Definitions

Hypertrophic osteopathy is a diffuse periosteal reaction resulting in new bone formation around the metacarpal, metatarsal, and long bones. Synonyms include pulmonary osteoarthropathy, hypertrophic pulmonary osteoarthropathy, and hypertrophic pulmonary osteopathy.

General Considerations and Clinically Relevant Pathophysiology

Hypertrophic osteopathy can affect all four limbs. It can be a paraneoplastic syndrome (e.g., primary and metastatic lung tumors, esophageal carcinoma, rhabdomyosarcoma of the bladder, anal sac adenocarcinoma, renal transitional cell carcinoma, nephroblastoma), or it may be associated with other diseases (e.g., granulomatous lesions, chronic megaesophagus, patent ductus arteriosus, bacterial endocarditis, heartworm disease) (Hammond et al, 2009). The precise pathophysiology of this disease is unknown. Alterations in pulmonary function have been suggested to increase peripheral blood flow, resulting in connective tissue congestion. The increased peripheral blood flow is thought to be neurally mediated. The periosteum responds by forming new bone on the cortical surfaces of the metacarpal, metatarsal, and long bones. This new bone may be diffuse or nodular. Histologically, the affected area is made of bands of new cortical bone that contain small, fibrous marrow spaces.

Diagnosis

Differential Diagnosis

This condition should be differentiated from bone neoplasia.

Medical Management

Treatment is aimed at the underlying disease process. Remission of periosteal proliferation may occur after resolution or resection of the primary lesion.

Prognosis

The prognosis depends on the possibility for complete resolution of the underlying disease process. If the primary disease can be resolved, the secondary hypertrophic osteopathy often resolves. Although clinical signs often disappear within 1 to 2 weeks after treatment, bone lesions may take months to remodel.

Reference

Definitions

Panosteitis is a disease of young dogs that causes lameness, bone pain, endosteal bone production, and occasionally subperiosteal bone production. Synonyms include enostosis, eosinophilic panosteitis, juvenile osteomyelitis, and osteomyelitis of young German Shepherds.

General Considerations and Clinically Relevant Pathophysiology

Panosteitis is an idiopathic entity causing endosteal and periosteal new bone formation. Osseous compartment syndrome due to a protein-rich, high-calorie diet has been proposed as a potential cause. Excessive protein may cause intraosseous edema and secondary increased medullary pressure and ischemia. Although some periosteal new bone is often evident, the predominant change is endosteal bone formation as the marrow is invaded by bone trabeculae. The marrow remains highly cellular with varying degrees of fibrosis, and no evidence of chronic inflammation, acute infection, or malignancy is noted.

Diagnosis

Differential Diagnosis

Panosteitis must be differentiated from other orthopedic diseases of large, immature dogs (e.g., osteochondritis dissecans, fragmented coronoid process, ununited anconeal process in forelimbs; hip dysplasia, osteochondritis of rear limbs). When radiographic evidence of panosteitis and other orthopedic diseases is present concurrently, panosteitis usually is assumed to be causing the acute clinical signs.

Medical Treatment

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.

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

Differential Diagnosis

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

Medical Management

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.

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.

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

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.

Reference

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.

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.

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