Outline of Veterinary Skeletal Pathology

contents Ch 3, p 1 Chapter 3, Page 2 Ch 3, p 3 



Outline of Veterinary Skeletal Pathology

Chapter 3 - Bone, Specific Diseases

D. Pig
1. Cortical Hyperostosis.
a. Incidence. Congenital cortical hyperostosis is an uncommon familial disease in pigs and is considered to have an autosomal recessive mode of inheritance.
b. Clinical features. Pigs are born dead or die soon after birth. Limb involvement may vary, but one or more of the forelimbs are always involved (fig. Ic-22).
c. Pathology.
(1) macroscopic appearance. There is enlargement of the limb due to increased soft tissue and increased periosteal bone beginning at the ossification groove. Enlargement of bone cortices are found in long bones such as the humerus, radius, and tibia (fig. Ic-23); the femur, scapula, and metacarpals are often normal. Muscle atrophy and subcutaneous edema are prominent in the affected limb.
(2) microscopic appearance. Bone lesions are limited to regions of periosteal modeling where a subperiosteal layer of woven bone radiates perpendicularly from the developing concentric lamellae of more normal diaphyseal cortex (fig. Ic-24). Trabeculae within the marrow cavity and the inner cortex appear normal. The excessive bone is deposited on the periosteal surface prior to birth, and longitudinal bone growth and calcification of bone matrix stops soon after the animal is born.

2. Osteochondrosis.
a. Incidence. Osteochondrosis is a common cause of lameness in young adults and older animals. When pigs are under market weight, the incidence and severity of osteochondrosis cannot be related to lameness. Lameness develops when older animals develop complicated lesions in a bone region that is weakened by osteochondrosis.
b. Clinical signs. Animals bear weight with stifle and tarsus extended. The stride is shortened, and the animal bears weight only on the toe. During walking, there is lateral swaying of the hind quarters.
c. Pathology. Lesions are found in the articular cartilage of the medial femoral condyle, the anterior trochlea of the humerus and the lateral aspect of the humeral head (fig. Ic-25). Physeal lesions that appear as disorganization and persistence of the hypertrophic cartilage zone are most common in the distal ulna and the proximal and distal femur (fig. Ic-26). Other changes are similar to those described in chapter 2.

3. Atrophic rhinitis.
a. Incidence. A common worldwide disease of pigs.
b. Clinical signs. There is sneezing, coughing, and nasal discharge as a result of inflammation and atrophy of the nasal turbinates.
c. Pathology. Destruction of the nasal turbinates has been produced following intranasal inoculation of toxins derived from Pasteurella multocida (figs. Ic-27, Ic-28). Mixed infections with Pasteurella multocida, Bordetella bronchiseptica, Haemophilus parasuis have been associated with the condition. Pasteurella toxin stimulates osteoclastic osteolysis and inhibits osteogenesis in turbinates by causing degeneration and death of osteoblasts (fig. Ic-29).

E. Dog
1. Canine chondrodysplasia.
a. Chondrodysplasia of Alaskan Malamutes is a disproportionate short-limbed dwarfism with normal body length that has autosomal recessive inheritance. In addition to abnormal endochondral ossification in which the physeal plate has somewhat of a rachitic appearance (figs. Ic-30, Ic-31), macrocytic hemolytic anemia and delayed sexual maturity also occur.
b. Chondrodysplasia of Scottish Deerhounds has autosomal recessive inheritance and causes exercise intolerance and retarded growth in pups. Kyphosis, limb deformities, and joint laxity gradually develop. The long bones and vertebrae are short, and there is delayed epiphyseal ossification. Chondrodysplastic cartilage is characterized by the presence of Schiff's reagent-positive mucopolysaccharide inclusions (periodic-acid-Schiff reaction).
c. Chondrodysplasia of Norwegian Elkhounds is a disproportionate dwarfism that grossly resembles that seen in Alaskan malamutes. Differences include shortened vertebrae, marked reduction in the depth of proliferative chondrocytes and the presence of intracytoplasmic, alcian-blue positive chondrocyte inclusions.
d. Pseudoachondroplastic dysplasia occurs in miniature poodles and has an autosomal recessive inheritance. Long bones and vertebrae are short with bulbous ends (figs. Ic-32, Ic-33). The maturation sequences in cartilage are delayed, and physeal plates have a stippled appearance when radiographed.
e. Multiple epiphyseal dysplasia is a rare condition of beagle dogs inherited as an autosomal recessive. Stippled mineralization of the physeal plates, similar to that seen in pseudoachondroplastic dysplasia, are characteristic radiographic findings. The stippling gradually disappears, and specific bone abnormalities are not seen in adult dogs.
f. Ocular-skeletal dysplasia is observed in Labrador retrievers. In addition to ocular defects, animals may have shorter than normal forelimbs and ununited or hypoplastic anconeal and coronoid processes. The abnormal gene has recessive effects on the skeleton and incompletely dominant effects on the eye.

