fracture (one-third of pat1ents). The prognosis rs very poor
Mesenchymal chondrosarcoma (Fig. 5.90)
Features are Indistinguishable from a high-grade conventional chondrosarcoma and include poor1y defined osteolysis, matrix calcifications, cortical expansion and v1olat1on and soft tissue mass. Most frequent s~es of rnvolvement are femur, nbs and spine
Occurs usually between 20 and 40 years of age and has a poor prognOSis. Metastases to lymph nodes and other bones 1s not unusual. Approximately 50 percent of mesenchymal chondrosarcomas anse 1n the soft tissues
Osteosarcoma (Figs. 5 9 1. 5 .92.5.93. and 5.94)
Co/1\ti!IIW!td osteosarcoma presenting as a poorly defined Intramedullary lesion most often originating in the metaphyses of long tubular bones with varying degrees of osteolysts and osteosclerosts is most charactensbc. The tumor may however be purely osteolytic or osteoblastic. Cortical destruction associated with an rnterrupted penosteal reactron rn the fonn of a Cadman's triangle or wrth perpendiCUlar ("hair-on-end" or ·sunbursr). tam1nated ("onron skin") or amorphous appearance is most characteristic Large soft tissue masses are commonly found in tumors w1th cortical violation. Most common srtes of involvement are the l ong tubular bones (BO '• 1 e&peaally the femur, bbia and humerus. Osteosarcomas are relatively infrequent in the pelvis, spine and facial bones. and rare in the remainrng skeleton. Tc cc.ngrrtft:f c n.
Osteosarcomas most commonry present in the second and third decades of hfe with pain, swelling, restriction of motion and pyrexia . Men are more frequently affected than women. In the elder1y they may be a complication of Pagers d1sease or radiahon therapy. Cinctl11c n.•lcCI.
...,.....
(ltg. 5.87)
taken for a ben1gn osteosclerotiC process
(wlllim·£.• on pug£ 104)
5 Localized Bone Lesions
103
F1g. 5 87 Clear cell chondrosarcoma An ovoid osteolytiC lesion (arrows) w1th slightly sclerotic border Is seen 1n the humeral head.
Fig. 5.88 Dedifferentiated chondrosarcoma. A well differentiated chondrosarcoma wrth e)tenSive matnx caloficabon IS seen in the diStal femur associated w1th a poorly demarcated expanSIIe osteolytiC focus wrth cortiCal VIOlation (arrow)
Fig 5.89 Dedifferentiated chondrosarcoma A focus of pc.mctate calcifications (arrows) 1n the humeral head Is associated wrth a hiQhly destructive perrnea11ve leSion w~h multiple pathologic fractures involving the proximal humerus shaft
Fig 5.90 Mesenchymal chondrosarcoma A highly destructhle leSIOn \vlth ext ~nsrve 1rreguar matrix calaf~eallon. cortiCal VIOlation and large sort tissue mass is seen orig1nabng from the lateral aspect or the femoral neCk and greater trochanter.
a
b Fig. 5 91 a, b Osteosarcoma (2 cases) A destruct111e osteoblastic leSion with extensive amorphous penosteal reactiOn and large soft tissue mass is seen in the proximal humerus &!aft A mixed. but predominantly osteolytic, relati\e poorly defined osteolytiC lesion wllh cortJcal violation IS seen 1n the diStal femur.
104
Bone
Table 5. 10 (Cont.) locali.t.cd bone lesions Otsease
Radtogra. htc Ftndtngs
c
Penosteal osteosarcoma (Ftg 5.95)
Oblong dense lesaon ansmg from the dtaphyseal surface of a long tubular bone wrth trregular thickentng and occasionally saucenzatlon of the adjacent cortex •s typteal A Codman's tnangle and radtabng or cloud-ltke osseous proliferation are frequerily assoetated. Femur t1bta and humerus are the most commoo Sites of tn-
Usually dtagnosed tn the second and thtrd decades of hie wrth better prognOSis than conventional osteosarcomas but worse than parosteal osteosarcomas. RadiologiC and histologiC features of penosteal osteosarcomas and periosteal UuxtacorbcaQ chondrosarcomas are sunilar tf not t
~olliement
Parosteal osteosarcoma (Ftg. 596)
A large rad10dense oval or round mass with smooth. lobulated or irregular margins attached in sessile fashIon to the ~dernai metaphyseal cortex of a long tubular bone "characteristic. A thin radiolucent line may separate the le~on outSide its attachment (pedicle) from the cortex which rtself may be thickened. With progres..ive enlargement the tumor tends to wrap around the bone. Ossiftcation within the tumor proceeds from its base to the periphery and may be homogeneous or contam radiolucent areas. Tumor extension into the medullilry bone is unusual. The most characteristic location 1s the posterior surface of the distal femur
Most common type of osteosarcoma arising on the surface of a bone . Affected patM:nts are adults most often in the third and fourth decades of hfe. Symptoms are typically inSidiOUS and tnclude patn, swelling and a palpable mass. The prognos... 1s better than tn both conventional and penosteal osteosarcomas DD.I'I>'I-Imi/1/UIIic llll'rJ.\1/i.• l!'.lt{icam (Figs 5.97 and 5.98) can be differentiated from a parosteal osteosarcoma by the demonstration of a fine radiolucent line separating the lesion in its entire length from the adjacent bone. Furthermore lhe ossification 1n myositis ossificans is evenly radtodern;e throughout the lesion and its periphery IS sharply delineated (mnlinuo on pcj!.e
Fig 5 92 Osteosarcoma A poor1y demarcated miXed osteolytiC and osteoblastic lesion is seen in the diac wmg.
Fig 5.94 Teleangiectatic osteosarcoma with aneurysmal bone cyst. A poorly defined slightlyexpanstle trabeculated. osteolytic leSIOn with cortical violation is associated with an aneurysmal bone cyst (arrows) presenting as better defined eccentric lesion v.rth •soap-bubble' appearance.
106)
Ftg 5.93 Osteosarcoma. A purely osteosclerotiC lesaon IS seen m the distal femur conSistent wrth a lowgrade tntraosseous osteosarcoma.
Fig 5.95 Periosteal osteosarcoma. An oblong dense soft tissue lesion arising from the postenor femur diaphySIS With doud-hke and radiating osseous prolrferation is seen.
5 Localized Bone Lesions
105
Fig 5 96 a, b Parosteal osteosarcoma (2 cases). a: A large heterogeneous ossified mass containing radiolucent areas originates from the posterior surface of the distal femur and wraps around the shaft causing the inhomogeneous appearance of the latter. The tumor periphery is irregular and poorly defined. b: A partly ossif.ed mass is attached by a sderot1c stalk to the irregular antenor cortex of the femur in the subtrochanteric area. The tumor ossification is concentrated around its stalk and gradually fades out towards the tumor penphery
b
a
Fig.5.97 Posttraumatic myositis ossifteans. Following a complicated distal radius shaft fradure extensive heterotopic bone formation developed around the fracture srte simulating a malignant osseoustumor.
\
Fig.5.98 Posttraumatic myositis ossificans. An ossified lesion with a complete rim of thin peripheral calcification ("eggshell calcification") is wrapping around the distal ulna. The lesion is separated in its entire length by a fine radiolucent line from the adJCicent bone.
106
Bone
T 11blc 5. I 0
(Clint ) l ocliii/Cd bone lesions
Disease
RadiOgraphiC Find1ngs
Comments
Ewing sarcoma (Figs 599, 5 .100,5.101, and 5 .102)
A poorty defmed osteolytic lesion with cortical ~iolation and large soft tissue mass is characteristic. In tubular bone• an Interrupted periosteal reaction of the laminated ("olllonslon") or less commonty perpendicular ("suntxnf' or "ha~r-on-endj pattern is characteristically aSSOCiated Saucerization of the cortex is a rare but relatiVely charactensbc mamfestat10n of the diSease. In flat and 1rregular bones osteosclerosis can be the dom1nant rad•ographoc feature The tumor can affect any bone, bU has a predilection for the dlametaphyses of long tubular bones and overall the low~;r half of the s~eleton. The most common locations lrtelude femur, bbia, humerus. pelvis and sacrum.
Usually diagnosed between the ages of 5 and 30 years (peak 10 to 15 years) with slight male predominance involvement of the tubular bones occurs more often in ch•ldren, whereas Involvement of the flat bones 1S rr10re comrr10nly found •n young adults. Patients present w1th localiZed pa1n and swelling occasionally combined w1th fever and leukocytOSis. The turr10r IS rare m blacks Pllmttlv& nec•ooctocbrn;,/ tumors (PNU} (F1g 5.103) have Similar histologiC and 1mag1ng features but epiphyseal Involvement pathologic fractures. and distant metastases occur more frequently when corr~ pared to EWing's sarcoma.
AngiOsarcoma
Solitary or multiple poorty or well demarcated leSIOns most comrr10nly located in the medulla or cortex of long tubular bones. pelvis sp1ne and skull Cortteal th1nn1ng or VIOlation and/or m1ld expanSIOn wrthout periost"•s Is occaSionally assoc~ated
Occurs in the fourth and fifth decades \'lith male predominance If multicentnc It may Simulate multiple myeloma metastases cystiC ang1omatos1s and cystic osteomyelitis (e g tuberculous or fungal). Homlltl{J/oondcll'tC'IIollw refers to a low-grade malignant angiosarcoma. Hemall{Jioperlcytoma IS a borderline malignant tumor. with sim11ar •mag•ng features
Presents as an expanSIIe trabeculated osteolytic lesion wrth cortiCa l th1n01ng and violation measuring up to several a>nbmeters 1n d~ameter or as a well marg1nated purely osteolytic focus wrth endosteal scallopmg. Rarely It may present as a sclerotiC les10n (e.g IVory vertebra) Most common locations are spme and pelvis Comphcabons 1n the spme •ndude transd1scal tumor spread and pathologiC fractures resulting sometimes 11n complete d1ssolut10n of a vertebral body.
Plasmacytoma may be considered a solrtary rr~anifesta bon of mu1t1piP myeloma with conversion to the latter occumng as late as 20 years after mrt1al diagnoSis Plasmacytoma affects younger pabents than mu1t1ple myeloma V>lth about half the pabents be1ng 50 or younger at the bme of diagnoSis It frequently presents wrth neurologic symploms and rad10graphteall)' rr~ay be miStaken for a giant cxll tumor.
(Fig. 5 1(]4)
Plasmacytoma {Ftgs. 5.105 and 5106)
(cont6HleS
Ftg 5.99 Ewing sarcoma. A permeative osteolytic leSIOn With COrtiCal VIOlatiOn and beg1n111ng laminated ("onionskm") periosteal reaction is seen m the proximal humerus shaft
on page JOB}
Ftg 5 .100 EWing sarcoma ExtenSive laiTIInated ("on10nsk1n1 periosteal reactiOn and cortical tunneling is seen in the prmomal femur shaft. while the permeative osteolytic leSIOn IS barely perceptible.
5 Localized Bone Lesions
107
Fig.5.102 Ewing sarcoma, Saucerization of the femoral cortex (arrows) is the only manifestation of the disease in this case
Fig. 5.1 01 Ewing sarcoma. A poorly demarcated mixed osteolytic and osteoblastic lesion involving the entire iliac wing is seen.
Fig.5.103 Primitive neuroectodermal tumor (PI\'ET). A poorly defined, mixed osteolytic and osteoblastic lesion 1n the distal tibia with cortical violation and beginning amorphous periosteal reaction on its lateral side and early laminated periosteal reaction on rts med1al side is seen.
Fig. S.104 Angiosarcoma. A poorly demarcated osteolytic lesion (arrows) with cortical violation is seen in the ilium,
Fig. 5.1OS Plasmacytoma 1n the ilium.
An expansile osteolytic lesion With trabeculabon 1s seen
108
Bone
Table 5.10
(Cont.) Localized bone lesions
Disease
RadtOQraphte F1ndmgs
Comments
MuHiple
Multiple well marginated ('punched out'") or poorly delineated osteolytic lesions of relatillely urnfonn size are characterisbc Endosteal sea llop1ng 1s typ1ca lly present w1th larger leSIOns In the long tubular bones. 0 1ffuse osteopen.a wrthoi.A well-defined areas of osteolysis IS another common presentation. Penosteal new bone formation IS exc:eed1ngly rare Focal or multiple sclerotiC lesiOns are an unusual 1nrtial presentatiOn. but may develop after chemotherapy 1rradiabon or pathologiC rracture Preferred locallons 11 order of decreasIng rrequPncy are 5p1ne nbs skull pelviS long tubular bones and claiiiCies (diStal end) Sp1ne Preferential osteolytiC destrucllon of the vertebral bodes. somet1mes associated with irregular thickening of the rema1rnng vertebral trabeculae relative o;panng of the postenor elements, scalloping of the anterior marg1ns of the vertebra l bodies (pressure eroSIOns from adjacent soft bssue lesions). and paraspinal or extradural tumor extension are common, Pathologic compreSSIOn fractures are a rrequent complication,
Occurs 111 patients over 40 years of age wrth male predol"'inance presentmg With bone pa1n. anemia hypercalcemia. proteinuria (roudmg Bence.Jonesproteons), and monodonal gammopathy (hiQh erythrocyte sedimentatiOn rate, abnonnal electrophoreSis) w.JIIk>nstmm's maaogloiJVIInerria presents With s1m1lar d1n1eal and rad1ographoc finchngs but the radiographic features are usually lessconsp1cuous
myeloma (Figs. 5.107. 5.108, 5.109, 5.110 and 5.111)
(corotkwes
Ql1
page 110)
Fig .5.106 Plasmacytoma An expansile trabeculated osteolytic leSion ("soap bubble appearance") originating from the scapular spine Is seen. Fig 6,107 MuHiple myeloma. Multiple well-demarcated ("punched-out") osteolytic leSions are seen on the vault of the skull
5 locali7ed Bone lesions
109
Fig.5.109 Multiple m yeloma. Numerous well to poorly defined osteoly1ic lesions are scattered throughout the pelvis and proximal femora .
Fig 5 110 Muhiple myeloma Patchy osteopenia and tiny foci of increased bone density are evident throughou1 the thoraco-lumbar spine besides several compression fractures.
Fig 5.111 Muhiple myeloma. Osteopema with a prominent vertical trabecular pattern ("corduroy" appearance) is seen in all vertebral bodies of the lumbar spine.
11 0
Done
Table 5 I 0
(Cont ) loealit:cd bone lesions R
M(.~
S<*t~ry.
(F~gs,
bl~hc 01
5.112, 5.113,5.1 14, 5.115, and 5.116)
Fonclong~
or nlOfe oornnlllftly.
mulrple mixed 01>t.x.lytoc-o61eoblios!JC
05leolybc, 05loolesions wdh pref-
Bone met.Jsla&e5
~re
by
r.u
the mos1
oornron
skeletal
lflllolvcflleflt ol the roo marrow contaming skeletoo ("Pine, pet•os. nbs, skul, fefll()(a and lu.meri) is cllmodcri:.hc Ocleolytic meta5lase5 may be well or
spread maltgnaf'CY oocunWJg e1lltCf by hetmlogenous or dwect IUJOOf e•lenbiOil. They mosl frequently OligOoolo from c&rLIOOIJT3b ol bceast, prosldte, king, kidney, thyroid and gul.lroont~id ltad Breast carcinoma
poa1y marginak'
061oolyloc
dill•. tho porJuvr ctcmenls incLding the pcdicllls are frc•qt. nllf olso 1rM>IIIed (DO mui!Jple myeloma). Purely ostoolyhr mettu:tases commonly arise from carcinOilla$
061eoblasloc,
eltlfltial
of lung. ~!dney, thyroid
nnd lymphoma Purely OSiooblasaro mo5t olton 3$SOCialod v•.th prostatic
mct.a&l- lund to be nuod, or lc6s coo""lOilly
purely
or OCIC'd: Ln.loc, often motemive end freqoofllly awocxuled vlllh polhologic fractures. Prostate caranoma mclat-lascs ~re ch:
may be expAO~
Paget's diS-
BroncflOQNIIC corcWJomR nv1astases are typically OSieolytrc or ITllxed and occahiOOally mpam;ile An eccentriC
phoma, a>rcincJij1,
erOSIOil
lr.
~~astasos
but also With Hodgkin's lymand medulloblastomas. Periosteal re-
ociiOOS ..re hf1Jhly unusu.ol 011 nnetaslahc d.sease except '" prObtatlc and br£!lomw,. N<:olher ~us expall!>ion 1101 wfl IISSUo rnuM>(l$ wu typioolly associated with bone n~tJtaol
oxu:pt on 11b k.>!>iorn., Obloolybc
meta>Jasas
of the external
("cool<~u·l>ito"
COilex of a long tubular bone Sign) • r«IG, but qude characterr:Jic for
a btonchogonJC caranoma m<:t.Jl.lasr:; manrf<.>l.liubbly) appcwunco.
f1on1 wrco10r~IS 01igrnatr11g in the kidney, thyrOid, lung ond li\ler ond osteoblastic metastases from prost<Jtic and bre.tsl a;orcinomos One or more sclerotic vertebral body
Guslrointcsltnol tract mctastaws 0011or the whole spec· !rum from purely oaleolylic to purely osloobi:Jstic. Mclaslasef> from colon or roclum curcinoma may oc-
(ivory vertebra) is ll1061 often caused by prostatic or b1oal.l etlfcrnomo metastases, but also found wi!h Hodg-
casionally r06()mblo an et.lOO&<Jrcomo burst periosteal roacbon.
kin's lymphoma and Paget's disease. Pathologic Ira<> lures ore a frequent ~lta•tion, especially in the spone
Mctoslahc bone diSOO$G \Wh untrnov..l primary most often ong11ntcs from prostate, lymphoma, breast,
Rtl$r-or- of An OE:Ieolytr. mf'tasii>SIS to treatment (e g. choo'lotherapy or radiation lhl'rapy) is evident by progr(!S$jv& sdrnDYi proceed11g from the penphery
lung, kidoc'Y, thyroid
towards the
011ntcr ol the leSKlll v.til
e~~entual
and depict a sun-
or colon
redudlon
10 ~o 01 disa PJ>oo;;u~ na~ of the 05leolybc focus The appearance o1 osleoscteIOft ol the dosee:;e, bd may also ond,.
ol pre-euslrng OSieOiybc not be identified on 1adl~ g1aplta. A posil"'o ltoatmunl response ol osleobla!>lic ~
aole a healng
r~nse
lll(.-t.lt.laseli II.at could ir rli&Uy &ion is evident
by deacaf>e and eventi.U disappearance
of tho aclorotJC focus
(contin006
Frg.5.112 Metastases from bronchogenic carcinoma. Scallorod predominantly ostoolybc metastases are soon In the thoracic spine with moin involvement of the ~hi podiote& and posterior E'II'ITlf'OIS of 110 and T11 (arrows) producrng an "empty •crteb
on
page 112)
Fig . 5 113 Metastases from breast care> noma Predorron.'lnlly 01>looblastlc 11'lUta..tasos Involving all vertebral bodies induding tho postenor elements of the lumbar sp100 lvOfY vertebrae are seen at l1 and l5 (arrows) ()! looblasloc foci (al'l'CN" hoods) are eviderd m the sptnous processes ol L2 and l3.
5 Localized Bone Lesions
111
Fig. 5.114 1\letastases from prostatic carcinoma. 1\lultiple bilat~ml cxpansilc and purd) o~tcoblastic metastases originating fi'Om the rib; ru-e f.ccn.
rig. 5. 115a. b M~tastasi;, from renal cell carcinoma before (a) and all~ (b) radiation therap). A purel) lytic. mar~cdly cxprulSilc ("blow-out") !c-ion is seen originating from the dol"\31 aspect of the proximal humerus !.haft (a). .\ftcr radiation therapy the lesion be<:rune partially o;,silied d~picting a tmbcculakd pattcm and a \\ell -demarcated ~!erot ic margin (b)
a
b fig.5.1 16 Cortical metastases from bronchogenic cru·cinoma. 1\lultiplc purely O'>l~ol)1ic lc'ion., arc seen in the cortex of the hhia TI1e largest lesion located posteriorly has l>roken through the cortex on both ib inner and outer •urface.
112
Bone
Table 5 10
(Cont.) Locali1cd bone
lc~ions
D1sease
Rad10gaph1c Andlngs
Comments
lymphoma (Figs 5117, 5.118, 5119, 5.110 and 5.121)
Preferential sites of 11111olvement Include spine, pelviS, scapula and ribs, In long tubular bones i1111olvement of the diametaphyses of the femur and bbta about the knee is most common, Non-Hodgkin lymphomo typ1cally presents as solitary or, more often, multiple poorly defined osteolytic les•ons, Hlsliocylic /ymphom.~ (pnmary or secondary) frequently has a mixed osteolytiC-OsteoblastiC appearance and may resemble Paget's desease without bony expansion, Purely osteoblastiC lesions are uncommon en nonHodgkin's lymphoma. Hodgkin's cisease of the bone IS always caused by secondary in~ol•ement . Its presentation ranges from purely osteolytiC to purely osteoblastic lesions. Diffuse sclerosis of a ~ertebral body (ivory ~ertebra) is not an unusual man•festatiOn Osteolytic leSions tend to be poorly defined and are aSSOCiated with periostitiS in one-th1rd of the cases
Secondary 11111olvement of bone caused by hematogenous spread or. less frequently, by d•rect rnvaSIOn occurs 1n one-th1rd of patients wrth non-Hodgken's lymphoma and 1n 10%wlth Hodgk•n's diseasP Primary bone lymphoma 1s much less common, accounts for approximately 5%of all primary malignant bone tumors, IS usually or the histiocytic-type (previously called retiCUlum cell sarcoma), and typiCally occurs en older p;•t•ents w1th a 21 male predom•nance. Butlattl; /ymiJIIOma presents as expansele ol>teolyt1c leSIOns associated with a soft tiSSIUe mass ln~olvement or the facel bones (especially the max1lla) Is most characteristic in children of tropecal Afoca Nonendemic Burkrt(s 1}-mphoma may be assoCiated w~h 1mrnune dysfuncl1on (e.g., organ transplantatiOn and AIDS). Myt;oos fungodos is a T-cell lymphoma wllh primary involvement of the skin. Discrete or poorly defined osteolytic lesions may be assoCiated in the appendicular skeleton
leukemia (Fegs. 5.122, 5.123 and 5.124)
Diffuse osteopen1a with medullary widening and cortical th1nmng 1n tubular bones and vertebral compresSIOns are the most common presentation Moth-eaten or permeative osteolySIS may be round 1n both tubular and flat bones. RadiOlucent and/or rad10dense metaphyseal bands. as well as peoosteal new bone formatiOn are parbrulalt)! common 1n children. Comphcalions may include Intra-articular and subpenosteal hemorrhages, septiC arthritis, osteomyelitiS, osteonecrosis and secondary gout GraooiOcytlc sarr:omos (chi;Jramas) present as Single or multiple, often expanslle lyt1c les10ns in the skull, sp1ne . nbs, sternum and long tubular bones, usually in acute myelogenic leukemia
Leukem1as are claSSified based on cell matunty (acute W1th Immature or blastiC cells versus chroniC with mature ails). cell morphology (myeloid versus lymphoid) or cell ongm (thyrnus-
(oonrtnues
F1Q.5 .117 Non-Hodgkin lymphoma A poorly defined (moth-eaten) osteolytic lesion (arrows) is seen 1n the distal femur.
on poge 114)
F~g 5 .118 NonHodgkin lymphoma (h•sliocytiC type). A mcxed osteolytic and osteoblastiC lesion wrth coarse Irregular predominantly vertical traberulallon involving both the vertebral body and pedicles of l2 (arrow) IS seen
5 Localized Bone Lesions
113
F1g.5.120 Hodgkin's diSease. An ivory vertebral body iS seen at l3 (arrow)
Fig. 5119 Non-Hodglon lymphoma (hisbocyllc type) A m1xed osteolytiC and osteoblastic leSion 1s seen 1n the 1hum The lesion d1ffers from Paget's disease by the absence of enlargement of the Involved bone Furthermore cortiCal VIOlation (arrows) is also evident in this particular case.
Fig 5.121 Hodgkin's disease Several relatiVely poorly defined osteoblastiC leSions are s;;en 1n the diStal femur and the pro)(IIMI tibia and fibula
Fig.5.122 leukemra Sderollc bands traverSing all metaphyses about both knees are seen in this child.
Fig.5123 leukemra. Innumerable tiny and poorly def111ed osteoly1ic and Obleoblaslic foci are scattered throughout the pelvis.
Fig 5124 GranulocytiC sarcoma (chloroma) A barely perceptive permealo~e o ~eoly11C leSion wrth pathologiC fracture (arrows) is seen invol~1ng the femoral head and neck.
114
Bone
Disease
Radio9ra hie Findinos
Comments
lange mans cell hisbocytoSIS (Figs 5.125. 5.126 and 5.127)
pteswts as solitary or. less commonly, mu1t1ple leSIOns with preferentia I involvement of skull, mand1ble. Spine, ribs and the diarnetaphyses (rarely epiphyses) of long tubiJar bones. Relatively well defined radiolucent areaswith endosteal scalloping v. ith or w•thout si!Qht bone expansion and periosteal new bom format1on are typical in the long bones and may mtmiC osteomyelitis or e~en Ewing"s sarcoma. lll.lell-defined iytjc lesions with or without sclerotic borders may be foond 1n the skull and pel\is. A rad10dense focus (button sequestrum) is frequently obse~ed 111 skul lesaons Larger osteolytic areas in the skull typically depd beveled edges caused by the uneven destructiOn of the 1nner and outer tables. In the mand1ble radiOlucent lesions about the teeth may lead to the "floating teeth" appearance. In the spine a col lapsed vertebral body (vertebra plana) with intact intervertebral spaces or, less frequently, a lytic and occasionally slightly expansile lesion involving the vertebral body and/or the postenor C'lemenls may be found
Langerhans cell histiocytOSIS compriSes three major cond1t1ons. I . EOSII>Ophio: granuloma is both the most common and most benign variant representing approKimately 70 ~ of cases. It IS usually d~agnosed between the age of 5 and 20 2. Hand-&NIIIei.Ctrrlstlo.lfl cJ/scllStJ is characterized by the tnad of exophthalmos, d~abetes inSipidus and large lytic skull les1ons ("geographic skutlj. 3 I.BIIetE~.Stwo ascase IS the acute diSSemll18ted variant 1n ch11dren IJfiCk r age 2 Bone lesiOns are less common, but may 1nclude mutt1ple widespread lytic leSIOns 1n the skull ("raindrop" pattern~.
