Differential Diagnosis in Conventional Radiology Francis A. Burgener, MD
Martti Kormano. MD
Tom1 Pudas. MD
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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.
C> 2008 Ceorg lhteme Vt'rlag, RlidtgerstraRe 14, 70469 Stuttgart, Germany http://www.thicml•.de
Th1eme New York, 3B Seventh Avenue, New York. NY 10001. USA http: Jwww.th1en1e.com Typesetting by primustvpe llurler CmbH. D-73274 NotLingen Printed in Germany by Crammlith, Pliezha~n ISBN 978-3- 13-656103-4 (TPS. Rest of World ) ISBN 978- 1-58890-275-7 (TPN. The Americas)
1 2 3 4 56
Important Note: Medicine is an ever-changing science undergoing continu.ll development. Research and clinical experience arc continually expanding our knowledge. in particular our knowledge of proper treatment and drug ther · apy. Insofar as this book mt>ntions any dosage or application. readers may rest assured that the authors. ed1tors. and publishers have made every effort to ensure that such references are in accordance w ith the state of knowledge at the time of production of the book. Nevertheless this docs not involve. imply. or express any guarantee or responsibility on the pan of the publishers in respect of any dosagl:' mstructions and forms of application stated m the book. Every uSt'r is requested to examine cart>fully the manufacturers· leaflet~ acrompanymg each drug and to check. 1f necessary m con~ultauon with a phy~ician or specialist. whether the dosage schedules mentioned therein or the contraind1cations stated by the manufacturers differ from the statements made in the present book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market. Every dosage schedule or every form of application used is entirely at the user's own risk and responsibility. The authors and publishers request every user to report to the publishers any discrepancies or maccuracies noticed.
Some of the product names. patents. and registered des1gns referred to 1n this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore. the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain. Th1s book. mtluding all parts thereof, IS legally protected by copyright. Any use. explo1tclt1on. or commercialization outside the narrow limits set by copyright legislation. without the pubhsher's consent. is illegal and liable to prosecution. Th1s apphes in particular to photostat reproduction, copying. mimeographing or duphcanon of any kind. translating. preparanon of microfilms, and electronic data processing and storage.
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 rtlc 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 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 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 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~n\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 lOlld left ptes 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 ep1phyIIO\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 osteompatlc 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) 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..unt'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 esPdmg 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
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'
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 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 whi" duonK Stlerostng-type 0\teomyelitis. Sc.lffosinq osteotn)'f!irti) of Gorrlos a lov.-grade chrOflk ioff!( tion not associ.Jtt..'
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 intrat;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 recro~\ 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.'
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.aphyses 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 (especiis.
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 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-booity 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
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 ,etriphrocakrno~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 lragm•-ntat1on of the JOint su1face (nl'd. fragmented c11ld latcrcJII}' diSplaced capitcJI epi~S is cU· soc1ated v.ith c1 ""1dencd and shortened femoral nPact1on 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 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 patnital heart d1sea\e) may re~ult in similar bony ma~~t>s
ch~ngf:d to the el 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 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 wroor 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£'
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()(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.rs). An obliqu.. fractuu. (not shown) occurs secondary to impa 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 Ur-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'ltIaccc.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..-r sublll'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 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 !
)
..-., ,......,
I b
a
\\'! \'(\~}.. ~I ?<J •
( (
~
~I ,(
.,..
(
r ~ ) I d
fig.4.8 Distal mdiul. fracturc&. a Colh · .fnl(/lllt Dor~ displacement nnd nngulahon apex ,·olar of distal fnt(!ncnt b Srmth fracturc Ve 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 pnt 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 (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). Frclculae 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 scn.
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.>died 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·HnolatN 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 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 ctress or torque cau
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. sesct 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 bonr.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 IIIO: t.\''b and a-tooblaJ.-
In rap1dl~ ~~twmg ltmll>n. II>l'
hutu.: frarnu.:t1t)
{M.:tlth... !-..h:lt.:c.l
(s.:qu~>'-1•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,
mlrandral aold l~ldu.'' ahM;,-..,.,,. Giant cell
gangba
tumnes. T) pical metaphy!iea/ l~ioot' mdtld.: tK•Jtol'- c.;ntcr \\ilh ••~;md to 11,., medullar) lanai and ""'rt""· T)pical centro/ k-,.iimplc ( uniumual) bu'k! ~)~ ..:u...bondromll.'>. lihoou:. d)•pl...,.ia and hone inlarcb. Eccmtric lesions induoc ruk.un,mal bone
''"'" giant iNt.' are n('lll()&,if\'ing fihn"'u.' and 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 indu& k.,.wr" I th• JMi< teal rl'nl3
d""'IIWid
1\s.~r«>tl~t
libruma (rl>tl' hi.,tioc)toma
(.' h( ·ndtt)~an.·(\llle:t
I ~n1rhorn"
I ang.. rhans ..:dl lushfKt of •xtemal cortl'x
r '
.te'
nl soft trssue nE'Oplasm or a~e~~ Subperio~teal
osteomyelitis
'>ubpenoste.al hl?mdtoma AvtJision franostcal ou~tacortrcal) chondroma Bizdrre parmtl'al osteochondromatous prolrfcratron (BPOP) Pcnosteal u~tO!cortlcal) dexp.m~oiE> trdbeculated oppE>arance 1\ ~l't'n origonatosteolytoc lesoon woth roap.tx. bl ing rrom the gredter trO 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 osteolytiast 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 characteristim 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.
Fnatcr tuberostty IS 1ncidentalty also present.
r.g
5.44 Enchondr-oma An Pxpansile I 1()0 wtth sl,ghtty \Cierotien tn the middlt> phc1Llnx of the thrrd frnger. ~teolyt 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 pathologorentlc!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 pssrve 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. ht: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 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 osteolytitases m.1y eventually de\elop in .about one-third of all chordomas.
Adam.Jnti· noma ( blutoma) (F~g. 5.75)
Su19le or multiple, central or eccentric, mult•locular, shghtly l'xp.lnsilc, sharply or poorly delineated osteston wtth reat t1ve surrounding sclerosis 1\ ~n 1n the tibia.
Fig. 5.76 Ameloblastoma. An expclnsilc. multiloculated, osteolytic lesion with both endmtal ~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'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 .
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,. Nion 1101 wfl IISSUo rnuM>(l$ wu typioolly associated with bone n~tJtaol!>iorn., Obloolybc
meta>Jasas
of the external
("coolito"
COilex of a long tubular bone Sign) • r«IG, but qude characterr:Jic for
a btonchogonJC caranoma mSIS 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 •crtebl~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-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 JoCarcoma 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 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 osteolytiet'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 frdents 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.L' (heredrtary or assoaated wrth nephropathy). J-i;rba'.< t'i.•uN (elbows. vi11Sis, knees and ankles) and lrmnlorgcd 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 dOSa!.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
""
/'ond) lwthropalhy (pslL~ mt1Ult ts: py0{!1..1lit: tuk'nulous fungal Gout Hydrox-yapalitcdq>r the !'>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 p1in1C>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 ttll: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 lttTflC r more loodt" ll.:t...:hcd C'f't.'ph)1•"' in
to -'C\crnl Cetllimetcrs
Reactive (productive) bony changes In OJ.I<Xlarthnti' t>l \\cight-hcm·mf.\ Jnmt~o 'dcr~o" of the -'Ubd1ondral bnc " lrcquentl) the h f'l r.uhographk ,;gn of the disease, 'ince the cHtL C\l
H\1)1)
Od1rono..,,.
Odtrono>is
lnlixtwus arthnl"'
lnlccttou• urthntts
A\-asculllt nnr(}!;t (o>tooo,uooi )
A\as.:ular tJ
-}XX:t Of the fL'Illml lltXK is h..1111cd /•1111/l' \\IIIJ!. Jt IS 1110,( tst lnllunutic 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~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>
CPI'I>
~t.h.:n~d~~.·rnm
11)1"' lit.Uillllns 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.
and O'>sofKaticn of both the intt>rspinous ligament ptoduteopcnta, 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 LSUe thickemng of dtgtls 2 and 3 (sausage fingers).