2. Fibrous osteodystrophy.
a. Incidence. Renal secondary hyperparathyroidism is common, and the disorder has also been termed renal rickets or rubber-jaw (fig. Ic-34).
b. Cause. In renal failure, inability of the kidney to excrete phosphates causes these ions to accumulate in the blood and leads to lowering of the serum concentration of ionized calcium. The damage to the kidney and inhibitory effects of increased serum phosphate decrease production of the active metabolite of vitamin D with subsequent decrease in the intestinal absorption of calcium. Hypocalcemia causes hyperparathyroidism (fig. Ic-35).
c. Clinical findings. Tests for renal function are indicative of severe renal insufficiency. Hyperparathyroidism in response to hypocalcemia causes marked resorption of bone, and hypocalcemia contributes to defective mineralization of osteoid (osteomalacia). Hyperphosphatemia is present throughout the course of the disease; serum alkaline phosphatase is also elevated. Unlike primary hyperparathyroidism where serum calcium is elevated, serum calcium may be normal or low in renal secondary hyperparathyroidism.
d. Pathology.
(1) macroscopic appearance. In severe cases, the bones of the head show pronounced softening, enlargement, and radiographically detectable rarefaction. The jaws become "rubbery" (fig. Ic-34). All of the parathyroids are grossly enlarged (fig. Ic-35).
(2) microscopic appearance. Lesions are those of fibrous osteodystrophy and osteomalacia with osteoclastic resorption, fibrous replacement, and production of woven bone trabeculae that fail to mineralize properly (See chapter 2). Since osteoid retards osteoclastic activity, osteoclasts are found selectively on mineralized surfaces, and unmineralized bone tends to accumulate. All bones are affected to varying degrees, but the lesions are most striking in the facial bones and the mandible. Metastatic calcification of soft tissues is a regular feature.

3. Panosteitis (eosinophilic panosteitis or enostosis) is a self-limiting condition of unknown cause.
a. Incidence. The disease is uncommon but is seen more frequently in females (ratio, 4:1), and it is more commonly observed in large breed dogs, predominately German shepherd dogs.
b. Clinical findings. The condition primarily affects long bones of young growing animals and presents clinically as an obscure, intermittent lameness affecting one or both forelimbs. The condition usually affects one bone at a time. Pain can be elicited by deep palpation, but there is no swelling or heat at the site. During the initial stages, some animals have fever, but there are few other signs of systemic illness. Lameness may subside and reappear in the same or another limb, and spontaneous recovery invariably follows a course of two to nine months. The ulnae and radii are most commonly affected. The disease appears to cycle back and forth between the forelegs and the hindlegs. In 20% of cases there is eosinophilia of the peripheral blood.
c. Pathology.
(1) macroscopic appearance. The condition is characterized by filling of the medullary cavity with bony trabeculae. In the initial stages, enostosis begins around the vessels at the intervertebral foramen. When the pain is most severe, there is little radiographic evidence of bone abnormality; but within 10 days radiographic density increases in the region of the nutrient foramen (figs. Ic-36, Ic-37, Ic-38). As the condition progresses, the patchy increased radiographic density of the medullary cavity increases greatly in amount. Longitudinal sections of bone show deposition of bone within the diaphyseal marrow. In the early stages this is a spherical focus. As the marrow cavity becomes filled, there may be a well-defined periosteal reaction of new bone.
(2) microscopic appearance. Histologically, the first lesion is seen on the medullary side in the region of the nutrient foramen (fig. Ic-39) where there is fibroplasia, increased vascularity and edema. A small central area of woven bone trabeculae is formed, and newly formed osseous trabeculae spread centrifugally from it within the marrow cavity, eventually stopping at the metaphysis. From the periphery to the center of the more fully developed lesion, there is an increase in bone maturity (fig. Ic-40). As the lesion begins to resolve, the more mature central bone disappears first, and the lesion can resolve completely.