AmyloidoSIS (FIQ. 5128)
Osteolytic lesions of variable size with endosteal scalloping Simulating multiple myeloma preferentia lly JoC<1ted 1n the proximal humerus or proximal femur IS the most common presentation. Subchondral amyloid depoN11on may result in avascular necroSis. PathologiC fractures are a relatively rommon complication Subchondral cyst formation and ewsJons 1n the hand and wrist associated With penarticular or diffuse osteoporosis may Simulate 1heumatoid arthntis, although ext~ Sl\e nodular soft !Jssue masses, welk!efined cys!Jc leSIOns w1th or WlthiOut surround.ng sderosisand preservatiOn of the JOint space are more characteristic for amyloidoSis.
Musculoskeletal abnormalities are the result of amyloid deposition 1n bone, synovlum and soft tissue. Prll7lolf'Y om}'loldoois occurs In patients above the age of 40 wrth male predominance It may be associated with multJple myeloma Sewrt<Jory am}'lvi<Josts IS assoaated Wlth chronic renal diSease, rheumatoid arthnlls, lupus erythematosus. ulcerallve colitis, chronic suppurative d1sease,and lymphoproliferatll!e diSOrders.
Brown tumor 111 hyperparathyroidism (Fig. 5.129)
S1ngle or multiple, occasionally eKpansile, weU to poor1y defined osteolytJc lesions of the axial and appendiCular skeleton. Eccentric or cortical location is not unusual Canmon stes of Involvement are facial bones, pelviS, ribs and femora llley may undergo necrosis tJnd liquefaction producmg cysts. or with proper treatment (removal of the parathyroid ade· noma} become mcreaSingly sclerotic.
Brown tumors are more commonly assoaated Wlth primary than scv:-v~
Ewtopt.tic granuloma
Spontaneous healing of a solrtary lesion occurs, typically progreSSing from the penphery towards rts center and eventually resulting 10 its disappearance or transforrnallon mto a sderohc focus.
(conl/nrf('.<
Fig 5.125 Eosinophilic granuloma. An irregular, relatively well-defined osteolytic lesion with minimal endosteal scalloping slight bone expanSIOn and beginning periosteal reaction on Its anterlof margirl IS seen 1n the proximal radous shaft
on (X>flf' 116)
FIQ. 5 126 EoSinophilic granuloma. A well deflrJod, trabeculated osteolytic leSIOn wrth sclerotiC margin and cort1cal violatiOn is seen 1n the 1llum.
5 Localized Bone Les1ons
115
Fig. 5.127 Hand-Schiiller..Christian disease. Large. v.ell- ~en 1n the vault of the cran1um 91~1ng the appearance of a conttn.,ntal map ("geographiC skull1
Fig. 5128a, b AmyloidoSIS (2 cases) . A large well-
a
b F1g 5129a. b Brown tumors m primary hype rpa rathyroldism. Muniple poorly to well defined osteolytic lesions, some w1th trabecuatton, are seen 1n the pelVIS (arrows) and t1bia . Most t1bial lesions are cortical based (a pel vis b· tibia)
a
b
116
Bone
Table 5.10
(Cont .) Localized bone lesions
Otsease
RadiOo' "' hiC
HemophiliC
Central (intraosseous) or eccentnc (subperiosteal). welldemarcated osteolytic leSion are often associated wrth either solid or interrupted penosteal reaction and a large soft tissue mas... Minimal to massive calcification wrthin the lesion is occasionally also encountered. Rarely. more than one bone contaans a pseudotumor Preferred locations are pelviS. femur t1bia and hand
leSIOns are late sequelae of intramedullary or penostea l hemorrhage occurring 1n fewer than 2 of hemophiliacs. Hemophilic arthropathy •nclud1ng dense jo1nt effusions and joint contractures. avascular necrosis espeaally of the femoral head and talus spontaneous fractures and soft tissue hematomas may also be evident
One or more cystac lesions often wrth partial calclfica lion may be found 1n the subchondral and deeper osseous areas Simulating enchondromas. larger intraos· seous calaficahons may m1rmc bone mfarcts. These find1ngs are most frequently seen 1s the hands and feet. Association \'1 rth cha ractenstic find1ngs of gouty arthropathy is d1agnowc.
Occurs 1n approximately 5 'lb of patJents with chronic gouty arthntls lntraosseous urate deposrtron wrth subsequent calclficabons usually ongmate from the adJacent JOint per~etrate the cartllagll"'ous surface and extend 1nto the adjacent spongiosa
Eatty sagns are nonspecifiC and 1ndude mottled osteopenaa . poorly defmed osteolyt1c lesion(s) or patchy osteopenac and sderobc areas F1ndings are however more charactenstac in an advanced late stage In the d1ametaphyses they include a serpiginous peripheral rim of sclerosis surrounding an oblong area of bone rarefaction Periostrtis and matrix calafications are frequently associated Intramedullary calaficabons are often the only Mdi ng and are typically shell-l1ke whereas the calclfacahons m chondroid matnx tumors tend to be Irregular and central and are surrounded by a rim of noncalclfJed often slighUy radiolucent tumor matnll Solid periosteal reactions and cortical thickemng may bf' assocaated with both condrtions but rn the case of chondroid matrix tumor suggest a lowijrade chondrOt>arcoma rather than enchondroma. Typacal findings or o&teonecrosis in the epiphyses include subchondral cyst(s) wrth sclerotic rim. arc-like subchondra l radiOlucency (crescent sign) subchondral fragmentation and eventually collapse of the articular surface. wrth considerable sderosis and secondary degenerative changes rn the affected jo1nt.
Osteonecroos can be dl\lrded 1n bone rnfarctron . occurrtrig more frequently 1n the metadaaphyseal regrons of long bones (e g. femur. humerus and tibia) than 1n the axial skeleton and in avascular necroSis involving the subartacular bone. Solrtary bone infarcts are frequently daagnosed as an incidental finding Osteonecroos may be idiopathic (25 ••) or associated wrth ho matological and reticuloendothelial diseases (e.g . ·'" I<· ctll and Gan/v\ chwL•I) collagen vascular dJSeases(e g lr•pr"' cry1hcmtllo.•r •}. trauma (e.g ~ub Wf•lul /up [ro
pseudotumor (Flgs. 6.130 and 5131)
Intraosseous tophus In gout
( I ic. 5 ll2)
Osteonec:ros1 s (bone Infarct and avascular necrosis) (Flgs. 5.133, 6.134,6.135 and 6136)
FlndiOVS
Comments
(WII/./ 1•('.<
Fig .5.130 Hemophilic pseudoturnor. ExpanSIIeosteolybc leSIOn with trabeculation developed in the greater and lesser trochanter as well as 1n the ischium and pubic bone adjacent to the compor~ents of the total hip prosthesiS 1nserted 12 years earher
(0/
f'q;C
I 18)
Fig 5.131 Hemophilic pseuooturnor. A large expanslle osteolytic leSIOn surrounded by a thin rim of solid "' ' bone formation (arrows) and contarnrlig extensive central calafacabons is seen in the IliUm
5 1oc.aliLed Bone Le!>iom
117
Fig 5.132 lntraosseous tophi in gout Wcll-0 'IT llcltf'd o~tt>O- Iytic: l~ion~ ~1th f"" ,t Cclkifi<.ations arc seen in thl' fourth and rifth ful<)CI' rcscmbl•ng enchondromas.
• I<J ~. 133 Osteonecrosis (bone infarct) Patch)' d• •m11 er-
fig. ~ 134 Osteonecrosis
hg. 5.135 Radiation osteonecrOSis. Extcn\1\1\. bone 1nlarction hmited to tilt> fof'ld of rrrad1atioo ~~ d1agno~toc . F1nd1ngs 1nclude wtdt"iprf'ad cdie lfocclhons rn the medulla and rrregulc1r tor· tical thickenrng w1th numerous round to oblong intrcJcorticallu cencies.
(bone infarct) An oblong shnlhke calcifKatlon 1\ """n 1n the distal t1bic1. A he.lhng dl\t.JI fibula fracture .Jnd oJ posttraumatiC osteochondrcJI defect in the medial talar dome are cJiso present.
alizatioo and poor!) ~11. ·d osteolyti<. l~iom seen in the distal femur are the ec1rhest radrographic find1ngs rn osteonccr
Frg. 5.136 Radiation osteonecrosis A dysplastic ostE'Open1c pt>l· \iS with extensn- c.tlc ofr<.Jt o s .and numerous pathologiC fr actur~ and bilateral dv.moldr ,..,._,~s of the feiTlOfal heads art: thE' coosequences of pdVtC uradicJtron durinq childhood.
118
Bone
T;Jbte 5.10 (Cont.) lucaliz. d b..ne lesions Disease
Radiographk Andings
Healmg or Oste<Xis ., 't1 c 111 J~ formatton may simulate healed fracchronic osteom)chtiS or o~n osteoid osteoma. respecture and tM'Iy. Demonstro~tlon of a fraHure hoe 1n an area of lostress fracture calized elliptical cortical thickening of a long tubular (Figs. 5 .137 bone (as opposed to a round or ovoid intracortical aband 5 .138) scess or nidus) is diagnostic. Pigmented vil- Sulx.hondro~l pressure erosions mdy lx> found at marlonodular syn- gins of "tight" joint\ slKh as !'tip. ankle. and wrist. They ovitis (PVNS) are caused by an ofttm shghtly dense o~ppeo~ri119 soft (Fig. 5.139) tiswe mass due to hcmosidenn deposition in both tilt• effUStl"'porosis and jo•nt space narrowing are typically absent. Pressure erOSions in the !..nee (most commor1ly in· valved joint) are uncommon. Ost~litis
Hematogenous osteom)lt'lrtrs present\ 1nitially in the
(acute) (Ags. 5 .140, 5.141 and 5.142)
medullary space with focal osteoporosis, endosteal sc.1l· loping. and osteolysis due to hyperemia. edema, abscess formation and trabecular destruction. Progression of the disease to the Haversian and Volkmann's canals results 1n cortical fissuring with subsequent destruction and sub· periosteal absc~s formation. A pcriostNI reaction (lam•· nated or, less commonly. spiculated) 1s a characteristic f1nding at this stage. After one month, a sequestration (detached necrotic cortical bone presenting as radiodense bony spiCule surroonded by gr c~ooL!tion tissue and newly formed cortical bone (•nvollKrum) may be evi· dent. An ope01ng 1n the involuuum IS termed a cloaca. Smus trach ledding to the skin surface are often evident. Occasionally intraO\\COUS 9c1s may be !>et'n. In both Ill· fants and ddults extensi<Jn of the disease process into the ddjacent joint is common whereo~s in childhood ( 1 16 years of age) the open growth plate represents an effec tive barrier to the spread of the infection from the metaphysis to the E'piphy~~~ and JOint, re~pectively. Osteomyelrtis from a contigUOtJs soft tissue infE'Ction typi· cally pre!>ents as focal osteoporosis due to edema with wbsequent cortical erosion. Periostitis is another less frequent initial frndrng . Cortical destruction and bone marnm infection w1th abscess forma tron may ensue.
Comments
In t e o~l>~enct: of proper chn1cal rnformat1on a hcafE>d frdultll'\9 in locali7ed bony expan\1011 o!l>d defOimltiE's can at times be difficult to d1fferent1ate from f•brous cly~plasra.
Monoarticular proliferative synovial disorder presenting with insidious onset of swelling. po~in of long duration and decreased range of motion occurnnq typically in young ddult~. A hemorrhagic (chocolate-l»own) joint effusion In the absence of trauma is characteriStic.
Affects all ages but is commonly found in children. dia· betrcs. and rntravenous drug ab~rs. Occurs by hematogenous route, spread from contiguou\ rnfection or direct rmplantation (punctures. penetrating injury and postoperative infection). Pyogenic O\tromyclitrs 1n children is most often caused by staphylococcus aureus. streptococci, escherichia coli, and hemophilus mfluen1ae. Gram· negative orgamSM~ 'lre not uncom· mon rn adults and intravenous drug •bt sci"'\ Tubi'rru/oos osteomyelitis (figs S 143 1nd ~ 144) arises most commonly secondary to serti• .. r· 1~ r.s S. naJ rn· 110ivcment accounts for approxtmately 50~ of ~Ictal tuberculoSis. Compared to pyogenic osteomyelitiS osteopr1rosis is more pronounced, whcreo'S n"'• bone formation is less externive. Tu~rculous dactylitis ("spina vcntosa") (f 19 5 145) r• fers to cystic expansion of the short tubular bones of the hands and feet with varying degrees of periostitis. Cystic tuberculosis pre!>ents as one or rnlJitiple well-defined o~teolytic foci without sclerosis preferentially tn the penpheral skeleton. Fungal osteomyditis (Fig. 5.146) rl" .embles a tuberculous infection. Sohtary or multiple (l'l'!( •lytic lcs1ons v.ith discretE' marg1ns. mrld surroundtng scleros1s and httle or no periosteal reaction are a common presentatron. (contmues on pog£> 120)
Healed fracture. A widened proximal femur shaft with mixed osteolytrc and osteoblas· tic texture is seen mim•cking f1brous dysplam. An ovoid wbchondral cy\t is incidentally set'n In the laterc~l aspect of the acetabular roof. Fig. 5.137
fig. 5.138 Healed stress fracture A locah7cd elhptrcal cort1cal thlck(>ning t\ seen in the medial a~pect of the proximal femur shaft.
5 Localized Bone Lesions
119
Fig. 5.140 Acute osteomyelitis. Patchy demineralization, and beginning endosteal scalloping, cortical fissuring (arrowhead) and laminated periosteal reaction (arrow) are seen in the radius shaft representing the earliest radiographic manifestations of acute hematogenous osteomyelitis.
Fig.5.139 Pigmented villonodular synovitis. Several well-demarcated defects (pressure erosions) are seen in the lateral aspect of the femoral neck and head as well as 1n the acetabulum where they induced a reactive sclerosis.
Fig. 5.142 Osteomyelitis in diabetic foot Besides neuropathic arthropathy manifestabons in the first and fifth toe, osteolytic destruction of the second toe including the head of the second metatarsal is seen caused by osteomyelitis originating from an infected neuropathic sk1n ulcer in the second toe indicated by a metallic marker
a
b
Fig. 5.141 a, b Osteomyelitis. A permeative osteolytic lesion with cortical fissuring and beginning sequestration of a large bone fragment in its center is seen in the humerus shaft (a). One year later an expansile lesion with extensive new cortical bone formation IS found (b) The lesion depicts endosteal sca llop1ng and contains the sequestered bone fragment (arrowheads).
120
Bone
Table 5 10
(Cont.) Localized bone les1ons
Disease
Radiogra hie Find1ngs
Commerds
Brodie's abscess (F1gs 5 147 and 5.148)
Usually solitary. lytiC and often elongated lesion v.ith sclerotic border typically in the metaphyses of long bones Epiphyses, diaphyses, flat and 1rregular bones (e g carpus and tarsus) are less common locations In the epiphySis a arcular we ll-def1ned osteolytic leSIOn 1s typical. In the diaphysis the abscessesmay be found In central, subcortica l or cortical locations. In the cortex the abscess is surrounded by periosteal new bone for mation simulating an osteoid osteorr~a or a stress fracture
Subacute pyogenic osteomyelitiS (smoldenng indolerd mfect10n), usuaMy of staphylococcal ong1n 1s common 1n children. 1n whom the lesion 1s typically located in the pro>c1IT1al or distal tibia metaphySis and somet1mes connected to the growth plate by a tortuous channel. HistologiCally a central purulent or mucoid fluid collection is surrounded by inflammatory granulation tissue and spongy bone eburnation The lesion may occasionally conta1n a central sequestrum
Osteomyel••s (chroniC) (Ff9. 5 149)
Thick irregular sc:lerobc bone wdh radiolucencies and e)tensi\e periostea l new bone forrr~ation is characteristic Signs of remaining actl\llty or reactivation include a change from the pre~10us exam, poorly defined areas of osteolysiS, th1n lammated penosteal reactiOn, poorly defined bony excrescences. and demonstratiOn of a sequestrum, sinus tract or son t1ssue abscess. Sclerosingosteom,.vmu, of Garre (Fig. 5.151 ) is a lowgrade infection without purulent exudate presenting as focal or circumferential cortical thickemng and sclerosis 1n the mandible (most commonly) or diaphyses of long tubular bones In the lat1er locatiOn osteo1d osteoma, stress fracture and Rt!l'ing':,; dsNJ.
LBto acquired S}P/1/Is resembles chroniC ~eomyelitis. ThiCkened sclerotic long bones caused by endosteal and penosteal new bone formation and 111-defmed lytic leSionc (gumma formatiOn) are charactenstiC Chtonk: recorrent mu#lfocal ostPOmy.,.tls (CRMO, c:flroole symrr""rlc pi.Jsma ceU osteomyehtJs) (F1g 5.150) pre~nts most commonly in children with a protracted chn1cal course and often symmetnc Involvement of the medial ends of the clavicles and metaphyses of long bones wrth a combination of osteolySis and osteoscleroSis and extensive penosteal react1on and new bone formatiOn SAPHO rynckome (synovitis. aane . pustulOSIS, hyperostoos, osterus) rr~ay be a related condibon EpldiJrm<;kf corciloma occurs 1n 1'1!. of osteomyel1bs at the of a chronicafty dra1mng Sinus and 1s eviderd as an enlargng soft bssue masserod111g the osteomyelitiC bone
nosis.
we
(contlfiUes
Fig. 5.143 Tuberculous osteomyelitiS A large multiloculated osteolytiC lesion without significant reactive scleroSis is seen in the acetabular roof and adjacent ilium. The mfect10n most likely originated from the hlp where signs of tuberculous arthntis including JOird spa~ narrowing and early eroSIVe changes 1n the femoral head are evident.
Fig.5 144 Tube rcolous spondylitis An erosive leSion on the antero-inferior aspect of LS is associated with marked diSC space narrowing between LS and 51
on PIIOf' 122)
Fig 5.145 Tubercolous dactytn1s ("spina ventosa") ExpanSIIe fusiform enlargement of the first metacarpal depicting a permeative osteolytic pattern IS seen
5 Localized Bone Les1ons
Fig.5.146 Funga l osteomy(coccidiOidomycosis). A solitary osteolytic lesion wrth discrete margin and mild surrounding sclerosis IS seen 1n the olecranon
F1g.5.147 Brodie's abscess An osteolytic les10n w1th sclerotic margin and multiloculated appearance is seen in the prox1mal tibia meta physis The leSIOn IS connected on rts superomedial border by an osteolytic defect (channel) to the growth plate.
ChroniC oste~ A th1ck sclerotic distal humerus shaft containing several rad1oluceoc~es is seen.
Fig.5.150 Chronic recurrent muMocal osteomyelitiS. A thickened sclerotic distal t1bla With severa l medullary and cortical osteolytic foci IS seen.
el~is
Fig.5.149 myel~is
121
F1g 5148 Brodie's abscess An oblong osteolytiC lesion with surrounding scleroSis and minimal periOstitis 1s seen 1n the distal tib1a
Fig. 5.151 ScleroSing osteoof Garre Circumferential cortical thiCkening and scleroSis IS seen tn the llbta diaphysis. myel~is
122
Bone
Table 5.10
(Cont.)
locali:~.cd
bone lesions
Disease
Radlograp.c
Gomam's disease (vaniShIng bOne disease) (l'ig.. .5.1.52)
ProgreSSIVe, ol!en maS&eve osteolySIS wrttlout attempt of repair (no penosteal or osteosclerotic reactiOn) spread•ng across)cunts or rntervertebral spacesiS charactensllc. Preferential locatrons are the hip and shouder rcg10ns, although any bone can be affected. Tapenng or pomting" of the long bones at the sites of osteolysis IS typical In the pE;I\IIS a rapidly destructive arthropathy of the h1p presenting w1th destruction of primarily the femur head must be drfferentiated. This condition may be idIOpathiC, may represent unusual aggreSSI\Ie forms of osteoarthrrtiS, osteonecrosis, CPPOor HADD, or may oocur after rntra-art1cular cortJcosteroid InJections l'mx~trol jmorl'i jo('{:/ l'cjicicrcy (Pf'i'f)}(Fig 5.153) charactenzed by partJal absence of the proximal femur rs dJagnO\oed 10 mfancy
Occurs sporadic at any age without sex predilectiOn, but IS usually dJagnosed before the age of 40 years H1stologrcally a oonmalegnant proliferatiOn of angromatous and fibrous t1ssue IS evedent . Other osteolySis syndromes diagnosed 1n infancy or chid hood 1nclude acrL' (heredrtary or assoaated wrth nephropathy). J-i;rba'.< t'i.•uN (elbows. vi11Sis, knees and ankles) and lrmpKfrwr.< (carpal and tarsal areas and elbows)
Fibromatosis
Solrtary or multiple soft tissue masseswith erosions of the adjacent bone or osteolytic lesions. Cortica l hyperostosis may be associated wrth bone involvement.
Variety of ben1gn, but often aggreSSive frbrous proliferations presenting in both children and adults as tumor-like soft tissue lesiOns. lnvolllement of the adj acent bone is not uncommon m infantile forms of the d1sease.
Symmetnc and slowly progressrve lytic lesions are found 1n the carpal and tarsal bones and the ends of long and snort tubular bones Bone deformities may eventually occur from pathologic fractures.
Rare hereditary disorder of ad1pose trssue affecting pnmanly the bones and brain Presents commonly tn the second or thtrd decade of life wtth painful bones and JOints and subsequently With presenile dementia.
Monostotrc or more commonly polyostotiC asymmetnc lesiOns wrth preferentia l 11wolvement of the pel\lis, femur, lrbia, spene, skull, scapula, and humerus The pattern of 1nvolllement ranges from purely osteolytiC (e g ., osteoporOSIS carcumscnpta in the calvarium, and V· or flame-shaped defect in the diaphyses of long bones) to purely osteosclerotic (e.g., ivory vertebra). The mi><ed pattern (e .g .· picture frame vertebra• and cotton v.ool" appearance of the skull) that is usually associated ~. rth bony enlargement, cortJcal thickening, and coarse trabeculatiOn represents the most common manefestabon In long bones the desease charactenstically progres~s from an eptphyses to the diaphySis Bone softening may result in bowing deformrties of the long bones, acetabular protruSion, b iconcave compresSIOn of vertebral end plates, and basilar mvagirJation Comphcatlons rndude cort1ca l stress fractures (s1ngle or multiple horizontal radiolucent lines in the convex aspect of the deformed bone (lateral aspect of the femoral neck and shaft, antenor aspect of tibia). transverse pathologic fractures, and sarcomatous degeneration.
Common disorder of m1ddle~ged and elderty pat1ents that 1s often dJagnosed as an InCidental findtng on radiOgraphs obtatned for unrelated ptUrposes The disease IS present m 1O'.lb of pat1ents over the age of 00 years and rare 10 pat1ents under 40. Laboratory f1ndrngs 1ndude elevated alkaline phosphatase and hydroxyproline levels in the serum and abnormally high hydroxyproline urine levels. Serum acid phosphatase values are normal Neoplastic trnolllement 1n Paget's d1sease includes sarcomatous degeneration, g1ant cell tumor, aneurysmal bone cyst, and supenmpoSition of metastases, multiple myeloma and lymphoma Sarcomatous degeneratiOn occurs rn approximately 1., of patients usually over 55 years of age Predomrnantly osteolytic osteosarcomas (60 • ). malignant fi brous h1St1ocytomal fibrosarcomas (25 %)and chondrosarcomas (1 0%) are the most frequent tumors found In sarcomatous degeneratiOn.
(Fig. 5. 154)
Membranous
lipodystrophy (polycystic
lipomem·
Findings
branous oslleodysptasla)
(fig.. .5 1.5.5)
Pagers disease (osteitis deformans) (flO. 5.156, 5.157,5.158, 5159,5.160, 5.161 , and
5.162)
(wulil.lti'~
Oil
pc.f!.C 125)
5 LocaliZed Bone Les1ons
Fig.5.152 Gorham's disease (van1sh1ng bone disease). Complete osteolySIS of the left prox1mal femur and beginn1ng osteolySIS of the left acetabulum and adjacent mnominate bone Without e1ther periosteal reaction or reactive sclerosis is
Fig.5.153 Proximal femoral focal deficiency (PFFD) Dysplastic acetabulum and absent proximal femur are seen.
seen.
Fig 5 155 Membranous lipodystrophy 1/'vell-df marcated cystic leSIOns are seen in the carpal bones.
Fig.5 156 Pagers d1sease. MO<ed osteolytic and oslt..'OSCierotlc form IS seen 1n the proximal femur and pelv1s and a predominantly osteolytic form With V- or flame-shaped osteolytiC defect (arrows) in the femur shaft.
