AFIP Wednesday Slide Conference - No. 20

February 10, 1999
Conference Moderator:
Dr. Steven E. Weisbrode, Diplomate, ACVP
The Ohio State University
Department of Veterinary Biosciences
Columbus, OH 43210
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Case I - N1893 (AFIP 2420927)

Signalment: Two-month-old, female, Blonde d'Aquitane calf.
History: The calf presented with severe lameness, swelling of the interphalangeal joints, and gangrene of the left forelimb and hindlimb. The calf had received treatment for pneumonia and septicemia at seven days of age. Lameness was first noted at five weeks of age.
Gross Pathology: The limb extremities were variably swollen with localized hair loss, ulceration, and sloughing of the hooves. Bony sequestra in the distal metacarpus and distal metatarsus of the left forelimb and hindlimb were sharply defined. Fibrinopurulent exudate was present in the interphalangeal joints of both forelimbs.
Case 20-1.Gross Images. The limbs in (A) demonstrate variable amounts of dry gangrene affecting only the hoof, hoof and toe, or hoof, toe, & metatarsal region of the leg. Note the sequestrum in the distal metatarsal bone of (C).
Laboratory Results: Salmonella dublin was isolated from the joint exudate and colon.
Contributor's Diagnosis and Comments: Terminal dry gangrene; Osteomyelitis and arthritis.
Etiology: Salmonella dublin.
Microscopically, necrosis and fibrinopurulent debris are prominent at the level of the distal growth plate of the metacarpal bone. Mature and fragmented neutrophils are common, fibrin thrombi are present in small blood vessels, and there is widespread necrosis of cartilaginous, osseous, and myeloid elements. Lesions extend into the epiphysis and diaphysis, and occasional clefts are present in the growth plate cartilage. The necrotic areas are poorly circumscribed by mononuclear leukocytes and dense fibrovascular stroma. Microscopic findings in other tissues included histiocytic foci (paratyphoid nodules) in the liver and crypt abscesses in the ileum.
Hematogenous osteomyelitis in calves frequently involves the growth plates of long bones and vertebral bodies. The increased susceptibility of metaphyseal bone has been related to local features of small blood vessels that favor localization of circulating bacteria, leading to thrombosis and necrosis. These features include loop formations, endothelial gaps, sluggish circulation, and lack of anastomoses.
Most cases of hematogenous osteomyelitis in calves result form infection with either Salmonella dublin or Arcanobacteria (Actinomyces) pyogenes. Advanced cases of Salmonella dublin infection sometimes progress to terminal dry gangrene. The gangrenous appearance of the extremities has been compared with that seen in ergot poisoning in this species. Records of previous illness, including diarrhea and septicemia, in affected calves and other problems associated with salmonellosis in affected herds are not unusual.
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Case 20-1. Bone. At the margin of the necrotic sequestra (left), which extends through the growth plate, there is a mixture of degenerate neutrophils, fibrin, edema, and cell debris (right).
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Case 20-1. Bone. The necrotic bone (right), and marrow is being replaced by neutrophils, macrophages and fibroblasts forming collagen (center & left).
AFIP Diagnosis: Bone: Necrosis, coagulative, focally extensive (infarct), with moderate multifocal chronic-suppurative osteomyelitis and physitis, and fibrosis, Blonde d'Aquitane, bovine.
Conference Note: Depending on the sections examined, conference participants identified many of the histologic features described by the contributor. Multifocally, the physeal cartilage is characterized by hypereosinophilia of the matrix, chondrocyte nuclear pyknosis, karyolysis, and loss (necrosis), with scattered fissures. Within some sections, variable numbers of viable and degenerate neutrophils, lymphocytes, and macrophages have infiltrated and disrupted the physeal cartilage and the spicules of woven bone within the primary spongiosa. Immature fibrous connective tissue, similar inflammatory cells and variable amounts of cellular debris have replaced the growth plate and primary spongiosa. In other sections, the predominant findings are extensive coagulative necrosis of cartilage and primary spongiosa bounded by zones of granulation tissue and small numbers of inflammatory cells.
Within the epiphysis of most sections, trabecular bone is frequently hypereosinophilic, and there is karyolysis and loss of osteocytes (necrosis). Occasionally, viable woven bone is found deposited upon spicules of necrotic trabecular bone, and diffusely there are increased amounts of mesenchymal tissue with scattered inflammatory infiltrates and cellular debris similar to that in the physis.