4. Hypertrophic Osteodystrophy, hypertrophic metaphyseal osteodystrophy. Hypertrophic osteodystrophy is an inflammatory bone disease of unknown cause.
a. Incidence. The condition affects young dogs usually of the larger breeds.
b. Clinical features. The spontaneous condition is characterized by clinical signs of pain, lameness, and pyrexia, and by swelling and hyperthermia of the metaphysis of the long bones. It frequently affects multiple bones and may be bilaterally symmetric. The condition is especially prominent in the humerus, radius, and ulna. Radiographically, there is frequently new bone formation in the periosteal region of the metaphysis of long bones, and a transverse line of increased density is observed next to the physeal plate with an adjacent metaphyseal radiolucent zone (figs. Ic-41, Ic-42). The costochondral junctions are enlarged with increased radiodensity.
c. Pathology.
(1) macroscopic appearance. The gross appearance depends upon the stage of the disease; but in earlier stages, sawed sections of long bones have a 1-5 mm wide transverse pale yellow zone with a soft, crumbly consistency on the metaphyseal side of the growth cartilage (fig. Ic-43). In more chronic lesions, the ends of affected bones are markedly enlarged by a thickened periosteum and by deposits of extraperiosteal bone and cartilage (fig. Ic-44). Dogs may recover from the disease and appear normal. In some instances, the bone metaphyses remain malformed, and the animal's limbs are shortened.
(2) microscopic appearance. Early microscopic lesions are those of acute inflammation in which the intertrabecular tissue of the primary spongiosa is infiltrated with large numbers of neutrophils (fig. Ic-45). Inflammation results in necrosis of osteoblast and osteoclasts lining trabeculae of the primary spongiosa, and necrosis of osteoblasts leads to failure of ossifications of mineralized cartilaginous trabeculae. Some of these mineralized cartilaginous trabeculae that are thin and elongated may fracture and cause an infraction (incomplete fracture) beneath the physeal plate (figs. Ic-46, Ic-47). Damage to the metaphyseal vessels prevents normal physeal plate cartilage resorption and leads to increased depth of the zone of mineralized hypertrophic cartilage. Inflammation of osteochondral junctions (osteochondritis) may be present despite the absence of gross or radiographic lesions. Osteomyelitis may be evident in the mandible, particularly in the dental sac, and the incisor and molar teeth may have a grey-brown color. Soft tissue lesions may include calcinosis in various organs including skin, heart, spleen, kidney and stomach. These are sometimes associated with suppurative foci. Hemorrhages are probably related to prolongation in blood clotting.

5. Craniomandibular Osteopathy (lion jaw).
a. Incidence. Craniomandibular osteopathy ("lion jaw") is an uncommon hereditary bone disease of unknown pathogenesis in young dogs (fig. Ic-48). The disease is autosomal recessive and occurs most frequently in Scottish Terriers, West Highland White Terriers, and Cairn Terriers, but has been seen in other breeds, such as Great Danes.
b. Clinical features. The disease is characterized by multiple bilateral exostoses (fig. Ic-49) of the mandible, and tympanic bullae of the temporal bone are involved with less regularity. Exostoses occur on the occipital, frontal, lacrimal, and maxillary bones. In some instances bones of the limbs are involved. Exostoses of the angular and condylar processes of the mandible and tympanic bullae mechanically obstruct the movement of the jaw, causing difficulty in eating, which is usually the first sign of the disease. As the lesions advance, it may not be possible to open the mouth more than 1 or 2 cm, and the mandible may approach twice normal thickness. The disease is usually first seen in dogs three to seven months of age and runs a course of intermittent progression and regression of the exostosis until 11 to 13 months of age when the disease ceases to progress and may recede completely.
c. Pathology.
(1) macroscopic appearance. The gross lesions involve the maxilla, tympanic bullae, occasionally parietal and frontal bones, and long bones. The long bones (figs. Ic-50, Ic-51) may have exostoses extending outward from the preexisting cortex, or finger-like projections surrounded by dense collagenous tissue may form metaphyseal osteophytes. The mandible is thickened through its width and length, usually from the middle mental foramen caudally. The greatest change appears in the region of the angular process. The lesions are, in general, bilaterally symmetrical. The tympanic bullae are enlarged 3 to 4 times normal diameter and are filled with solid deposits of new bone. Each bulla is usually fused with the adjacent angular process of the mandible. This fusion obviously interferes with the movement of the mandible.
(2) microscopic appearance. The microscopic lesions in the mandible consist of bony proliferation on the periosteal surface and internal replacement of compact cortical bone with osseous trabeculae (fig. Ic-52). In some instances, osseous proliferation is not accompanied by inflammation; however, quite often, active areas of ossification or bone remodeling are associated with suppurative foci. In other regions, trabeculae are separated by highly vascular fibrous stroma, which contains a mixed inflammatory cell population of macrophages, neutrophils, lymphocytes, and plasma cells. A mosaic pattern of irregular cement lines (reversal lines) is characteristic of the newly produced trabeculae. The prominent cement-line pattern in trabeculae of the enlarged bone gives evidence of previous intense remodeling activity (fig. Ia-39). Necrotic bone is observed in some trabeculae.