123
Fig 5 154 Fibromatosis. Osteolytic leSions with pathologiC fractures are seen in the distal tibia and fibula 1n thiS aggresSIVe 1nfanble form.
F1g 5 157 Pagers diSease. MD<ed osteolytic 1nd o 1to. lerot1c form is seen en the dl:olal femllf and prox1mal llbiCI F1ndings 1nclude bony expansion, coarse trabeculation thiCkened corhoes, bow1ng deformrt1es and a pseudoarthrOSJ& 1n the distal femur.
124
Bone
Fig 5.159 Pagel's disease. An t>nlorgcd voo1cbral bOOy wrlh coorsc voo1ocal striations and scholoc ("pic> lure frvn>e voo1ebrai IS seen
,.,.,og;,.,..
., l3.
FIQ 5 158 Paget's disease SciNOiic skull b~~se, thiCkened vaun (espea«ll)l lhe innfl!' table ol the frontoponetal bone) and mul"'le ~leroloc foci ("COlton woor appcardnro) are dkl{lnosbc.
FIQ 5.160 Pagct"s disease. A slightly enlarged -IVory vertebra• os S'*'ll al L4 .
Fig. 5.161 Aneurysmal bone cyst In Pagers disease. A welklema.rcaled corticol lefJon (arrow) wtlh 6Cicrotic border originates from the anterior cortex of the distal femur wilh characteristic findings of Pogct'& dtSCuSG.
Fog 5.162 Osteosarcoma 11 Pagel"s dosease A hugo, piU1ry ~ofoed soft hssue mass is seen origonahng from ltoe de$lruded pJmmal femur IJ~nR around the hemiarthroplasly. Characterishc features of Pagch dOS<>a!.e are prest:nl 11 the right hemipeMs and lemur.
5 LocaliZed Bone Les1ons
125
Table 5. 10 (Cant) Localized bone lesions D1sease F1brous dysplasia (Figs 5163, 5.164, 5.165 and 5.166)
Comments Solitary or multiple often shghlly e•panSIIe radiolucent ~ons that may ha~e a hazy quality ("ground glass" appearance). The matnx may also be umfonnly dense. partially calcified or ossified. or thick dense bands may be present. A curvilinear sderobc rim may outline lytic leSions. The monostotic fonn (75 X) commonly involves a rib. femur. tibia humerus and mand1ble. whereas the polyostotic form (25 X) frequently involves the skull and facial bones. pelvis. spine and shoulder girdle beSides the long tubular bones. PolyostotiC fibrous dysplasia may be unilateral or bllater~JI and may affect several bones of a single I mb or both bmbs. Solitary leSions 1n the long bones are located 1n the d&aphyses or. lesscommonly. metaphyses. Bovnng deformities are frequent 1n the polyostotic fonn
Usually d&agnosed before the age of 30. In the McCt,,w-.llhn~hl syndrome precocious female sexual dcveloproont and cafe.au-lait spots are associated wrth the polyostotic fonn. DO Vn,mtihH~ttlll· to.~i-•. where more irregularly contoured and darker cafe-au-lait spots are frequently associated with similar bone lesions 0~.11ji·u/K j,J"·c•l. ll.\ are closely related to fibrOUS dysplasia and occur 1n the facial bones (especially mand1ble) and tubular bones (especially anterior aspect of bbia) In the tatter location they are also referred to asn.,tmfihrrlltJ dn-rlrmn (Fig 5.167)
(COII/1/UI{',\
Fig.5.163 F1brous dysplaSia Slightly eKpanSIIe. inhomogeneou leSIOn with "ground glass" appearance that IS parbally surrounded by a sderobc marg1n is seen in the proximal
femur
""
/'
FIQ 5164 FibrOUS dysplasia. A slightly e pallSIIe septated osteolytic iesion is seen in the dJSial humerus. Sderotic expansiOn IS evident 1n the prox1mal ulna Or,teolytlc leSions With endosleal scalloping are present 1n the mid ulnar shalt.
126
Bone
a
Fig. 5.165a, b Polyostotic fibn and beginning bowing deformity is also evident in the femoral neck and intertrochanteric area. b
Fig 5.167 Osteofibrous dysplasia. An expansile multiloculated osteolybc lesion is seen originating from the anterior cortex of the tibia shaft that appears somewhat irregularly thickened A healing pseudofracture (arrow) is also evident.
Fig 5.166 Fibrous dysplasia. ExtensiVe miXed osteolytic and osteoblastic lesions with trabeculation and calcrfteations are seen in the ilium and hip. Coxa vara deformity ("shepherd's crook") is also evident.
5 LocaliZed Bone Lesions
Table 5.10
(Cont)
loca li:~cd
bone
127
l~ion s
c
Disease
Radiographic
Sarcordos.s (Fig 5 .168)
A solitary or multrple osteolytiC lesionswrth a coarsened or lace-work trabecular pattern that may be associated with endosteal scalloping or cortiCal VIOlation wllhout penosteal reactron ISthe most common presentation. Purely osteolytiC ("punched-out") cysbc lesions or purely osteo~rotiC foa are lesscommon presentatioriS. The hand IS the predomrnant ~te of rnvolvement. v.tlere acrosderos.sor aero-osteolysis may also be present.
Osseoussarcordos.s is uwally assocrated w1th erther sl
Presents typically as scaUoped osteolytic lesion wrth or
Forergn bcldy reactiOn to wear debns of prosthetic components such as pol)methylrnethacrylate cement. polyethylene arid ~hcone. Rarely an mlt(Jn.«crntJ jorur,n />()(II' gm1,dm"ft IS found that IS not assoaated w1th JOint replacement surgery or any other known cause of accidental forergn bcldy implantatiOn.
Parllculate disease (Frgs 5169. 5170, and 5171)
Ancllngs
wllho~ sclerotiC margrns about a prosthetic com-
ponent Larger expensle lesiOns may become trabeculated and eventually break through cortex wrthout rncrtmg a periOsteal reaction.
Fig.5168 a, b Sarcoidosis. Multiple osteo lytiC lesions wrth a honeycomb or lacework trabecular pattern, some of which dePICt endostea l scalloping or cortica l v1olat10n wrthout penosteal reaction are seen rn the hand (a) and foot (b)
a
b
Fig.5 .169 Foreign body granulomas An expariSrle trabeculated IP' ~on~ rth sclerotiC margrn rs seen rn Ilk proxrmal femur shaft wrapprng around the ferooral component of the total hrp prosthesis. A similar smaller second leSion rs evident JUSt below the acetabular component
Fig 5 170 Particulate disease. An aggressille osteolytic lesiOn with deliCate trabeculatiOn and cortiCal VIOla· liOn rs surrourldmg the loose femoral component of the dislocated total hip prosthesis. A similar second lesion wrth bony expansron but wrthout cortiCal VI· alatiOn IS found around the loose acetabular component
Frg 5 171 Foreign body granuloma An oblong eCt"".entric lesion v.rth sclerotic marg1n resemblrng a non~fyrng fibroma IS seen 1n the posteuor a sped of the diStal femur metaphysrs (arrows). No history of accidental foreign body implantation was available '" thiS case
129
6
Joint Diseases
A ruultit11dc of rudiologic dlaltj.:~o:s o~o;cw in mticular disorders. No single mdJOgJaphic lindlng i!. ho\\ cv cr diagnostic for a S)A:dhc arthropothy, since md1vidual lcsioiL-; in many conditions appcur !-.imilur. 'J11e wmhination' of variOlll; mdiologic pammctcrs may lc;1d to an accumtc diagnosis, especially \\hl..'lt Jll.'ltUlL1Jt dinicul and luhoratory lindil~gs are taken u1to COJNd<.:rahon. llte time and se<JUC!Il:C of arthritic abnormalities obscnod mth respect to the evoluhon of the dtscas.! may also om..,- unportant clu..-s to the corrcd diagnosis. l-or example n mpidly propn.:s.,in!! dcstruchvc arthntic process 111\'0h·ing a smglc J0111t JS VIrtually dtagnost1c lor septic (pyogl:'lllC) arthnhs. ('~o:rtmn diM:I any arthmpathy 1111L"t mcludt: tht: lhllo\\ m~· u1h:na I Number of Joints mv oh oo (monow11cular vt:rslL' polyurtt<:ulur). 2 Distnhution Jk'tlcm ol unohed JOints '\ joint spate "1dth. 4 I msion 5 Subchondral cysts. 6 . hagm<.11tation of suocbond al hone and k><1sc mlm·articular Osh.:ophy to~•". entheS(>pathy, tlt!ri<>~titis). l\. 0~1l:'r j.:t:nCTaliied). 9 joint ddonnitic:- 10 CJI(liKlroc and penartkular soft ti.,,uc cukificatiow.. II joint c11usiott' and par.Htrtkular S(>l\ hs.'liC a0<1onnalit•c.,..
Monoarticular arthritis
Cl••blc 6 .1)
Anarthritic p1occss mvolvm!' usmglcjoinl t'wnunonly fow1d in iltfcctiotL" wthnli". glk' arthritis jou1t space IIUITO\\ ing, joint dl'u-;ion and petiartu.:ulm o~tcopomsis arc chmadcri~ticalh Jllt..oo;cnt in the cud~ ~tagc followed by poorlY dcfmcd bone dc:-.tru1.tion. Smcc pcnmticular osll:'Oporosis and jou1l space nanowiu!! me not )ltt....oo;cnt in gout, ostcomtluitis and uvusculur nccn>~i~. cv cty monoarticular di:;casc dcpictil~g U1c:;c two wdtogwphic ubnonnulitics must be considcted ulleclious Ul OJigm until pto\Cil other\\ isc. OsS(,.'()l)l; erosiotlli and cysts in gout arc shurpl'r marginated as opposed to U1e poorly ddiiwd bone d<.'Struution 111 mfcctious arthriti.-. Ostcourtluitis s..'Condarv to tJ mu11u nwv at times be dif· ficult to dtllcn.11lJHtc lwm gmit 111 ~1null jomt~ · \\lthout JIOP..'~" clinica) his!O!) and lahont(OIY fmdings, SIIICC OSS<."'Oll~ CfOSJOilS may s-imulate post-tr:mmutit dcii.'Cts. AH1scular tl'..'Cmsis u1 the early stage prCl'ol..1tl:- \\ltl nonnal mdiograplnc fmdings. SubMxjtu.;•ntly pollhy hK1.1ll lUld sc:btltic.: llrCII~ may re SC..'I..'Il in the slihchondml hone on om: ,ltk of;uomt lolto"cd by a dtagnostlc an:-hkc sulxhondrnl lucl:'IIC) (cr~cnt sign) and C\"Ciltuall} hagmet1tation and wlhlfhC ofthc 111voln:d hone.
Polyarticular arthritis
('I ahlc
c, 2)
Rhetmlatmd wthnt1s. s..-ro11q;ahve :-l>ond) lwthropalhy (ps<'rialic arthnh:-. Rl.'itds s~ndroJIIC, ankvlosmg S')1ondy-
Table 6.1
Monoarticular disease
luJl.'C lit.>lL~ mt1Ult ts: py0{!1..1lit: tuk'nulous fungal Gout Hydrox-yapalitcdq><'slltc>n clL<;ca.<;C (I lAO< l) TrdlUUatic wthntis Sccondan· ost..:oarthntis A \a~ular l tu:msis (osh.:<>li<.'CIOsls) l'igml:'Ili<.XI 'illonodularsy. noV" it is ·~ noviaio~h:ochoudwmatosis
( >stcochondnti:< t.hss..'l·ans
Table 6.2
Polyarticular disease
(}.,k"\>arthnlls
l:.rl:*n costet)(lrthnhs RhctUllatoid arthr itis Psoriatic.: urthntis Reil~o.'J's sy1Klrmnc 1\n\.:~ lo~ingspoudy hti.-;
litis and cntcropathic arthropathy), gout, calcmm pyTophosphatc dihydrate C!)stal dcpooit1on di.~se (C. PPO), ostcoarthnlls and ncun1p;tthk arthwp:tth) urc the most common polyarticular JOIIll diS(lfJ)(lrl>sis, 111ld lu:-ift >nn soli ti~'id arthntis An t:n1st\ t: arthritis pwct:s.' mv<>h 111g 0t1lh :-ynov i.1l and libmcartilagt:noll~ JOmts (t:g. pub1c sylllJ'hysis und m:muhriosktnal
130
Bone
Tablc 6.J
Distribution
pattern~
of
l)()l~ at1icular
di!leaM.'S
Bllateral
sym-
metric
Prinuuv ost=1hntts Erosh t.'Osk'tlill1hntis Rhcumatmd m1hnlis 1\nk.)losin~svond\ litis CI'I'O llcmcx:hrom:nosis Ochronosis Mull1C<.-''l1tric ret k ulolust101:\ l
arthnhs Systanit- lupus t.or:-tkmatoslb Sclt."T(>d<.Tllla t.lultiplcq1iph\ ,,,[l[~·splasHt
Asymmetric
Scwndan ostcourthnt1s Psoriatic w1lmti-. RCitds s~ ndrome Gout
Distal Inter-
Osteoarthritis hosi\ t.·ostu1mthrit is Psorialk: arthritis Gout Mulhtt.11lrit J<:tK.uk>hbtiol:\ to:-is Sdcnxknna -
phalarlg@al joints (hand)
ProxJmal lnlerphala~l
joints
(hand)
Ostcoru1hntis Erosn cost..:oarthnt is Rhctunatmd urthnt is Psonahc arthritis Gout MulticCiltric reltculohishocvtosis Sclcr<xlc.:nnu Su:onuw: ost\.'tlattlu it is Rh.:unwtoid arthritis Gout (PPO Ik111<'1;11r<'tMhllit~
juaouJ's urtlu itis Sysk11uc lupus '-'ll-tllulwtosw. First carpometacarpal joint
Common
car-
pometacarpaljolnt Midcarpal
joint
RadiOcarpal )Oint
Ostcoorthrit is Rhclunatoid arthrilts Gout Systemrc lupus ._,ythem111oM1S Rhewnatoid mtlu it is Gout O.t.xllll11U1hs (sct•1~1otm1l(!fiotmpc zoidaljoi11t) Rhcwnatoid m1hntis (i.ndudmg triquctropisilonn jomt) Gout (PPl) (swphollliJX'/t<•lr.JJlC7<•niJI JOint) Sccoudar\
o~k~'lillthnhs
Rllcwnatoid mtluitb Gout (PPO I h.:mocluomato~ts Distal radiOulnar joint
Rluunutoid m tlu ills Gout SdlcrodCima
jomts) und tl1e ligamentous alluclml\.1tl'- in the pchiS. f\.1nur· and c<•kanctL' in an ollc.:n a ..-,nunclric liL.J11<>n ~~ d1 m~<:t.:ri~ tic f(•t a !'-C!H!Cg!lll\c spondylartllmpatJty ·nm. dt.tgnosis is further slll'flJllltll\ ut ru t.-arly stage muy t<-"M-1nblc osteoarthritis and (1'1'0, but c'tcushc stlcro~is lL"-WwatcJ witl1 joint frag.mcntahon, lwdurcs <md sublu,utiomJdislocations is \'irtuully dia~nostiL in u mo1c adumct.'\1 wsc.
Distribution patterns of articular diseases (fable 6.1) S)tnmctnt joint imoht.wcnt is t\')>k:al of rho.:tumrtoid artllritis, primarv ost...-ourtluitis, (PPO and tK:UJ< puthit: urt1m•rli.tt11~. \\h\.1CU." an a,!·nunctril dtstribut1<'n of the af(~.X;too _tomts fit\ Or:, t11c diagnosis of a !'>Crtlll\.'gUti\c ::,pond)btrthWlXtlh\ S'-'\:<>tlililry ost.xllll111ritis und ~t>nt In the hmtd noncroshe arthritic chW~j!Cs invol\ 111!1 U1e dislui interphulungcal joints suggest:-. ost'-'r the !'><.'Cond and thin! metittiiTJl<'Phabttlj!cal jomts and t1lc radioca!JX!I JOin!. lnmh·etnCill of 111~.; metacarpophalangeal jomts is COlllDlOn m hc>th rhelUtwtotd and pMmatic arthritis, but these joints nrc usually Sl"l;.lfW by botll JlOilllll)i und eJOSI\C osteoarthritis. In the \\1i~t erosh·c arthritic changt.'S '' ithout site prcdik'\:tion me \cry LOIJUllOll in rhclUnutoid wtlmtis und gout und less lrequcnt in psoriatic m1htopatlw 13ot11 p1in1<1JY ostcourthritt:. tuld (PPO ha\'c a pr..xlil~.X;llon lor the fust ca'rpomctaeaqllll jornt mtd tile joint bet\\ C\.11 the sca1~1oid and trJ)lC/Illm·tiitllCIOid. In the lb<.>t prim~ ostCOOJ1hritis rs t\Titully locat..xl in botl1 t!K fiN mctalar'>O~eal jomt (h. llu\ rigidw.), \\)l\.1\; it lllil) be a~-.ocialcJ witll hallu'l. Ht4:tL'i dcfonnitv, and 111 the lin-t taNOmctatur:-al joint Rhctmwtoid ur1hritis tt•mmonl) all'Ccts t11c mterphalangc.:tCiltiall) am:ct any jmnt <>I the forefoot, but the mo~t severe changes commonlv o~:x;ut in the metatarwphalmlj!cal joints and the mtct)11{ahmgc.:<1l JOmt of the gro.::tt l<>c <•out ~10ws a predilcctton lor the ln:-.t mctatarWl~UJI:mgcttl J(llllt ;md to a lesser dt."gr'-'\: the rntt.•rphal;mgeal JOillt ol the gro.::tt toe, ti'IC metattNOrhalallg..:
6 Joint Dtseases forefoot and midloot um he um.x.t4.xl. Neumr~ttlm: arthropathy in diahet~ muy tmolve the mctatuNJphalangeal jomts and all jomts of the mtd fo<>l and hindlll. as \\ell as the posU.~UJX:rior a'1x:.:1 oflhe calcat1ClL'i thut abuts the rctrocalcancal bursa. Rctrocakancal burs1tis IC<Jd.-. ll• wtilatcral or bilat4.Tctl 4-Tosions at this sit.. 111 rlu.:umutoid arthritis. LocaliLcd 1etrOUtkanwl burstlis not rdato.Jd to a systo.:mit ru1hritK. pnx:e-..-. j, ll.11nw Hagunds syndrome (IIi!- (, I). ·1 he co1 dition is aggmHtlu.l h~ u Jll'<'mino.:nt hrdllCe at the ~kro-supenor u~pett of the calwneus (Hal)lund's delonnlty) I he hallmati. olthc ~'l'lmtoguli\e SJ'll•ndyloorthropathies arc tlufl)r pcnost1tis aboul the postcnor and mtenor aspect ofthe calcaneus mtd tTol~<.lhn-.t-d Sl)llrs (t"'ttcsophytcs) at the attaclunent or tllc Achllks tendon and plantar aponeuroSIS (1 ig. 6.2). Lroswns ut tltcsc sites us \\ell IL' ncar tl1e retrocalcancal bursa m.: not u dominant JUdiO!(Htphic fcatut.: in tha;c conditions. lnostcomthriti:-. \\ell-defined and typicall) narrow-has..:d calc·pace a11d patdlofc1noml _toint ) '' ith mu11\cd joint >opaco.: narro\\ing, OstcoporO,IS !Uld O.:Cil!>ltlll!> IS\ irtuaJh dtagnosliC Of rheumatoid arthritis. A lritomt"'rtmo.:nt.tl dtstnbution may also he found in ~-roncplli\ c ...pond\ larthro]1(1thies, hut the m\OI\'ement 1s lreqll4-"1111~ Us)mmdn<.: 1md 14....._, S<.:\4-Te than m rheumatoid arthntis tutd p.:riost.:<~l nC\\ bone lomwtion may be (rOnowx:cd. In ostcoarthritl<; the medial compartment i:; 1). pt<.:aU~ more SC\ 4-Td:V ull'ctto.Jd than tlte latcml compartm4.nt resultin!! frU.JU4.11tly in \anL~ lkfonnitv Sig.nifitant d..:-g4."1lCrati\o.: tbat~o.:s in tltc patdlofemcwl joint tna) be ao;.!!T4-'Ssion of the arthntic process mdudmg o~'Ous d.:slntchon and tmgmcntation favor the fomtcr dtagnosis lso latt'() dt"gt'llemlt\'e-hke arthropathy of the patellolcmoml toint should also mise the possibilil\' of CL>PO. Neurop11thtc urtltropathy ts choractcriLcd by disoJBaniLution of one 01 botl1 knees induding sublll'illliou, fmgmo.:utation and o.::\teu~ivc stlerosts. In tl1c hip tllc Jliltlcm oftomt spate los.-. ma.,_ be u:-.eful to ditlerentiatc Huious mtkulm disca:-.es Citcwnfcrentiul (a\lal or ~:om:entric) los.~ of1oint sJlrdl neck (Frg 6.4) t'tn:wnli.1'4.1tltal los.-. ofJomt 'll1tte is a~iated \\llh riJCtunatotd artltntts \\here hoth htps are affected m symmclrk. titshtOil. A umlatcrnl (monoarticul..'l!') concentric Jos.o; ot JOIIlt SJXICC sugg4.~ts an mtectious proccs.<; but ts also foWKI mth td10putluc chondrolvs1s of the hip. In anl.:ylosing spondvliti:; u similar bilateral concentric JOint space los.-. is fowtd ILS Ill rho.:wnutoid Urtllfi(j,,, but the Jli'<.'SCllte of OSlo.:oph\ (O~is, lOlllllll.,lting 011 the supcroJat..m) a:.-po.x;t of the funOhll head and pwg 1cs....mg to " toliar about tl1e ft11t<•ml head-neck jlUttlion, is distindhc 11f the fomtt.T disord~r llip unoho.:nK1tt 111 both Jl~>li!ttK: urthriti.-. and ReiIds s-yndrome 1s 'mular to ank;.losing stxnl(}'ylitis but un-
131
• ..., • '
•
fig () I Haglund's sy11dromc • \k1tsl\ ct.'!'IN\ e ch:mgo.:s m tlte JlOS(<.'I1lSli!'<.'TiOr !t~JX."'d (lf the OIIWIII.!ll-. Hre II !><X:Iall.'o \\llh new h~1ne fimnation and l<x:alitcdsoft tisMto.: mas.' :::..x:<>1'lllar. to ro.:tmcalcmlCIII bw"JSitis.
