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Conference 11 12 December 2007 The Armed Forces Institute of Pathology Department of Veterinary Pathology WEDNESDAY SLIDE CONFERENCE 2007-2008 Conference 11 12 December 2007 Moderator: Dr. Steven Weisbrode, DVM, DACVP CASE I – 306729 (AFIP 2840709). Signalment: 1-year-old, female, boxer, canine History: Th e do g presen ted to a referral ho spital for chronic (greater than one month duration) grade II out of VI lameness on the left hind limb with a sho rt stride and mild muscle a trophy. Physical exam revealed pain on manipulation of th e left stifle, m oderate left stifle th ick- ening, and mild decreased range of motion. Radiographs revealed a fluffy proliferation in th e reg ion of th e left stifle fat pad, and thickening with slight mineralization of the medial aspect of the joint. A percutaneous bone core biopsy was performed and was consistent with multifocal osteocartilaginous m etaplasia. Due to th e dog’s ag e at 1-1. Left stifle, boxer. The medial trochlear ridge is the ti me o f the in itial b iopsy (9 months), it was reco m- moderately proliferative and expanded by osteophytes. mended that su rgery to rem ove th e lesional tissu e be Photograph courtesy of Dr. Brian Huss, Vescone postponed un til sym physeal clo sure occurred. The dog (Waltham, MA) and the Angell Memorial Animal Hospi- returned for arthrotomy 5 months later. At surgery, mod- tal, Pathology Department, 350 S. Huntington Ave., Bos- erate degenerative join t di sease (fig. 1 -1) w as noted ton, MA 02130 with numerous osteophytes on the medial trochlear ridge. A bony mass was present that incorporated t he m edial Gross P athology: Tissu es sub mitted fo r h istologic joint ca psule from t he l evel of t he proximal t rochlea t o evaluation consisted of a 5.5 x 3.5 x 2.0 cm and a 2.0 x the tibial plateau and from the medial collateral ligament 1.5 x 1.2 cm piece of hard, nodular, whit e-gray tissue to the patellar tendon. The mass was seen to be contigu- lacking orienting anatomic features. ous with the patellar fat p ad and both the cranial medial and lateral menisci. The joint capsule was removed with Laboratory Results: Aerobic culture of the joint at t he the mass (excision was complete grossly). time of initial core biopsy was negative. 1 WSC 2007-2008 Conference 11 eases. In this condition, detached fragments of cartilage Contributor’s Morphologic Diagnosis: Synovial osteo- or subchondral bone become implanted within the syno- chondromatosis vium and incite the formation of chondrometaplastic nod- ules. With the secondary form, there is little to no cyto - Contributor’s Comment: The submitted specimen con- logical atypia, and the condition usually responds favora- sists of sections of joint capsule that include the synovial bly to surgical intervention, provided that the initial joint membrane an d f ibrous layer . Th ere is a poorly d eline- disease is not allowed to progress. ated, e xpansile, m ultinodular m ass com prised of broad trabeculae of woven and lamellar bone that are lined i n In the past, an attempt has been made to apply the above- many areas by a si ngle layer of osteoblasts. In most ar- mentioned classificatio n to canine p atients with osteo- eas, these trabeculae arise from foci of collagenous tissue chondromatosis, bu t th is h as p roven t o b e d ifficult, as via e ndochondral ossification. Hem atopoietic cells and many lesions in the dog do not fit all the criteria of either adipose tissu e are presen t with in t he in tertrabecular classification. In the present case, there was no apprecia- spaces. ble cellular atypia seen and there was evidence of degen- erative joint disease. This would be most consistent with Synovial osteochondromatosis, or synovial chondrometa- a classification of secondary osteochondromatosis. How- plasia, is a proliferativ e disorder of undifferentiated stem ever, the patient had no history of trauma, and the lesion cells of the synovium. The proposed pathogenesis is the was confined to one stifle jo int. Th is is m ore typical of transformation of fibroblast-like cells under the influence the primary form. A lack of cellular atypia argues for the of extracellular chondroid matrix material into chrondro- secondary form, but cellular atypia may not be seen in all blastic cells. It is th ese tran sformed cells th at are b e- primary cases. T he p resence o f degenerative joint dis- lieved to give rise to th e characteristic cartilaginous nod- ease is not in of itself an adequate criterion for the secon- ules. These nodules may grow and project out form the dary form, as th e formation of osteochondromatous nod- synovium on delicate vascular pedicles, or as seen in this ules can lead to degenerative