The disease is self-limiting, so treatment consists of controlling pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) (see Table 34-4 on p. 1221) usually are administered during acute episodes of lameness. Exercise restriction is recommended when the animal is lame. Owners should be warned of the likelihood of recurrence, but the long-term prognosis is excellent for complete recovery.

Surgical Treatment

Surgical treatment of panosteitis is not indicated.

Prognosis

The disease is self-limiting, and most animals eventually have normal function of affected limbs without evidence of pain. However, the disease may continue to affect different limbs, causing pain and lameness until the dog reaches maturity. Clinical signs rarely persist after maturity.

Note • Advise owners that panosteitis may recur, but that it usually resolves by the time the dog is 2 years of age.

Craniomandibular Osteopathy

Definitions

Craniomandibular osteopathy (mandibular periostitis, lion’s jaw) is a proliferative bone disease of immature dogs involving the occipital bones, tympanic bullae, and mandibular rami.

General Considerations and Clinically Relevant Pathophysiology

The cause of craniomandibular osteopathy is unknown. It is most often recognized in West Highland White Terriers, Cairn Terriers, and Scottish Terriers. A genetic predisposition is suspected in many breeds; in West Highland White Terriers, it is thought to have an autosomal recessive inheritance pattern. A similar syndrome (calvarial hyperostotic syndrome) has been reported in Bullmastiffs (McConnell et al, 2006). Craniomandibular osteopathy has been associated with canine leukocyte adhesion deficiency in Irish Setters. A link to canine distemper virus has been postulated but is not supported by epidemiologic studies.

Proliferation of new, coarse, trabecular bone occurs adjacent to the mandibular rami, occipital bones, and tympanic bullae in affected animals. This new bone formation causes irregular enlargement of mandibles and tympanic bullae. Existing lamellar bone is resorbed by osteoclasis and is replaced with new bone that expands beyond the periosteal borders. Osteoclastic destruction of the original lamellar bone is accompanied by invasion of inflammatory cells (i.e., neutrophils, lymphocytes, and plasma cells). Normal bone marrow is lost as it is replaced with a vascular fibrous stroma. This proliferative stage of disease occurs when the dog is approximately 5 to 7 months old and is accompanied by intermittent fever, discomfort when eating, and pain when the mouth is forced open. Owners should be warned that multiple relapses may occur; however, bone proliferation decreases as dogs reach maturity and physes close.

Diagnosis

Clinical Presentation

Signalment.

Although young West Highland White Terriers, Cairn Terriers, and Scottish Terriers are most commonly affected, this disease has been sporadically reported in other breeds. Clinical signs are usually first noted when the dog is 3 to 8 months of age. Males and females are equally affected. No seasonal distribution has been noted. Calvarial hyperostosis syndrome has typically been considered to be a disease of Bullmastiffs.

History.

Owners often note that the animal is reluctant to eat, drools, and has trouble chewing food. Pain is often evident when the mouth is opened.

Physical Examination Findings

Affected dogs have bilaterally enlarged mandibles and tympanic bullae. In severe cases, fusion of these structures may occur, preventing the jaws from being fully opened. Pain on opening of the mouth and intermittent fever (body temperature reading of up to 104° F for 3 to 4 days) may be observed.

Diagnostic Imaging

Skull radiographs reveal increased irregular bone density of the caudal mandibles (84% of cases), including tympanic bullae (51% of cases) (Fig. 36-3). Sometimes lesions are confined to the mandibles (33% of cases), and occasionally they are confined to the base of the skull (13% of cases). The calvarium may be thickened. As dogs reach maturity, the edges of the new bone become smooth and affected areas shrink.

FIG 36-3 Lateral radiograph of the skull of a dog with craniomandibular osteopathy. Note the areas of periosteal proliferation.

Laboratory Findings

Specific laboratory abnormalities are not seen. Blood cultures are negative.

Differential Diagnosis

Craniomandibular osteopathy must be differentiated from infection (i.e., abscesses or osteomyelitis) and primary bone neoplasia.