I ig.6.2
JnJ1ammator> calcaneal spur (entl1csophyte). A broad-l'll't~ plantar ct~ll:mte
l1g 6 l I)t-gcncmu' e calcaneal s~trs (enthc!>sk1l<'tly und phmtnr 11(l011C.:UIOSIS infcrtOJ1) ( otC:I()llll.!l;ill)')
Fig 6.4 Cin:wnti:n:ntial I<JS-'> of j<1illt SJl
132
Bone
l1g.6.S A~ymmelric loss OfJOUlt Sj"XKe NatTowmgol the joint ~pale is limited to the superior (wcight-b.:arlltg urut of the hip rutd ts ns:;oti;tt.xl with rcacti,·c sclcroSJs and sulx.hondr.tl cyst fonnatton (ost..:oarthritis) ·
I ig.6.6 I latchet sign. Aneros1on limited to the lateral aspect of thl humeral head (arrows) produces a delonlllt:> r<.'llliJliscent of a liutdlet ll1i.., fmding i ... twic.all\ tl'-'><" wtl.'d w1th ankvlosing. spond:.litis or l~al arthritis ru. in this ca.o;c. It should not be confuSl."Xl \\1th a I hii-Sachsclefcct sccondnf\ to nn ant..:rior shoulder dishll:lltKln.l <><"-Cmtra-articular hony fra~'lmmts (IIITO\\heads)and a
common In ('1'1'0 wulateral or h1latcml conumtric loss of joint spalC is lls.-;()(:t.tted with sclerosis. osh..'n. l'mtJ IL'lO acetabu/1 (M:C I ig.(>.IKI\htis. osteoarthritis (m.xlihtuneral joints comhmed '' 1th \\ 1dcnc..\l <.,TOdc..'d HUOIIliOduvicular joint:; is chuructCtish<. fm lhl.'lliiiiJtoid mthrilts. Ankvlosing S")Xmd) litis p1c..-scnts 111 similar fa.>hion. but u latgc bony defect (e1os1on) on Ute supcrolutt:wl aspu:t or the humeml head. tile "hatthct" dcfounity (fig.6.6), the ui~IICC of ostcopo10sis and the pres<.1ll:c of bon) pwliferation about the OS..'>l-'OU.' cwsions m..: duc.:s to difll:rl.1ltiatc it from rbcwuatoid arthnlls. Sc\eJc o:,tcoarthrit•s in the gk110lmm..:ntl jt,int is lL,tmlly "-''><X:IJt.xl with pr<.'\ tou.-. truwna or O\crtJ:>C and is U~crclbrc most on._,. wulutcJUI 1\crvmiotJ.l\ ic.ular joint lkgc..1lelpur.; protrudiltg infi..'l'iorly from this joint !Ul() the udjac.:c..'llt unden;urfucc of the ucJQtlllon. In CPPOan ad\'anccd degc..'IJCI,IIJ\ c-like process in U1c glenolnuneral joint may be us.'>otiatc..'d wiU1 chondwcukmosis. Calcilllll hydro:\)"£1)'lttite crystal dqXJsition dtsuL..c (111\00) presenting initioll;. '' ith cloud-like caltllications m the rotator cuJI or suhacronual buNt may (rOgrcs.-; to u dc...,1mch\ e arthropathy of U1e glcll<>humt.ntl JOmt \\ith chrun~.. mtator cuJf tear, the so-call.xl Milwaukee shoulder s;.11
Joint space width (Tables 6.4 and 65) 1\nalys•s ol the \\1dlh ot the JOint space may pronde llll)JOrtant clues m the dill"crential diagoos1s of arthnllc disorders. In these condihons the joint space may t>c nmnlw<.'Cl, nonnal or \\ldl.'IIC..'CI l'urthermore jomt sp.-1cc namm'ing may he synunctnc or !I~> mmclric and occur c:rrlv or h•te Ill the dis)"lfOCCS.' S)~llmetnc JOint space los!.. 111\0h mg an entire joint emlv Ill the dJ=tsc procc...., 1s suggcsll\c ol an mti:chou.., or inllummatory arthritiC d1soulcr. An as) nunetric joint spa~c narro\\ing mlhe large jomts ol the hmcr c:\tremit;. is indk~tti\e of ost~Xtrthritis. In U1is wnd1tion suldl(llldml sclchlsis usual lv precedes a mdiol!l,tphict•ll) a]'l'let:iablc joint spuc:c los.-. AdHmccd c..Tosi\C m dl."'uncti\e joint di~1sc '' 1U1 tdati\cl~ well-lilllintmncd joint spu..:c and Joint imohement sugl!c.."'ts gout and asy mmclllt ostccmccwsis, Jcspecti\'cly. A wid..:nw joint space is typiwllv uss<x: iatw with lurg.e joint effusions, especially in c:hddrc..'ll, mKI hunathrosis secondary to tmwna. hemophilia or oU1cr blc..'Cding disord<.TI. Joint la.xit~ in ncuromuswlar di.'>C>rc.lcrs fre<Jucntly pn~cnl'i with a '' idcuw jomt ~llllCC too. 1\ droopilif shedder (Fig. 6.8) is an ntl\.:nc•r "sublu.'-Ution" or tile l•u1 1crul hcuJ t
ease
fip,.<•.7 Milwaukee shoulder ( lmld-liko::Hicllile~tionin the rotator cull' and subatTornial bursa ))fOJc..'Ctinp, bd\\c.>.:n the dis1al auomion w1d luuueral head arc a'-'>tll:iat.xl with dc:structi\c ~hould..:r urthntis and chronic rotator culf tear endcnt bv the dccrca'l.'d d1stancc between humeral hc;.td and inkTJOr ~ ol the lttT<'minn
6 .lomt I )Jsea~'S
(eg. in intra-articulm J)l(l'llllrdl.,. ulll:ding the supporting mw«:ulalur.: or any direct inl u.ry of Ute capsule or rotator culT itseu·. Tnk! ~ublu,<Jt ion:-. tmcl di~lo<:atiotl.'-. lYptcaUy pte:scnt al.w as JOint SJ'tl:>tdunt>lc \\ld1.11ing <>t'thc JOIIll sJ'rio~til.: arthropatlt) \\hen se..-ere deslrudror of the sulxhondml hone is pre;enl This cot~ht.ion hits to be drlli.:r...,lliat...xl lrom S.XJUclllo! ofrcs.xtion arthroplast ics wnsistrng <>1" rCJilr hotlt mtKular ~urta.:cs in an mll.,-phalwtgeint. A 1ridmed acromiocla\ ic.:ui<Jr JOIIII (I ig. 6. 9) rs a frctJill-111 findu1g 111 r!K.:tunal<> icl arthriti.:- tmd ~>riatic lUthtlll)itlh~ . hut abo crtcountcrcd in infectiow.. arthnti~. tnnmutllt· S<:l)itflltKlll post-trnumatic ost.:olys1s (e.g \\l.'lf!.hl lillers). uc.:mmt<>plast~ \\ rth r=tion of Ute distal cla\Kic, arK! hyiX'fJ"li.U
Erosions (Table 6 6)
133
Ftg.6.8 Oroop1ng shoulder A large hpohemarthrosrs with fatblood level (arrows) secondary to a nondr.;placed greater tuberosity fracture produces 1nfenor sublu~ahon of the humeral head evident by the increased dtstance between the latter and the inferior aspect of the acrom1on
Marginal articular cr osi<m~ at oss.:ous surll.K!.'l> Utal do not pos.'>Cs.'> protcchvc cartilage we typicul for early rltetunatoid arthritis (Jig 6. 10). lltc erosions typically arc poorly ddinccl and witltoul !,J;lctotlc margin. In llte hand and wnst S)-lnmelric unohemcnl With prcclill'Ct1on fm the pro,imul inlerphalmtgcHI and mclitcafJll>phal;mgcal joints. trapc;ium, capital.: scaphotd, lrKJUctrwn und p1:-.rfonu. and boUt Ute
Table 6.4
Narrowed joint space
OsteoarthritiS (often o"~mmctn... tn wc•ght-beanng )Olnls) Rheumatoid arthritiS
Fig 6.9 1/Vtdenrng of the acrom1oclavteular JOint IS caused by erOSIOn of the d1stal clavtele and to a let'.~r degree the distal acromion (secondary hyperparalhyroldt5111).
Psonallc arthntls Reiter's ~ ndrome Ankylosrng spondyhlls (1'1'0
Hemodlromatosis
HM.OO Ochronosis Infectious arthnlis Hemophilia Mult•ple eptphyseal dy<>plaSJa Endstage of any arthnlte process
Table 6.5
Widened joint space
Subluxatton or dtslocallon (congenatal, traumatiC) Hemarthrosrs
Of
large JOint effusion
Jomt laxrty (neuromuscular, traumatiC)
PsoriaSIS Nel.l'opathlc osteoarthropathy Aacmegaly Pigmented vdlonodular syno' rtiS Syno\ ral osteochonclromatosrs Syno\ ial neoplasm Resec!ton arthroplasty
Ftg.6.1 0 Erosions in rheumatoid arthritiS. MuHtple preferentially marginal erosrons~ rth symmetnc dtslnbulton and charactenstic localization (spaTTing or the dt&tallnterphatangeal JOints) are seen
Bone
134
Table 6 6
Erosions
I rost\cosk<~rlhnhs Hheum
Anhlosrnp;ponth hits
IL\<X> Atn) ImdoSis
Mmtkl.'lltnc rdiculdu,hot~ toSJs IJUl.\.I!OUS
~c il>rOlkrma
r\1\S,pt<.'S.'>IIIC eto,.ions) '}ll0\'ialos1cochondmmah •ts (I'I Cs~;ure ero~tons) Artiwlw tlcft..-.h sit, tUiatitlf CHI;.it\JI'i 111 (1'1 '0. osl<.'(lllL'\:W!->is. Ost~;
fig.6. 11 hos1on~ in pl-l.matic arthrit1s Mulhplt: marginal erosi<•n!->IHC urth tingl.T
radial ruxl ulnar stv)ol(.l 1s <:ham<:tm;.tic A pooily defined monom1icu1ar crOM\ c arthritic proce-.-. suggt:!->ls an mfectimt<; etiology. In p:-•oriallc arthmp:.th) (Ftg 6. 11 ) margmal cro;.iorb chamctcri;.ticall~ an.: as.'-<x:iatcd witi1 adJaCt:tlt hnny pmlilerntion C\ idcnt a' irrctzular c'\LTenc (lf more eccentnc eros10ns \\1lh <.ek'l"oiJt· margm and n
Subchondral cysts
I !'Ill-ions u1 gout [u:wlric cr()!.ions \nth O\ ..,... hanging edge (arro\\) and a~'od,ttl.!ll soh riJ.!.( 12
u. .'ll('
ma'' h
~'(·n
hg 6.B Fragmentation of the articular surface u1 frostbit..:. fmg11~<.1\WltOII t>f the distal art KUI|
'I he n.1nammg less expoM:d tingl.b \\ere ull
(Tublc 6.7)
Single or mulhplc rudioluct'llt lesions witi1 sclerotic margins arc conunonly found "1th ost<-'C>w11uills. (PPO. and ostoonecrosL'> (rig. 6.14 ). In botl1 osteoarthritis and osteonecrosis thc!>C cy~ts me typicullv locutcd \\itilin ti1e pr~urc SC!!lllCnt of the .1oint whe1<:as in (PI'O titcy urc morc \\1desprcad w1d licquently unusuullr large A subchondral cyst occu,ionally L' ti-..: -l.'jUcla of 11 bone injwy tiun becomes c\'idmt O\ t'l' u pt'l'iod of month:; after the traumatic episode (lrawnuti<: <:~ st). h1 rlleWimtmd arthritis ti1e subchondml <:y;.ts lr<XJll<-'1111) oripin;~te in the chondro-ossoous jlmction and do not dt'iJtd a ~urrow1di.ng sclerotic IDllfgllt An mlrao~...._'(lll~ gun~tlion Jli<-X11L., us a solitary subchmldml cvsltc lt:hlon \\ith !-t:lcroti<: mmgu1 UJl\Wherc in the subchondml bone of u ~Hnl ll(Jt anl.'\:k'tl l'l\ an urthritit: pn:x:~s. f urtht..'llllOIC Sll!xltondra) C} sb Ulll be m.itnicl.:d by i.ntrdO,....._'Oil' !!<'uty tophll'i. u Brodie's ullSCI..'-' and \ ariL1~ of Il<-'Oplasms (e.g. chondwhl.tstoma g1w1l ~:ell tlllllor. utlr'dO!>scolJs Jipoum. clear tell chondrosaJwtna. and ::.kektal mctastuscs )
6 Joint D1seases
135
Fragmentation of subchondral bones and loose intra-articular bodies (fahlc• 6.1\ nnd 6.9) ol tl~<
Fragmentation
.lrtillllar
>lorfa.:c
(rig.6. 15)
i.• com-
mon!) "'"l'Ciakd \\ tth CI'I'D, ....t~'''""'"'"i<, neuropathic artlltopath), tar a.h:u~<:,d 01 t.-oartltritL'!. .tnd trauma (~teochondral fracture"") ""ullin& fr\:Cju,ntl) in (>flC <>r more loodt" ll.:t...:hcd C'f't.'<>ph)1•"' in <'"'looarthriti.' Ill&) abo lcaJ to kll>MO inlr.t-.lrtk.ul.~r lll>dic'!l. Joint 11.:!l'tf\k.-tion l'C<:<>nd:u~· I<> I') <'(<'1lic or holx-rc'Ul<>u-' arthritis lllll) al'o he ""·ociatlitJ~' C'f'1oochondral fmctun: fragment ma) I'r fred) me>hilc in the joint In S)'Tl<'' ial ol'tc<>di~ located ''ithm and nrNllld the mH>I\cd joint and ranging 111 "'e is. t·hara'-·tcnstil'
ff(lfll
11
lc" mi lhmdcr<
to -'C\crnl Cetllimetcrs
Reactive (productive) bony changes In OJ.I<Xlarthnti' t>l \\cight-hcm·mf.\ Jnmt~o 'dcr<>~o" of the -'Ubd1ondral b<>nc " lrcquentl) the h f'l r.uhographk ,;gn of the disease, 'ince the cHtLml cartilaee dcreneralion
Table 6.7
Fig.6.14 Suhchondml c"y>-1 111 a\n.,..ulnr nccmsis (o~teonecrosis) A ~·~tic le-t<>n 111th -'CII.'r<~t marc•n '-' .c-;;n 111 th~ \\etghtbearing r<>rti<~l of the ddonned and f1illlcncd fcmomt head. Secondruy dcg'-·ucJ4tiH: c.:hungc" im.-ludin~ rcnM·•dcling and nc\\ borlt.! fom1ali<>n (huttrcssme) nl<>nr the mcdml n rc.t of the fcmnmi head and nee!- (arrn\\s) arc aiM> C\l
Subchondral cystic lesions
(JOtll
CI'PO Ann lc-tdosts A\
~.,.I \lllhotrt
1'""1-tmnm.otic
scCrthnt1s
lktUOJ~ulta
lnkdious (llrodt,'s • 1..c~ s) lr•tra<)l.....:HL' ganeliN• llltraOS.,C(•lfS
lt['<'lllD
hone in ost~oorPig.6.1S FrngntL'Illalion ol Mtlxhondrnt thritis. D.:gcncntii\C <:han!''" in the \•etght hc;lrinr, I'Klt1ion nf ti>C hip are '<:en including Mtbdwndral <.:)~>1 fn and beginning fragmentation of h••lh a.:ct.thulm d<>ll'" lllld fcllll>t,ll head.
(hondr<•l•la,hll!l.t Giant <·ell tunwr
1\ lc\aslasis
Table 6 8
F ragme ntlltlon
of articular surface
Table 6.9
Loose intra--articular
Ost.:oorthnti!-
(ad\luKcd
lutrn-artJwlar lo a..1t." (),.t~oorthnt~<
(a•h llll~cxl
••as•)
CPPD
t ~)
CPI'l)
11:\DI>
H\1)1)
Od1rono..,,.
Odtrono>is
lnlixtwus arthnl"'
lnlccttou• urthntts
A\-asculllt nnr(}!;t (o>tooo,uooi )
A\as.:ular tJ<.-.:tm.u.
l\curopathi.: O!.l~uartlm~llllh)
l\
().;tc<'Cll<'ndriiL<
O,k
d"'-'
S~110\ ial
("""·"'"•"
1'6t,oanhrop:lth) dL'--.:~an.'
<1!.1Ccll.h<mdn'tn8IOMS
bodies
136
Bone I if!.6. 16a b Ostcoph)'1<>:.is in osteoarthritis M.ll"glllaao!>Ctcopb:.1cs ili'C ,.,.....,, u tl1e putcllokmoralJomt. b: A central {mlLTKlrJNIIt) (l~te~>ph~tc (arm\\) pr.:;.crtts l'-' hutton-lil.c t:\lTCStL1lle originating fnnn tire Mtbdt<>tKlwl l'<>ne largdy tlL1tlt
II'
b
a
rig(>.J7 EntltL'SO~thy in DIS! I htcn~i\cwcll-de lin<."nmJI ~ruilioc.ioinb.
crut onl) lx: apprcctatcd when n substanttul loss of cartilage has occurred rcsultmg m JOIIlt space nru·mwing. Osf('opl(vtosis (I i!!.6. 16) ts the hallmark ol pnmun· 1md sccondarv · de!!em:mli\e jmnt disease Afar~ina/ o.~te~phvtc•s dc,clop .in the pcnphcry of the articular surlacc of rqomt ruld appear as hps ol new hone. I .:ss common arc (c•untd (mtcrt6r JOint) ().f'l(\11'\ awcaring as button hl.e (lf 11. t OOil\ <."'\Cn..>scenccs that may be demarcated at thctr ro -4.~ ll\ r~manl~ of the origin.tl cartilage simulating occa,,. •null} ioosc mtm-articular boda.:s. I uth(.\C>patl(l' refers to bony prohiCmlion at the stte of osS<.'<>tLs lttl;tchm~t of ligaments nn<.l h..,Kions l'nthesoph)-1e> lltg ( 17) arc commonly found \\1th ~rnm..'f:!all\c spondyloarthropathics and dithL<:e tdiopathtc :-.kcletal hyperostosis (DISII) In the spme these condthon~ me chamch.:risticallyl IIS.<;(lCIIIICd with synde:.TJtOphytcs {osstfkaltons Of the OUter portton ol the annulus fibrosus) 01 J'l<'lmvet1cbral osstfication, r~"l'lC(thelv. '!he thm and \L'Titealh onente<.l sYmmetric s)nd.:snl<;phytes in ank~ lm.ing ~ll<'t~d\ hits cnterop;tthic.: sr<md)larthropathy dtlkr from the hroaJer asymmetric S)Jl(h.."SSltophytes ol JN'!'I
and
sharp!~ nuugmatcd lL'- opposed to the mtlammutory cnthclo.(lphytcs lt~<;(KIIItt:d With tl1e SL'rOIIL'glttt\C SJls commonly a-;S<xial<.xl \\1th JX'nostitrs (pcrio~leII on the l'tedial 11>-}XX:t Of the fL'Ill<>ml lltXK is h..1111cd /•1111/l' \\IIIJ!. Jt IS 1110,( t<'tnllllllil~ <>h-en ed \\ith osk'oarthritb and <"t<.'(lllL'\:msis, hut (l{Crd ma
Osteopo•·osis ln hpcrosi.s) <'t Clltts<."r gcnewliL<."~•rtmtt mdiogruphic feuturcs of rltt..wuatoid, )l)<>g<.1lle. and tuhcrntlolls
6 Joint D1seases
137
arthrilt~ Th~ w1hltlJ16lhie~ hU\e to be dilll:n:ntiat..:d from rdlc' ~vmputhctic d~·~troplw (Sudcd.':, ~toodv~llophv) and tnmsil-111 ll.'t,!ltcoporo~is Wlpapl, i~ ioiut al-tJOnnalilic:,. (}.,tcoJX>ro~is typil:all~ lli nt>t a Jcatwc ofosll.'tlWthritlli, CPPO,gout ml
Joint deformities Sublu,ahons and dislocations arc conunonh cmt<;ed b~· trnuna hut nrc also as..'>OCiated wtlh congL1Ul.ll tmd dc,clopmentul dis.!a~'S., neuromuscular dLSOrdcrs and most arthropatJua>. 1\11 l.TOSl\C arthritic proccs.-; IIS.-.o<:UIIOO With multiple joint d.:fonnitics suggcst5 the diagnost ol ctlhcr rhl.'\unatoid :u1hrihs or a seronegall\ e ~-rondy larthro)~th~ such as psorwtic arthritis. The hand ddonmht-s as~iatcd \\lth tl~-;c diseases flrC depicted in hg 6. I K Sumlar hand and \\nst dclonnillcs 111 the absence of crot-1011.~ may be lound \\1th systcrmc lupus erythematoSJL~ or jncwud's arthritis secondary to rhl.'llmaltc lever Common toe dclimnitics include hallu' Hllp.us (HI Ipus delonmty 111 hrst metatarsophalangeal jomt), hrunmer toe (hypere,tendcd metatarsophalangeal, lle,al JYO'\Imal mterphoJI:mgt:.•l, h)lX.T.:,tcil svn:adml! of the metatarsals. lateral de\ iahon of the lir-;t to fow1h toes in the metatarsophalangeal joints, and cod-..-up toe (hvpcrc,tcndl.'tl mclatan;ophalanp.cc1l joint with subluxation of the phalan' abo\C tl1c metatarsal hcc1d) arc also fTl.'qUentl~ as.-;(X iuiL'tl. SubiLL,alion as.~ociatcd with urtiwlar f.ragmcnlilllOtb <'slL'ophytoslli and ebunwtlon is most fn_'qu.:ntly fl!tmd 111 neuropathic arthropat11y.
Chondrocalcinosis and periarticular soft tissue calcifications (I abies 6.10, (· lt and 612 ) Caktlkatton ol artrcular cartilage is tCilncd chondrocalcmosrs (hg (lliJ) It ts the ha llmark of calcmm pyropho~vhate dihydrate crystal dcposttion d isease (CPPO) llo\\ever clJOndrocalc inosi~ du.: to pyropl10!.1'lhatc and les.-., l'rl.'lJUently otl1et crystals 1s also as.<>OCiated "~til man~ other wndihons. most c<,mmonly \\ ith primary and tX>st lnllunutic pcriarticulru· calcification. urc 1\l)ical for calcitic tendimtis and bur~itis, rcs!X-'Cti\'cl\'.
r,_
Joint effusions JOIIll ctltrsron;; ar.: commonly assocmtcd \\1th s·yno,·ral intlarnmalton :u1d lr.•uma In the absence of an lllJlll) a large mcn<>artrcular _tomt ciTtL"JOn suggests an inli:l:t1ous artiiritic
Fig.6 18 I land dclonnitie::. in inllrunmatory lUthritis. 1.11\ J1Cra.1l.n:;ion ru1d .. ublu\.alr<>n of the distal phalWl.' of the thumb. 2. HypcrC'\1CJ"Lo;JOil at mkrphalrmgcal JOml and lk'\.ion ut the hrs"'t mdilCafJl<'J~lalant-:ccll jomt (f-,h:.qJcd def<,nnity <·r hitchhrkds thumb). .l. II)'JlCIC,lCihln olmctacarpophalmtgeriatic artlllliJ16thy tlliln mcwnatoid arthritis.
Table 6. 10
C hondrocalclllosis
Ostl.'OWtbrihs (pn1nmy , ~c.:
llt.,nochromai<Jl;Js \\ Jlsou's dL.;cao;c
r.Arr Ochrmosis ACI(>llll.."g!tl) (h;olosis
prou.-s.-;. JOIIll cfl'usio11~ cw1 onh be dillcrL'llti;,~tcd from puruarticular wll ti.-.:.u;,; S\\clling. when tht cap:,ulc of tl1e af. fcctcd joint is s<.:parntcd by u layer of fut from U1c :;urroluiding ti........ucs. llli.'i is the ca'iC in the elbow, hlll.'C utd wilJC \\here joint elli.L\ions c1m l-e reliably di:Jgfloscd b~ com t11-
138
Bone
'
fi .6. 19 ~ccn m
""
Chond~alcinQSil\ in CPPO. f""~~ calcification i' lhc l.tl :rnl and lo a le-;scr d~grcc medlitl meni,ctL<.
He 6.21 Son lt!-."ue catcifi· cat ion in ' dcrodcrtllll ~' '"'"' Dh«ll 11~<: ... t.:cranoo nnd &•"-•I asp<'CI <'f the ~ 'l.imal ulna.
I ig.(..2(l (.'nlc11ic tendinitis A I<'Cah7cd cnklli.:;oli<'n ts't'en m the •upraspinald' k 1oc.lon (aiTNil>) Of the rN,•It•r LUll htnillkr taluflcalil>ll i' Ill'<> llf"'""' in the long bicq" hem! kn\1 head).
l'lldi<•graph~
h
(Fig. 6.22)
Massl\c
1<•int
ctlu,i<•oh
1113)
caw-.! 1\ld~nint <•r J""'lld<"'ublu 'l.ation <•I th.: inH•h cd JOllll '-llJwuldd") l'l' \\iduung of Ilk' dL'iat~<:.: h.:h>.:nn m a largc mdio.:arpal j<·int dlil'll•n (l1~ 6.22d 1. . \11.:1 an mtm-arucular fractur.: a lipoh.:lllartlm.,.is c'llll be b~
diagm-...:<.1
(mo.
i
the
prc.,<'IICC
~obtained
of a fat-hi< ~>
lc\ d
\1 hen
lb.
\1 ith
horiLontal b. am IL'dmiqu... Ocll~'i<•null) intru-articular gos i.' abo found in the ah-,'ttcc of JX'rlltnlling IIIJUI').' roiiO\\ ing a frn,1111'\! (>I ~~~ l<><:ation gaJl rndi"!'ntPh
may accumulal ~
mtr<>C<'>l)
in lhc jo1nt. b.'id~'
hlood
in the fom1 of one or " "'"' air I'K1hhlcs a~ a intrn-articular pr~'tlrc Such a pncumo-
and hone marro\\,
rc~ull of nccntiw hcmar1hr"'i' or ('ll•UmolipOI~o?martlrrC•"s, 1'\."f'CCII\ C1) L< part~<:ularl) <·oom1nn m the hip. A l')"l\<~lil· arthnt" .:au-.ed b) a f,3S-pwdu< me (ll'ganism ma) aJ,., Jln""<:l>l \\lth a large Joint dlll,i<·n .:ontaining gas. '!hi_, «•llllllK n llil> to he dill~-
Tllblc 6 12
Perillrticular
son
l i!>!>UC C
1'<.,1-MUtlc,ll h•l"' tit\)1 l'aral~'"'
1l1..:ran.ll ir~JU~
T able 6. 11 ~L'CIKUth\.,;
lnterYertebral
disc calci f tcalton
1-i,I'U. d·~.•.:a.-,...._
(aktli< l•ndi itL' aJ'KI bun;it"'
(1'1'1)
POO.J.IIIlUntall~
11\1>1>
CPI'I>
~t.h.:n~d~~.·rnm
11)1"' lit.Uillll<»i'
l l)l•
I'Wll('lq;m (• g. JX•ll<>lll)dlli>.) Spmnl hL
mll:nnm:dOI)
\."Onnedl\e
ti..,~u«.:
(c g. rotlf:CIIIIJI Nlf£U:al Iratiinlcc1iou; dq;m•IDII\c, I>I:O.H)
D
\!1lk-alkah ~\llllrnn~c ( al, in(lf;i~ cin.,ull
id<'O.IS
dL,~asc:-.:
:ulll renal <"t~O
II\ I~ •fMI.Ilh\ n>ldl'lll
\111~ l<•ld
lie
and <'lhcr
II) ('CI pnrathyrnidi"n
. \cu uncgal)
Ill
(~>peciaU} tul..:rullt•us)
lnfc'-11l•tl' arthrit "
llcntt.~hn•l1ilhJSi:o-.
and ltmlOf'llhs
hunc f~,t rna-
Ci joint Di~eases
139
F1g 6.22 a, b, c, d joint effusions a: Elbow: V1suahnt1on of the postenor fat pad (arrowhead) is diagnostic. The anterior fc1t pad can r>Orm<~lly be ~een. but 1ts elevat1on by the Intra-artiCular flUid may product> a "<>all~ conftq ''a liOn (arrow) lnd1Cat111e of an ellu\100. A radral head fracture is also evidt>nt. b: Knee Flurd accumulation m the su· Pfclpatellar bursa (arrow~) thclt connects Wlth the~ 1e • diaqnostk. The joint effusion (curved c1rrow) may abo displace the inferior patcllc1r lcJt pad .mteriorty. A fat-fluid (blood) level (arrowheads) can be seen m the SUPfapatellar bursa 1n a post-traumatic lipohemarthrosis. when the examination is ~rformed With horizontal beam techmque. c: Ankle· A larger anterior (arrOW\) and smaller postenor (arrowhead) soft trssue bulge IS charactenst1c. d: Wnst· Antt>nor subluxat100 of the p~s1form IS caused b). the largt> h{'fTlarthros1s in the radiocarpal joint secondary to intra-articular fractures of the d1stal radrus and ulna.
a
b
c
d
entia ted from a transient. linear or cre!.<:ent-~haped intr.!-artJcular vacuum phenomenon (gd~ in the intrd-drticular cavity) that is an occas1onal mc1dental finding ( Fig. 6.23) indicating the absence or.! ~•gmficant joint effusiOn. Gas within a meni~cus or diM 1!1 usually as~l(lated With degenerative disease
Para-articular soft tissue abnormalities (Table 6.13) Fus1form para-artiCular soft ussue swelling commonly occurs w1th rheumatoid arthritiS and psoriatiC arthropathy, whereas sausdge hke swelling of an entire digit is quite chardcteristiC for the latter condition. Subcutdncous nodules are frequently associdted w1th rheumatoid arthritis (fig. 6.24) dnd are charactcnstiCdlly loc<~tcd in dor~l and ldteral dspects of the fingers. about the olcuanon. i~chial tuberosities. femordl trochanters and the Achilles tendon region. Gouty tophi presentmg d\ noduldl soft ti\sue md~\e~ are commonly found rn the knees, hand.-., anl-les, elbows and may rarely Cdletfy. In o ... teodrthntiS of the h.md Heberden's nodes dbout the d1stdl interphal<~ngcdl JOints and Bouchard's nodes a bout the proximal interplwlangeal JOints are posterolateral soft tissue nodules wh1ch in a more advanced stage may be dSSOCidted with d bony outgrowth (osteophyte). The differentidl diagno.m of artiCular di~orde~ is discussed 111 Table 6.14.
fig. 6.23 Vacuum phenomenon. A ues
joint effusion.