changes within the adjacent case, may form a more broad-based nodular mass. When synovium. Regardless of the classification scheme used, their base is narrow, they often break off and form loose the prognosis for dogs with this condition appears to de- bodies within the jo int. Th e cho ndrocytes o f th e l oose pend on the degree of degenerative joint disease noted at body are nourished b y th e syn ovial fl uid and thu s will the time of surgery, as well as th e ability to perform total continue to form more cartil age m atrix an d in crease in synovectomy with removal of any loose bodies. R ecur- size. Th is will often result in degenerative joint disease rence with incomplete removal of the affected synovium due to physical damage to the adjacent joint capsule and and/or l oose bo des has been re ported. C omplete articular cartilage. If t he nodules remain attached to the synovectomy m ay be i mpossible, however, a nd t empo- synovium (as was seen in this case) th ey will often un - rary rel ief has been reported wi th l oose body rem oval dergo e ndochondral o ssification with t he formation of alone. Th e dog in th is report was doing well (no lame- broad trabeculae of bone. In dogs, the disease is usually ness reported) 2 months post-surgery. seen in medium to large breeds, and has been described in the scapulohumeral, coxofemoral, talocrural, and stifle Differential diagnosis should include severe degenerative joints. Th ere is usually no history of trauma or pr imary joint disease, osteochondral fract ures secondary to degenerative joint disease (such as osteochondritis disse- trauma, osteochondritis dissecans, and neoplasia, particu- cans). larly chondrosarcoma. In humans, osteochondromatosis is uncommon and most AFIP Diagnosis: Joint capsule (per contributor): Osteo- often occurs in the stifle joint of middle aged males. The chondral m etaplasia (osteochondrom atosis), di ffuse, condition in humans has been classified into primary and marked, Boxer (Canis familiaris), canine. secondary forms. The p rimary form is described as the spontaneous formation of i ntrasynovial no dules in an Conference Comment : T he co ntributor gives a good otherwise no rmal joint. It is us ually confined to on e review on a poorly ch aracterized, rare cond ition in ani- joint, most commonly a larger joint (e.g. knee, hip, shoul- mals. We essentially agree with the contributor’s diagno- der, elbow, and ankle). Histologically, the primary form sis of osteochondromatosis, although we prefer the termi- has been described as foci of chondrometaplasia that con- nology of osteochondral metaplasia to describe the mor- tain ch ondrocytes with cellu lar atyp ia. The recurren ce phologic lesion. rate with th is form is con sidered high. Secondary syno- vial o steochondromatosis is a similar co ndition th at fol- Osteochondral metaplasia can occur within any synovial lows trau matic, d egenerative, o r inflammatory joint d is- lined structure, such as a joint, tendon sheath, or bur sa.4 2 WSC 2007-2008 Conference 11 Ectopic ossification of these structures requires a v ascu- peared less dense and slightly lytic? lar su pply, and the presence of d etached osseous bod ies (joint mice) implies a previous attachment to the synovial Histopathologic D escription: The femoral head has a surface. normal sh ape an d t he articu lar cartilag e is microscopi- cally normal. There is variable lack of differential stain- The underlying cause of osteochondral metaplasia in ani- ing in m arrow, bo ne lin ing cells an d osteocytes in ter- mals is no t known. Due to t he relativ ely li mited re- preted to be artifacts of decalcification. Th e marrow is sponses of the joint, it can often be difficult to distinguish mostly fat ty wi th l imited hematopoiesis an d a reas o f osteochondral metaplasia fro m ot her disease pr ocesses acute hemorrhage. At the deep specimen margin there is that resu lt in i ntra-articular jo int bodies such as osteo- bone debris within the marrow spaces that is presumed to chondrosis or chip fractures.4 reflect method of surgical removal since no sawing was done to the specimen once received. There are shredded There is so me v ariability in th e slid es. M ost slid es ex- fragments of hyaline cartilage present on the deep margin hibit lamellar bone formation, and only a few slides ex- in what would be the location of the growth plate. Com- hibiting bo th la mellar and chondroid bo ne formation. pared with a no rmal active growth p late, the cartilage is Lamellar bo ne is form ed by end ochondral ossificatio n hypocellular an d ch ondrocytes are present in irregular with a sh arp l ine of demarcation between cartilag e and groups (fig.
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