6. Calvarial Hyperostosis. A hyperostosis of the frontal and parietal bones in Bull Mastiff puppies. The condition was recognized recently in different areas of the US and may be hereditary. Affected animals show extensive swelling of the cranium between six months to one year of age. Dogs may have fever, lymphadenopathy, leukocytosis and eosinophilia. The hyperostosis extends outward, and the cranial cavity remains unchanged. During progressive stages, biopsy shows a remarkable subperiosteal proliferation of woven bone trabeculae. Secondary remodeling of woven bone occurs after periods of proliferation, and lymphosuppurative inflammation may be present. When the animals become mature, cranial swelling remains stable and begins to regress.


7. Legg-Calve-Perthe's Disease. Idiopathic necrosis of the femoral capital epiphysis.
a. Incidence. Although femoral neck fracture and slipped capital epiphysis can cause necrosis of the femoral head, the cause of femoral head necrosis in Legg-Calve-Perthe's disease is different. It is seen almost exclusively in small dogs, most commonly in terriers and poodles.
b. Clinical signs. Lameness of insidious onset in dogs 4-8 months of age.
c. Mechanism. The condition is most likely the result of ischemia due to intra-articular pressure caused by obstructed venous drainage.
d. Pathology.
(1) macroscopic appearance. Bone necrosis leads to collapse of the humeral head. The articular cartilage becomes wrinkled, and the humeral head is flattened (fig. Ic-53). A longitudinal section shows an articular surface with a concave contour overlying pale cancellous bone.
(2) microscopic appearance. The initial lesion is necrosis followed by lysis of bone of the femoral head (fig. Ic-54). Continued growth of the growth zone beneath articular cartilage without endochondral ossification causes increased depth of the growth cartilage and causes the joint space to appear widened in radiographs. In the repair phase, there is proliferation of vessels and mesenchymal cells at the margin of viable and dead bone with replacement of necrotic tissue by creeping substitution (see response of bone to injury).

8. Osteochondrosis.
a. Incidence. It is an infrequent cause of lameness in young dogs, usually affecting only the larger breeds.
b. Clinical signs. The condition has an insidious onset and causes persistent lameness in animals of 4-8 months of age. It may involve shoulder, knee, or hock. Lameness is unilateral, although the lesion often is bilateral. Pain is elicited by hyperextension or hyperflexion. Joints may be crepitant, and there may be muscle atrophy. The shoulder is most commonly affected, but sometimes the stifles are involved.
c. Pathology. Lesions in the shoulder are typical of osteochondritis dissecans as described under "pathologic conditions")(figs. Ib4-7, Ib4-9, Ib4-10).

9. Retained endochondral cartilage cores. Bilateral forelimb deformites with retained cartilage cores are seen in giant-breed dogs usually within the distal ulna. Histopathology shows a localized central thickening due to the accumulation of hypertrophic chondrocytes that fail to mineralize properly (fig. Ic-55). This condition may represent a variation of osteochondrosis.


10. Diffuse Idiopathic Skeletal Hyperostosis (DISH). The cause of this rare condition is unknown. Although it is not caused by administration of excessive vitamin A, it has similarities to feline hypervitaminosis A. The canine disease is characterized by progressive development of para-articular mineral densities along the joint surfaces of the appendicular skeleton (fig. Ic-56); progressive osseous fusion of the ilium, pubis, femur, and ischium (fig. Ic-57); and progressive flowing ossification of the dorsal spinous processes of cervical and thoracic vertebrae (fig. Ic-58). Progression of ossification leads to para-articular joint fusion and almost complete ossification of the metaplastic cartilage. Intra-articular structures are spared.


11. Neoplasia. Osteosarcomas occur most commonly in the metaphysis of long bones in older large dogs. Less than twenty percent of osteosarcomas occur in the bones of the head. Chondrosarcomas occur most frequently in the head or sterno-costal region with lesser numbers in the fore and hindlimbs. Both osteosarcoma and chondrosarcoma may begin in the nasal cavity or sinuses. Multilobular tumors are seen on the parietal crest, temporo-occipital region and the frontal sinus.

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