Analgesics (see Table 34-4 on p. 1221) should be given to control pain until the animal reaches maturity. Severely debilitated animals that cannot open their mouths enough to eat solid foods require oral fluid nourishment or a feeding tube. Although antibiotics and corticosteroids are often administered during febrile episodes, they will not alter disease progression.

Surgical Treatment

Surgical therapy is not indicated. Surgical resection of bone bridging the mandible and tympanic bullae in dogs with severely restricted jaw motion has been unsuccessful; however, rostral mandibulectomy may allow the dog to lap gruel. Affected dogs should not be used for breeding purposes.

Prognosis

The prognosis is guarded until the extent of bone production is known (i.e., at maturity). Excessive bone production, leading to fusion of mandibular and tympanic bullae, can restrict mandibular motion sufficiently to prevent dogs from eating. These animals are often euthanized.

Note • Warn owners that multiple relapses may occur until maturity.

Hypertrophic Osteodystrophy

Definitions

Hypertrophic osteodystrophy is a disease that causes disruption of metaphyseal trabeculae in long bones of young, rapidly growing dogs. Synonyms include skeletal scurvy, canine scurvy, Moeller-Barlow disease, osteodystrophy types I and II, metaphyseal osteopathy, and metaphyseal dysplasia.

General Considerations and Clinically Relevant Pathophysiology

The cause of hypertrophic osteodystrophy is unknown. Proposed causative factors include vitamin C deficiency, oversupplementation of dietary calcium, and infectious organisms. A link to canine distemper virus has been postulated but is not supported by epidemiologic studies. Experimentally, vaccination protocols have been associated with the development of hypertrophic osteodystrophy in Weimaraner puppies; however, no specific vaccine has been identified (Crumlish et al, 2006). The pathogenesis is obscure, but an apparent disturbance of metaphyseal blood supply leads to changes in the physis and adjacent metaphyseal bone, causing delayed ossification of the physeal hypertrophic zone. The acute phase lasts about 7 to 10 days. Affected animals show signs ranging from mild lameness to anorexia, pyrexia, lethargy, severe lameness, refusal to rise, and generalized weight loss. Clinical signs may wax and wane.

Note • Affected animals may be very ill, requiring intense supportive care.

Grossly the metaphyseal regions of long bones are widened with perimetaphyseal soft tissue swelling. A line of separation of metaphyseal trabeculae is present parallel to the growth plate. Histologic microfractures of trabeculae are evident and are surrounded by inflammatory cells and necrosis. Failure of bone deposition on the calcified cartilage lattice of metaphyseal bone is evident.

Diagnosis

Clinical Presentation

Signalment.

This disease affects young, rapidly growing, large breed dogs, and males are affected more often than females. Clinical signs are usually first noted at 3 to 4 months of age; however, they may occur as early as 2 months. Relapses may occur as late as 8 months of age. The highest incidence is in the fall. Weimaraners may be at increased risk.

History.

An acute onset of lameness is often reported, and puppies may be so severely affected that they refuse to walk. Inappetence and lethargy are commonly reported by owners. A history of recent diarrhea may precede the onset of lameness.

Physical Examination Findings

Findings on physical examination range from mild lameness to severe lameness affecting all four limbs. More severely affected animals are often unable to stand or walk. Long bone metaphyses are swollen, warm, and painful on palpation. Swelling is often present in all four limbs; however, forelimb swelling may be more obvious, especially in distal radial metaphyses. Severely affected dogs may be depressed, anorexic, and pyrexic (body temperature of up to 106° F).

Diagnostic Imaging

Radiographs of affected long bones reveal an irregular radiolucent zone in the metaphysis, parallel and proximal to the physis. This gives the appearance of a double physeal line. Metaphyseal flaring with increased bone opacity occurs because of periosteal proliferation in later stages of the disease. This reaction subsides with time but may leave a permanently widened metaphysis (Fig. 36-4).

FIG 36-4 Radiograph of the distal radius and ulna of a dog with hypertrophic osteodystrophy. A parallel lucency proximal and adjacent to the physis is typical of this disease.

Laboratory Findings

Laboratory abnormalities are not usually found. Hypocalcemia has been noted in a few affected dogs, but its significance is unknown. Bacteremia has rarely been reported in association with hypertrophic osteodystrophy.