Based on the histologic findings of extensive coagulative necrosis of cartilage and bone with surrounding fibrosis, several conference participants favored an ischemic etiology, such as ergotism, over an infectious agent. Several participants had difficulty distinguishing inflammation from bone marrow myeloid elements, and did not identify a major inflammatory component within the lesion. In the submitted gross photos, a cross-section of one of the limbs demonstrates necrosis and lysis of bone, and the inflammatory process extends outward into the skin. The gross findings and the microscopic pattern of inflammation and necrosis suggest an embolic bacterial etiology rather than an ischemic process, such as that found in ergotism. Those sections dominated by coagulative necrosis and extensive fibrosis may reflect the histologic appearance of "dry gangrene" discussed by the contributor in association with Salmonella infections of bone.
Bacterial osteomyelitis develops either by direct implantation into the affected bone, as may occur in trauma, or as a result of hematogenous infection. Hematogenous infections occur most frequently in neonates or juvenile animals and children. In children and animals, the most frequent sites of inoculation are areas characterized by rapid growth and increased risk of trauma, such as the growth plates located at the proximal and distal aspects of long bones.
The microvascular anatomy of the metaphysis is unique; large caliber veins with little collateral circulation are present, which leads to marked slowing of blood flow and increased susceptibility to thrombosis and colonization by hematogenous bacteria. Thrombosis and venostasis of the metaphysis seem to be important in the development of osteomyelitis in adult humans, and are most frequently associated with trauma.
Salmonellosis may lead to thrombosis as a result of endotoxemia. Bacterial lipopolysaccharide induces vascular dilatation, pooling of blood, activation of platelets and leukocytes, complement fixation, and release of vasoactive amines, leading to thrombosis. Thrombi in metaphyseal vessels serve as foci for bacterial implantation in septicemic animals, with subsequent development of osteomyelitis. An acute, neutrophilic inflammatory response follows bacterial implantation, with production of fibrin and exudate. Continued exudation and inflammation cause increased tissue pressures due to edema. The inelastic nature of bone complicates and exacerbates the increases in tissue pressure, resulting in greatly decreased blood flow to the affected area, ischemia, and necrosis of bone and cartilage. This mechanism probably explains the findings of dry gangrene and coagulative necrosis in bacterial osteomyelitis. Extensive osteonecrosis interferes with the penetration of antibiotics and frequently complicates the treatment of bacterial osteomyelitis.
Contributor: Department of Veterinary Pathology, Faculty of Veterinary Medicine, University College Dublin, Shelbourne Road, Ballsbridge, Dublin 4, Ireland.
1. Firth EC, Kersjes AW, Dik KJ, Hagens FM: Haematogenous osteomyelitis in cattle. Vet Record 120:148-152, 1987.
2. Morgan JP, Van De Watering CC, Kersjes AW: Salmonella bone infection in colts and calves: Its radiographic diagnosis. J Amer Vet Radiol Soc 15:66-76, 1974.
3. O'Connor PJ, Rogers PAM, Collins JD, McErlean BA: On the association between salmonellosis and the occurrence of osteomyelitis and terminal dry gangrene in calves. Vet Record 91:459-460, 1972.
4. Palmer N: Bones and joints. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th edition, vol. 1, pp. 101-109, Academic Press, San Diego, CA, 1993.
5. Bullough PG: Bone and joint infection. In: Bullough and Vigorita's Orthopaedic Pathology, 3rd edition, pp. 107-121, Mosby-Wolfe, London, England, 1997.

Case II - 980264-5 (AFIP 2641219)

Signalment: One-year-old, male, European cat.
History: The cat was referred to the Department of Medicine at the Ecole Nationale Vétérinaire d'Alfort because it had developed numerous firm growths over the right and left scapulae, the right ribs, and the pelvis beginning at six months of age. The animal was anorectic and thin, and it had locomotion problems. A radiograph confirmed the clinical examination, and after several days, the animal developed a low and irregular femoral pulse. Vessel compression was excluded as the cause of the pulse irregularities, and the cat was electively euthanized.
Gross Pathology: At necropsy, many masses were observed. On the left and right scapulae, we observed three masses of almost 8 cm in diameter with irregular margins. The masses were heterogeneous in color, being white on the periphery and red-gray in the middle. The masses were coalescing and hard. On the right ribs, we observed only one mass, which measured 8 cm in diameter and involved the three first ribs of the right hemithorax. We could see the remnant of one rib in the center of the mass. The other aspects of this mass were similar to the first one. On the pelvis, we noted a single mass on the right ileum measuring 4 cm in diameter that compressed the pelvic vessels. This mass was heterogeneous in color with a hemorrhagic center.
