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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.
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v
Preface
Convt>nllonal r.ldtography remains the backbone of our ~pe cialry desptre the advent of newer and posstbly more exCiting tmagmg techmques such as computed tomography, magnetic resonance imaging, and, most recemly, posttron emtsston tomography. In contrast to many of these newer methods. conventional radiography ts pract1ced not only by rad10log1sts but also by a large number of climcians and sur geons. Wtth each examination. one IS confronted with radiologic findmgs that require interpretation in order to arrive at a general dtagnosttc tmpresston and a reasonable dtffcrenttal diagnosis. To assist the film mterpreter m .Jttammg thts goal. this book i~ b.l!>ed upon radiographic findings. unlike most other textbook~ m radiology that are disease oriented. Since many disec1ses present radiographtcally m a v.Jnety of mantfestations. some overlap in the text •s unavoidable. To minimize repetttton, the d ifferential diagno~is of a radio graphtc findmg is presented in tabular form whenever fe.Jsible. Most tables hst not only the various d1~a~es that may present radiologically m a specific pattern, but also de scribe in succinct form other characteristi(ally cJSsoctated radiographic findings c1nd pertinent clinKal data. Rcldtographic illlustration~ and drawings are included to demonstrate visually the radiographic features under dtscusston. The transition from film to digital radiography hcls had a great impact on conventional radiology smce the publication of the ld~t edit ton. Th1s ch.1nge, however. did not .1ffecr the w.1y radtologtc dtagnoses are ascertained. Sinn~ the publication of the last edition the n.1mes of a few diSOrders have ch.1nged (e. g., hl\tiotytosts X is now known as l.angNhans tell hi~tiotytost\) and a few new diseases have been recognized (e. g., femoroacetabular impmgement and severe .!Cute rt>sptratory distress syndrome or SARS). These facts were taken mto con~iderarion in thts new edttton. The chap ters "locali1ed Rone Lesions" and "jmnt Dtsease~> have been completely 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 s with age, increasing from mfancy to age 3'5-40 and then progressively decreasing at the rate of 8 % per decade in women and 3% in men. The rc1diogr.1ph1c findmgs of o"teopenia are loss or hone dens1ty and cort1cal thmnmg. Osteopema may either be generalized or localized. and 1ts differenrral diagnos1s 1s d1s cussed ~eparatcly m Tables 1.1 and 1.2 . In osteoporosis, a combmat1on of loss of bone density and cortical thmmng may result man apparent mcrease m den· sity of the cortex and vertebral endplates, that appear as
thin, sharp lines (Figs 1.1 and 12). Bone resorption occurs preferentially in the transverse trabeculae, while the trabeculae along stress lines are accentuated. Resorption of all trabeculae in a vertebral body produces the •empty box" sign. As a result of compression fractures the vertebral body may depict a dep•eso,ed endplate or become wedge-shaped. biconcave (fish Vt'rtebra) or umformly compressed (pancake vertebral body). Cartilaginous (Schmorl's) nodes are causc·d by displacement of a portion of the intervertebral di~c into the vertebral body W1th the exception of osteogrnem lmperfecta, bones do not bend m osteoporosis. A pred1spos1t10n towards fractures. however. exists in the brittle bonrs. especially in the vertebral bodies. ribs, hips and wri\tS. fracture healing is delayed and the callus formation poor. Abundant callus forma tion 1n osteopenic bones may occur, however. with exogrnou~ (iatrogenic) or endogenous (Cushmg·s syn· drome) hypercortisolism and osteogenesiS 1mperfecta. In osteoporosis. sl.'rum calciUm, phosphorus and alln 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~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('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 acal 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. .hn 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 rrogeneous eprp~eal dys· plasia associatE'OrdE'r has ~en compdred with the "flowing of wax down a burning cdndle.· Note also tht> mvolvemt>nt of the small osteoma-lokt> protrusions from the proximal phtllanll of the third fingPr (ulnar sodt>) and the moddle phalanx of the folJrth finger (radial side).
2
Fig. 2.12 Osteoma All abnormally dcn~e lc~ion with ~tructure- lt>ss appt>aranct> is characteristiC In this rase. thE' mtt>oma originated from the outN tablt> and could f'a~ily be palpated.