Ftg.6.50 Enteropathtc arthnbs (Crohn's disease). Bilateral fused sacrodiac JOirtiS and deliCate
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 erffi'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. Socond0Ciated 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~Jsit."m
d:s~.luomlltosi.
sophyles 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 !>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.JE>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-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(' 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)
(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 &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.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 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~ cn)·-like arrearance and arc com· 1110111) dt'flla~
. \fk1' I'•Mt) tile affect~ arttcular 'urf3C'eng ~ Mnatn or,-..,I' ular and ahlonnal m "'-'~ mod th, JNDl' ma) app.:ar tl"pla.>IJ< ll'lll :tf'llllllf dtan~;<s (•r•MI 1-ca~ms t< • rt~t)· •l'•ttU mall plaslt< ~hall o\\ :tc'\.tal>ult h: I hl.th no! d) pia Ittchldl'Ol
tim~
MO»t cmc
Rhcumatt>id arthnlls S) !'lemic lupu' en•lhc>tnai.m
(arru\\>) tvod \aM.ular cnl.ofkationl>
in h)-
dd~....:t
tn
oUlC.,tlu:r.
194
Bone
Coni> Periarticular ~on l t!>Sue calcification or osstflclltion
Tllblc 7..1 \~1
l.d
l>t-.ordcrs l'cnantclll:tr ~·akt'icd lump ao:.«Xiatcd \\tth rhctgc 195)
O.:muttOtll)O>.itil, in u dtild. Pet i.utiwlu• ti ·II• calcification.' around tl~ll ptc'-Cnt o-
(Fig. 7. 16)
twn. ~~o~1 \."'tlnm1on in lr~'" ()nl) t.:~nall r-.nentat;~..: uf thl-...~ tumono an: inlnt·arti'-ular "Ill\: pcriat1u.11la.r mas..' t'~hu1 u. ntan1' l.'Hk1ti~ fkds. but n< I c:\11\t .ttkolil'l otlen of the hurme 111 the ,,.;nil) of joint- (h op, l ll ""· >lwuldcr) or ne~r ht•ll} pn>hohu anc:t.,.. It tk~a'Ciib.
ovoid calcifications sues of the leg.
Ftg 7 21
l\l)nf~Jiuc II)JVWlcemw $plllmmes
l cka)-rr.~l
I U\\t.:r cxtrL·mtlu.:
ancry.
hg 710 !-.ft-lt"l'UC cak1ficallm ""'ocinlcd "tth ,-aricose \~in,_, &>th Q"llil'llh-) a1KI .:akili d phkbolith:, (arrO\•) ar~ ~w.
2 03
8
Skull
Calcifications Cakific.:ations are a wmmon fmduJ!t on ~kull mdiogruphs. With computed tomography, many more calcifications \\ithin the ~kull can be .lppru:J.Jto.:d that l..~ape dck-ction \\ith plain him mus purhon) 13-m•algnugha nnd &.:nt,Jte r.uch.:us
1\ calcrfied pmcal 1~ li11md 111 5
• \
6
' • ~ 12 , \
shape ol the calc•lication arc taken into account Scatt.:rcd
intrdCcrc.:lTul taluficahons are virtuall) lunitCl! to a 'anc.:l) of infectious J)IOtcsscs. tuberous sclerosis and mclal>tatK: corcit•11 min stone") Cerel·ml 1/l(arcl.\ may rarely calc•f~ al:-.. Suhcluml und lt..~~ lre.~ in tlu.~ group, ulthough otl)(;t vual encc.-phalitides (e.g. JX>Iio. lwrpt!.\, and rubella) ha1c ht..X.'!l tmplicated as a cam.e of intracerel>ral calct!l\:allons. ll1e mctdence of calcilicatton in C'ftom~uhc di~1se ts c.-stnnutc.'c it)(;llidul m the dillercntial diagnosis of mtracramal culcthcHtKms It may pr.:;...'Tlt lh a $ingle nodule. or less commonly a~ multiple calctli...' not ha\c a JWl.t\t.'lllriwlar dL'>tr bullon. and can abo be lound sublentoriall:. (c ll dl.'lltall! nude•) Cak1licutiIL'> occur abo m the rosa! g~mglllt Sm:tll H!\!:IS ot localvc..'tl hyperost(l>;)S of the sl.."1lll ar,;: often !l:>.OCtalcd \\ith tuhcrom; sclerosis, mxl may actuall) be lOnfu.-.u.l "tth mlrocen:br.tl caletfication:;. In neuro/il>mnatrut~ gnumlar unilutcrnl or bilateral lcrnpornl lobe cukifkuti
Vascular Markings. Sutures. and Fracture Lines
fig.8.16 Prinlill) h\ poporutll) milanl m llOSJhon and thus relath·ely ca~1ly rc..>cogtlV!tble. l'occluoman (oraclmol(f) granulations, \\hich arc amclmoid C'\1enstotlS projecting into the lwnen of the main sm~s and aJJaccnl \cnous lakes, may L"ffO S4: II\(>)
cent lines. wh1ch aro.: ollen lhllicull to ditlcrcnli:tle from vascular mrukmgs and sutwc:; A kx:a/i;:ed inctt'ase in m.1rolar marl.inp..~ c.tn be a 'CIY important finding in the dwgnosis of " mwinp.ioma ''hen the incrca!>Cd HI:;(;Ular mutiJ.ngs arc w •>eJ,Ilo..'d \\ 1th u calcified lesion or a locis. II 8 Skull
213
I •s !\ 2:1 Osteoblasllc metasw~ fmm brc::1't mrcirK'ma RNmd lesins
hg.!! 24 Chronic osteomyelitis. A detect (HIT\\s) M.'\.'11 in the front< I 0011~.: \\ 1tl !Kltuu:nt sd.:r~i.s
Diffuse Sclerosis of the Skull Vault A d11Tm.c inCICit'-C in hone dc.'tl!'ity or lhe lr.Jllilllll 11111)- he caused h) an abnonnal osteoblastic respon!>.II0\11 I'Cm Uudu.,,~~ tb.~m.l£' (gc11cmhAxl cort•cal
hg.8.25 Radiation os1con~"f0~-is Fxiert,l\C mixc;'\1 I)-Ill' :md sckmlic !lone 1moiH'l 1L'lltJs t.) (I•Jg. lU2) 1-ngelnullm-Canmmfi dJSC.plSI>. ("c.:l \\ool" appt~Jmnt-e, l1g 106) In the )01\C
sclerotic ph:•sc, a lllllloon th1ckcmng or the cal\ arium c.:an he found ,,,th los.' ot' 8 Skull
219
l•r.IU!t
Primary hypCfJ>nmthyroidism I hid,cnmt d the cnl\'arium "ith grnnnlar '"-""''11ica1K>n ("'tunc:. a triangular shape (am)\\ s). J Lesion originates limn the diploe. Symmetrical l'llll;ton and l"'\paru;ion of both labks ro.:sull 4 Ll-:.lonoriginates from the tnl'IUI1J:!CS or brain. Ana\innstc deled i:, produced on the tm\Cr table.
I ig.8.41 Uutton sequestrum. A rndJOden!.l: locus is seen within a h l.tt tturuallo.:hlon (eosinophilic g.r.muloma).
to the Cl:ntcr of the lesion An erosion alot1g the out.:r table mdicatcs a !':Calp lcston, whereas an croston on the UU\CT table rellet:b an mtracranial al:lwmmlitv. I 'llllnlitle lesions orig.matin!! m the diploe erode and'or displiM; both itu11.-T and utl'T tables (fig. 8.40). Trlracramal/e.\/0/1.\ eroding tht: \'auh or lllt~ of the sl.ull tmd with cosmopluhc gmnulonms, 1111.-'tnsta~ (csllo.!Ctall} from breast cruunoma), 1--pitlh hem1ahon of men1nges w1th or wtthout bra1n. Ctan/IJin bitiwm refers to a congenial midline defect wrthol.C herniation.