Differential Diagnosis

This condition should be differentiated from septic arthritis, septic physitis, and panosteitis.

Medical Management

Analgesics should be administered to control pain (see Table 34-4 on p. 1221). Occasionally, severely debilitated animals require fluid support. Corticosteroids, antibiotics, and vitamin C have been administered but have not proved effective in shortening the course or severity of the disease. Bacteremia should be ruled out before corticosteroids are administered.

Prognosis

Most animals recover fully within 7 to 10 days of the onset of clinical signs; however, multiple relapses may occur. Occasionally, severe debilitation or multiple, severe relapses cause owners to request that affected animals be euthanized. Interference with normal physeal development may cause permanent deformity of long bones.

Note • Warn owners that multiple relapses may occur and that deformity of the long bones may occur.

Reference

Crumlish, PT, Sweeney, T, Jones, B, et al. Hypertrophic osteodystrophy in the Weimaraner dog: lack of association between DQA1 alleles of the canine MHC and hypertrophic osteodystrophy. Vet J. 2006;171:308.

Bone Neoplasia

Definitions

Primary bone neoplasia arises from cells located within the bone structure. Metastatic bone tumors are those that spread to bone from other primary locations. Primary and metastatic tumors may occur in the appendicular skeleton (i.e., long bones) or the axial skeleton (skull, vertebrae, ribs, and pelvis).

General Considerations and Clinically Relevant Pathophysiology

Primary bone tumors of dogs include osteosarcoma, chondrosarcoma, fibrosarcoma, hemangiosarcoma, giant cell tumor, liposarcoma, periosteal osteosarcoma, periosteal fibrosarcoma, parosteal osteosarcoma, osteoma, multilobular osteoma, multilobular chondroma, osteochondroma, and chondroma. Primary tumors of the appendicular skeleton of dogs most commonly arise in the distal radial metaphysis, proximal humerus, proximal or distal femur, and proximal or distal tibia. Benign bone tumors (e.g., osteoma, ossifying fibroma, multilobular osteomas and chondromas, osteochondromas, enchondromas, chondromas) are generally slow growing. Depending on tumor accessibility, complete surgical excision of benign bone tumors is usually curative.

Osteosarcoma is the most common primary bone neoplasm in dogs, accounting for approximately 85% of skeletal malignancies; 75% of osteosarcomas originate in the appendicular skeleton (Tables 36-1 and 36-2). The front limbs are affected twice as often as the rear limbs. In dogs less than 15 kg, 60% of tumors originate in the axial skeleton. (Withrow and Vail, 2007). Primary osteosarcoma of extraskeletal tissues is rare but has been reported (mammary, subcutaneous, spleen) (Withrow and Vail, 2007). A genetic cause of osteosarcoma appears likely based on experimental and clinical studies (Withrow and Vail, 2007). Osteosarcoma has been associated with fractures and metallic implants and may also occur within radiation fields following radiation treatment of soft tissue sarcomas.

TABLE 36-1

Malignant Bone Neoplasia in Dogs

TABLE 36-2

Malignant Bone Neoplasia in Cats

Osteosarcoma is locally aggressive, causing bone lysis and/or production. Metastasis is common and usually occurs early in the course of disease. Although fewer than 15% of affected dogs have radiographically detectable thoracic metastases at presentation, 90% die or are euthanized within 1 year of diagnosis because of complications associated with pulmonary metastasis. Improved chances for survival are possible with amputation or limb-sparing procedures combined with chemotherapy.

Note • Osteosarcomas arise most commonly in the metaphyses of the proximal humerus, distal radius, and distal femur.

Osteosarcoma is the most common tumor of the axial skeleton. Of 116 axial osteosarcomas evaluated, the most common sites of occurrence were the mandible (27%), maxilla (22%), spine (15%), cranium (14%), ribs (10%), nasal cavity and paranasal sinuses (9%), and pelvis (6%) (Withrow and Vail, 2007). Because osteosarcoma is the most commonly diagnosed bone tumor, it is used as the model for evaluation, diagnosis, treatment, and prognosis of bone tumors in this section. Although the work-up needed to diagnose neoplasia is similar for all bone tumors, treatment and prognosis vary depending on tumor type (see Tables 36-1 and 36-2).