F1g 2 14 Parosteal sarcoma Th s ~terlor cortiCal tumor of the distal fl'mu d1c1~ ~ s pre-..:nt• cl' c1n lneqularly defined sclerotic les1on tn thi ••mt .o~terio. projection (vit>Wed fact'-on) . The lateral prOJt'Cllon of th1s sarcoma l'i shown 10 F19 4 49
O~trm< lrrosis
19
Fig. 2.13 Osteosarcoma. A rc1ther homogeneous sclerosis of the d1stal ft>mur spanng only a sn1.1ll port1on of thf' subchondral bone in the latercJI femur condyle IS seen.
Ftg 2.15 Ewing's sarcoma A rel.lt111ely poorly def111E'd sclerotiC IS ~en n L3 '1\1{)1· j • posterKJf two-thtrds of the lt('rte· bral bocly c1nd J".'Ciocl.,s.
lesion
20
Bone
Table 2.1
(Cont.) Solitary or Multiple Scattered Osteosclerotic Lesions
Disease
Radlographk Flndir.gs
Ost~
Poor!) dl fmcd .m·~ of oncrt>awd density WJth ondi!>- In childr.-n, l._;_.kemta, nl'tlroblastoma, and EWing's hnrt or kist trabe< ular ~tructu rE'. With increase tn sarcoma ml'tastascs must be considered. although suE'. adjacent mE'ta~ta'>es may coalesce, r~ulting fi- thf>~e le\ion\ are more commcnly lytic l.lfofore ncolly tn mo\t doffuse sclerosis. Wtth the exceptton of trNt fJ1Cflt ts lnstttuted. renal and most thyroid r arconomas whi" duonK Stlerostng-type 0\teomyelitis. Sc.lffosinq osteotn)'f!irti) of Gorrlos a lov.-grade chrOflk ioff!( tion not associ.Jtt..'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.'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 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 w, pE'Ivis. lower t.'ultiplt> and often skeletal hyperostosis) extremity (commonly symmetrical (Fig. 3.32) patella and calc 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 CIaccc.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 \\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 ?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). Frclsent 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) If 19 25. os ve'>dlrclnum (....._ 26. os wneonavrtulare medrc!le 27. ses 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
,
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 hand or rn the ~kult. Tht> lesion may be expam1le With thinning or destruction of the cortell. Sk~olllc\lon~ u~uxlf'nd thro11gh ont> or both tab~ . All 1m'9ularly shap«:t button sequestrum 1s usually present in larger skull lesions.
lliuLIIy dld\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 characteristimur.
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 ckmcuito"
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~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.pKfrwr.< (carpal and tarsal areas and elbows)
Fibromatosis
Solrtary or multiple soft tissue masseswith erosions of the adjacent bone or osteolytic lesions. Cortica l hyperostosis may be associated wrth bone involvement.
Variety of ben1gn, but often aggreSSive frbrous proliferations presenting in both children and adults as tumor-like soft tissue lesiOns. lnvolllement of the adj acent bone is not uncommon m infantile forms of the d1sease.
Symmetnc and slowly progressrve lytic lesions are found 1n the carpal and tarsal bones and the ends of long and snort tubular bones Bone deformities may eventually occur from pathologic fractures.
Rare hereditary disorder of ad1pose trssue affecting pnmanly the bones and brain Presents commonly tn the second or thtrd decade of life wtth painful bones and JOints and subsequently With presenile dementia.
Monostotrc or more commonly polyostotiC asymmetnc lesiOns wrth preferentia l 11wolvement of the pel\lis, femur, lrbia, spene, skull, scapula, and humerus The pattern of 1nvolllement ranges from purely osteolytiC (e g ., osteoporOSIS carcumscnpta in the calvarium, and V· or flame-shaped defect in the diaphyses of long bones) to purely osteosclerotic (e.g., ivory vertebra). The mi> 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
""
/'n clLdC and is U~crclbrc most on._,. wulutcJUI 1\crvmiotJ.l\ ic.ular joint lkgc..1lelc nmnlwrthnt1s
lktUOJ~ulta
lnkdious (llrodt,'s • 1..c~ s) lr•trat,ll head.