Epidermoid (Fig. 841)
Solitary 1yttc and often expansile lesion meaSUlng up to several em tn diameter Its borders arealways weU-marg1nated and may be scaUoped and sclerotiC. OccaStOnally, a button sequestrum can be found.
BeOIQn tumor caused by either posttraumabc Implantation or congemtal inclUSIOn of epldPrmal elements Appearance vanes considerably wtth c;rte of olig10 (e g , scalp, diploe, or dura; see FIQ 840)
Dermoid
Srnal radiolucent defect without sclerotic margin. usually occumng tn the midline.
Bemgn cyst1c leSIOn caused by congenital u1Ciusion of elements from all dermal layers
Araclwloid cyst
Smooth defect, often wrth a thin sclerotic lim.
Usuauy congenrtal, rarely traumatic or 1nftam· matory 1n ongm. LOQ.:Iized pressure causesthinr>tng and outward bowing of the c;kull (see also posttraumatiC [leptomeningeal) cyst 1n th1s table)
Primary bone tumors
Solrtary. rare
Usually mtxed lyt1c-sclerotte or pl'edommantly sclerotiC appearance
Usually multiple; 1rregular, til-defined radio lucenCies ("moth- eaten") dear-d by multiple areas of cal\lanal th1nnmg
Round midline defect 1n the F1g.8.46 Menlngoenc~alocele. frontal bone wrth the meningoencephalocele ev1dent as a softti"c;;;aJt,) 1113 11\."'i.
Fig 8 47 Epidef"mokls (2 cases), a A relatively small lytiC leoon" nh slightly sderoiiC margins IS seen. b A large defect wrth scalloped marg1ns containing Irregular bony fragments IS evident
8 Skull
223
a
b
Ostec>l) tic mt'h"'"'''" (3 cases) a Mulbple wregular. and part1ally cont:uent raorth
8 Skull
paru.ion (fig. 8.57). lk>lh o nonnall) tilted >din nnd a >upcrinlpO'>ed bon) >tmclurc (q; frpont;.\ t"'tun:. l'to.:lllllillilnlin of the oor-um >ella n .. ult ~cast<MtBll) frm th.: c\lcmin of n largo.: ~plt.::noid • inus into 111, d~U[cd an erial 11) p.;n.-n•ion. of t)._ .attu. ~~ um sdl.t oc.:uts
1'-' (!>ltnion e>l dt>r"llll \nl ·ritlll"" I h
bcgm< "ith erosion f the anterior
.:mcx e>l th< OON IIlt , proceeds to the floor f the th~
llallo.mcd ~dl.t \\ ith utkkrcutting of li!C anterior duwid J'fl>o. lutcqwl dowm,ard disploc.:ment tic. '"'' n1rc ofien ,..; liar dtangcs indil.tinguish.•J.Ic frCe "'"" the >tra •chtcning nnd p:u1tnl d..'1\\~\~r. a odtdi\d) 'maU pituilar) adcnma can eca'lonnll~ prt>r loM•il "'lh 111\.: ~u...- <J.-,.trui\cl~ found m tl1is urea Vutuallv all dlJ;()nkrs presenting cbcwhcre in the ::.1-.clcton \nth ol>lc.:obla.stic lcsiolLS or diOIL...:: ost~kru::.is muv lmc.he the loa...:: of the skull also. This is u purticularl~ o::ommon lindiJ~g in ull col-.:;titutional disca.~ as.',(l(;illtl.'tl '' 1th o::.t'-~>l-llcrosis (fiJ.!. 8.(>6) for a complcte iliJlcrcntiul thagiKlsi,.,, t11e rc..tdl1 i:. referred to Chaplt:r 2. Meningiomas n111y ar1sc trm \ariu.; lcl(;ations at the base of the ,)..ull "'lch a-. 1..nbnlill1n pl.tlid 111cxes'>'-'S. and petro us bone. They CHLLse a locahtl'tl thid.l.1llllg and sdi!Til~>ts of the im oh ed bone (Fig R67). I m:-ions ot neighboring bony stmctures may also be as~c1atcd. 1>11lC.:rcnttation from localued libmus d~ l-lll:hlfl can he dillKult hut tile Jm!SI.'rlce of 1lm1or calcilicahon and the dcmonstmhon or trabeculae in the thickened sclcrollc bone nn: only tound \\lth tnCIUngtomas and may help to distinguish these two entitles. CarcitKJnms originating 111 tl1e car, sphenoid sinus, and nasopharylt'\ cmd imading. the base of the skull 1ue usually destmctive, but IIUI) bcwmc !.elerotll uller radiothempy. Lymphoepitheliomas (nonkcmtmitmg. MJLwtllOLL~ cell carcinoma~) of the twsoplwry tl'\ 01 parunu~l sU1lLSCS occu.-,ioually produce a IOCIIlitcd !.ell..'rolit h:actiou iJ1 ti'k.: udjaccut 0011c lx:forc ruw treatment has lx.-cn instituted. Low-wade fll;d c/J'(JIIic il!fi.·ctiw,\ in the sphenoid l'inus wtd mastoid' produ~c loc&litcd SlleroMs wmbi11Cd witl1 poor pnclUlli.ltil.allon or the urea 1\ locahtcd S'-k.'foslli iu U1e middle car may he caLL-.cd I~~ c hmlllc inllanunal!on. Sclerotic changes in p~ in th~ fiont.ol hone the \ault of the
Scku~ic·
change•
cau.pl.l'ia kull \lith cxt"'"'ion onto the lwntul l><Jne ;, """" TIK: trubcwlnr pattcm in both the sdcrotic nnd "gnmnd !)las.,' ap· pcarinc nrc,,. " chnroctcrist ically cflnccd.
u,...
Fig.K69 PogtllC and orllltal enlargernt-'111 can he f(mnd (l"ig. R,70) ·r he dtsc:ts..: mny nlso he bilateral and erode the chnmd procCl>scs and the tip of the
hg.}; 71 Acoush. T\\o large ruca:. of desunulating biL.ttcrnl choleslo.:atomas ar1.: t-een in tl1c pclrou' bon..., (arrows). On the left stdc. the l\llnor had t-.ecn re1110\cd one month earlter \\ilh a surgtcaldeh..x:t r.:mmmng that is illlJXk>:-thk to dLili.:r..:ntiatL from the otiguwllL.,ion slnt... t ion
arc locally invasi\'e chemodectomas arising l11e chcmon.:cL·ptor organs locat.xl III tl1e ju!(ular fossa or rarely in the hypotympanum of the mKldlc car '/ he glomus jugularc twnor LTodcs the jugular foramen :md the interior it'-lXX:t ofthe nudpctrous py=id 111 the early stage. \\ hcreas in a btc.:r stage tl may ex1end mto the mrddlc car and the postcnor fossa \\omen are three times more fh:qucntly at:. fixtc..x.l than ltlL'Il crated Wllh !l dense relroscllar calcification lhat is found Ill 70°/o of pall~.:nt s (l 'ig. 1\73) J\,kningiom:~s and ghomas may erod~.: mto the ha:.c: of the skull causmg a localual bone destntclton although ru1 area of innca~ hone density is a morc wmmon mmufestallon in the limncr ttunor... Cardnomas (f the nn.~nT.. panu.(Nrl ,tionall~ with lcsioll!) locutc..'d pol>lo..norh in the orbit Xeuro.fibromalrui~ can b.: a.'>.-.ociutcd witl1 wlilatcral orbitnl cnktrgcmcnt. !urge l;.tic udi.:ds in the orbital roof. walls. and floot. ~..·nlwgctncnt of the opt it cwtal 01 sUlll., inlo ~guming at the 1atmt1 \I all
Rare. In mwint;i•·mos mido.llc 1.,..__-a.