140
Bone
Ta~e 6.13 Para-articular soft tissue nodules and swelling
Ostcoarthriti\ ,Hel:x-rden's nodes, Bouchard's nodt.~. bunion) Rheumatoid arthritis (fusiform soft tissue swell ng and rhcumatrnd nodules) Rheumatrc fever (srmnar to rheumatoid arthritis) ~latrc arthntls (fUSiform soh tr~sue swelhng and sa~;..age frnger) Gout (tophi) Multrcentnc retrculohrstrocytosrs (skrn nodules and xanthomas) osteoarthropathy lnfectrous arthrrt~ (fusrlorm soft trssue swelhng and abscess formation) Trauma (fmrform ~>It trssue swdhng) Foreign body granuloma (YOiar) Neurop.~th1<
Hemophilia (hematomas) Amyloidosis Pigmented vrllonoclular synovrtrs
Fig. 6.24 Sub
Sarcoidosis (subcutant'OUS nodules) Synovial cyst Ganglion Myosrtrs ossifrra"' (o\sifrro) Calcinosis clrcumscripta and tumorahs (cakilrt."
6 Jo1nt Diseases
Table 6.14
Different ial Diagnosis of Articular Disorders Character1sbc
Rheumatoid arthritis (RA) (Figs. 6.215,
6. 26,6.27, 6.28,6.29, 6.30, and
6.31)
141
Loc:lltlon
Symmetric polyarticular Involvement of the synovial joints of the appendicular skeleton. Hands: Metacarpophalangeal and prox1mal Interphalangeal joints in duding 111terphalangeal JOints of the thumbs v.1th relative spanng of the distal Interphalangeal JOints Wrists Distal radioulnar JOint in· cluding ulnar styloid radiocarpal JOint including radia l styloid process and pSiform tnquetra joint Feet: Medial aspects of the metatarsal heads except 1n the fifth diQII, where erosions on the lateral aspect may be the earliest manifestation Interphalangeal JOint or great toe (med1al aspect) and calcaneus (erosions at insertions of Achilles tendon and plantar aponeuro&S) AaormocteviCUiar JOint (resorption of distal da~1des) Glenohumeral JOints Elbows Hips (circumferential loss or joint space and protrusio acetabuli). Knees(symmetnc Involvement of the medial and lateral compartments) Ankles CerviCal Sp!l'lP SubluxatKlns (anterior, lateral or vertiCal at C1-C2. less frequently at one or more subax~allevels). Vertical subluxation (telescoping) at the C1-C2 level may result 1n basilar invagination Mu~ilevel subluxations produce a "doorstep" or "stepladder" appearance
Racliogfaphlc
Findings
FuSiform periarticular soft t~&&ue swelling, regional osteoporoSis and JOint space narrowing assoc~ated with marg1nal and central ero~ns are the hallmark of the d1sease.lhe f1rsl eroSK>ns are frequently found 1n the metacarpophalangeal and pro•1fflal Interphalangeal JOints of the hands and the ulnar styloids Besides marginal eroS~ons originating typically in the bare bone areas or a JOint without protective cartilage coverage, compressive erosions due to collap&f" of osteoporobc bone and surface erOSions due to resorpiKln of bone beneath mflarned tendons are also encountered. Syno~o-rtl5 resulting 1n nuid accumulation in jo1nts, bursae and tendon sheaths is more d1fficult to appreCiate with conventional radiographic technique Progression of the d1sease leads to complete destruction of the 1nvolved JOints and eventually to bony fusion, though the latter is rather uncommon. Subluxations and d~catKln are frequent. In the hands nex1on and extension contractures resu lt 1n boutonniere or swan neck deformHies of the fmgers, hitchhiker deformHy 1n the thumb and unar devia!Kln 1n the metacarpophalangeal JOII'It!' In the wnst both volar (palmar) ftex10n 111stabtbty· (VISI) and dorSiflexiOn Instability (1'151) occur besides dorsal subluxatKln or the diStal ulna Erosions may progress to extensive osteolysis in the distal clav1de elbow and distal ulna. A chronic rotator cuff tear e~o-ident by progressive elevation of the humeral head (nai'TOWing of the space between humerus and mfenor surface of the acrom1on that typically becomes concave) 1s common in the advanced stage In the spine dif!use narrowmg of the disc spaces and facet joints w1thout osteophytosis is charactenstic.
Commenb
Type Ill hypersensitivity connective soft tissue diSOrder with female predominance presenting cl1n1cally with mommg sl1ffness, para-articular soft tissue swelling, especially or the wnst, hand and teet, and subcutaneoU& nodules at dorsal pressure points (e g. olecranon). High sedimentation rate and poSitive rheuma· toid factor in 90 ' are characteristic laboratory findings Extra-articular manifestations (75 ••) are found 1n the lung (pulmonary fibroSis and rheufflatold nodules), pleura (unilateral or, lessfrequently, bilateral pleural effusions, usuaDy not associated With parenchymal lung disease), cardiOvascular system (peri· card1tis, myocarditis, aortitis and vasculitis), and lymphatic system (mild adenopathy and rarely splenomegaly) In ()l f o(' r lu. JI/11(/(0UI onhnll> (FIQ. 6 32) well-defined subcortiCal lesions often With sclerotic fflarglfls are the dominant radiographic feature, often in the absence of significant osteoporosis, JOint space narrowing and erosions. In th1s condition 50 of pat.ents are seronegative and there IS no sex predilection Felty ..yndrrmc: Rheumatoid arthntiS assoaated Y.llh splenomegaly and neutropenia Sjogren's.' " d11 nK. Connective t1ssue diSOrder With keratoconJunctllirtiS sicca, xero~omia and articular find· ings similar to rheumatoid arthritis.
(«>t'l mlle.<
on rag<
I U)
142
Bone
Fig.6.26 Rheumatoid arthntis Osteopenia and erosive arthritic changes are assoaated w1th lingf'r defonnrt1es 1nclud1ng hitchhiker's thumb, swan neck deformities 1n d1g1ts 2 and 3, and boutonniere deformity in digrt 5.
Fig.6 25 Rheumatoid arthntis Osteopenia and erosive arthritic d1anges 1nvolv1ng the hand and wnst w1th spanng of the d1stal interphalangeal JOints are seen.
a b
Fig.6.27 Rheumatoid arthr~is Severe osteopenia and erosive arthnbc changes are aSSOCiated w~h subluxabonsldislocahons and ulnar deviatiOn 1n the metacarpophalangeal JOints 2 to 5, ulnar subluxatiOn in the radiocarpal jo1nt and scapholunate dissociation.
Fig 6.28 a. b Rheumatoid arthribs (2 cases) a Shoulder· Extensive erOSI\Ie d1anges In the glenohumeral JOint and resorption of the diStal davicle are seen b Elbow. Jomt space narrow1ng and early erosions are evident
6 Joint Diseases
Fig 6 29 Rheumatoid arthritis. ConcentriC (axial) joint space narrowing is associated wrth obleopenia, erO"~ions and small subchondral cysts. Beg1nn1ng osteophy1osis IS indicative of early secondary degenerative changes.
143
Fig 6.30 Rheumatoid arthnbs. Small eroSions (arrow) with minImal surrounding sderoSisare ~n 1n the posterosupenor aspect of the calcaneus Generalized osteopema and a large ankle joint effusion (arrowheads) are al::oo evident.
Fig.6.32 Cystic rheumatoid arthnhs. Small well-
144
Bone
Table 6. 14
Coni
Disease
Characterisbc Location
Radoographic Findings
COmments
Juvenile rheiXIlato•d arthritis URA. chrontc Juvenile arthrrbs) (Ftgs 6.33 6.34 6.35 and 6 36)
Symmetric, polyartiCular Hands (metacarpophalangeal arid tnterphalangeal JOiniS) Wnsls, Feed (metatarsophalangeal, ~nter phalangeal arid 1ntertarsal JOints). Knee:; Hip:; Elbow:; Cel'\llcal sptne Temporomandlbt.lar JOint
PeriartiCular fuSiform son ttssue swelbng, osteoporoSis and joint subluxations are common. Similar to rheumatoid artlvihs of the adlJI (RA) In contrast to the latter JOint space narrooing arid erOSIOns are late manlfestabons 1n JRA,1ntra-artteular bony ankyloSis, penosbiiS and eptphyseal compression fractures are common and synovial cysts are rare . Growth diSturbances mclud1ng eptphyseal enlargement and edher o"ergrowth or urldergrowth of long bones w1th reduced diameters (overconslricbon) are charactensttc
Rheumatoid arthrrtJs tn pabents under 16years ofagewtth female predommance Three types are d1fferenttated 1 Juvenile-onset adult type rheurnatold arthritiS (15%) 2. Juventle-onset ankyloSing spondylItiS (5%) 3 Sblrs drsease (75 %) SystemiC andtor artiCular symptoms wrth negattve rheumatoid factor Three subtypes a) Syslem•c dtsease Acute febnle onset wtth sktn rash, generalized lymphadenopathy, hepatosplenomegaly, pencardllts and myocarditis are usually assoctated w1th mtld articular mantfestallons b) Polyarticular dtsease. c) Para-artiCular or mono-arttcular dtsease, Usually conrmed to large JOints. Assoctated iridocyclitis may lead to blindness
D•ffcrcntml Diagnosis of Articular Disorders
(contmues
0 11
pogc 145)
Fig.6.33 juvenile rheumatoid arthrHis Osleopenia , j,oint space narrowing and overgrowth or the eptphyses Including widening of the intercondylar notch in the d1slal femora are seen.
Fig.6.35 juvenile rheumatoid arthritis. El
Fig 6 .36 Juvemle rheurr~atold arthritiS A completely fused (sp4ne with uniformly marked disc space narrowing and severe osleopenia is seen.
6 joint lJiseases
145
Table 6.14 (Cont.) Differential Diagnosis of Articular Disorders Disease
Characteristic location
Radiograph!< Andings
Comments
Ankylosing spondylitis (Ag.6.37, 6.38and 6.39)
Symmetric ill' •I• ment of ~yn OIIial and fobmcartolagenous pnh and sites of ligamentous and tendonous attachments (enthe~s). Sacroiliac joints lumbar sptne Thoracic spine Cervical sp1ne (late) Tendinous insertioo in pelvis ("whiskering") P\Jbic symp~s Hops Shoulders Stl:'rnoclavocular JOints
Bilre.lrOSIVe chanq<'\ progress from loss of articular dd•nitioo to superfteoal erosions, fraying of thP subchondral bone and wldC'ning of the joint. Pro· liferative bony changes progress from focal sclerosis of the subchoodral bone to irregular booy bndges and eventu ally complete ankylosos. In the spine syndcsmophytes (thin ver· tocal ossifications of the outer fibers of the annulus f•brosus) connecting the anteroor and lateral cornC'n ~ulung eventvally on a bamboo sptne formation and straightening (~quaring) of the anterior vertebral margins are di· agnostic. Other fondongs oocludf' Illcreased ~erosis of the comers of the vertebral bodoes ("shiny comer" sogn). discal ballooning (btcoovex shape of the disc Sffondary to osteoporosis), "dagger" sogn (ossofocation of the inter· spinous ligament prodU(ong a central radiodense line oo frootal radoographs) and "trolk'Y track" sign (three vertical lines on frontal radiographs related to the ossifications of the interspinous lig.lmenh and apophyseal joints). The hip Involvement i\ typically bi· lateral and symmc-tric woth coocentric joint space narrowing and osteophytosis. In tilt> \h01•klt>r diffuse joint space narrowong and erosrve changes predominantly on the superolateral aspect of the humeral head that m.JY progress to complete destructoon of that part ("hatchet" sign) are characteristic.
Chn;nk onOammatory disease pri· marily affecting the spine woth male predom1naoce of 4:1 to 10:1 and chnkal on\rt with low back pain and ~tolfne\s at the age of 15·35 year~. Histocompat1bil'ty antigen HLA-827 os posrtive tn 9f,%, Three tomes le~s commoo on black~ than Cauca\ians. SymmetrK bii.Jteral involvement of joints and sotes of ligamrnto~ at· tachment wtth subtle erosiOns and new bone formation (osteitos) With prefcrentoal involvement of the axoal skeleton and I.Jrge joints os charac· teristk. Erosive lesions in the spine at the discovertebral junction are termed Andt.nson lesoons or, when located on the anterior margin, Romanus W\1011\. Complication\ of the ankylosed spine mdude fractures typically through a fused dose. Oue to their lnnab•hty these fractures are assocoated wtth ~•gnifKant morbidity and mortality. especially on the cervical reg1on. Hand and wnst involvement occurs in 30% of patoents. but os rarely a dominant fe.Jtur e of the disease. R.ldiographic findings in these locations are similar to psoriatic arthrop.1thy.
(continues oo
poge 147)
fig. 6.37 Ankylosing spondylitis. Symmetroc bilater.JI sacroiliitis with erosion~ and joint space narrow1ng, mild concentric (axial) narrow1ng of both hip~ .Jnd exten>ove fluffy enthe)Opathy aloog the 1schoat1c bones are charactenstK
146
Bone Fig. 6.38a.b Ankylosing spondylitis. Fusion of the lumbro~l fused sacroiliac joint'> and O'>sofKaticn of both the intt>rspinous ligament ptodu
b
a
Fog 6 19 Ankylosing spondylitb. •nerali7ed O'>teopcnta, fu. sion of thf' lc""' I 1mb in both hips wtth m1ld ptotrusto acet.Jbuli on the nght sode. erosoon and blur· ring of the subchondral bone with adjacent ebom.lllon in the pubic symphysis, and extensive fluffy enthesopathy along the ischiatic bones and greater trochanters are seen.
6 Joint Diseases
Table 6.14
147
(Cont.) Differential Diagnosis of Articular Disorders Comments
Psoriatic arthritis (Figs.
uo.
U1 .U2, 6.43,6 .44, 6.46 and
U61
Asymmetnc polyarticular Invo lvement of synovial and flbrocartilagenous joints and srtes of tendinous and ligamentous attachments (entheses) Hands: Distal interphalangeal joints. prox1mal Interphalangeal joints, metacarpophalangeal joints and tufts (tuftal resorption is almost always assoaated with na1l Involvement) Feet Interphalangeal JOints, metatarsophalangeal JOints and
tufts. sacro~ICICJOints
Stemocla\icutar jo1nts Acromiocla~icular joints Spine Calcaneus Pubic symphySis
FuSiform soft tissue swelling about the Involved joint or. less commonly. sausage-like swelling of ent1re digit is typical Osteoporo::>is IS not promtnent or absent. Diffuse loss of jo1nt space (Similar to rhe'--llaloid ar· thnbs) 1s characteristic, but 1n the small joints of the fingers and toes considerable widening of artiCular space 1s not uncommon. EroSive/destructive changes tend to progress from the JOint margins to the center. "Pencil-in-cup", or ball-1n-cup·, "cup.and-saucer" appearance are qute characteristic 1n the d1g1ts. Bone pro~feration is typically associated with erosive changes and may produce irregular excrescences With Spiculated appearance Exube· rant penostitiS and new bone forma lion 1n an entire phalanx may result In an 1vory phalanx . Bony ankyloSIS IS qurte common man advanced stage . especially 1n the hands and feet Enthesopathy (bony proliferatiOn at ligament and tendon attachment s.tes) occurs at the posterior and inferior surfaces of the calcaneus, femoral trochanters, the ischial tuberoSities, medial and lateral malleoli, olecranon radial tuberosity and about the knees including the petella . Deformrt1e,:; 1n the hand and feet are less frequent than 1n rheumatoid arthntiS. SacrolliaCJOinl Involvement tends to be bilateral but often somewhat asymmetnc. Findings mdude erosions, scleroSisand v.idening or r~ar rowlng of the joint space, whereas complete ankylosis is relatively rare In the sp1ne thin and curvilinear to thiCk and fluffy paravertebral OSSifications may be found w1th preferential Involvement of the lower thoracic and upper lumbar spine . They may Involve only one side of the sp1ne. or when bilateral, may be asymmetric (DO: ankylosing spondyfiiiS). In the cerv1cal spine extensive prohferabon along the anterior surface and both narrowmg and sclerosis of the apophyseal JOints are charactensllc mamfestations.
ArthritiC changes are present 1n leS& than 5 •,, of patients with psoriaSIS. Skin disease 1s present in 85 '• of patients with arthritic onset, but occasionally arthnbs rr~ay antedate der· matologiC81 changes. HLA B271s positive Ill 80 % of patients whereas the rheumatoid factor IS negative Types: 1) True psonahc arthritis (polyarthnbs wrth d1stal Interphalangeal JOint Involvement) 2) Seronegative polyarthritis simulating rheurr~atold arthritis (DO; Psoriasisv.llh COincidental rheumatoid arthritis). 3) sacrollubs and spondylitis 4) Penpheral arthnbs and sacro1hit1s (comb1nal10n of types 1 and 3) Rad1ograph1c features that differentiate psonatlc arthnt1s from rheumatoid arthntis in the hand Include: 1) Lack of osteoporosis 2) Tunat resorptiOn . 3) Asymmetric dlstnbution of Joint involvement 4) Involvement of the distal mterphalangeal joints and relatiVe sparing of the wrists. 5) Occasional Widening of the articular spece secondary to destruction of margln81 and subchondral bone 6) Bone prol1ferat1on mclud1ng elCuberant penosleal reachoo. ankyloSIS and 1vory pha lanx format1on 7) sausage-finger
(cmtuurcs on
rage 150)
148
Bone
Fig.6.40 Ankylosing spondylitis. Erosive arthritic changes are seen in the hand and wrist that are indistinguishable from psoriatic arthritis. Fig.6.42 Psoriatic arthnbs. EroSive arthnt1c changes mvolving pnmanly the prox1ma l and d1slal mterphalangeal joints and the wrist are seen. The marg1ns of the eroSions are frequently Indistinct because of the a~iated new bone formation. Bonyankylosisof the diStal Interphalangeal JOint of the 1ndex linger is also evi-
dent
F1g.6 41 Psoriatic arthritis. Erosrve arthntiC changes w1th both asymmetnc dlslnbution and severIty of JOint involvement in both hands and wrists are seen.
6 Joint Diseases
149
Fig.6.44 Psoriatic arthrit L<. I rosioot< associated with hone proliferation are seen in the nnerphalangeal joint of the great toe, the lir;t tarsometatarsal joint and the dislocated metatarsophalangeal joinb 2 to 5. Tuflal erobiom; are abo evident in ~' l)ra1 toe-s.
Fig.6.43 Pl.oriatic arthritil,. Sever<: dc-,;tmction of the ~ubchon dral hone i' sec11 in the hand mtd wri't leading to con~oidcrabk widL1ling of the articular space in sc,·cral fingers
l'!;oriatic arthritis. frosions ofthe bone adjacent to the spaces of (4{5 and (5{6 '"th Oufly ankrior ~yn de:mophy1c fonnaticm mtd begioming bon) bridging. Fig.6.45
int~r\ert~bral
fig.6.46 Pwriatic arthritis. fu>ion of the lumb.tr spine by large asy11llllllric s~ ndcl>mophy1•~ i!, seen. t\arro\\cd bilatcoal .acroilioc joint< with early ero•ion' and mild rcacti'c <elcro•is on the right sod.: ar.: also pre<><:nt.
150
Bone
Table 6.14
(Cont.) Differential Diagnosis of Articular Disorders (
Rrilt>r'~ ~' n dNlmf' (triad CJ11111Juith. umhrltl.., a nd C'Ql · jun<1hlth.) (Hr-. 6..a7. 6.411 Mnd 6.49)
t:nlrropollhk· artllrltk (t~ 6.~1.
6.!11 and 6.!12)
'1111ract~ rl14k·
lonltlon
( fllll iUftlb
Usually asymmetnc polyartiCular irl\lol\lement of synov1al and fi· bfocart1lagenous JOints and eotheses wrth preferetlbal Involvement of the lower extremity. Foot· Metatarsal phalangeal and mterphalangeal JO•nts mdudmg sesmoids calcaneus Ankle Knee Pubic symphyses Sacroll1ac JOints Sp•ne Hand (espeaally proximal interphalangeal joints)
PenartiCUiar osteoporOSIS may accompany acute ep&sodes, but IS not a prominent feature of the chroniC stage Lossof jo1nt space and ei"OSIOns are more frequently found 1n smaller than larger JO&nts Superfaal bone resorption also ocrurs beneath Inflamed bursae and tendon sheaths Fluffy penosteal bone proliferation IS charactensbc, espeaally m the posterior and plantar aspect of the calcanei, ISChial tuberOSities and tro. chanters, but also 1n the metatarsal, metacarpal and phalangeal shafts, the malleoli and the knees Sacroiliac JOint InvolVement is common (in excessof 50%m advanced disease) and 1s usually bilateral symmetric or asymmetnc. Osseouserosions associated wrth adjacent SClerosis varying from m1ld to severe pre· dom1nate charactenstically on the Iliac Site of the JOint In the lower thoracic and upper lumbar spme thin or th1ck vert&cal OS· seous bndges may extend across the 1ntervertebfal diSC and •nrt&aU)' are separated by a clear space from the lateral marg1n of the ad,acent vertebral bod1es. Sp&nallrl\lolvement IS typK:aDy asynvnetnc.
Peak onset ocrurs between 15 and 35 years of age with male predominance HLA-82715 posrtl\le 1n 75 ~oof pabents Transm1ss10n occurs 1n association v. 1th e1ther epidemic dysentery or se)'ual1ntercourse Urethribs 1s frequently the 11nlt.al man1festat10n Associated mucorutaneous leSions'"" dude balanitis C1rc1nata and keratOSIS blennorhag1ca 1n soles and pa lms ConJunCtiVItiS may progress to uvertes and keratitis Seventy percent of patients develop radiographiC bony alterations Acute attacks may be assoc1ated with soft tissue swelling and osteoporOSIS Rad10graph1c features of Rerter's syndrome are virtually IndistingUishable from psoriabc arthrrt1s. Compared to the latter condrtion preferential involvement of the lower extrem1bes, less frequent Involvement of the Spine and relatively rare bony ankyloSIS of the small JOints of the hands and feet are favonng the d&agllOSis of Rerter's syndrome
Monoart1rular to bilateral symmetriC Sacro1hac)01nts Spme Knees Ankles Feet Shoulder Elbows Wnsts Hands
Central type Symmetnc lrl\IOIIiement of the sacroM&ac joints and spne indistinguishable from ankylosmg spondylitis. Peripheral type. Monoart1rular or pauaarticular acute synovitiS presenbng w1th son tiSSUe swelling and penarticular osteoporoses A close temporal aSSOCiation between exacerbabon of Intestinal and arthrrt1c fmdmgs is characteresllc Chron1c changes are rare and Include joint space narrowing, erosions and cyst formation mimicking rheumatoid arthritis. Clubbing of fingers and rarely pertostlbs of tubular bones s1mulat1ng hypertrophic osteoarthropathy may also be found.
The 1nadence of arthritiC changes· Ulceratl\le cohbs 12% Crohn's desease 10% Whipple's dr.;ease 75% (predomlnanUy penpheral type) Salmonella 2% Sh.gella 2% Yer51n1a 30% lntesbnal bypasssurgery 3% Hepatic disease (cirrhosis, hepatrtiS) 2% (excluSIVely peripheral type) PancreatiC d1sease 1% (exclusively penpheral type, associated osteonecroSIS COmmon) Intestinal infections caused by sa lmonella and yerS1n1a may also cause sepbc arthrrt1s and osteomyelitis by hematogenous spread (continues on page 152)
6
Jo111t Diseases
151
b Fig 6.47 Reiter's syndrome. Ero sions wrth partial destructiOn of the metatarsal head and beginning flufr;,: bone prollferallon are seen In the S" metatarsal phalangeal JOint. Joint space narrowing and begmning bony proliferabon without eros10ns are evident in the Interphalangeal joint and metatarsophalangeal of the great toe
Fig 6 48 a, b Reiter's syndrome ExtenSIVe fluffy penostttls IS seen tn the medial aspect of the diStal t1b1a metaphysis and about the lateral malleolus In a, and about the posterior and Inferior aspect of the calcaneus In b
Fig 6.49 Reiter's syndrome Erosivearthntlc changes .vtlh bone proltferabon are seen 1n the se~eral JOints of the hand and the wnst Note also the diffuse tiOfl li:>SUe thickemng of dtgtls 2 and 3 (sausage fingers).