(hondrCtcopb:.1cs ili'C ,.,.....,, u tl1e putcllokmoralJomt. b: A central {mlLTKlrJNIIt) (l~te~>ph~tc (arm\\) pr.:;.crtts l'-' hutton-lil.c t:\lTCStL1lle originating fnnn tire MtbdttKlwl l'ne largdy tlL1tlt lltg ( 17) arc commonly found \\1th ~rnm..'f:!all\c spondyloarthropathics and dithLn of the distal phalWl.' of the thumb. 2. HypcrC'\1CJ"Lo;JOil at mkrphalrmgcal JOml and lk'\.ion ut the hrs"'t mdilCafJlpeciaU} tul..:rullt•us)
lnfc'-11l•tl' arthrit "
llcntt.~hn•l1ilhJSi:o-.
and ltmlOf'llhs
hunc f~,t rna-
Ci joint Di~eases
139
F1g 6.22 a, b, c, d joint effusions a: Elbow: V1suahnt1on of the postenor fat pad (arrowhead) is diagnostic. The anterior fc1t pad can r>Orm a "all~ conftq ''a liOn (arrow) lnd1Cat111e of an ellu\100. A radral head fracture is also evidt>nt. b: Knee Flurd accumulation m the su· Pfclpatellar bursa (arrow~) thclt connects Wlth the~ 1e • diaqnostk. The joint effusion (curved c1rrow) may abo displace the inferior patcllc1r lcJt pad .mteriorty. A fat-fluid (blood) level (arrowheads) can be seen m the SUPfapatellar bursa 1n a post-traumatic lipohemarthrosis. when the examination is ~rformed With horizontal beam techmque. c: Ankle· A larger anterior (arrOW\) and smaller postenor (arrowhead) soft trssue bulge IS charactenst1c. d: Wnst· Antt>nor subluxat100 of the p~s1form IS caused b). the largt> h{'fTlarthros1s in the radiocarpal joint secondary to intra-articular fractures of the d1stal radrus and ulna.
a
b
c
d
entia ted from a transient. linear or cre!.t'l mlle.
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 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~;ult h: I hl.th no! d) pia Ittchldl'Ol
tim~
MO»t cmc
Rhcumatt>id arthnlls S) !'lemic lupu' en•lhc>tnai) 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~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)nr.~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 mtatK: corcit•11 sts (!.Caltcrcd nodulwcalcilicatiotlli 1-3 mm in diat~ll:tt..-r) . lrichino.sis (puntlatc calcifkations of 1 nun r lt.."l'-') and para~onimiusis (punctate to cn>tic. ofl1-'lt in dusto.:r.; and me 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 cukifkutilanl 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 \\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'r•:r lrwi77:CIII of lrrpvr'(lft:llryroidOJm and richJJ OlA) ..t.u incJu.:, u ,: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--pitng 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 radin nnd a >upcrinlpO'>ed bon) >tmclurc (q; frpont;.\ t"'tun:. l'to.:lllllillilnlin of the oor-um >ella n .. ult ~castltnion 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 fr~cnnilll~ not more than 5 mm abo\e U1is line
Sclerosis of the Base of the Skull 111e foii0\\1llf!. dJO'crcnllul dmgnosis ts linutoo to those discases that Clthcr lh:qucntlv imohc tl1c base of tllC skull or arc C\.cll!l>i\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>tllC 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 Acoushtionall~ 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\ I the aJja~"ll fwntal >llllh and liiUlll•lllul cd[, i' c\ idc11t.
""II
Fie,th 0Jb1ts
I'
as,t>ciat,tJ
U~ •;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~>latn ho"c'er, ~ llc.:n a d..l»-c l>n (O!ol :1lah:ral \\llh 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 [ragmphrc los.-; of lanuna dura ol~:n·~..xt in Pagel~~ dtsca.w• (l1p I J .4),fibrous dyspla.\ia, and osteomalacia is common I) the n:sult of both bone rc~orption and !ielerosis. The \\idlh of a nomtal Jlottc that i• fl>nn•..t in the pcricnl11el n
poor!~
to wcll-ddined detect around the
lelc~ lt.
mm~ent.
ral lxxhcs must be 'isthlc (lll rudiographs In a cas.: \\h(.'ll good quahty mdiogmphs :1,\l'Ctl
left atlanto-
ftg. 12 4 Hyperc\1cn\1'l lind ctlcd ll>r1c" (a ptdure lrnm.: :tppry aprearanlnlllion of the left tKcluhuhun, iM:hium, and puh~ !ll>nc. lismcllat..:d r~:ri u,tcul readu>n j, ..:en mill\• II IU11111r 1\ 11h h1'1"h~"111 dlllr •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
Hypefpmy 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 populahpanSion 111 7tel::e:\ S)ndrome ma~ occaSior\811) catLlXIllSile 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~ ~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: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. 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 ' 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. Bowc