thol ·~ ir;inJl< ln>nl the
(hnmlvrhohc :tJ,llas nn: lhc •«'()t>tl ont-..t romn)(-t\ cint.d '"'" an) nt.1>;~; lC!.ion (e>rt>it.1l dysrh.,a) .,.,,,rs, 1\,un hlOri>•lal •~~ in llu: 01bit. \\'ilh hcuhng, "ilhcr !-polltancott,l) or ancr !hemp), the murflll t1f lhc h.~ic.m may hen.tl~d
com~ ~krohl l1u..: h.:~wns ~.:un \ar'\' ctm~adcrnhl} in :--itc and seem lo ha\e a predil..'n fnr the oool' and lmeral \\all of the orb1t. of the (ondilloll'o cat~'ing a mt•r.: l<x-ali;ed cnlarr=('flt ophc canal and '"J".'rwr t>rlJ
10
Nasal Fossa and Paranasal Sinuses
The par.ntlNll ~illlL~ ((llhist or the front.tl Sllltl"> •;pllt:llOid smtL'r the und,:r-;t.mding of the dt.'\ elopment and "l~•d olany pathologic pmces.o; J>nemnalization and cxpanston ol the sinusl.'l> me u wnstanl fettture of actomeg.a/}, hut as an t~>lat Hto\\-{)UI
hn~tun:
of the tell ortut
,\ rotwoid soft-
ma:,, (am>\\) hall!~'nl' '''"n th~ kll ~nlrnt n>l i.' th~ nh
radiograplu
n ho"c'er, ~ llc.:n a d..l»-c l>n (O!ol : ~h.:"' lunwrs ar.: wn• ran: ;ond mdud iUl"l{'t1hR»na.
Hnrc. A ll age~. Benign mewnc~nnnl nwpla.wnv are en'
IC'-s c()fllmon.
j rnwzi/c czngio(ibroma: Ili~1l~
\aSf the ma,iJiarv an11a ant..~ 1i01l) Of in\ad.: tho;; adJa.;,nt 'inu.,...,.. orhl< and c H'TI 11.... lnle~' ""') pmoe I hirh-h~nk.1ll of the a.
u,.,
d) ~f'l.u>ia.
(conlzn11cs on par,c· 2-11)
10 Nasal Fossa and Paranasal Sinuses
rig.IO.J O.,t~oblnstic mcta;tasc• hom bo.;ast otW)cd tit.: floor of the pihntary ft""""l.
hg JO b
!\oo-H~in'
SUre eros10n ()Jt,,.,l(,., v.h1ch are also most commonly found 1n the frontal SinUS. have a much greater denSity than mucoceles and ::Jlould not be oonfused \'•llh Uhe latter (F 1Q 10.18)
FIQ 9.6) Fracture (see
F~g
10 1)
Localized submucosai hematoma may simulate polyp (e g., blowout fracture; polypoid mass on antral roof). A1r-fiuid (blood) level may be present Partial to complete sinus opacification may be found in en acute fracture or as sequela of an old fracture . Complex facial fractures iroclude bltNotil fractures of tilt u btl (see Fig 10.2), trtpod fraciiiHc (Fig. 10.19), and I< {t>tt [ra. uround the j<m:. rna' be cmt-.cd b' the ~nc wnc.hti.elclllhc.: Ill ll!!in t hm\c\ ~'1'. be approct;Jted \\ith comCiltional " my kduuquc. rnld ru.Juirc special d.:ntal ftlms with high r..:!iOlution lot propl.T c\ aluatiotL I:xccs~i\e bone fCSill']>liOll an>Utrd the fions Dcnlul granuloma; 2 pcricxlontul l)Sl (occasionally conun nmg small root remnant}, J d~..ntigi..WtL' nsl. 4 primordial c~·st, S "floating teeth" (e.g., ~..~ 'inoplulic grmmk>ma): 6 odontoma. 7 umcloblasloma
fig. 11.4 Pagel's
disease.
Thid.cni.ng und sl01..rvsis of tlJC H•~' of the lanuna dum around
mondtblc rcsult..:d m IY>f'O.\Is of any ctiolog:- (c g., scntlc, ~tcrotd themp), Cthhing's s~ndromc), but in th~ ca'4.~ r.:~nnants ol' the lamina can olk'n strll be rccogm7cd tmk~" the ostcoporoSils has pn't!rC~'-Cll so far that the wrrccl diagnosis can easily be ~,..,t.rhhshl..'tl by other mdrogmphic lindings. In both pcriodontos rs (non-mllrunmatorv, dcgcncmll\e) and periodonlitt.\ (intlummalory), rcsorptron of hone including the lamina dum occurs charactcristicalh around the neck and proo.:rmal part o l tlte root of a tooth wlulc the kmuna dum around the a1x:' rmwll\.~ mtact If tlte Jlfl'lC~' pn'lCccd. to a periooontal ah.~cr.\\, n...".(''rpl!on of the enhrc lumu~;r dura combmcd \\1th \\1dcnmg ol tlte pcriodonL1l memmmc space may be loond The mdrogmphic absence oflantina dum is not onlv the result of 1ts r~>rption but may aLetatcd mth resorptiOn ol the larmna dum ts a SC\ ere mllamnwtron such as periodontal ah.~cenoJmg ""' , k-.iom. compoM:d of aboonnaU) dcn,c l>ottc that i• fl>nn•..t in the pcricnl11el n
poor!~
to wcll-ddined detect around the
lelc~ lt.
mm~ent.
f a prinoan tc.11h arc li•und "ithin the k-,iion cmt l-.: lound wiUt an .:nl:lrging t..:\1-l.
[(tnll~ mt tl1~
rcp.u.tthc
prl't.:~'
ft,llo\\ing the rc!io-
lutiun l)l a tl\:'ri ..tpU..1t1 uh-.los. 1\.lt"t c~'>llllllC>II ,..,,t t>l ta\1 I p othdot•u-lmc'tl "'~· u.'uaU) 'ituaJ~d at the apex t•f th..: rt~>l. Acquired and probabl) ol uoll.utuotatf the last molar j, '-"CIL
I ig.l1.7 Rl'<doual C)'l '\ C)'he ""' n w olh .... kml~ord..-r L' '-<ell on llo.: lllil\JIIa (arR•\\). lrrq:ular thid.uoing and l>Ckro.i... of the ldt I ud} and ramu. ot II~ mandibk o< also C\·odcnt due to 5clcmc'Jltitcn>t"' C)1'1. A 'harrl) delined h too.: k• '"" c.:ntainine a molar cn•wn o' ....-en 1111 ''" rng the ldi l>t>d) t>f the nw>diHc.: .
250
Bone
Table 11.1
(Cont.) Differential Diagno sis of lytic lesions in the Jaw Radloel~
~
.-ance
Comments
Purely lytle. v.ell-marg1nated, unilocular, round or oval lesion most commonly located postenor of the thord molar 10 the angle or ramus of mandoble.
Develops from embryonal tooth sac before any calcified slructt.res have bf>en form-ed
Radoolucent. often multi loculated lesion with smooth or scalloped border located 10 the body or ramus or the mandoble Occt.lrs frequently in conJUndoo wilh Impacted tooth. Differentiation from an amelOblastoma os often not pos51ble .
Account for 5 to 10% of all jaw cysts and have a high recurrence rate Multiple keratocysts can be found on Gortw,.s syndrome where they are associated With nevoid basal cell caranomas and son. !Issue calafJCations Other bony abnormahbes onclude smal flameshaped cyst1c leSions and sclerotiC foa , bofld nbs and anomahes of the spone and harlds.
Assural cyst
Most commonly located in midfine of mandible or maxolla (e.g., mcisive canal cyst or nasopalatine cyst). rarely lateral (e.g. • globulomaxillary cyst between lateral incisor and canine tooth).
Arises from the epithelial remnant of an existing fissure or suture (srtes of embryonic fuSions).
Solitary bone cyst d the mandible (trau-
In general relatively poorly defined and orregular radiOlucency of varying siz-e usually located in the body of the mandible. larger lesions characteristically have a scallop-ed superior border that app-ears to undulate around the roots of teeth into the interdental bone The teeth are neither splayed nor loosened
Occurs most often on younger persons. History of trauma often present ("traumatiC" or "hemorrhagiC" cyst). May regress spontaneously
Unolocular or more commonly multilocular cystic (bubble-like) app-earance often with coarse trabecular structures foiling m part of the cystiC cavrties SIZe vanes from 1 em to huge tumors causng corllcal expansion or destructiOn wrth deformoty of the face Rarely,a small h.mor rTIImiCS a somple cyst
Most common tumor of the mandoble that can occur at any age but os ~ually doagnosed after 30 years of age local mvaSion onto surroundong structures and even dostant metastases occur Adenoam&'otYastoma (Fig 11 .13) and ame/otYasbc fbroma are rare tumors occumng both on the first two decades of lhfe They are chnocally less aggresSIVe than ameloblastomas Clusters of calaficaiiOns and retaoned teeth may be found on these leSions.