Ftg.6.50 Enteropathtc arthnbs (Crohn's disease). Bilateral fused sacrodiac JOirtiS and deliCate <;yndeo'"'Oohyte formation tn the lumbar spme are e~ldent
152
Bone
Table 6.14
(Cont.) Differential Diagnosis of Articular Disorders Radiographic
A ndlngs
Comments
Disease
Charactenstlc
Jacc:oud's ar-
Btlateral symmetnc Hands
Bilateral symmetnc deformtng nonarthropathy Ulnar deviation and flexion deformrttes of the metacarpophalangeal JOints espeCia lly 1n the fourth and fifth ftnger are charactensbc. HypereKtenston of the Interphalangeal JOtnts may be aSSOCiated joint space naiTOWing and eroSIOns are lyptcally absent Foot Involvement wrth lateral devstton and subluxation of the metatarsophalangeal joints IS less common
Post-rheumatiC fever arthropathy RheumatiC fever IS cnaractenzed by fever. cardllts and polyarthnt1s followmg an epsode of beta-hemolytic streptococcal Infection. ReverSible nature of the artiCUlar deform•tes IS charactenst1c, but occaSionally deformrt1es may become fixed .
Btlateral symmetric Hands Feet HipS Knees Ankles Shoulders
Bilateral symmetnc deforming nonerosive arthropathy of the hands occurs 1n 25 ~ of pattents. Sublu~atton of the metacarpophalangeal JOints with ulnar deviation, swa n-neck and boutonntere deformities of the fingers and hyperextension of the Interphalangeal JOint of the thumb are characteristic. JOint space narrowtng and erosions are rare Occasionally hook erosions on the radtal and volar aspects of the metacarpal heads are found, presumably produced by capsular pressure. Associated foot abnormar.~~t.s may 1n etude hallux valgus deformty. metatarsophalangeal joint subluxations and splaying of the forefoot. In· stabilly in knees. shoulders and atlanto-axial joint may also be present. Osteonecrosis is. beSides deforming nonerosive arthropathy, the other classic feature of the disease occurring in up to 40 of pattents. The femoral heads are most commonly affected srte. but humeral heads, femoral condyles, bbaal plateaus, talar domes and the small bones of hands, wnsts and feet are also frequently Involved. Signs of avascular necrosis tn these JOints and cystic changes in the carpa l bones are the corresponding radtographic features Acrosclerosis and tuftai resorption complete the radiographiC picture
Relatively common connecbve tissue diSOrder With 10:1 female predominance and typcal onset during cnildbeanng age Three ttmes more common m blacks Laboratory find1ngs Include antinuclear DNA antibodies (87' ~ LEcell formation (78 •). hypergammaglobullnemta (77 · •·l anemia (78•,) and leukopenia (77• ) NonspectfiC bilateral polyarthralgia involving hands, wnsts. shoulders and knees is present 1n 90 9o or pat tents. Myosllis and spontaneous tendon rupture are common and usually assoaated wrth systemic or local sterOid therapy. Soft tissue calcifications occur, but are much lesscommon than in either scleroderma or dermatomyositis. Osteomyellbs and sepllc arthritis (bactenal and mycotic) are relat111ely frequent comphcattons Both steroid adm1111strabon and renal diSease are maJOr contnbubng factors to the susceptlblhty for Infection. The deformtng noneroSNe lupus arthropathy d1ffers from Jaccoud's arthropathy in the hand only by the Site of Involvement In the former a" metacarpophalangeal joints tncludtng the thumb are typically involved, whereas the latter has a preference for the fourth and fifth finger.
thritis
Locatton
(Feg.6.S3)
Systemic lupus erythematosus
(l'ig. 6.54)
erosi~e
(continues on page IS4)
6 Joint Diseases
153
Fig.6.51 Enteropathic arthritis (Crohn's disease) Erosions with fluffy spiculated bone proliferation are limited to the greater tuberosity
Fig.6.52 Enteropathic arthritis (Crohn's disease). Juxta-articular osteoporosis and scattered early erosions are evident in the hand and wnst best apprec~ated 1n the volar aspect of the Interphalangeal joint of the thumb and the ulnar aspect of the fifth carpometacarpal joint. Nonspecific arthritis with para-articular soft tissue swelling is seen in the distal interphalangeal joints of the third and fourth fingers
Fig.6.s3 Jaccoud's arthritis. Ulnar deviation without erosions IS seen in the metacarpophalangeal joints. It IS most severe in the fifth digit where it progressed to complete dislocation.
Fig.6.54 Systemic lupus erythematosus Ulnar deviation in the metacarpophalangeal joints and hitchhiker's deformity of the thumb are seen.
154
Bone
Table 6.14
Sclerodermll (Fig 6.55)
(Cont.) Differential Diagnosis of Articular Disorders
Monoarticular to bilateral symmetric. Hands (distal and prox1mal interphalangeal jo1nts and metacarpophalangeal joints). Wnsts (first carpometacarpa l JOint and distal radioulnar JOint) Stemodavicular joints Acromioclavicular joints Mandible (thickening of the periodontal membrane resulllng tn a widened periodontal gap between the tooth and the mand1ble IS a charactenstic findtng).
Acro-<>steolysis and soft bssue calaficattons are the hallmark of the dtsease Resorption of the tufts leads to ''penciling· of the phalanx. Calclftcahons present as small punctate deposits at the phalangeal lip to more wide spread conglomerate deposits with periarticular distribution. Acrosclerosis (hyperostoSis of the tuft) associated with soft tissue atrophy is another presentallon Nonspeafic articular •nvolvement of the hands and wnst may eventually progress to erostve destrudl\le changes wrth or wrthoot tntra-arttcular calaficat10ns. Involvement ranges from monoarticular (e g first carpometacarpal joint) to bi lateral symmetrical. Foot abnormalities are less frequent and usually limited to the metatarsophalangeal jotnts. Thinning of the 1.d to 6" ribs posteriorly and resorption of both the proXImal and dtstal ends of the claviCle and the diStal acromiOn can also be found
Autoimmune d1seasewrth 3:1 female predom•nance and peak age of 30 to 50 years May be assoc1ated w1th CRESTsyndrome (Ca lcinostsof sktn and subcutaneous tissue, Raynaud's phenomenon, Esophagealdysmotilrty, Sclerodactyly and Telangiectasia). Musculoskeletal abnormalities of scleroderma associated wrth other collagen vascular dtsease (e g. rheumatoid arthritiS or systemiC lupus erythematosus) IS referred to as m1xed connectllie t1ssrue d1sease or overlap syndrome, respecllvely Soft tissue calcificatiOns frequently occur also about large JOints (DO · Mllk-alkal• syndrome, hypervttamtnoSis 0, renal osteodystrophy and tumoral calcinosis) . Dcrmctmny(lsl/i.\ (Fig 5.56) presents wrth sim1lar radiOgraphic features as scleroderma, but both extensive linear subcutaneous and Intermuscular fascial plane calcif1cabons are typical for the former diSOrder.
Hands \M"ists Hips Knees Ankles
Nonspecific (periarticular soft tissue swelling, osteoporoSis and JOint effusions) or absent.
Po(nrrtCiiiiS JdJ
F!nJhema Familial
~
lterra..-,
.._
(Fig 6.57) Relapsing polyChOndrRis
Bilateral asymmetric SacroUiac joints (unilateral or bi· lateral) Hips Knees
Osteoporosis Epiphyseal overgrowth in chtldren ArtiCUar erosions, sclerosrs and fusion may eventually develop.
Rare genetic disorder predommantly 1n Sephard1cJews,Arrnenians and Arabs presenting w1th multtple episodes of fever assoaated With pentombs, pleurlltS and synovrt1s
Btlateral asymmetric Sacroiliacjoints (unilateral or bt· lateral)
Bilateral sacro1lntis with JOirll space loss, erosion and eburnation without spinal alterations Nonspecific findings in penpheral joints, sternoclavicular joints, manubnostemal and costochondral JUnctions rang1ng from usually mild nonerosive to occasionally mullllabng arthnbs. Extra-artiCUlar findtngs tnolude tracheal stenosis and calcifications of the auricular cartilage .
Episodic inflammation of cartilaginous tissue (e g. external ear, nose, larynx, trachea, nbs and JOints) and ocular structures (e g conJunctiva, sclera and urea} occurring tn all age groups w1th peak In fourth de· cade
Monoarticuiar or oligoartiCUiar Knees Small peripheral jo1nts Sacroiliac joints
MonoartiCUiar or oligoarttcular tn· vol\lement with penartiCular soft tiSSUe swenmg and osteoporosis and rarely joint space narrowing and small erosions
Tnad of recurrent oral and genrtal ulcerations and ocular Inflammation cl1aracteristic. Occurs at al ages (peak age 30 years) with male predominance.
(fig. 6.S8)
Beh-er s syndrome
(Figs 6.59 and 6.1101
nodo.IUII
(umtitu/a on
p
6
Joint D1seases
155
Fig 6 56 Dermatomyositis. Extensive subcutaneous and intermuscular fasc1al plane calcifiCations are evident.
Fig.6.56 Sclefoderma. Osteopenia. soft tiSSUe calclf1C8hons and resorpbon of the tufts 1n the thumb. mdex and middle finger are seen The small cyst1c lesion 10 the diStal aspect of the first metacarpal IS an InCidental fincl1ng most I kely represenbng a small enchondroma
Fig.6 57 Familial Mediterranean fever. Osteopenia joint space narrow1ng and early erosions are seen in both sacroiliac JOints.
Fig.6.58 Relapsing potychondrltls. Ear1y erosions w1th react1ve sclerosis are seen in both sacroiliac joints
F1g 6 .59 Beh-et's syndrome. Mtrumal scattered erosive change.. an: seen 1n the ~. rist with the largest erosion be1ng located 1n the ulnar styklld (arrow).
F~g.6.60 Beh-et's syndrome Early erOSIOns are seen tn both sacr01hac JOints (i p n ~n•s as •n F1g 6.59)
156
Bone
Table 6.14
(Cont.) Differential Diagnosis of Articular Disorders
Disuse
Characteristic
Hemophilia
Bilateral, not always symmetnc Knees Ankles Elbows
(Fi~'
6.61
and 6.62)
Gout (Figs. 6.63,
6.64,6.65, 6.66,6.67, 6.68 and 6.69)
Location
Monoart•~lar or asymmetric' polyartiCUlar Involvement typiCal Feet Involvement of first metatarsopha langeal JOint most charactenstic With erosion frequently located on medial or dorsal aspect of fir'>l metatarsal head. Other metatarsophalangeal jouts. interphalangeal JOints. tarsometatarsal JOints and ~ntertarsal joints may also be affected. Hands D1stal and proximal Interphalangeal JOints are most commonly Involved. but metacar pophalangP.al JOints and wrn:;ts may also be affected Elbo\'11>' Bilateral olecranon burSitiS v.1th er<>ffi'e and proliferatiVe changes 1n the adjacent olecranon VIrtually pathognomonic. Knees 5aCrO~IBC JOints
Radiographic
Findings
Commenls
Dense appeanng (hemosiderin depoSition) jo1nt effus.ons and periarticula r son llssue swelling, osteoporosis. joint space narrowing, cartilaginous and osseous JOint destruction with secondary sclerosis. osteophytos1s and subchondral cyst formatiOn and epiphysea l overgrowth (secondary to chronic hyperem1a) are charactenstic. Widen1ng of the Intercondylar femoral notch and squanng of the mfenor pole of the patella, tobtotalar stanling 1n the ankle and widemng of the trochlear and radoal notches of the ulna 1n the elbow may be aSSOCiated. lntraosseous hemorrhage may lead to osteonecrosis (especially 1n the femoral head and ta lar dome) and hemophiloc pseudotumor formation simulating a vanety of bemgn or mabgnant leSIOns and infectiOns.
Occurs In approximately 1 1n every 10,000 males due to X-hnked defociency of coagulabon factor VIII (hemophilia A, 90 • of patients) or factor IX (hemophiUa B or Chrn.tmas disease, 1OCb of pabents). Von \Nilk·brand's disease(autosomal dorrnnant v.1th factor VIII and platelet defic1ency1 may occasionally present w1th s1mdar features m both genders Rad10graph1c features of hemophilia and JUVenile rheumatoid arthritis 1n large joints are v1rtualty indistinguiShable. Involvement of the spine and hands, bony ankyloSis and growth 1nhib1bon are however findongs only associated\'< ith Jllvenole rheumatoid arthritis
Erosions caused by toph1 may be
Hyperuncemia IS the hal mark of the dosease Deposition of urate crystals occurs in para-artiCular soft tissues,joints and bone causing inHammation and destruction The disease is caused by either overproduction of uric acid or decrease in renal urate excrebon. There IS a 20:1 male predorrnnance vnth the first attack occumng typiCally in the 511> decade of hfe, although any age IS possible, 1n women the diSease commences m the postmenopausa l penod. Stages· 1) Asymptomatic hyperuricemia 2) Acute gouty arthritis. MonoarticlJiar or polyartJcutar attad<s pre::.en!Jng w1th pall'l. tenderness and swePong, but usually without radiographic bony abnormality. 3) Chronic tophaceous gout [).!velops eventually in fewer than half of the pahents w1th recurrent acute attacks. Socond<~ry gaut rarely causes radiO· graphically apparent arthropathy and IS assocrated wrth myeloproliferatiVe d.< orders and sequelae of lhe1r treatment and w1th chronic renal fa11Ure. Le~oan synd'cme: X-hnked enzyme deficiency of uric acid metabolism presenting With mental retardation is associated w1th self-mutilation (amputation of fingertips), gouty erosions and retarded skeleta I maturation SDtumJno gout is a comphcabon of chrornc lead porsoning caused by contamonat•on of alcoholic beverages Type 1 fJ(ycogM starage cb>nse may also be associated with gouty arthntis
intra-<~rticular, para-<~rtlcular or at
a considerable d1:>lance from the j oint and are typically surrounded by a sclerotic border producing a "punched out" appearance. An elevated bony spicule may form ov"'r the erod1ng tophus producIng the "overhangong edge" Sign that is found 1n almost half of the cases and quite char-~ctenstoc. Bone proliferation may occaSionally produce club-shaped metacarpal metatarsal and phalangeal heads ("mushrooming"), enlarged ulnar styloids and th1d<ened diaphyses Tophllyptcally present as eccentric juxta-<~rtocular. lobulated son t1ssue massesoccaSiona lly containing calcitic deposits Intra-osseous calcified tophi may mimic enchondromas in the hand. Calcium pyrophosphate deposition d1sease (CPPD) IS occaSionally assocrated presentong wrth chondrocalcinoSIS of the meniSCI of knee . pubic symphySIS and Inangular fibrocartilage of the wrist. Osteonecrosis 1s another associated complication
(continues on t><'lfl(' 159)
6 Joint Diseases
a
157
b
Fig.6 61 a , b Hemophilia. Erosive/destruclr\e changeswrth subchondral cyst formations are seen in the elbow m anteropostenor (a) and lateral (b) prOJections Fig.6.62 Hemophtlia. Osteoporosis, widened tntercondylic notch and joint space narrowmg and destruction of the adjacent bone are seen bilaterally Furthermore extenSIVe reactiVe scleroSis with subchondral cyst formabons is present 1n the lateral compartment of the left knee .
Fig.6.63 Gout Well defined erosions w~h small bony spicules associated with a soft t1ssue mass are seen in the diStal Interphalangeal )Oint Osteoporosis and jomt space narrowing typJCally are absent.
F1g.6.64 Gout. A large dense soft bssue masssurround1ng the diStal Interphalangeal joint of the fifth finger where small subchondral and marginal erosions are seen . the latter with tiny overhang1ng bone spicules EroSIVe and cystiC changes wllh beginning bone proliferation are also seen in the wrist and distal radioulnar JOint, most notably 11 the prox1mal aspect of the triquetrum
158
Bone
Fig.6 65 Gout. A large erOSIOn With conSiderable amount of new bone formaliOn is seen on the medial aspect of the first metatarsa I head and ned< without involvement of the artiCUlar surface of the adJacent JOint Only min1mal erosive/cystiC changes are seen in the other metatarsal heads and about the interphalangeal )Oint of the great toe
FIQ.6 66 Gout. A large soft trssue mass with scattered calcifications is SPen eroding the adJl!cent olecranon.
Fig.6 67 Gout. A large tophus (arrows) wrth sclerotic margin is seen 1n the patella. Jo1nt space narrowing with small erosions and subchondral cysts and reactive sclerosis is seen 1n the medial compartment of the knee
Fig.6.69 Gout and CPPD. A multiloculated cystiC lesion in a slightly expanded lunate IS associated with chondrocalcinosis in the tnangular fibrocartilage. A smaller cyst with sclerotic margin is evident 1n the distal aspect of the triquetrum.
Fig 6.68 Gout. Well defined erosions of varying SIZesand large cysts with or without sclerotic margins are seen m the distal tibia lateral malleolus and talus
6 Jo1nt Diseases
Table 6.14
159
(Cont.) Differential Diagnosis of ArticuL1r Disorders
01sease
CharactenstiC location
Radiogra otlic F•ndinQs
C«lmments
Calcium pyrophosphate dihydrate
Bilateral and symmetnc dlstnbution. Knees Wrists Metacarpophalangeal j
Chondr()calclnOSIS is the hallmark of the dr.;ease and refers to hnear or punctate calcifications of both the fibrocartilagenous cartilage (e.g. menisci of the knee . triangular fibrocartilage of the wrist. pubic symphysis. annulus fibrosus of the intervertebral disc. and acetabular and glenoid Ia bra) and the hyahnc cartilage (e.g. wrist knee. elbow hp and shoulder) The calcification~ 1n the fibrous cartilage tend to be Irregular, thiCk and snaggy and m the hyahne cartilage thm and hnear Synov1al capsular tendinous, bursal and ligamentous calaficahons are frequently associated Arthnt1c changes of CPPOand osteoarthntis are very similar and include JOint space narrow1ng and subchondral sclerosis. In C PPO.however, subchondra l cysts tend to be larger and more numerous, and subchondral bone collapse and frag mentati()n with formation of 1ntra -articular loose bodies are much more common, wf1ereas osteophytosis IS often less prevalent. CPPOalso tends to affect JOints that are not commonly involved in osteoarthntiS, such as the metacarpophalangeal JOints. mdcarpal and radiocarpal compartments of the wnst. el bows and shoulders In the knee the med1al compartment 1S most frequently invollled, sm1lar to primary osteoarthritis. but ISOlated Involvement of either the patenofernoral or lateral compartment is somewhat suggesti\e of either CPPOor post-traumatic osteoarthritis. In the wrist a predilection for the radio· carpal compartment results 1n "degenerati\le" changes between the distal rad1us and the proximal carpal rOIN. The scaphoid moves proximally and appea rs compressed and deformed by the adjacent rad1us, whereas the lunate moves distally and hereby producmg a "stepladder'' appea rance. Th1s pattern 1s also referred to as scapholunate advanced collapse (SLAC)and, beSides CPPOis also found a sequela of occupational or accidental trauma Isolated "degenerative' changes in the second and third metacarpophalangeal j
Most common crystalline deposition arttvopelhy affect1ng prlmanty the middle-aged and elderly population w11hout sex predolection. Chn!Cany CPPOmay be asymptornabc or mmic ostcoarthnhs, rheumatoid arthnlls. neuropathiC arthropathy or gout, the latter beg1m1ng frequently referred to as pseudogout CPPOis usually idiopathiC, but a hered1tary form IS also recognized A vanety of d1seaseshave been aSSOCiated w1th CPPOincludmg osteoarthnhs. dl8betes mellitus, gout, hyperparathyroidiSm, hemochromatOSis, and \Nilson's disease ChondrocalcinoSJs may be found 10 both pnmary and post traumatic osteoarthritis and thus the demonstration of car· tilage calcifiCation should not automatiCally lead to the d1agnosis of CPPOarthropathy partiCularly snce the accumulation of other crystals than calc1um pyrophosphate dihydrate (CPP)might be retpom;lble for t~ findmg Wfsoo's dsease (hepatolenllcular degeneration} IS a rare autosomal recessi\-e di$E!asevnth e~ceSSI\e oopper retention caused by the 11nabHIIy of the hver to excrete it 11nto tl'1e bile It presents wrth degenerabve changes in the bra~n. especially the basal ganglia. hepatiC cirrhoSis and doagnostiC green~-brown Kayser-Fleischer corneal nngs Articular changes in the mPtacarpophalangeal JOints, wnst, hand. foot, hlp, shoulder, elbow resemble CPPOor osteochondnhs d1ssecans Additiona l radiographiC findings Include osteoporOSIS and fluffy new bo ne formation at sites of capsular, ligamentous or tendonous attachments. In the spine wedged vertebral bodies w1th Irregular plates and Schmorl's nodes simulate Scheuermann's dr.;ease.
crysta l dep()siion disease (crrD)
(Figs 6.70 6.71 ,6 72 and 673)
(oonllnues on page 161)
160
Bone Fig 6.70 CPPD. ChondrocalanosiS of the tnangular fibrocartilage associated with severe arthritic changes in the second and third metacarpophalangeal JOint IS a characteristic presentation. Other typical finchngs seen in this case include calcifications of the lunotriquetral figament, JOint space narrov.mg 1n the radiOcarpal and scaphotrapeZJotrapezoidal JOints, tmy, beak like osteophytes on the radial side of the second and third metacarpal heads and capsular calcifiCations abo~ the third metacarpophalangeal )Oint
Fig 6.71 a b CPPD Faint calcifiCations in the triangular fibrocartilage are aS1>0Ciated with adVanced arthntic changes in the radiocarpal JOint mcludiOQ scteros1s and compreSSion of the pro••mal scaphoid that appears embedded in the distal radius and Increased scapholunate distance This pattern is also referred to as scapholunate advanced collapse (SLAC) Mult1ple small cysts 1n other carpal bones and 'degeneralr.le" changes 1n the scaphotrapeZJotrapezQidal )0111t Without involvement of the first carpometacarpal JOint are also seen in (a). One year later Significant progreSSion of the arthntJC process •nclud1ng a new large subchondral cyst forrr.allon 1n the diStal rad1us 1s seen 1n b
b
a
FIQ.6.73 CPPD. Disc space narrowing with faint calcifications of the intervertebral discs, sclerosis of the ad)8cent plates and mild osteophytosis IS """(11.
Fig.6.72 CPPD. Chooclro<:aldnoSIS 1n the mensci and calcifications of the JOint capsule and collateral figaments, respectively, are seen in both knees,
6 Joint Diseases
Table 6. 14
(Cont.
16 1
Differential Diagnosrs of Ar1tcular Drsorders
Disease
ChatactCJ.,hc
loc.ltoon
Calcoum hydroxyap
Tendons
Perlortrcular
Bursae
RadtOgrapluc
Frndrngs hydroxy
(HA)
crystal
Joirrt ca psulo
Cl \ll>tul <.lcposdion I!> found 111 calctfrc tcnd<mrt"' ..nd bun.itis. H ir moch
deJ)06rtiOfl dl&886e (HAOO) (Figs. 6 .74 6 75 and 676)
Shoulder
moou conwnon HA depo611ion
than inlta-urUcular and rumoU always
Periorticubr and lfJOtTl011
mon bctwoon 40 and 70 ycer. of age. SyrJ1t toms tion
~,,
freqt-lly
assoaaltld resultmg rn ' J tx• "" ,.. go ..toon of the humeral head v rth
tlOSSILie erosaon of the lldja<xr•t inlenor aspect of lhe actomiOil and di!Jal cktvoclu. Tho coodJtion rs /omtt/ cuff tour tutluvp
shm./dcr smdrome. HAOO may also involvo tho knoo
(oft, n ~m~od to tho later ol compartf11('flt). hip, clbo ' and tho 1-ITif II Jill~® of tho hands and fllE't
include
pain,
tend~~·
ness. loall ed
pr~
the latter lnlra-ortiClJLlr HA oocurnulation leeds to pnl space narro•~ng. df>c;truchon ol St•l> cllroodral bone. subch<>odrnl .nero~. rntra-artic'ular df'br'IS nnd jOint drsorganl7atron In lhe shouldf'r a cllronic rotator cuff tear h; 11111ar1ably
HAOO ,,fleets both men l>nd is particularly com-
HA depOO!s are llOWE'\'er P I'IO loond rn a"}'ll..,tomnbc
ppl!lhy snnul;ltes CPPO, but does noc prOduce the charact~ns tic calcof1Cahorl6 found in chondroc.
HAOO
cinosil;. Cloo
irrtra..artrcular
opacotios nlily IIOW6\er be e~rdont " ' HAOO In miu·d wlcium
plwspiUJ/c
dq>~Jsit."m
d:s<ir.,tod syllO\'io l fluid . This cond ito on is oot uncommon Gnd should he oxpoctod when mdiographrcnlly cllondrocolcinosis ond periortw::11l:u cnlrofiCltions are prEl&ent to a
un~w
extend
(("(lnJinl!c.< on f'l•g'
Fog 6 74 HAOO (Mrlwaukee shoulder). Rotator cuff rolcrftcaIrons aro B&tiOCialed with a chrome rotator cuff tear evrdcnl by the wpctior rnigr.>tion of tho humcr.JI hood with mart
Fig.6.76 HAOO (housemaid's knee). Muhiple calctftmtl()l'lS noted on ..n enlarged subrutaneoos rnfra patellar bursa
are I >
Fig.6.75 adjacent
HAOO
(trochanteric
to tho gooater trochantor
bursohs) A calcllication "' ~><.'