Case 20-2. Gross images. This composite photo illustrates the external, surface, and cross-sectional views of the multinodular growth of cartilage-covered bone typical of this disease which, in this cat, affected the ribs, both scapulae, and pelvis.
Laboratory Results: None.
Contributor's Diagnosis and Comments: Feline osteochondromatosis.
Microscopic examination revealed a tumor-like mesenchymal proliferation consisting of chondrocytes forming a rim of hyaline cartilage surrounding spongy bone. The cortex of each growth was irregular, and the spongy bone had trabeculae supporting fatty marrow. Remnants of cartilage persisted in the osseous mass. The histological picture suggests a peripheral chondromatous proliferation followed by imperfect central endochondral ossification.
Osteochondroma is an abnormal cartilaginous growth with endochondral ossification. The term osteochondromatosis indicates that there are multiple lesions. This disease is reported in dogs, cats and horses. There is no sex or breed predilection, but it is consistently observed in adult animals. According to Pool (6), feline osteochondromas usually have a biphasic pattern, with a cover of cartilage giving rise to a bony base by endochondral ossification.
In man, the origin of osteochondromatosis is probably hereditary or congenital. Particles resembling feline leukemia virus and transmissible feline sarcoma virus have often been detected in the lesions found in cats with osteochondromatosis; their etiologic significance remains unclear.
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Case 20-2. Bone. Irregular endochondral bone formation occuring deep within cancellous bone. Dark cells in the lower right are osteoclasts.
AFIP Diagnosis: Scapula: Osteochondromatosis, Domestic Shorthair, feline.
Conference Note: Osteochondromas are cartilage-capped, partially ossified protuberances or exostoses that are usually multicentric, but may occur singly. The condition occurs in cats, horses, dogs, and humans. The disease in dogs and horses differs from that in cats in clinical presentation, skeletal distribution and proposed cause. The condition in dogs, horses, and humans is inherited as an autosomal dominant trait. Tumors occur on the long bones of young animals, are thought to arise from dysplastic or ectopic growth plates, often become progressively larger as the animal matures, and cease to grow at skeletal maturity. Tumors do not occur on bones of intramembranous origin, such as the skull or scapula. Usually, the lesions in dogs and horses are of little clinical significance unless there is mechanical interference, although malignant transformation to chondrosarcoma or osteosarcoma may occur in long standing lesions of adult animals.
In contrast to dogs and horses, tumors in cats arise after skeletal maturity, are distributed randomly throughout the skeletal system including intramembranous bone (e.g. the skull), demonstrate progressive growth similar to a neoplasm, and proliferating cells located at the surface of lesions may contain viral particles that resemble feline leukemia virus and feline sarcoma virus. The tumors are thought to arise from periosteal mesenchymal cells in lesions of intramembranous bone. Malignant transformation of benign lesions and appearance of new lesions may occur in cats, heralding a grave prognosis.
Histologically, osteochondromas of dogs and horses recapitulate the zones of development found in the normal epiphyseal growth plate. Microscopic examination reveals a variably thick cartilage cap with scattered areas of mineralization covered by a thin layer of fibrous periosteum. The cap of hyaline cartilage is bordered at the base by regularly arranged cancellous bone which is produced by orderly endochondral ossification in actively growing lesions. Trabeculae of cancellous bone are separated by marrow elements. In old lesions in adult animals, extensive endochondral ossification may result in little or no cartilage remaining at the apical surface. Feline osteochondromatosis differs microscopically from the inherited condition in young dogs and horses in that the cartilage is irregular, chondrocytes are haphazardly arranged, endochondral ossification is less orderly, and the hyperplastic periosteum may directly form bone.
Contributor: Ecole Vétérinaire d'Alfort, Laboratoire d'Anatomie Pathologique
7, Avenue du Général de Gaulle, 94704 Maisons Alfort, France.

1. Newell MS, Roberts RE, Baskett A: Presumptive tenosynovial osteochondromatosis in a horse. Vet Radio Ultras 37:112-115, 1996.
2. Pool RR, Carrig CB: Multiple cartilaginous exostoses in a cat. Vet Pathol 9:350-359, 1972.
3. Magnussen KL: What is your diagnosis? (Osteochondromatosis in a cat). J Amer Vet Med Assoc 210:1733-1734, 1997.
4. Hubler M, Johnson KA, Burling RT, Francis DF, Ratcliffe CC: Lesions resembling osteochondromatosis in two cats. J Small Anim Pract 27:181-187, 1986.