Somitar to ameloblastoma, but more dense when the charactensllc honeycomb appearance is present wrthon the lesion.
Clinical behaviOr SlrTIIIar to ameloblastoma: locally mval>ive and tendency to recur
Primordial
cyst
(I ig II '.1) Keralocyst
(FIQ 11 .10)
matic cyst) (Fig. 11.11)
AmeiOblaSloma
(adamantinoma)
(F19 11 .12)
Calcifying epithelial odof!logellic · (Pincl:lorg tum«)
(F19 11 14)
(contrnues on page 252)
I I Ja\\s and Teeth
Fig 11 9 Pnmorchal cyst A well-defined cystiC leSion ts seen tn the angle of the left mand,bje
251
Fig 11 .10 Keratocyst A lyl1c lestOn w1th parttaUy sclerotic border (arrows) IS seen 1n the body of the left mandoble
Fig. 11 .11 Solitary (traumatic) cyst of the mandible. A poorly· defined radiOlucency wtth scalloped marg1ns mvolvtng large portions of the right mandibular body extends supenorly between the roots of the teeth
Fog. 11 12Cular spasm ot \anahlc chology. may be dt1llcul1 to (.'\'!tluatc m films taken on ~ Suck\ tal•lc. 'l11c true cxk'llt of anteroposterior cunc:;. ru; \\ell ns c\entual lateral cunatur'-~ (scoliosis). is better '-"'alu<Jtcd inu wctghtbcaring stunding) position. if such po:-.11Jtrlt,iOtl or pwlape·.c. MRI ~]l(lUld be ~ F a rdc•~'IK.C point fot di1l'erential diagnosts. a l'he <JCdflliOI'llle 11re stmunari7w 111 table 12 4 A ll se' CJI cc:n kat \CJ1d>ral lxxhcs must be 'isthlc (lll rudiographs In a cas.: \\h(.'ll good quahty mdiogmphs rdc ullacl
,~ .. II fradurc
l '""
all) ,t,tbk. T) f>C IH: An•biun . in 25-50 t. of
frndurc {•f tl..: ru d 1 the atla< (fir. 12 4)
,,f
t rul ..t,lnl fradur.:- L' {•Jt,n "'" onh m th.:- t•blk1uc 1i.:\\, I~IJk1al 1118\ Ill: """" in lat,ral \i..:\\. In ll\l'"lk~it•ll I111Clur, lb.. Jll"ll'ritor lragm,•ll of the ardr c•l the .!tl.., L' an~;~latcd and t•r dj,placo.!d tJc.,\\11\~arili. In h)f"L....,t.:\.l~r~u. m fr.lctun.::. th4,; fJO:"l~ricll frapll,nt ol II> Inch •lk uld he dllfcrcrrlratcd '""" a fra.:tllf:1,\l'Ctl
left atlanto-
ftg. 12 4 Hyperc\1cn\1'me RadiOgraphic Find1ngs
Comments
Burst fracture of 0 - (7
On lateral v1ew burst fracture is charactenzed by an antenor wedged deformity or vertebral body and retropu~on of a fragment from the posterior supenor marg1ng of vertebral body On AP view \'1iden111g or mterpediCUiar distance may be seen.
Fracture mechaniSm IS ident1cal to Jeflerson fracture . but fracture happens at tl1e lower part of the cervical spine. Burst fracture IS stable, if posterior ligaments are 1ntact. Burst fracture becomes unstable rf postenor 11gaments disrupt. CT 1s recommerlded for eva1uat100 of spnal canal
FlexiOn tear drop frach.re (see Fig 4.23)
Rad1ologal features of flex100 tear drop fractures mclude bi\ckward drsplacemerrt of fractured vertebral body postenor diSplacement of upper column, wldemng of 1nterspmous spaces, and kyphotiC deformity of the cerval spne on the lateral ~leY- On APv1ew wK!emng of 1nterlamnar spaces. a sagrt1al spirt fracture through the vertebral body arK! one or both lam1nae IS often seen
The flexion tear drop fracture IS a spec1fic form of burst fracture USually accompanied by spnal cord mjury FleKIOO tear drop fracture IS highly unstable About 15•, of all cerviCal fractures are flexiOn tear drop fractures
Extension tear drop fracture (Fig 12.7)
Lateral view of the spine demonstrates the tear drop fracture of anterior inferior comer of vertebral body arK! there is no subluxation.
Extension tear drop fracture is usually stable, but may be unstable at the lower part of the cervical spine The most common location IS at the level of (2-3 Defect 1n the oSSificatiOn of the endplate may simulate fracture
Endplate compression fracture (Fig 12.8) Ante nor Lateral Postenor
Endplate compression fractures are usually hyperflexiOn inJunes that leave the posterior height of the vertebral body normal while the anterior vertebral hetght decreases. In thoracic and lumbar vertebrae an Increased den54ty or diameter and lrregulanbes of the anteriOr marg1n of the vertebral body may be assoe~ated. \l\ilden1ng of the facet JOint spece may be present m acute trauma
If the antenor vertebral height 1n the cervical spine IS 3 mm less than the posterior height. a compresSIOn fracture Is suspected. In thoracic and lumbar spine. this measurement IS not valid because many d1seasescause wedge-shaped or colapsed vertebrae (e.g . Scheuermann's disease). Compression fractures are common in the lower cervical spine arK! in the lower thoraCIC spme CompreSSion of the postenor mrenor rnarg111 of the vertebral body is hl<ely due to an e:denSJOn Injury.
May resemble SIITlple d1slocabon in the lateral "racture of the pediCle may be better appreCiated 10 the frontal VIew
Neural arch I& the most common Site of a fracture 1n cerval spne. The artiCular prllar IS parbcularly vulnerable 1n fractures
Obhque or vertiCal avulsion fracture of the llp of the spinous process of C6 or C7 (occasionally T 1-13).
caused by a repeated sudden load on the flexed spne. Must be differentiated from hyperflex1on fracture, 1n v.h1ch the fracture line I~ more honzontal.
Fractures of the pecicte neural arch (Ag. 12.9) or artJcular process Clay-shovele(s fracture (see Fig 4 22)
v~ew.
(Ce>llfl/111('.\ 011 Jlns may involve more than one level.
A hemtvertebra may cause encroachment of the neural canal. Unlike fractures hemlliertebrae are outlined by a cortical margtn. Absent pedocle (usually cervtcal) may Slmulate an e~pandong mass tn the onterv ertebral cana or metastatic destrucbon of the pedlde Heml\iertebra or "butter!ly" vertebra of the thoraCIC or tO\IVer cerviCal regton may be part of a neurenteriC canal anomaly (fiStula. stnus or enteric cyst) or more rarely associated Wlth pulmonary or cardtac anomalies. Severe forms of sacral hypoplasia may be associated with major anomalies of the gastrointestinal and genitourinary tracts. NarroWing of the arch associated with enlargement of the neural foramen is usually due to a neunnoma (Fig. 12.27) or neurofibroma (Ftg 12.28).