162}
(arrow)
162
Bone
Table 6.14
(Cont.) Differential Diagnosis of Articular Disorders Chllracterlstlc:
Hemochromatosis
LQ{.AIIIon
Metacarpophalangeal JOints Wrists
(I og. (• 77)
Comments
is an onhented diSOrder wrth abnormal iron deposa!Jon resultong m arrhosrs. doabetes slon p!Qmentahon and heart failure It has a 10 1 male predominance wrth symptoms occumng alter the age of 40 years Secoo<Jaryi.'CmtKimm./aJ/S osassoaated Vltth an mcreased ontake of oren such as multiple blood transfuSions on myeloprohferatory dosorders and refradory anemias. An arthropathy 'IS found In approxomately one-third of patients comrnencong typocally m the small joonts or the hands and eventually progres::.ing to the large joints
In the spine widespread, often laminated disc space calcifications mvolving both nudeus pulposus and annulus fibrosis with predilection of the lumbar spine is most charadenshc. Associated findings mclude mal1<ed uniform asc space narroWUlg at all levels. multiple vacuum phenomena and osteoporosrs. Progressivedoscal ossification and bony bridging eventually results m a bamboo sp~ne. Exlrasponal manifestations in large JOints resemble CPPD Fondings Include asymmetric or symmetnc )Oint space loss severe subchondral sderosos. and eventually collapse and frag · mentabon of the articular surface with intra-articular loose bodoes In contrast to CPPDsubchondral cysts are absent or onconspicuous, whereas severe onvolvement of both the sacroiliac JOints and pubic symphySis with eburnation and fragmentation IS suggestive of ochronosis.
Rare heredrtary metabolic dosease woth inab4hty to metaboliZe homogentiSic acid that is excreted by the lodneys The urme os colorless when passed but darkens when exposed to hght Ochronollc pogmentatoon of the ears and sclera is usually first observed at the age of 20 to 30 years. Symptoms and signs or ochronotic arthropathy usually appear on the fourth decade or life.
seo
Ochronosis (alkapllonurUI)
(rig. 6.78)
Bilateral, not always symmetric Spine
Hops Knees Shoulders Sacr01hac JOints Pubic symphysis
.'ntnlll") /11. mt>~.luomlltosi.<
Fondings are almost identocal to CPPD ondudong chondrocalc~nosos, but are commonly assocoated With a more uruform loss of JOint space and osteoporosrs Charadenstoc onvoo\ement of the metacarpophalangeal JOints (primanly 2D and 3<"- lesscommonly 1". 4· and so·~ ondude symmetnc JOint space loss. sderosos. subchondral cysts, and fragmentation or flattening of the metacarpal heads Compared to CPPD,the 4•• and metacarpophalangeal JOints are more frequently onvolved, uregular beaklike osteophytes on the radial aspects of the metacarpal heads are more prevalent. the wrist Involvement tends to be more widespread with doffuse affection of all modcarpal and common carpometacarpal joints, but woth relatiVe sparing of radoocarpal compartment.
(continues on page 164)
6 joint Diseases
163
Fig. 6.77 Hemochromatosis. Symmetric joint space loss with mild subchondral sclerosis and large beak-like osteophytes (arrows) on the radial aspects of the metacarpal heads are seen in the second and third metacarpophalangeal joints.
F1g. 6.78a, b Ochronosis. Marked uniform disc space narrowmg with rrregular and slightly sclerotic endplates. discal calcificatron and multiple vacuum phenomena i~ seen in anteroposterior (a ) and lateral (b) projettion throughout the lumbar and visualized lower thoracic spine. The syndesmophytosis in this case is rather minimal. Grade 1 anterolisthesis of l5 against S1 is also present secondary to spondylolysis at l5.
a
b
164
Bone
Table 6.14 (Cont.) Differential Diagnosis of Articular Disorders Disease
Characteristic Location
Acromegaly (Feg. 6.79)
Hand~
Bilat._..JI
~yrr .net1ic
Fl:'et Mandrble Spine Sort tJSsue thickening (heel. phalc~nge))
a..&ographit. findings
Cornmoc-nli
Hands and feet. Soft timJe thlckcnlrlCJ of the phalanges. joint spc~ce widening (espesophyles at ligament and tendon at· tc~chment sites. Spine: Enlarged intef\lertebral di\c, increased anteroposterior and lc~teral dic~meters of the vertebrc~l bodies with exaggerated con~ity of their posterior aspects. Premature osteoarthritis with promi· nent osteophytosls is seen at a Iiiler stage, especially in the weight-bear· ing joints and spine.
Hypersecretion of growth hormone dlJe to eosinophilic adet'oma or hypPrplasia of the pituitary gland leads to gigantism rn the tmmature skeleton and acronlf'9aly in the milture skeleton. Strmulation of endochondral ossifiedlion results In enlargement of tt1e costochondral junctions (acromegalic rosary). Strmulation ol pPno~tcal bone formation ~ctds to enlargement of the mandibl<.>, phalanges, metacarpals, metatarsals and various tuberosities. Cclrtllaqe prolifer at1on results 111 wid('rred articulc1r .1nd Intervertebral spates.
Amyloidosis (Figs. 6.80 and 6.81)
Monoarticular to bilateral asymml:'trk Hand Wrists ShouldNs Hips
Articular involvement rncludes asymmetric soft tissue masses, periartrcu· lar osteoporosis, erosrons and cystic lesions with or without ~lJrroonding sclerosis and presef\lation of the jornt space. joint contractures and subluxations may also be present. Avascular necrosis may complicate amyloidosis in larger JOints. Periarticular amyloid nodules or masses are frequently observed about the olecranon. shoulder. hand and wr1st, where they can cause tl'-e carpal tunnel syndrome. Osteolytic lesions prodi.King endosteal !><.alloping and. occasionnerCJiized osteoporosis are additronal manifestations.
Pnmary .arnylo1dos1S occurs without dis£>ase or is associated With multiple rrtyf'loma. Secondary amyloidOSIS is associated With varrous chronrc diseases Including rheumatoid arthntis. sepsis. inflammatory discrd£>rs such as Crohn's disease, neoplasm and chronic ht.>modialysis. PrimCJry amylordosis is more frequent in men with an onset between 40 and 80 years. Amyloid joint d1sease shares many radrographlc features with goot, xanthomat~is and pigmented viUonodular syn0111tis.
Multicentric: reticulohis tiocytosis (li·
Bilateral symmetric H;mds f£>et Wrists Shoulders
Predilection of the tnterpllcllang£>al joints of the hands and fpet With erosions originating at thP JOint margin~ and spreading centrally associat('d with soft tissue nodule~ is characteristic. The erosions are well circum scribed resembling defect~ ~PPn in gout. The joint space is fr£>quently preserved. Osteoporosis and new bone formatron CJre alxent. Progre~ sion to arthritis mutilans IS seen In about one-thrrd of C.J<>E>S. Severe eros1ve destructive changes in the cervical spine, CSpi:'Ciall~ tht> atlantoaxial joint is also a common manrfestation. Er~lons and bony ankylosis may be ~ in the ~roiliac joints.
UrxomiTlon systPmrc dis£>ase of unknown caus(' With female predominc~nce and typtcill on~t>t in middle age. In ilpprcximately two-thirds of pat1ent~ polyarthritis is thl' fir~t manrft>\tatlon of the dtsease. followc·d aft('r months to years by eruption of red to purple skin nodules measunng up to 1 ern 1n diameter. PatrC'nts may also rev('al xanthomas pr!'ferl>ntrally rnvolv•ng the eyelids. Abnorm.allaboratory findrngs include .anPmra. hyperchol~terolemia and t>levatE'd erythrocyte S£>dimentation rate.
poid derma toarthritis) (Ag. 6.82)
[I bow Hips Kni:'CS Ankles Spine Sclcroiliac joints
coexi~t('nt
(contmues on page 166)
6 Joint Diseases
165
F1g 6.79a, b Acromegaly Soft tissue th~ekemng of the phalanges JOint space wldenrng (espeaa lly metacarpophalar~geal and metatarsophalangeal JOints) enlarged tufts and bases of the terminal phalanges and promment metaC8fP81 and metatarsal heads are seen rn the hand (a) and foot (b)
F1g 6 81 Amylordosis In chroniC renal failure Poorty defrned osteolytic leSIOns are seen in acetabular dome. femoral head and proxomal femur shaft In the former two locations the lesions are surrounded by an irregular and poof't demarcated sderosrs
Fig.6 80 Amyloidosis Osteopema and multrple carpal cysts wrth relatively v.ell preserved joint spaces are seen in the wrist
Fig 6 82 MultiCentric retlculohrstlocytosls Soft tissue nodules (wMe arrows) are associated with marginal erosions (black arrows) in the proxrmal and distalmterphalar~geal joints of the index fir~ger.
166
Bone
Table 6.14
((onl )
Differential Diagnosis of Articular Disorders
Disease
Charac:Wrlstlc:
Osteoarthritis
I'm ·r.ry· n.•lc{l(,f1/U71ts: Jcnnt space loss, subchondral scleross. Ohgo-arllcuar to polyarttcu- cyst formation and osteophytos.s are the lar, often bilateral and relahallmark of osteoarthntiS tively symmetnc The JOint space loss 111 we~ght-beam1ng Hand {Interphalangeal articulations typically 1s asymmetnc and JOints rarely metacarlocaliZed predominantly 1n the area that is subjective to excessive pressure (e .g pophalangeal JOints) \Nnst (first carpometacarpal supenor or we1ght-beanng portiOn of the JOint, scaphOtrapeziO-trapehip, medial compartment of the knee) . Subchondral sclerosis typically rs conf1ned zoidal JOint) to the area of joint space narrow1ng wrth H1p progressive obliteration of thrs space . The Knee Foot (first metatarsosclerosis may extend both verttcaiiY and phalangeal JOint. tarhonzontally 1nto the adJacent bone. sometatarsal JOints and Subchondral cysts (geodes) form with1n talonavicular JOint) the pressure segment of the subchondra l bone. The cysts commonly are multiple, Acrom10davicular JOint and of variable size and depict sclerotiC margins. They mayor may not communi cate with the joint. Osteophytosis: Marginal (peripheral) osteophytes are most common, developing as bps of new bone around the edges of the articular cartilage. Central osteophytes are button-like or flat excrescences within the articular surface denuded of cartilage. Thiekemng of the intra-articular cortex on the med1al aspect of the femoral neck IS termed buttreSSing and represents a penosteal osteophyte Capsularosteophytes onglnatiOQ from the capsular attachment srtes may be found in the Interphalangeal JOints produetng the 'seegull s.gn" as dorsal talar beak in the talona~1cular
(degenerative joint disease (..-tgs. 6.83, 6.S4,6 .H.."', 6.86,6 .fol7, 6 .8t!.6 .H9 and 6.90)
LocMion
Rldloer.,t~~c
)Oint
Findings
Comments .
Osteoarthnhs IS by far the most comrr10n joint d1sorder, one of the most comrr10n chronic drseases 1n the elderly and a leadIng cause of d1sab1lrty There rs a poor correlatiOn between clm1cal symptoms and radiOgraphiC findings The correlatiOn between JOint degeneratiOn and advancmg age IS not finear. Rather. an age related predisposition to osteoarthntiS appears to Increase exponentially after the age of 50. Osteoartlv1bs refers to degeneratiVe di~ ease of synov~a l jo1nts Abnormaht1es. hOwtover, predominate 1n the cartt1ag1nous and osseous tissues, whereas alterations In the synovium are generally mild. Pnmary (idiopathic) osteoanhrnis occurs in the absence of any underlying abnormalrty· Secondary osteoarthritis refers to joint degeneratiOn produced by a pre-exIsting condrt10n . Scwudan· o.•fcmrthrili~ (Figs. 6.91, 6 .92 and 6 93) 1s assooated With pre-exrsting art1cular di!>f!ase or deform1ty, trauma and chronic overuse and thus frequently ln\Oives art1cular srtes that are not commonly affected 1n primary osteoarthnbs Secondary osteoarthritiS may follow mflammatory or mfect10us arttv1trs, eptsodesof mnor or maJOr trauma . and congemtal disorders ChroniC athlebc and occupatiOnal ovei'IJ$e rs assooated with JOi nt degeneratiOn at specifiC locatiOns: \Mlrkers usn1g VIbrating or pneumatiC tools (e g miners or J8ckhammer operators) develop arthnbc changes in the elbows, wrists and hands (especially carpal cysts), ballet dancers in the ankles and feet football and soccer players in the ankles, feet, hips and knees. cyclists in the patellofemorel JOints. boxers and wrestlers in the hands, wrists. elbows. and baseba ll players 1n the shoulder and elbows. Sacmltt;C:Jtdnl.\ (F1g 6.94): Besdesfocal or diffuse, well-
DegeneratiVe enthesopathy may produce bony excrescences In the trochanters and ischial tuberosities and spurs in the calcaneus, pate lla and olecranon. Bony prc>liferation may be seen at syndesmotiC 1n,,.,.tion •it.,_ Flattening and collapse of the articular surface may become apparent in a more advanced stage which is not always caused by the development of secondary avascular necrosis. Both joint effusions and synovial proliferation are not prormnent features 1n osteoarthritis. large effusiOns should suggest an inflammatory, infectious or traumatic arthnbc process. CompltcatiOns of osteoanhntrs 1nclude malalignment (e .g varus or, less commonly, valgus deforrmty· and lateral sutr luxabon 1n the knee, lateral displacement of the ferr10ral head, radial subluxation 1n the first carpometacarpal JOint. and radial or ulnar deviation in the interphalangeal Papu iJr c.htmlf I(' <•.•two1thnr~ of till.' hip refers to an osteolytic destruction of the joints) and the formation of loose Intraarticular cartilagenous or osseous bod1es. h1p v.1thout osteophytosis Within weeks. BesK!esosteoarthntis, CPPD,HADD and osteonecrosis have also been implicated (Fig . 6.95).
(continues on ptJgc 169)
6 Joint Diseases
167
Fig.6.84 Osteoarthritis. Advanced degenerati\e changes including JOint spa<:f' narrow1ng, scleroSis, subchondral cyst formation and mild lateral subluxation are present mthe f1rst carpometacarpal joint
Fig.6.83 Osteoarthntls. Arthritic changes including JOint space narroWing and osteophytosis are seen in all Interphalangeal JOints, he first carpometacarpal JOint and the scaphotrapeziotrapezeidal joint whereas the metacarpophalangeal jo1nts are spared. Osteopenla and a fracture or the base of the prox1ma1 phalanx of the fifth finger are incidentally also present. Calciflcallon of the triangular fibrocartilage is also evident.
Fig.6.85 Osteoarthritis. Joint space narrow1ng 1n the superolateral aspect of the hlp IS associated with adjacent subchondral cyst formatiOn 1n the acetabulum and femoral head Considerable osteophytoSlS 1s also seen 1n the acetabulum.
Fig.6 86 Osteoarthritis. JOlnl space narrowing hmrted to the ,. eight-bearing port1on of the hip aSSOCiated wrth subchondral scleroSIS IS seen New bone formation (bUttress~ng) along the medial aspect of the femoral head and neck is also evident (arrows).
Advanced degenerabve chang~ wrth Fig.6.87 Osteoarthritis. fragmentation of thP subchondral bone of both the femoral head and acetabulum 1n the weight-bearing porbon of the hlp IS evtdenl
168
Bone
Fig.6 .89 Osteoarthntis (hallux ngldus) Advanced degenerat111e changes w1th joint space narrowing, extensive subchondral sclerOSIS and osteophytoSIS are seen 1n the fir& metatarsopha langeal JOint
Fig.6 .88 Osteoarthritis. Ad\lanced degenerall\le changes with JOint space narrowmg, sclerosis, osteophytoSis, subchondral cysts and loose bod.es 11'1 the Intercondylar notch are seen 1n both knees.
Fig 6 90 Osteoarthnbs Hypertrophic degt:nerallve changes with Inferior spurring are seen 1n the acromiOclavicular JOint causing Impingement on the supraspinatus muscle and tendon (1mpmgement syndrome)
FIQ 6 91 Post-traumatic osteoarthnbs. Chondrocalcmosis in the lateral meniscus, a large Intra-articular loose body (arrow) and a shell-like ossification (arrowheads) along the med1a l femoral condyle (Pelligrlni-Stleda ossification) 1nd1cative of a chron1c rr~ed1al collater 11 ligament 1njury are seen.
Fig 6 92 a, b Chronic overuse osteoarthntis a Javelin thrower. Degenerat1ve changes Including subchondral sclerosis, mild osteophytosis and healed fracture of the bp of the olecranon are seen 1n a J811ehn thrower b Jackhammer operator Multiple carpal cysts and early degenerat111e changes in the radiocarpal and distal radiOulnar JOints are seen in a pat.ent wrth normal bone mmeralization.
a
b
(>
Table 6.14
Cant
DISease
Characterishc locat1on
D1fferent1al
Rad1ograph1C Fuldmgs
Erosive osteoarthntJs (FIQ 6 96)
Bilateral symmetric Interphalangeal pnts of the hand
F1nd1ngs of advanced osteoarthnbs Uomt space narroWing, subchondral sclerOSIS and prom1nent margmal osteopnytes) are assooated with eroSIOns llley commonly originate 111 the central portion of the jo1nt as sharply marginated defects Their central location differs from the marginal erosions seen in rheumatoid and psoriabc arttvitis. Progre'>SIOO to bony ankylosis is not infrequent In contrast to psonatic arthritis the diStnbutlon pattern tends to be bilateral symmetnc
Jo1nt Diseases
169
D1agnos1s of Micular Disorders
ts. Presentsctmcally With acue ,nflammatory eprsodes 'ncludlllg pa1nful Heberden's and Bouchard's oodes {marginal osteophytes and son bssue tljckenmg about the distal and proximal Interphalangeal JOints, respectiVely) 111 women (male, female ratio is 1.1 0) May be assoc iated With pn· mary (non111Hammatory) osteoar· thnhs m other pnts of the hand and wnst
(c mllmue.• 1>11
Fig 6 93 Post-trat.mabc scapholunate advanced collapse (SLAC). SCleroSIS and compres. 10n of the prox1mal scaphoid secondary to a healed fracture, scapholunate diSSOCiation. and proximal migrabon of the scaphoid v.rth obliteration of the radiosca· phoid space are seen Mild compresseon, rotatiOn and sclerOSISof the lunate wrth degenerative changes In the lunocap1tate jo1nt are also associated.
1 O)
Fog.6.94 Osteoarthnbs In the sacr04hac JOints. B~ateral welldefined subchondral saeross\1 rtholA eroSions oc JOint space narrol.\ing is seen.
FIQ 6 95 Raptdly destructrve osteoarthntis of the htp B~ateral osteolytic destructiOn of both ao tabula and femoral heads IS seen On the right Side the procei>S 1s further advanced and uwotves also the femoral neck. Fig 6 96 Erosive osteoarthnbs Jo1nt space narrow1ng, subchondral sclerosis and osteophytoos are associated in several interphalangeal JOints with central eroSIOns Degenerative changes with small subchondral cyst forrnat1on are also seen 1n both first carpometacarpal joints
pc1~c
e>
170
Bone
Table 6.14
(Co nl ) Differential Diagnosis o f Articul ar Disorders
01sease
Charactel'lstl<:
Degenerative disease ot the spine
MICidle and lower cerv1cal sprne Lower lumbar sprne
(Fll.."- 6.97. 6.98.(~ 9'), 6.100, and 6.101)
loca tl o n
RadloQra ·Ill<:
Comments ,
Andi11QS
Degeneration of the rntervertebra l diSC (mtwchmlliroM.<) may present With tl.
COnditions aSSO()iated v. 1th degeneratrve d•sease of the sptne 1ndude costovertebral osteoarthr1hs. Baastrup's disease and Bertolotti's syndrome. CoJio~trlt b~td wlwtu·thrit s: The costovertebral jo1nts are located between the head of the nbs and the vertebral bod1es and between the ned<sand tubercles of the nbs and the tranS\Ierse processes DegeneratiVe changes. predominant m the art1culabons of the 11.. and 12• nbs, 1nclude jOint space narrowIng, bony ebumat10n and osteophytosis and may progress to complete bony ankylOSIS With pagetoiCI appearance of the postenor port1on of the affected nb. lJtl(i.\lrup'., tb.\1'11.'1 : Extensive disc space loss or excessive lordosis of the lumbar spine leads to approximation and contact of the onen unusually large sprnous processes DegeneratiVe changes including reachve sclerosis and osteophytosis may develop between the "kissing sprnes" and may be assocrated With consrc:lerable pa1n. Hcr/('/{1/11'< .
(Will/lUI(~
/J/1 fX/f.C
r2)
F;g. 6.97 a, b Degenerative disease of the spine (spondylosis deformans ~ Anterolateral
osteophytPSis throughout the lumbar spine is the dom1nant radiographic manifestation seen in anterolateral (a) and lateral (b) projection
a
b
6 Joint D1seases
Fig.6 98 Degenerative disease of the spine (osteoctlondrosis). Narrowing of the Intervertebral space with relatively littl e osteophytosis is the dominant radiographic manifestation best seen at L4t5. Lesssevere disc space narrow~ng with calcification of the posterior longitudinal ligament (arrow) that IS postenorly displaced by the bulging diSC and small anterior osteophyte formation 1s seen at L314
171
Fig.6.99 Degenerative disease of the spine (spondylarthrosis and Baastrup's disease). Spondylarthrosis. Degenerative changes in the apophyseal (facet) joints presenting w1th jo~nt space narrow ing, bony eburnation and osteophylosts are seen 1n all segments of the lumbar sp1ne Baastrup's d1sease Degeneratrve changes lnduding reactiVe scleroSis are also seen between the unusually large spinous processes (arrows) which appear 1n contact w1th each other f'kissmg spines').
Fig.6.100 Bertolotb's syndrome. Parttal sacrahzahon of LS is seen Degenerative changes bet\·-1e~m the enlar~d left transverse process of th1s transrt1onal vertebra and the adjacent sacral WIOQ are evident by the e)tensille scleroSis at U1e contact Site of Ulese two parts.
Fig.6.101 a, b DegeneratiVe cervical spine disease Disc space narrow1ng wrth mild osteophytosis 1sseen between t.J \ f' r, and (f> (arrows) Small osteophytes (arrowheads) protrudmg posteriol'tj 1nto the spenal canal are seen 1n a. Encroachment of the nght neural foramina by small osteophytes (arrows) ong1nat1ng from the uocovertebral (luschl
a
b
112
Bone
Table 6.14
((ont.)
Differential Diagnosis of Articular Disorders
Dlseas~
Charaderlatic:
omuse Id-Iopathic skeleUI hy·
Spme (espectally lower thoracic and upper lumbar area) PelviS Calcaneus Patella Olecranon
~rostosls
(DISH, For· estler's cis-
easel (Figs . 6.102 and 6.1031
Loatlon
Radlog~
Flnclngs
Diagnostic criteria in the spine
Comment I In·
dude: 1 . Flowing ossifications along the an· terolateral aspect of at least 4 contiguous vertebral bodies 2 Relative preservation of the d1sc space and absence of Slgmficant degenerative signs such as reactive scleroSis and vacuum phe· nomena 1n the Involved segment 3 Absence of bony ankyloSIS m the apophyseal JOints and no ev1dence of sacro1li1t1s Pelvis Bony proliferation ("'whiSkerlng") in the Iliac crests, ischial tuberosities and trochanters. Broad osteophytes at the lateral acetabular edges, 1nferior portions of the sacrOiliac joints and superior aspect of pub4c symphysis. OssifiCations of iii· olumbar, sacrotuberous and sacroiltac ligaments. Enthesophytes Without adjacent reactive bone sclerosis or eroSions at numerous sites, most commonly in the calcaneus, patella and olecranon
Common OSSifying diathesis characterized by bone proliferation at sites of tendinous and ligamentous attachment (entheses). Presentsusually v.rth m11d symptoms of restricted spinal motion and tendinitis m patients over 50 years of age wrth 3:1 male predom1na na> The cause of DISH IS unkno\'m It msght be considered a hypertrophiC variant of spondyloSis deformans. Bony hyperostoSIS of the spme somewhat Similar to DISH 1s aSSOCiated v 1th endocrine disorders such as acromegaly, hypoparathyroidism and diabetes mellitus HyperostoSIS of the sp1ne and ligamentous calt~ficallons are also found wrth fluoroSis, but the latter cond1t1on IS associated with diffuse osteosclerosis of the axial skeleton . Prolonged therapy for skin disorders w1th retinoid drugs (e .g . Acutane ), wh1ch are chemiCally sim11ar to v1tam1n A, may also 1nduce hyperostoSIS in both the axial and appen· d1cular skeleton . Excessivehetero topic bone formation after prosthetic h1p or knee replacement is frequently ob&erved wrth DISH. O~·•f•c·cnwn of t he !'WI< n or longmuJ, . ~rllillt;mllc nt
(01'/.L)
(F1g 6.104) affects the cerviCal spsne and IS often assocsated wrth DISH (cont .m~es
<'11 page
r
.J)
6 Jomt Diseases
173
Ftg 6.102a, b DISH. Huge paravertebral flowtng ossifications wrth preservation of the diSC spaces are noted throughout the lumbar spine 1n anteropostenor (a) and lateral (b) projection Note also the absence of bony ankylosis 1n the apophyseal (facet) JOints and the normal sacro1llac JOints
a
b
F1g 6.103 DISH Symmetrical bony proliferation ("wh1skering") is seen in the 1hac crests. greater trochanters and to a lesser degree tn the ISChial tuberoSities.