5. Doige CE: Multiples osteochondromas with evidence of malignant transformation in a cat. Vet Pathol 24:457-459, 1987.
6. Pool RR: Tumors of bone and cartilage. In: Tumors in domestic Animals, Moulton JE, ed., 3rd ed., pp. 168-172, Univer. of California Press, Berkeley, 1990.
7. Brown RJ, Trevethan WP, Henry VL: Multiple osteochondroma in a Siamese cat. J Amer Vet Med Assoc 160:433-435, 1972.
8. Jones TC, Hunt RD, King NW: Skeletal system. In: Veterinary Pathology, 6th ed., pp. 841-842, Williams and Wilkins, Baltimore, 1997.
9. Palmer N: Diseases of bones. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 1, pp. 129-130, Academic Press, San Diego, CA, 1993.
10. Bullough PG: Cartilage-forming tumors and tumor-like conditions. In: Bullough & Vigorita's Orthopaedic Pathology, 3rd ed., pp. 107-121, Mosby-Wolfe, London, 1997.
11. Slayter MV, et al.: Bone and Joint Tumors. In: World Health Organization International Histological Classification of Tumors in Domestic Animals, 2nd Series, vol. 1, pp. 6, 22-24, Armed Forces Institute of Pathology, Washington DC, 1994.

Case III - A44016 (AFIP 2638315)

Signalment: 18-month-old, female, ostrich (Struthio camelus).
History: The ostrich was presented for slaughter at a Texas slaughter facility. No antemortem abnormalities were noted at the slaughter facility. No other clinical history is available.
Gross Pathology: Per the submitting inspection veterinarian: "suspicious mass, 15 cm long by 8-9 cm wide, in the right pelvic area arising from the right iliac wing; mass appeared balloon-shaped with bony deposition on the caudal end, and a large soft tissue growth with a thin bony covering on the cranial end. The mass was attached to the ventral surface of the vertebral column in three areas by firm bony attachments." The frozen tissue, submitted on request, had central white to tan somewhat fibrous soft tissue with irregular lightly reddened areas dispersed throughout. There was a thin, white, irregular bony capsule (1-3 mm thick).
Case 20-3. Gross Image
Laboratory Results: Several immunohistochemical studies were performed on sections of the mass.
1. Muscle specific actin and vimentin antibodies did not work on ostrich control muscle.
2. Smooth muscle actin was negative in ostrich tumor tissue, except for smooth muscle around scattered vessels.
3. Cytokeratin, neuron specific enolase, and S-100 protein were negative in tumor tissue.
Contributor's Diagnosis and Comments: Giant cell reparative granuloma of bone (iliac and subvertebral, young ostrich, female).
Iliac, subvertebral mass: There is a dense fibrous capsule of some section borders which contains individualized and flattened bone multifocally. There is abundant, moderately cellular stroma with flattened to plump spindle cells and abundant mature collagen. Multifocally, there is a lightly basophilic matrix that stains with alcian blue for mucopolysaccharide. Scattered foci of more dense homogenous eosinophilic stroma with embedded nuclei are noted. There are discrete islands of multinucleate giant cells that have approximately 6 to up to 30 nuclei, and abundant eosinophilic cytoplasm. These cells surround and are occasionally found within small non-muscular vessels. The cytoplasm occasionally contains iron positive hemosiderin material, or has small cleft-like vacuoles. These latter cells often have light blue staining of the cytoplasm with alcian blue. The vessels are variably congested, with some small foci of hemorrhage and a few hemosiderophages. Trichrome staining reveals abundant collagen throughout, positive staining in more homogenous stromal areas, and occasionally centrally around multinucleate giant cells.
The lesion, as grossly described and as examined histologically, is most consistent with a giant cell reparative granuloma of bone. The islands of giant cells associated with and within vessels with an abundant stroma and collagenous and mucopolysaccharide rich matrix differentiate this from a giant cell tumor. In giant cell tumor, the giant cells are more dispersed, there is less matrix, and the stroma is usually mononuclear in type with some spindle cells and significant mitotic activity. The difficulty of finding antibodies which work in this species, and the inavailability of some specialized antibodies, precluded any further immunohistochemical staining of the lesion at this time. Further examination of this lesion is to be performed for publication of this lesion in an ostrich (unreported as to my knowledge).