MyelocM Hemlmyelomenlngocell'
Hem/myeocele Closed spinal dysraphlsms Llpomy~
Findings
LtpOmyelomenlngo-
celr Meningocele (Figs_ 12.22 -12.23)
Myelocy.tocele
Comments
Spino blfldo (I ig. 12.24) Tight filum termlt!Oh Vertebral hypoplasia and asymmetry (Figs. 12.25-26)
lateral hemivertebra results in scofiosis Postenor hP.mlliertebra tn kyphosis or gtbbus Postenor hemtVertebra tS usually dtsplaced approximately 3 mm postenorty from the neighbonng vertebral bodtes Hypoplasia or absence of a pedtcle or lamtna may also cause scoliosis
(oontonuos on page :!SO)
Ftg 12 22 Multiple clefts 1n the pastenor llt!Ural arches (arrows) and w odenmg of the sptnal cana l due to mentngocele
Ftg 12 23 Meningocele. Defects tn the neural arches are wide and im olve three lumbar and all sacral segments
Fig 12.24
Spina blfida occulla of LS
Spine and Pelvis
279
Fig. 12.25 Multiple segmentation anomalies throughout the spinal column Not a Single normal vertebral body ts present Rib fuSions are an assoctated finding
Fig 12 27 Narrov.tng and erOSion o the arch of the aJ. 12.40 and 12.41)
ll(t\\lJll... t..:akifiudiun and ~iricatiQn along tl11: an~ ap,.-,;1!; of 4 or mor, contigoous ,,·rkl>rul l>tl '-Cal and ""croilia.; j< •i11t m.anikst.•ti•-• at.: abl..lll. :O.Iu.t ml bodk-;,. 111.:} ar. ll'IUI1J) COIIIIIIUOll' \\ith the Corte" Of Clldplatc Ulld lht.:rc i~ tK' nar1·t\\ \ ing \)f the di:-.k !>~pace. 01
i\dd•ti!;." i~ unknown. but the u•ndition l•Ol.11 al:~'QJJ1)ani~o.."S ar1hrq>:1thi"". kTct,.,., and other di."'A."''· 'lhc nl) ~'Qn.oJlUlt a:;. w..i.-.tK·n ;_, t-ld.r llj;C. g.nuall) ""'r 50. IO\lnlllion of the left tKcluhuhun, iM:hium, and puh~ !ll>nc. lismcllat..:d r~:ri u,tcul readu>n j, ..:en mill
Ftg 12 50
Mx~
lytic and sclerotic do-
struction \• II IU11111r 1\ 11h h1'1"h~"111 dlllrine and Pelvis
c.
ndngs
Disease
R.ld:ograph
HI.Wlter"s syndrome
HypoplaSia of the ped1des and widening of the 1nterped1culate spaceS\\ilh postenor vertebral scalloptng may be present.
(mucopolysaccharldo-
slsll) hg. 1266) Mofqulo's
syndrome (mucopolysacchandosls IV) (Fig. 12.67)
Un11 ersal vertebra plana shO\' a central ante nor beak en contrast to the 1nfenor antenor beak seen 1n Hurtefs syndrome. Other sp~nal findings include hypoplastiC dens v.ith atlantoaxial mstabiht)'. dorsolumbar rotary kyphoscoliosis, and increased lnterpediculate distance as well as small sacrum with a narrow ovoid pelllic inlet and wide acetabula.
ts
The mfenor beakii"IQ of ovoid bodies d st1ngu1sh thiS cond1t1on from MorCI\liO's syndrome Huntefs syndrome IS radiOlogiCally Similar to Hur1efs syndrome, but ha&a sloWer rate of progreSSIOn. Mamfests clm•cally dunng the second year of life
The pat1ents excrete keratan sulfate 1n the unne The trook IS short, v.hereas extremlbes are relatively norma I There 1s usually no mertal retardallon, but mulbpte deformitieS of the extrem1bes and pigeon breast a e present Spondyloep1phyt;eal dysplasia congenita can be d1fferent18ted from Morquio's syndrome by absence of corneal cloudmg and mucopolysacchanduna and by manifestations present at birth, although sp1nal changes are 5lmliar In these two conditions
Proget"ia
The vertebral bod1es retain the1r Infantile central notchmg Bilateral coxa valga is constantly present
A rare disease of unkown etiology characlenzed by dwarfism and premature aging Beaked nose, receded ch1n, and baldness are typical
Arachnodactyly (Mar· fan's syndrome)
Lumbar vertebrae may be abnormally tall. ilium may be vertical with wide pelllic cavity \Mdening of the sp1nal cana l and posterior scalloping of vertebral bodies are noted ScolioSis is common
An autosomal dominant growth disturbance caused by failure to produce normal collagen Long slender metatarsals. metacarpals, and phalanges are charactenst1c
Homocystlnurla
Flattemng end biconcavity of osteoporotic vertebral bodies are a d1stinctrve difference to Marfan's syndrome
A hereditary, somewhat heterogeneous condition. usually a lack of enzyme cystath10r11ne beta syn· thetase . One third of pat1ents show changes si1111lar to those seen m Marian's syndrome.
Neurofibromatosis
Radiographic findings in the spine are multiple. Kyphoacohosis wrth dysplastic vertebral bodies, eroSIOn of 111tervertebral foramina due to "dumbbelr neurofibromas and postenor scalloptng of the \ ertebral bodies wrth or w1thout rneningooeles are commonly observed. Several other spinal or pelv1c anomalies are encountered, but they are not dl8gnostic of thl& disease.
A hereditary di&turbanoe of mesodermal and neuroectodermal tissues Neurofibromas, smooth marQinaled cafe-au-lart spols on the sk1n, and bone deformities are characteri&IIC find1ngs
(liOn Recldlnghausen's clsease) (Ag 12.68)
(continues
F19 12.66 Huntel's syndrome A h}'poplasllc venebra w1th characlenstic infenor beak and kyfaSIS is seen
Fig 12 67 Morqulo's syndrome. UmversaUy flat vertebrae have a central ante nor beak
on poge 300)
Spine and Pelvis
299
b
Fig.12.68a. b. c Neurofibromatosis. a AP projection shows scoliOSIS and nb abnonnahties (arrows), b Lateral pro,~ect10n demonstrates posterior sea lloping of vertebral bodies. Slightly enlarged neural foramina at the thoracolumbar region. c Oblique view of the cervica l spine demonstrates dysplastic cervical vertebrae w~h scoliosis and wide neural foramina .
c
300
Bone
Table 12.8
(Cont.) Differential Diagnosis of Disease with Generalized Involvement of Both Spl ~ C> •J • .. lvls Comments The vertebral bodies are osteoporotic and have a nonumform biConcave conf~guration. ScoliOSIS and protrusio acetabuh are common.
An 1nhented autosomal dom1nant connectiVe t1ssue diSOrder The congenrtal form IS present at birth; the tarda form may rnan1fest 1n puberty or adulthood. OsteoporoSis, multiple fractures, bow1ng of the long bones and blue sclera are charactensiiC
The sp1ne is radiolucent even 1n young adults. The trabecular pattern is coarse , producing areas of In· creased and decreased bone densrty Vertebral bo· dies tend to be biconcave A cupl1ke depreSSIOn Involving the central three-f1fths of both upper and lcw.er endplates of several vertebral bodies IS typical In children. the antenor ~ertebral notch may be exaggerated,
A condition 1n which the red blood cells assume a sickled configuration at reduced oxygen tenSIOn . An abnormal hemoglobin SIS Genet1cally transmitted. The sgns and symptoms of ~IC~Ie-cell d•sease are due to anem~a e g , rapid destruction of abnormal erythrocytes
BICOncav•ty or vertebral bod~es is not a feature or thalassemia, but loss or densrty and coarse trabecular pattern may be seen 1n spine and pelvis
A heterogeneous group of microcytic anem1as based on a decreased rate of synthesis of one or more hemoglobin polypeptide chains. Heterozygotes are mildly affeded. The radiOgraphic changes in bones result from erythroid hyperplasia of the marrow.
Cr.einism (congeniUI hypothyroidism)
KyphOSIS, flattened vertebral bodies. and increased width of .nterver1ebral spaces. An upper lumbar vertebra may have a wedge or hook configuration (sail vertebra) .