F1Q 6 104 Ossification of the postenor longitudinal l1gament (OPU) is seen 1n the cervteal spme (arrows)
174
Bone
Table 6.14
(Cont.) Differential
Diagnosis of Articular Disorders
Disease
Characteristic Location
Radiographic Findings
Neuropathic osteoarthropathy (Charcot joint) (Figs. 6.105,
Congenital Indifference to pam and menlngomyeloceles: Knees Ankles lntertarsal JOints Synngomyelza Shoulders Elbow& Tabesdorsalis H1ps Knees Ankles Spine Diabetes mellitus: Midfool Forefoot Leprosy· Hands Feet
Persistent joint effusion. often with Hypertrophic bone changes are caused by repetitiVe traumalmicrotra~.KM with attempted cartilaginous and osseousdebri (detritiC synovitis) resUting from frag- repa1r AtrophiC resorptiVe changes are caused meritation of the articular surface are by sympathetiC dysfunctKln resultmg in hyperemia and bone resorptKln Congenital causes earty find1ngs. More advanced abnor1ndude myelomen1ngoceles and congenital lflmalities include progressive rapd bone resorption or extei"ISIVe JOmt de- dlfference to pa1n. AcqUired causesanclude bra1n and cord 1n1unes or tumors, synngomystruction Y.lth marked sderosis and osleophytOSIS. Intra-artiCUlar O&SeoUS elia. tabes dorsalis. diabetes mellitus and lefragments. subluxations. massive ef prosy . . Ltwl neuropathic o" fectKlus processes are frequently sulion of the end or phalanges metacarpals and penmposed on the neuropathiC metatarsals rewlting 1n "llcl<ed candy stick" al>" changes in the diabetic foot. pearance are charactensbc.
6.106,6.107, 6.108,6.109 and 6.110)
Comments
(((>11/ i/UIC.\
011
page J76)
F19 6.105 Neuropathic ost eoa rthropathy (s yringomyelia). AdvaTICed arthnbs with destruction of the glenoid tritra-artlcular fragments sdleroSIS and osteophytosrs IS seen. Superior m1gration of the humeral head 1nd1catmg a chron1c rotator cuff tear is also evident.
6 Joint 01seases
175
Fig.6.106 Neuropathic osteoarthropathy (syringomyelia). A completely diSOrganized elbow with mu~1pte fracture fragments and exteOSI\Ie sclerosiS IS seen
Fig 6.107 Neuropathic osteoarthropathy (tabes dorsalis) DestructiOn of the ankle subtalar and talonavicular JOints v:Jth collapsed plantar arch and extenSive 5(;~ ·ros1s r.; seen
Fig.6.108 Neuropathic osteoarthropathy (congenital indifferenceto pain). Extensivesoft tissue swelling isassociatedwith multiple fractures in the d1stal tibia and talus angular deform1ty of the ankle numerous loose fracture fragments sclerosisand periostitis.
Ftg.6 109 Otabebc foot ~~ultlple healing fractures with exteoSi\ie callus formation 1n the m1d and forefoot are aSSOCiated w1th a collapsed and disrupted l.lsfranc JOint Artenoscferobc calcifications characteristically are also present
Fig 6 110 leprosy Multiple subluxatiOns-diSiocabons and extensve osteolySIS are seen 1n the forefoot resu~1ng 1n a tapered appearance of many metatarsals and phalanges (iicked candy stick" appearance).
176
Bone
Table 6.14
(Cont) Differential Diagnosis of Articular Disorders
Disea se
Characteristic
PyogeniC (septic) ar ·
Monoarbcular
thritis (F1gs. 6.111 6112,6 .113
a nd 6 .11<1)
1-iip
Knee Sp1ne
Location
Radiographic
Fmdings
Every monoarticular inflammatory arthritic process should be considered Infectious until proven otherwise. Acute stage· Para-articular soft tiSSUe swelling. JOint effuSIOn (frequently producing widemng of the JOint space 1n children) and JUxta-articular osteoporosiS followed by d1ffuse JOint space narrOWing due to rapid destruction of the articular cartilage and marg1nal and central bony eroSions. Subacute/chronic stage· Subchondral bone destrucbon w1th reactrJe bone sclerosis secondary degenerative changes and eventually bony ankyloSIS may be found In the spine disc space narrow1r1g and loss of normal definition of the adJacent endplates progressing rapidly to frank destruction of the subchondral bone plate or enlarging destructive foci is characteristic. After 2 to 3 months reparative changes become evident in the form of reactille sclero sis. In children a hematogenous in fection of the intervertebral diSC alone ("d1skitis") Without Involvement of the neighboring vertebral bodies may occur as long as the blood supply to the d1scs rema1ns 1ntact. DiskrtiS may occur 1n adults by direct 1noculabon of the offendmg agent dunng d~agnosllc or SLI'g~cal procedures Sacr01hac JOint 1nfect1on lypteally IS umlateral d1fferen118bng 11 from many other arthribc processesthat are frequently bilateral
Comments
A hematogenous tnfection-induced arthnt1s 1s e1ther caused by direct infiltration and subsequent multiplication of the VIable organiSm or v. rthout d1rect contam1nabon of the JOint The latter IS referred to as reactn'C' llrthnfl< and found With rheumatiC fever and Lyrr~e d~Seasevmere 11t IS caused by an ant.gen-mediated 1mmune response to the offending orgamsm A sympathebc )Otnl effuSIOn adJacent to a srte of lnfiammabon may al50 m1m1c an acute infectious arthnbc process /lm111, of mfuttm'·' ,oud cmllllmmatwll Include ftfmt.lof.~fiiOI<.\ .1pn·ad ctlltltl!tlfll,,, ·'!"l'tl(1 (intra-articular extension of osteomyelitis or neighbormg soft tissue abscess)and tlirlCt imp/wtJ(IIton (penetrating trauma or iatrogenic procedure) In infants and children monoart1cular involvement of the knee or hip is the most common presentation In the adult the lumbar spme and knee are the most common Sites of Involvement Common organiSms 1nclude staphylococcus aureus and streptococcus pyogenes at all ages hemophilus influenza tn children , and neisser~a gonorrhoeae (often more than one JOint lfii'Oived) and brucella 111 adults A prompt and definrte diagnoSis requ~res an arthrocenteSIS blood cultures and posSjbly bone biopsy (spme)
(C'OIIIIIU/(',\
on
{JOg£'
r f!)
<• Il l a, b Pyogenic (septict) A JOint effusion evident by the slight lateral subluxation or the femoral head 1s the only abnormality seen in a Six weeks later narrowmg of the joint space. espeaally med~altj, due to destruction of the artiCUlar cartilage and poorly def1ned mixed osteolytiC and osteosclerotiC areas m the femoral neck and adJacent shaft are seen in b. I•~
arthritis.
6 Jo1nt Diseases
177
Fig.6 .112 Pyogenic (septic) arthritis. Joint space narrowing With destruction and fragmentation of the subchondral bone in the medial talar dome and adjacent tibia plafond 1s seen. Begmn1119 periostitis in the distal bbla and fibula is a~oo evident
Fig 6 11 Ja b Pyogenic (sepbc) arthlitls Jomt space narrowing and poorty def1ned osteolytic and osteosclerotic lesions are seen in the femoral head and pro~1mal neck 1n a. One year later marked diSease progression With destructiOn and fragmentation or both the femoral head and acetabulum, osseous debns accumulation 1n the h1p w1th lateral subl~at10n of the ferrK>ral head, extension of the osteomyehtJc process 1nto the rntef1rochantenc area and begrnnmg repa1r (scleroSis of the acetabular roof wrth adjacent ~teophyte formation) is seen 1n b 8
b
Fig 6.114 Diskitis. Narrowing or the Intervertebral space between LSand 5 1 with slightly irregular adjacent end plates and marked sclerosis or the adjacent bone is seen.
178
Bone
Table 6. 14
(C'o nt.) Differential Diagnosis of An icular Disorders
Disease
Charactenstic LocatiOn
Rad!O{PPhic f indings
Comments
Tuberculous arthnbs
Monoart~eular
Tuberculous spondylitis most commonly affects the thoracolumbar area. It may 1nvolve more than one Intervertebral diSC and has a predilection for the anteriOr aspect of the vertebral body ExtensiOn 11nto the adJ8cent ligameris and soft trssue IS frequent allowing osseous or disc invasion at distant sites or leadmg to the formation of a psoasabscessthat tends to calcify. A gibbus deformity in the thoracolumbar area may be the end result In the appendicular JOintS PhemiSter's tnad IS characteriStic consiStmg of JUxta-articular osteoporOSIS, marg1nal eroSions and gradual narrowmg or the jOint space. Compared to a pyogen1c arthr~is a delay in destruction of the articular cartilage or intervertebral d1sc, absence of reparative sclerosis, and cal cification of the associated soft tissue abscessesare all suggest1ve of tuberculosis
Skeletal tuberculOSIS can affect persons of all ages, but less than 1r;, of pabents Infected With tuberculoSis have bone or joint ma111festabons TubE:rcoloUli spondylitiS 1s the most frequent skeletal manifestation presenting w1th an lllSidious onset of back pain, sliffriess, local tenderness and poSSibly fever. Appendicular tuberculous arthritis may present wrth pa1n , sweh1ng, weal
Monoart1colar Large appendiCular JOints Sp1ne
Jo1nt Involvement is usually caused by d1rect extension from an adJacent osseous focus and rarely by d1rect hematogenous implantation. Soft !issue swelling, effusion. joint space narrowIng, erosions or bony destruction, v.rth or without osteoporoSIS are ob· served in these cases
Usually in patients with compromised 1mmune system Cryptococcosis, North American blastomycosis, cocadiOidomycosis, hiStoplaSITlOSIS, sporotnchosis (especially hand and foot) . and candKhasis are common organiSI'Tis MIJCtxa foot · Single or mutllple osseous defects to extensrve destrucbon wrth penost1tis and scleroSIS leadng to extenSive mira-articular osseous fusion ("meltJng snow' appearance) .
Viral arthntis
Monoart~eular to polyarticular Penpheral JOints Often poly a rt~eular
Nonspeafic joint effusion wrthoul bony Involvement. ChroniC arthropathy following rubella vaccmat10nfinfect10n IS occasiOnally seen resembling JUVemle rheumatoid arthritiS
Transient arthntiS assoaated wrth rubella , mumps, mycoplasma Infections. and hepatrus. Osteomyelitis and arthritis (suppurative and nonsuppurative) were 1n the past wellknown complications of smallpox (variola).
HIV infectron
Oligoart1cular to polyarticular Knee Ankle Foot Hand
Reiter's-like asymmetnc oligoart1cular or polyarticular mvolvement of pref· erentialty the tower extremity with considerable erlthesopathy, espeaalty 1n the foot (AIDS-foot) Penpheral arthropathy sim1lar to psoriatiC arthritis is also found . Involvement of the axial skeleton with the exception of the sacro~iac joirrt is uncommon.
HtV shares certam aspects of cellular 1mmune deficiency elements wrth seronegative spondylarthropathies such as Reiter's syndrome and psoria-
(Figs 61 15, 6116 and 6 .117)
Fungal ar-
thniiS {Fig 6. 11 8)
(AID>)
(Fig. 6.119)
Sp1ne H1p Knee
~~s
Septic, tuberculous and fungal arthritis are not uncommon in AIDS patients either (Figs 6120 and 6 121) This mfecll\le arthntiC process Ill monoartlcular and beSides the knee and the sacro111ac JOIIlt the larger JOintS of the upper extremity and the acromiOclaVICUlar and sternoclaviCUlar jo1nts are frequently affected
(cwJitutt.\ o n JK11(( 180}
6 Joint Diseases
179
Fig.6 115 Tuberculous spondyl~is Marked dlbC space narrowing and a destructrve les1on with fragmentation aflecting the anterior aspect of the adjacent two vertebral bodies resulting 1n focal kyphosis (g1bbus cleformrty) IS seen at L112
Fig.6.116 Tuberculous arthntis. SeverelocaliZed osteopema associated w~h JOint space narrowing and mu~iple small erosions IS seen in the wnst mvoiVII"lQ the radiocarpal intercarpal and carpometacarpal joints The normal contralateral wrist 1n thiS pat~ent differentiates this condilion radiographically from rheumatoid arthritis.
Fig.6.117 Tuberculous arthmis. Juxta-articular osteopenia. JOint space narrowing and a poorty defined erosion (arrow) in the lateral aspect of the femoral head are seen.
Fig 6 118 Fungal arthntis A well defined triangular osseous defect with sclerotic marg1n 1sseen in the greater tuberosity: Several poorty defined osteolytic lesons w~h surrounding sclerosis 1n the humeral head and glenoid are also seen in this patient wllh AIDS.
F1g 6.119 HIV 1nfectton An erosi~e lesion (arrow) v.rth mnllmal spiculated ~w bone formation is seen 1n the superolateral aspect of the calcaneus.
180
Bone
Table 6. 1-l
('ont
Disease
Charactensbc location
RadiographiC Fmd1ngs
Comments
Pigmented v1llonodular synovrhs (PVNS) (Figs 6 .122, 61 23 and 6124)
Monoarticular Knee H1p Ankle Elbow Wnst
Dense appeanng soft t1ssue swellmg around the invol\ed JOint due to hemosiderin depoSition 1n synov1al proliferation and joint effusion. Pressure erOSIOns and cysts are common m JOints with light capsule (e.g hip ankle. wrist) . Osteoporosis and lntraartia~lar calcifications/loose bodies are absent. Joint space is preserved until very late 1n th<> diSease.
Highly vaSaJianzed tumor-like synOVIa l proliferation with multinucleated g•ant cells 1ngeshng he· rnosidenn Occurs typaiiV 1n adults 1n the 3m and 4 decade of life. HernormagiC (chocolate-bfown) effuSIOns 1n the absence of trauma are characteristiC.
Synovial osteochondroma -
Usually monoartJcular OccasiOnally bilateral Knee Hip Elbow Shoulder
Multiple calcified/osSified synovial nodules or loose bodies rang1ng 1n SIZe from a few millimeters to severa l centrmeters are charactenstiC Onethird of chondromas are not calafied. Lesions may cause pressure ero~ons in the adjacent bone (e.g . hip) and Widening of the joint space No osteoporosis IS evident. Secondary osteoarthritis occurs in advanced disease from chronic mechanical 1rnta lion by the loose bodies Malignant transformation to chondrosarcoma IS extremely rare.
Presents1n the 3.dto 5t decades of life v. rth chroniC JOint pam, limitation of motion and lod<mg With 31 male predominance SyriO\IIol cllotldtomotapiDsia occasionally occurs in the elder1y patient with advanced primary osteoarthritis causIng chron1c synovial mftammation and subsequently secondary osteochondromatosis Differential d1agnosis includes synovial homtJil(}toma lipOma ortx>roSOI'ns and pigmented villonodular synovitiS.
IOSIS
(Figs 6.125, 6.126 and 6 .127)
D•ffcrcniJal Diagnosis of Articular Disorders
(con6nuos
on page
182)
b
Fig.612Qa, b septic arthntis 1n AIDS (2 cases). a \/Videmng of both sacroiliac joints caused by erosion and destruction of the adjacent bone with extensive sclerosis 1s seen The bilateral involvement is unusual for septiC arthrrtls b Destruction of the subtalar joint is associated wilh extensive sclerosis pr1marily of the cai-
a
can"'lL"-.
Fig 6.121 Tubera~lous arthritis in AIDS OsteolySis of the prox1mal pha lanx of the filth finger with a coarsened reticulated pattern reminiscent of sarcoidosis is seen extending into the proximal interphalangeal JOint
6 Joint Diseases
181
FIQ 6.122 Pigmented v~lonodular synovitis ExtnnSic pressure erosions present as scalloped extrinsic osteolytic leSions in the lateral aspect of the femoral ned< and acetabulum.
Fig.6.123 Pigmented vdlonodular synovibs. Multiple lobulated cystic leSIOns often With m•mmally sclerot1c margins are seen 1n the humeral head, acrom1on and diStal claviCle .
FIQ.6124 Pl{lmented vdlonodular synov~is A large son mass along the d~ .tal ulna outllroed by two metalliC skin markers ts associatedwrth mulllple eros10ns·cyst1c leslons1n many carpal bones and the bases of metacarpals 3 to 5.
Multiple OSSified FIQ.6.125 Synovial osteochondromatosis. loose bodies are &<)en 1n the knee joint, suprapatellar bursa and popliteal (Baker) cyst (arrow)
Fig 6 126 Synovial osteochondromatosis Mulbple calcified or oSSified looS~. bodies are seen 1n the glenohumeral ,0111t 1ndud1ng the axnldiY and subscapular recesses.
Innumerable small Fig.6 127 Synov1al osteochondromatosis calcified oo...e bod1es are ..cen in a hugely enlarged h1p JOint
182
Bone
Ttible 1;. 14
((.;o. ' )
er ....,
1
1agn
•
rs
Disease
Charactensbc Locahon
Radioga ·hie Findings
Comments
Osteochon· dritiS d•sse· cans (osteochondral fracture) (FigS 6128, 6129, 6.130 and 6.131)
Knee . Medial femoral condyle Lesscommonly lateral femoral condyle tibia and patella Talus· Lateral and mPdial dome Elbow: Capri• ·Dum Shoulder; Humeral head and glenoid
Osteochondral fracture with characteristic location. The spectrum ranges from an 1n situ lesion wrth 111tact arbcu1ar car· tliage over a detached osteochondral body still located 1n the ong10al prt (mouse bed) to a completely detached osteochondral fragment (mouse) away from the prt evident as a subchondral defect with sclerotic margm. Soft b&SUe sv•elling and jolllt effusions are frequently associated. Knee: The most common location is the nonweight-bearing portion of the medial femoral condyle at the Intercondylar notch (70 '•} Other locations in the knee include the we~ght-bearing portions of e1ther the medial or lateral femoral condyle and rarely the anterior aspect of the lateral femoral condyle and the media l facet of the patella
Presents most commonly in male adolescents and young adults with pain aggravated by motion, chcking and locking or maybe asymptomatic. It represents a subchondral fat.gue fracture but a Slf19le traumahc e~ert IS occaSIOnally 1derit1fied (espectaUy 111 the talus) A pu-ely carblag1nous lesion cannot be apprec1ated by plain film radiography and requ1res MR imaging or CT arthrography for accurate diagnosis. Avascular necrosis of the knee may also present wrth find1ngs resembling osteochondritiS d1ssecans but in this condition frequently both knees or both condyles 1n the same knee are affected
(wnllllllt'.' \>n pll~e 183)
Fig.6.128 Osteochondritis dissecans. A 1 em oval shaped bony fragment (arrow) is seen in an osteochondral defect (prt). located dassically along the lateral nonwe~ght-beanng segment of the medial femur condyle. At a later stage, the bony fragment rr~ay become dr.r lodged from the pit and found as a loose body anywhere in the knee joirit.
Fig.6.129 Osteo· chondritis dissecans. An osteochondral defect extend1ng from the lf'ltercondylar notch to the weightbeanng segment of the medial femur containing two osteochondral fracture fragments (arrows) is seen (extended claSSIC variant).
Fig.6 .130 Osteochondritis dissecans. A radiolucent line separates an oval shaped osseous body (arrow) from the med ial talar dome. The leSion IS referred to as in-Stu when the articular cartilage covering the osseous fragment remarns 1ntact
Fig 6 .131 Osteochondral fracture An acute osteochondral fracture (arrow) is seen 10 the lateral talar dome In the su" acute/chrome stage this lesion may be impossible to differentiate from osteochondritiS dJSSecans
6 Jomt Diseases
T
~
6 14
(C
'ff r.. t
183
~
Drsease
Charactenst1c location
RadKJC¥a ; hic Firid1n95
Comments .
Avascular necrosis (osteo necrosis) (Figs. 6.132. 6.133, 6.134,
Monoartx:ular. occaSIOnallly bl· lateral H1p
Articular involvement affecting only one site of the joint is cha racterisbc. In an earty stage plam film findn'lgs are absent or nonspeCific and tnclude mixed lybc arid sclerottc changes producing a mottled appearance of the subchondral bone with preservation of the JOint space An arc-like subchoridra l lucent line (crescent Sign tn femoral head) is more specific. Progression of the dtsease results 1n subchoridra l cyst formation, fragmenta bon and eventually collapse of the affected e piphysis. At thiS stage loose intra-articular bony frag ments are frequently present The endstage IS severe secoridary osteoarthrrtis In-volving the entire joint. Post-traumatic avascular necrosis is most frequent in the femoral head (subcap ital fracture, dislocation, or slipped capital femoral epiphys~s). talar dome (talar neck fracture), humeral head (anatomic neck fracture, or severe fracture-dislocation), and proximal pole of scaphoid (scaphoid waist fracture).
Forearty diagnosiS of avascular necros1s either rad10nudide bone scmbgraphy or mag-tet1c resonance tmag1ng IS reqwed Pnmary avascubr necrosas IS uncommon tn the adult e~cept 1n the lunate 11\icr./-()c{J< di.iS of the kru·c (SOf'IC) USU· ally occurs 1n pattents ove r 60 yea rs of age wllh female predominance It presents v. tth nattemng of the weight beanng portion of the medial femoral condyle Involvement of the lateral condyle, tibial plateau or both knees are all uncommon Progression of the disease results in further depressiOn of the affected condyle with tncrcased sclerOSIS and possible loose body formation. More recently a stress (insuffiCiency) fracture rather than osteoneci'OSIS has been impticated as cansat1ve factor for this condition.
6 .135, 6 .136, 6 .137 arid
6.138)
Knee Talus Scaphoid Shoulder
(conlinun n1 f>tl~t 1115)
Ftg.6.132 Avascular necroSis Eartya>~ascular necro~ presents ~tth mixed lytic and sderobc changes in both femoral heads without alteration of their shape. An arc-like subchondral lucent line (crescent sign) seen in the right femoral head (arrow) IS a more specific findmg arid iridicates pi'Ogression of the dtsease Sequelae from bilateral core decompression are ev ident by the obltque tracks extend1ng from the greater trochanters to the femoral heads. Post-traumabc dtastaSisof the pubiC symphysiS IS 1nadentally also present
FIQ.6133 AvasctJiar necroSIS An arc-like subchondral !l ucent line (crescent sag-t) is seen (arrows) .
184
Bone
Fig 6.134 Avascular necrosis. Fragmentation of the femoral head .n the wetght-bearing segment results in flattening and collapse of the femoral head. F1g.6.13S Avascular necrosis LocaliZed fragmentation or the humeral head in Its superomed1al aspect is seen. The osteochondral fracture fragment with crescent sign resides in an irregular pit with sclerotic marg1n. A large subchondral cyst infero-lateral to the pit is also evident.
Fig 6 1136 Avascular necrosis. A large detached osteochondral fragment isseeninthe welght-beanng portion orthe sclerotic medial femur condyle 1n this patient w1th systemic lupus erythematosus.
Fig.6.137 Idiopathic avascular necrosis of the lunate (Kienbock's disease). A compres=oed sclerotiC lunate with several small cysts is seen.
Fig.6.1138 Spontaneous osteonecrosis of the knee (Ahlback's disease). An irregular osteochondral defect with sclerotic border is seen in the weight beanng portion or the med1al femur condyle
6 Joint Otseases
Table 6 14
(Coni .) Di ffcrcmmt Dtagnosis of Articular Disorders Ra
1\lultipk epiphyseal
l'ol)olrtKulat . l ilat .rul t:~r
lltp~
~pond)
K.lh.:QI
l<xpiph~ ~cal
\ni.J..'!> Slwuld.:n \\ n.-.ts
J)~pl:osia (~tg.
6.1W)
185
>\1lltudric
findin&>
fpiphys,al c"tt.:n> of long bot"-"' ar, lal~ in app.:aran.:.: and lragJu,nl..-d .\h~ <"-silication thC) ha'" a ntul· l>cn)·-like arrearance and arc com· 1110111) dt'flla~
. \fk1' I'•Mt) tile affect~ arttcular 'urf3C'e<' <>I' tile le>ng ~ Mnatn or,-..,I' ular and ahlonnal m "'-'~ mod th, JNDl' ma) app.:ar tl"pla.>IJ< ll'lll<'l"al '"'ad, and n•nd)k' an: natktJcd and oftt S.:c· <•ndru)· t*koarthriti' ;, pr.'l'mt l>cf<'f'C the 1 d <>r 41h decade of ltk
1k1crogcnc<'l'" IV'"'I' • f d) •pla'ta., \\llh 1111111111:11 h> :t<.'(·d >f'llllllf dtan~;<s (•r•MI 1-ca~ms t< • rt~t)· •l'•tt<J/1"$< tclutndmts, Jll'
atod Aft)
pkaw (dd.t)<-..1 au.! hat,;llllllkd '""T'Jlll) al ,,~ifit.:uti(m r~..~uhing 4.."'-.:nIUotll~ in tK>rtn.tl l1ip. hil.otcrnl in 50% <•f ca<e~)
(ctmlimtc.f on page 186)
a
c
b ftf- 6. 139 a. h. c lipond) locpiplt)'clll d)splasia tarda (XIink<'U mall <) It, k "'" me a....xo.,t.-d \\ilh mild!) d) >plaslt< ~hall o\\ :tc'\.tal>ult h: I hl.th no! d) pia It<' l.nc..,. \\lth I-
,h.,
l(l\\ iokr.:<'ltd) far fl(>tch<'> and h)p< f'l il'l" tohoal '!'"~<'" are ""'" c: O)"rbstk: Hrt<>di..., "tth dt;uoct