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Case 20-3. Tumor. Normal bone is replaced by streams & bundles of spindle cells and multifocal clusters of multinucleate giant cells.
AFIP Diagnosis: Bone (right iliac wing, per contributor): Fibroma, with numerous osteoclast-like giant cells, ostrich (Struthio camelus ), avian.
Conference Note: Conference participants were divided on the interpretation of the microscopic findings and the nature of the lesion in the bone of this ostrich. Like the contributor, some participants interpreted the mass as a reactive fibrous lesion with scattered clusters of multinucleated giant cells and spicules of mineralized lamellar bone. Other attendees identified a neoplasm of fibrous tissue composed of spindled cells arranged in haphazard streams and bundles with aggregates of large multinucleate giant cells within a dense collagenous matrix. Multinucleate cells contain up to 30 nuclei and have vacuolated cytoplasm. Rare mitoses were noted within the spindled cell population. At the natural margins of some sections, the spindled cells extended through and multifocally effaced the preexistent cortex. In some areas, small amounts of hemorrhage and hemosiderin are found in association with the giant cells. Inflammatory cells are absent.
Members of the Department of Orthopedic Pathology interpreted the lesion as a neoplasm within the fibroma "family." The growth characteristics of the tumor, with an expanding shell of bone and low mitotic activity, suggest an indolent lesion. Scattered aggregates of osteoclast-like giant cells are found in some human fibromas, but they are not as numerous as in this case. The orthopedic pathologists considered the giant cells an intrinsic component of the neoplastic process rather than a secondary reactive phenomenon. Differential diagnosis for similar lesions in humans would include osteoclastic fibroma and variant fibromyxoma (both of which are oral, head, or neck lesions), and an unusual desmoplastic fibroma.
Human giant cell reparative granulomas (GCRG) represent reactive, non-neoplastic lesions thought to occur as the result of intraosseous or subperiosteal hemorrhage. While the lesion in this ostrich does share some microscopic features with human GCRG, such as the presence of hemorrhage and hemosiderin within nodular clusters of multinucleated giant cells in abundant fibroblastic tissue, GCRG does not extend through the cortex of the affected bone. Additionally, there is no zonal orientation of the lesion in the ostrich that would suggest a reactive process.
Contributor: United States Dept. of Agriculture, FSIS, OPHS, Pathology Russell Research Center, College Station Road, P.O. Box 6085, Athens, Georgia 30604.
1. Fechner RE, Mills SE: Tumors of the bones and joints. In: Atlas of tumor pathology, 3rd series, Fascicle 8, pp.173-186, Armed Forces Institute of Pathology, Washington DC, 1993.
2 . Trigo FJ, Leathers CW, Brobst DF: A comparison of the canine giant cell tumor and giant cell reparative granuloma of bone. Vet Pathol 20:215-222, 1983.
3. Ung F, Kasey K, Keith D, McKenna MJ: Giant cell reparative granuloma of the temporal bone: Case report and review of the literature. Otolaryngol Head Neck Surg 118:525-529, 1998.
4. Kenan S, Lewis MM, Abdelwahab IF, Klein M: Subperiosteal giant cell granuloma. J Bone Joint Surg 76:810-813, 1994.
5. Bullough PG: Benign non-matrix producing bone tumors. In: Bullough & Vigorita's Orthopaedic Pathology, 3rd ed., pp. 405 , Mosby-Wolfe, London, 1997.

Case IV - 98-1975 (AFIP 2641612)

Signalment: Canine, German Shepherd Dog, male, seven months of age.
History: The dog had lameness of the right foreleg of two weeks duration. A firm to hard, 4 x 6 cm mass was palpated and removed. The mass appeared to be adjacent to a cervical vertebral process on the right side. Two days post surgery, the dog was no longer lame.
Gross Pathology and Laboratory Results: None described.
Contributor's Diagnosis and Comments: Fascia adjacent to cervical vertebrae: Calcinosis circumscripta (tumoral calcinosis), chronic, with chondro-osseous metaplasia.
The lesions of tumoral calcinosis and calcinosis circumscripta have been reported in dogs, horses, monkeys, man, and recently also in cattle and cats. Sites of occurrence in the dog include cutaneous or periarticular locations in footpads, bony prominences of limbs, cervical vertebral region, tongue, cheek, and pinna. Cervical juxtavertebral lesions have occasionally been associated with compression of the spinal cord and ataxia. An intramedullary case and a lesion involving synovial tissue have been reported. Large dogs account for about 90% of canine tumoral calcinosis cases, with German shepherd dog being most commonly affected.