The changes are not present at birth Sail verte-
Ostlopetrosis (Albers·
All bones may be 1nvolved . wrth loss of diStlnd1on betv..-een cortex and medulla, The vertebrae and pelv1S may be un1formly dense or there may be a 'bone-wrthin-a-bone" appearance of the vertebral bod1es Increased densrty of endplates may give rise to "sandwich vertebrae: Similar alternating bands occur In pelvis, too
OsteogenesiS imper-
t.cbi (F1g. 12.89)
SICkle-cell ......,.. (F1g. 12.70)
Schollberg (Fig. 12.71)
dis.Ht
brae occur also •n achondroplasia, Hur1e(s syndrome and Morquio's syndrome Hereditary failure of absorptiOn of pnmary spongiosa. The congenital form IS .nhented as an autosomal recessrveand IS mamfest at birth The tarda form tS dominantly 1nhented. d 1nteally benign and asymptomatiC 1n 50' Anem•a IS a common chmcal symptom. Somewhat similar, osteosclerosis, but wrthout bone-wrth.n-a-bone and wrthout anemia, IS seen in a rare hereditary condrtion called pycnodysostoSIS In osteopo1klloS1S, the sclerotiC patches tend to occur around acetabula but not 11n the sp1ne. whereas osteopath~a stnata may 1nvotve both pelvts and spine {COfllnlfls
on p..'lfle 302)
Sptne and Pelvis
Fig 12.69 OSteogenesis lmperfecla Radiolucent spine. biconcave lumbar vertebral bodtes.
301
F1g. 12 70 Sicklecell anemia. Cuplike depressions 1n the central endplates are dearest in the thoracolumbar reg1on.
FIQ. 12.71 a. b OSteopetrOSIS a Umformly dense vertebrae and nbs 1n a child b "Sandv.ICh vertebrae, Increased density of the end plates
a
b
302
Bone
Table 12.8
(Cont.) Differential Diagnosis of Disease with Generalized Involvement of Both Spine and Pelvis
Disease
Radiographic
MyelofibfOSIS ( myefo. scteroslsl (Fig. 12.721
Vanable degrees of osteosclerosis are seen 1n 50._. of patients The spme and pelvis are often ln~ol~ed. The 1ncrease of bone density may have e1ther trabecular or "ground glass" pattern and it may be patchy.
ProgreSSive fibrOSIS of the bone marrow w1th a lellkemoid blood picture (splenomegaly) and osteosclerosis, usually 1n patients O\er 50. The condition rs often preceded by polycytemia vera.
Mastocy1osis
Spme and pelviS are commonty affected, sllOWing a miXture of sclerosiS (erther diffuse or trabecular) and osteoporoSIS of the cancellous bone
Abnormal number of mast cells 1n sk1n, resulting 1n 1.1rrb1hcated pap1.1les Anelllla IS common Bone marrow Involvement results 1n sclerosiS
Irregular patches of osteosclerosis without bone enlargernerrt or coarsening of trabeculation. leSIOns 1n the ihum are cerrtrally located; pelvis and lumbar sp1ne are mvolved in 40 •
A familial defect of ectodermal development. Adenoma sebaceum of the face, ep1lepsy, merrtal deficiency, hamartomas of the kidney, and small scattered intracranial calaficatlons are common.
Vertebral bod1es show dense end plates and a subcortical radiolucency
ExceSSI~e•ntake of vltam•n D. Metastatic calclflcallons are common (Chapter 7). IdiOpathic hypercalcemia 1n a chronic form may also cause periphera l cortical scleroSis of vertebral bodies.
Thicken1ng of the trabecular pattern of the vertebral bodies and pelviS (also ribs and clavicles) is followed by dense, un~form, symmetncal scleros1s. Osteophytes are charactensllcally large and sclerotic. Bones may be widened. Calcification of the iliolumbal and sacral ligaments IS common
Exces51ve1ntake of fluoride, which inh1brts normal bone resorption
(urtiCAria
ptgmentosal (h•• 127') Tuberous sclerosis
(rig. 12 74)
HypervitaminOSIS
0
Fluorosis (R g. 12.761
Findings
Comments
(continues
FIQ 12 72
()11
rcge 304)
Myelofibrosis. Patchy scleroSis of the pel~1s. lower lumbar spme, and upper femora The pattern m~mics widespread osteosclerotic metastases (e g , carcmoma or prostate) .
Spine and Pelvis
Fig. 12.73 Mastocytosis. The vertebral bodies show patchy sclerosis
303
Fig. 12.74 Tuberous sclerosis. Irregular patches of sclerosis are present around the pelvic rim, sacroiliac joints, and in the sacrum and lumbar spme. A scoliosis is an associated finding in this case.
F~g.12.75 Fluorosis Dense, umform sclerosis of the lumbar spine.
304
Bone
Table 12.8
(Cont.) Differential Dingnosis of Disease with Gcncrnh1cd lm oh cment of Both Spine and Pch is
Hypefpdk fuo.t my 12- 15 and trisomy 17-18 s-yndrome~ us well as in a number or ran: osleoclx>ndn)(l;.svlasia,
Rib delormihes ocwr m 2H'' ol the populah<m The socalled cerncal nb ma) be a su1x:mmm..'!"'.u-y nb origmatil!f lcd in 1:--s.>sm..._.., and U1c clinical and ro.:>.cmhle mucopoly;;acchandoses). radiolog1c lindings Patchy <JStt.'(J))(1T(lSts munickmp mc1astatic di:-.ease comhim:d '' tth rib \\tdcnmt• ma\ he pr.....-..cnt in Goll(her's dt.~eme and Viemmm-/'I(A dt.\mW Rib \\1dcmng may he a feature in se\cr&l olhcr mre slc..xx.hondrodysl>lasias as \\t:ll
Hg. 13.4 Achondmplasia. 'lltc ril~:-arc \\ide and :-hort.
In osteopetrosis (Allx:rs..Schonherg disease), the nbs and clavicles arc mulonnly dens.; The stcmal ends may be \\10Cncd. Unilonnly dc·nsc ribs arc commonly cat&.' 6 em) sohtary C'>lXIllSile lesion~ are encounlpv, 'lakayasu~~ arteritis, urtcriosclt.'fOsi.s oblitcrall.'.) • pulmonary oligcn11,1 (lelltllop;y (4F'aflot,ahscnl pulmonary arlct.y or pulm011ary atrcsto or slcnosts, pscudotnmws arteriosus, L'hslcin~~ anomal): pulm011GI)' (TIIIp!Jp;ema) pulmonary or imercostol nr1cn0\cnous malfonllalion • obstructions of the supcnor l'('lla cam or .mhclm•ian rem neurofihroma/o.m or inl~'l'Costu l neurinonw (hg. 13.3) • pcnost.:al IITC@Uinrihc- municking nh notch~ occur 111 h)1'1t'rpamthyroidt.lllt, 111herou.1 ,\C·Iero.\1,\, thala.I.Wnna, collagen dtseaw.l, und ~llneltmt.., \\tiliout an~ l.nown reason (idiopathic noldllllf.!) Notching of ~upt."TK>r su1 fi•c.:e of nbs lllU) c.:wr in certain COIWI.."C:Ii\ e li:-..,uc diM.:c.:lUllilll.id artlJriti...,, S"''~ lemic lupus crvUlCillillosu::., sclcrodt.'l1tJU and Sjogren's syndrome. Supt.Tior ~urfac:c nokhi1!! nJU~ <X«.:lu in h:'tpt.'fparo~Uluoidhm., llt.lll:PJibl\lOIUIOSIS. r~tric:li\1! IWJg disca:;c, poliom~eliti:-, Murfun's s:--ndrome, 1ftd;•~ tCinc-shapcd chest with relatively
sh01t ribs (long trulilaglllotL'> ~mcnls), 1dativelv ~mall scapulae.