Histologically, osteosarcoma is composed of anaplastic mesenchymal cells that produce osteoid. Histologic subgroups include osteoblastic, fibroblastic, chondroblastic, osteoclastic, poorly differentiated, and telangiectatic osteosarcoma. An inflammatory component is often present in fracture-associated sarcoma (i.e., a sarcoma that arises in the diaphysis of a long bone at the site of a previous fracture), reflecting altered healing patterns and chronic inflammation associated with these tumors.

Osteosarcoma accounts for 70% to 80% of primary bone tumors in cats. Osteosarcoma occurs more commonly in the hindlimbs of cats and may have a lower rate of metastasis than in dogs. Cats rarely have evidence of metastasis at presentation (Withrow and Vail, 2007). Multiple cartilaginous exostosis (MCE) is a histologically benign disease of cats that occurs after skeletal maturity, in contrast to dogs, in which the disease occurs before growth plate closure. MCE is likely of viral origin in cats, most of which test positive for feline leukemia virus (FeLV) antigenemia.

Diagnosis

Clinical Presentation

Signalment.

Large and giant breed dogs have the greatest incidence of appendicular bone neoplasia. The median age of dogs with osteosarcoma is 7 years. A small early peak is seen in dogs 18 to 24 months of age. Large size is a greater determinant of risk than breed, although Greyhounds, Rottweilers, and Great Danes have been shown to be at increased risk (Rosenberger et al, 2007). Males may be slightly more commonly affected than females (1.1 to 1.5 : 1). Primary bone tumors of the axial skeleton are more common than appendicular tumors in small breed dogs. The median age of affected animals is 8.7 years. The mean age of osteosarcoma in cats is 8 to 10 years. No apparent breed or sex predilection has been identified in either species.

History.

Dogs with primary bone neoplasia affecting the appendicular skeleton are usually examined for lameness and/or localized limb swelling. Pathologic fracture may cause acute, severe lameness. Dogs with primary bone tumors of the axial skeleton usually have pain, reluctance to walk, and visible swelling. Clinical signs may be acute or chronic and progressive. Signs of axial bone neoplasia depend on the location. Neoplasia of the skull may cause difficulty eating and visible swelling. Neoplasia of the spine may lead to pain or neurologic deficits.

Primary bone neoplasia in cats may cause deformity and lameness. MCE may result in pain and rapidly progressive swelling. Common sites for MCE include the spine, scapula, and mandible.

Physical Examination Findings

Dogs with appendicular tumors are often lame. The limb may be enlarged and firm. Systemic signs of illness (e.g., fever, anorexia, weight loss) are uncommon in acute stages of disease. Tumors of the axial skeleton are often palpable as firm swellings. Tumors affecting the vertebral column may cause acute signs of lameness or paralysis. Respiratory abnormalities associated with pulmonary metastasis are rare until late in the disease. Cats with primary appendicular bone neoplasia exhibit lameness and painful firm swelling. Cats with axial neoplasia may exhibit difficulty eating, neurologic deficits, and firm painful swelling.

Note • Lameness is often the first sign of appendicular bone tumors.

Diagnostic Imaging

Radiographs of affected bones and the thorax should be evaluated. Radiographic signs of osteosarcoma include cortical and trabecular bone lysis, periosteal bone proliferation, and soft tissue swelling (Fig. 36-5). Thoracic radiographs should include a dorsoventral or ventrodorsal view and both lateral recumbent views (i.e., right and left lateral views). These radiographs should be carefully evaluated for evidence of tumor metastasis. Alternatively, contrast-enhanced computed tomography (CT) of the thorax can replace survey radiographs; CT is more sensitive than radiography in detecting small metastatic lesions. Although radiographic signs associated with primary bone neoplasia cannot be differentiated from those associated with fungal osteomyelitis, coupling radiographic signs with signalment and history can help determine whether neoplasia should be considered likely. Ultimately, histopathology is necessary for confirmation. If limb-sparing surgery is being considered, magnetic resonance imaging (MRI) should be used to determine the extent of the disease.