With rare exceptions, tumoral calcinosis lesions appear grossly as hard, spherical, nonpainful, subcutaneous or periarticular swellings which are often large and encapsulated, and which usually exude a granular, gritty, white, paste-like material on cut surface. Early lesions appear histologically as multifocal subcutaneous accumulations of amorphous lightly basophilic material which is periodic acid-Schiff positive, stains brown with acid orcein Giemsa, and can be shown by von Kossa stain to contain calcium. Within the basophilic material, hemorrhage is occasionally seen, and fractures or fissures are seen commonly, but inflammatory and fibroplastic responses are negligible. Intermediate lesions are more likely to have fully mineralized areas within the amorphous material, which is surrounded by mild to moderate granulomatous inflammation and fibroplasia. Late lesions are associated with marked granulomatous inflammation and fibroplasia, with macrophages, multinucleate giant cells, lymphocytes, and a few plasma cells and neutrophils. Inflammatory cells are arranged around mineralized centers in palisading granuloma fashion. Although these centers are generally acellular, they do incorporate some macrophages, fibroblasts, and histiocytic giant cells containing phagocytized mineral. Granulomatous areas are separated by thick connective tissue septa. Cartilaginous or osseous metaplasia is seen in 56.9% of late lesions. Very old lesions are multilocular, with thick connective tissue trabeculae, and are characterized by completely mineralized areas without much active inflammation.
Several possible etiologies for tumoral calcinosis have been proposed. These include: repetitive trauma with dystrophic mineralization; cystic dilation, hyperplasia, and mineralization of apocrine glands; collagen vascular disease; and local or systemic metabolic disorders. In humans, normophosphatemic periarticular tumoral calcinosis is strongly associated with previous trauma. In dogs, renal failure is associated with footpad lesions. In hyperphosphatemic tumoral calcinosis patients without renal insufficiency, there may be an inherited proximal tubular defect that causes excessive tubular reabsorption of phosphorus.
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Case 20-4. Cervical vertebra. Multifocally areas of endochondral bone partly replaced by granular mineralized debris are surounded by macrophages, foreign body giant cells, and fibrous connective tissue.
AFIP Diagnosis: Cervical vertebral fascia (per contributor): Granulomas, calcareous (calcinosis circumscripta), with fibrosis and chondro-osseous metaplasia, German Shepherd Dog, canine.
Conference Note: In most cases, canine calcinosis circumscripta probably represents dystrophic calcification, since it occurs in sites that are often affected by trauma or in which trauma is known to have occurred, such as ears that have been cropped. The reason young, large breed dogs are predisposed is undetermined, but their active calcium and phosphorus metabolism may be involved.
In humans, tumoral calcinosis is reported most frequently in individuals of African descent, especially during the first two decades of life. The disease presents as large, firm, irregularly shaped, mineralized masses, usually located in the vicinity of large joints such as the hip, lateral shoulder, and posterior elbow. The lesions are usually asymptomatic and only rarely cause discomfort. Occasionally, ulceration of the overlying skin with secondary bacterial infection and fistula formation occurs.
Contributor: Department of Veterinary Biosciences, The Ohio State University, 1925 Coffey Road, Columbus, OH 43210.

1. Lewis DG, Kelly DF: Calcinosis circumscripta in dogs as a cause of spinal ataxia. J Small Anim Pract 31:36-38, 1990.
2. Marks SL, Bellah JR, Wells M: Resolution of quadriparesis caused by cervical tumoral calcinosis in a dog. J Amer Anim Hosp Assoc 27:72-76, 1991.
3. Scott DW, Buerger RG: Idiopathic calcinosis circumscripta in the dog: A
retrospective analysis of 130 cases. J Amer Anim Hosp Assoc 24:651-658, 1988.
4. Smack DP, Norton SA, Fitzpatrick JE: Proposal for a pathogenesis-based classification of tumoral calcinosis. Intern J Dermatol 35:265-271, 1996.
5. Jones TC, Hunt RD, King NW: The skin and its appendages. In: Veterinary Pathology, 6th ed., pp. 849-850, Williams and Wilkins, Baltimore, MD, 1997.
Conference Coordinator:
Ed Stevens, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
* The American Veterinary Medical Association and the American College of Veterinary Pathologists are co-sponsors of the Registry of Veterinary Pathology. The C.L. Davis Foundation also provides substantial support for the Registry
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