l1g. IJ. IS Hurlds s:-.ndrome. 'f he clot\ idcisshort and lh!d., U1e nl'S f the ~llpllla llnd humeral q>lpln ~is,
1 he ch:l\ ide 1s fomlt.'tl li mn lhtt.'C SCJ'I.tmle o:-..,lfkation ccntI..TS. If one or mo1.: of thcm ll>lthscnl, h\I'Xlplasia or absence or U1e clavide c.:ttu:» 'f Ius is 11 chataderil>lic findit~g it1 cleulocrr111ial dv.\0.\losi.\ (hypopl,1sw or absence of elm iclc:s, deft.'tli\'e os...,i(kalion of 1111: culnuium, spina bifida, hypoplastic pelvic bones with scptualion of pubic symphysis). The ch~.--st IIlli~ b..: c:one-shupcd w1d ribs muy be short but oilicn\isc nonnal it1 d cido. !\ n(.lc (superim smlitu:) ,..hould be distiltgui.•.,hcd fmm intlammutory cwMon Wides1)rt!lld M./utl.\/.1 of the dm 1tlc may be due to chronic ().~teomyeltlis (llg. n 17) or Paf_et~ dt. of peetee' n nile; ma:o. ha1 e a tntlllllllbl. t>ngin (fig. anomul~
I he stt.nnun ts' i.~twhzed on lateral plam hlms but is USlwlly poorh shown m anteroposterior or oblique views. Fusion anomaltcs ol the stcnml scgmcnb (ltg 13.22) arc common and ore sometimes seen in association "ith oth1.:r mtomalics. mdudmg congenital heart di&as.: 'Ote most conunou anolllilly isjitsion of the manubriosternal synt.hondro::.is. with or witl10ut u sv nchondJ osis between lite first and st.-cond sq?,nlt.'llt of lite hod~ lite stenu.un. fusion of the numubrioskmal s·HtchondJllSts ma~ also be the end result of ank}• o~ing .spondylili.\, d~nos1crnul sync:ht.ndm: not articulute 11 ith the p.k11oid foSl:a 1\
fig 14 2 1\.nterior dislocation ofthc humeral head 1\ith cbarncto.:ri • It mcdwl arK! inferior displacemo..11t
comprd 1!,l'llll /a.mm. One measurement U."'-'l.·m\ll\' (0.'¥.(}()(/-Sch/al/er disease), 01 the infLTior o:-.,thwtion cc11t..:r of the pat.:lla (Sinding-Ian.en-jolum.t:ondmy to;1n-em/e rlwumaloid arthritis or to pmc'Sts of the qtwdnccjls mwi\:le in poltomyelilis. lncongrtl l)' (!fJKtleflar motion, c. g. lateral dislocation and tilhng ur.: more common tmd unportunt abnonnalttics. Thetr demonstmhon 1s bel-l done with cross sectional images using cr or MRiat llC'\ton less tlum 30 degrees, since plain films arc inscnstli\c The patella mm be ahs..'ltl or hypopla~tic . 'lbis is ll!>lJally due to huwlilat)' onycho-o.\ll'ody.1plasia or nail paid/a syndmmr (Fi~. 14 7), \\lm:h ts diUtildcri!L-d b) tli!K homs and SO.:\ era! oll1cr abnonnalitie: I lypopla.-..u of ll1c patella is occa~ionally ti!IX>rtccl in a:-.~)(.iuhll "tlh aulX.q11talos~ndac l~ ly. <md iipLt~ia of tltc llitlc!Lt in as..-.ocialion with bittlllt'tuled dll'arjism, lit IIIT!/if>t'(malo.'l.\ und poplitml ptery-gium .~vndrome.
fig. 14 6 DctcmnnatKln of the postlton of patella The measurements should lx· done :.t llc"on 1-o.:t'''-..:n 20 to 70 degJI:!eo., 1. •~ tK>mlllil\ hct\\o..\:11 0 1-i and I 2. I '<Jtdl~ alta ~ d· > 1.2. putdla J'Tolullformities confined to tile distal half of tht' trbia as· sociated with lcxali1ed cortkal thkkening and solid periosteal reactron c.Jn be found in trop~col
Echinococcus rarely involves bones. Bcsid('S the sprne. pelvrs, and sacrum, the long bones may be affected with multiloculatcter due to decre;~sed mt'dulklry cavity while the width of the wrtex i\ rl'latrvely little affect('d.
Osteomalacia (Fig. 14.11)
Bowing deformrtles occur, besides in the pelvis, spine. and thorax. particuldfly 10 the lower ex· tremities. The cortex rs thinnt'd as in osteoporosis, but bone deformities. pw~Jdofractures .and poor defimtion of tht' Inner cor tll.JI margin and trabeculaE' help to dofft·rentiate osteomalacr.J from osteoporosis.
Bowing deformities are also a common feature in rickets of any ctiolcx;y.
Hyperparathyroidism
Bone deformities similar to osteomalacia occur in .Jn advanced stagE'.
In renal osrrodystropfry (secondary hyperparathy· roidism) bone deformities may be scconddry to both osteomalacia and hyperparathyroidrsm.
P~'s disease (Fig. 14.12)
Bone cleformities are common in the lov.t!r ex·
Common cause of bont> deformrtocs rn the elderly p.:1tient. Here-ditary hypffphosphatasia ("juvenill' Paget's drsease"), which occurs rn children. prest>nh charac· tcristically with bowing .1nd thickening of all long bones in the upper and lower extremrtil's.
Fibrous dysplasia (Fig. 14.13)
Markt'd cleformitics of the long bones occur, p.:1r· ticular1y in the pol~totic form. where the boot' rnvolvernent rs gt"Oerally more extensive. "Shepherd's crook" deformity (upper femur). corti· cal thickening. widt·ning of the bone. and ac.cen· tudted or abnormdl trabt:culdtion may be present. srmolar to P.Jgtt's dheasc. The presence of radiolu· cent or cyst-like lesion~ or "ground-glass" appear· ance of the in110lved bone are useful in differcntidtrnq fibrous dysplasi.a from Paget's disease.
In contrast to Pagt>n disease, fibrous dysplasra rs usually diagnosed rn children and young adtdl\. Skin pigmentations ("cafe-au-fait" spots IMth irregular outline) and sexual prematunty in fem.Jies may be present in the polyostotic form (A/bright's syndromE').
Neurofibromatosis (Fig. 14. 14)
Overgrowth of the long bones may result rn bowed appearance. The f,bula frequently rs slender (overconstricted). Pst'ud.lrthrosrs (espt>eially of the tibia) is common wrth thrs presentation. Bowcick (Fig. 14.26)
langerhllns
diSNse
cell
histiocytosis (histiocytosis
X)
Fibrous dysplasia
(lig. 14.27)
(J ig. I 4. 29)
Flnclngs
D n:sistuzl ricket.,.
(wr:lira £.\ on ptlf.C 328)
Extremities
b
a Fig 14 25a, b Gaucher's disease a Prox1mal femur: Avascular necrosis or the femoral head and increased patchy sclerotic areas in the proximal femur are seen. b Distal femur: "Erlenmeyer flask" deformity of the distal femur and osteoly1ic lesions in the distal femur and proximal tibia are seen. Irregular sclerosis in the proximal tibia metaphysis is caused by old bone infarcts
Fig. 14.27 Fibrous dysplasia. Widening (undertubulation) of the humerus shaft with thinned cortices and "ground-glass" appearant('(' is steosclerosis (particularly in the metaphyses) and "Erlenmeyer flask" deformities occur in the distal femora. Dense metaphyseal bands and corbcal lhtckening are frequently associated. Soft tissue calclficallons may also be present
Ctinical mamfestahons tndude an elfin face, mental and phystcal retardation and neonatal hypercalcemia . Supravalvular aortiC stenosis and hypo· plasia of major vessels are frequenUy associated. HypeMramiiiOiils D may produce a Stmolar radiographic and clonical picture
(Williams
syndrome)
Ftg. 14 30 Lead poisoning. Splaytng of the metaphyses is assoctated with dense trans~erse metaphyseal bands
Extremities
Table 14.3
3 29
Narrow Diametaphyses (Overconstriction or Overtubulation) ~.JOograptk
r·
ngs
ComrMnts
Hypopituitarism
Proportional dwarfrsm often with overconslricted tubular bones and delayed eptphyseal closure.
Hypogonadrsm and other endocnnological diSturbances may concur
Tubular stenosis (Kenny-caffey disease)
CNerconstricted tubular bones show symmetrical endosteal thickening and narrowed medulla. ScleroSis of the calva num and coxa valga may be associated.
ProportiOnal dwarfi6m. Tetany 1n earty 1nfancy from hypoca lcem~a
Progeria
El