Outline of Veterinary Skeletal Pathology

contents Ch 2, p 7 Chapter 3, Page 1 Ch 3, p 2 



Outline of Veterinary Skeletal Pathology

Chapter 3 - Bone, Specific Diseases

A. Horse
1. Fibrous osteodystrophy. This condition was originally described by the name of Bran disease as it occurred when horses, owned by flour-millers, were fed almost exclusively bran, a cheap by-product. Similar changes can be seen when animals fed grain are supplemented with hay of poor nutritional value rather than alfalfa that is high in calcium.
a. Clinical features. Changes in the head and facial outlines are commonly the first signs of the disease; it has therefore been called big head (fig. Ic-1). The disorder is the result of feeding diets low in calcium and high in phosphorus. Clinicopathologic findings may reveal hyperphosphatemia and hypocalcemia, but compensation may occur through the action of parathyroid hormone on bone and the kidneys. Serum alkaline phosphatase concentration is elevated.
b. Pathology
(1) macroscopic appearance. The sharp features of the head, especially in the region of the zygomatic arch and upper and lower jaws, become rounded and indefinite, giving the appearance of more swelling than really exists (fig. Ib2-11). Dissection shows a rather uniform thickening and rounding due to diffuse proliferation of imperfect bone in the subperiosteal region. The teeth may loosen and fall out. There is also lameness and a general tenderness of the joints.
(2) microscopic appearance. Classic lesions of fibrous osteodystrophy with osteomalacia are most obvious in facial bones and the mandible (fig. Ib2-16), but the lesions are generalized throughout the skeleton.

2. Salmonella infection is a frequent cause of acute osteomyelitis that affects the long bones of foals (fig. Ic-2). It is characterized by necrosis and formation of sequestra in the epiphysis below the growing articular cartilage or in the metaphysis below the physeal plate.


3. Equine cervical vertebral deformity is a common cause of ataxia in young horses. The condition is often associated with degenerative arthropathy secondary to osteochondrosis (see below). Pathogenesis of the condition is incompletely understood, but maldevelopment of the cervical vertebrae causes narrowing or functional stenosis of the spinal canal. Spinal cord injury causes incoordination, principally affecting the hind limbs. Although the shape and characteristics of each cervical vertebra varies among individual foals, the cervical deformity is divided into two main categories.
a. Cervical vertebral instability. Occurs in animals from 8 to 18 months of age. There is dynamic compression of the spinal cord by the vertebral body when the neck is flexed (fig. Ic-3). Characteristic findings are symmetrical overgrowth of the bilateral articular processes and enlargement of the epiphyseal end plate of the vertebral body. This narrows the diameter of the vertebral canal during neck flexion, usually from C3-C5.
b. Cervical vertebral stenosis. Hypertrophy of the ligamentum flavum, fibrocartilaginous hyperplasia of the ligamentous attachment, and fibrous thickening of the joint capsule of the articular facets is associated with asymmetric overgrowth of these structures and results in stenosis of the spinal canal (figs. Ic-4, Ic-5). Dorsal or dorsolateral compression of the spinal cord occurs regardless of neck position. Lesions are frequently located at C5-C7.

4. Angular limb deformity is lateral deviation of the distal portion of the limb, originating in the distal radial physis, carpus or distal metatarsal physis, and it is seen more commonly in foals than other domestic animals (fig. Ic-6). It may be present at birth or be acquired later in life. Causes include uterine malposition of the fetus, trauma, poor conformation, and hypothyroidism. Foals with hypothyroidism have mandibular prognathism and delayed ossification of carpal and tarsal bones. Growth and modeling of cartilage prior to formation of the primary ossification center or of the physeal plate or AE complex (fig. Ia-13) of the epiphysis directly controls the bone's size and shape. If there is abnormal development of the chondral model, ossification only adds support to form an abnormally shaped bone. Conditions such as malunion of fracture, osteochondrosis, or premature arrest of growth on one lateral side of the physeal plate can produce a varus bone deformity. Increase compressive loads on a portion of the physeal plate can increase or decrease local cartilage growth depending upon the load magnitude. If local growth is increased, there is correction of the original deformity. If growth is decreased, the deformity is magnified.


5. Osteochondrosis.
a. Incidence. Osteochondrosis is a frequent cause of lameness in young horses (fig. Ic-7). The femero-patellar and tibio-tarsal joints are most commonly involved. Other joints commonly affected include the shoulder and metacarpo-phalangeal joints. The condition is frequently bilateral.
b. Clinical signs. The joint is distended with synovial effusion in animals 6 months to 2 years of age. Lameness may be mild to moderate. It is exacerbated by exercise.
c. Pathology. Lesions have been described in chapter 2. Typical equine lesions in the femoral head are illustrated (figs. Ic-7, Ic-8, Ic-9, Ic-10, Ic-11).

6. Epiphysitis is a generalized bone disease of growing horses that is characterized by enlargement of the physeal region in young animals. This condition is a misnomer in that it is not particularly inflammatory and is not caused by an infectious agent. It is associated with osteochondrosis of the physeal plate.


7. Neoplasia. Osteosarcoma occurs much more frequently in the head than in the appendicular skeleton. The most common site of chondrosarcoma is the rib. Ossifying fibroma is seen in young horses in the mandible, maxilla or nasal sinuses (fig. Ib6-6, Ib6-7, Ib6-8, Ib6-9, Ib6-10).

B. Cow
1. Chondrodysplasia of calves is an inherited condition that has several morphologic forms. The number of gene loci are uncertain.
a. Bulldog calves (fig. Ic-12) usually are aborted before the seventh month. The animals are grotesquely malformed with protruding tongue; thick, rotated and abducted limbs; absent hard palate; and umbilical hernia and protruding viscera. The trait appears to be incompletely dominant.
b. Brachycephalic (snorter) dwarfism (fig. Ic-13) is common in beef breeds. Inheritance appears to be recessive and produces a very pleasing phenotype in heterozygotes- a short-legged, compact appearance. Snorter dwarfs have a short, broad head that bulges; nasal occlusion; protruding mandible; and malocclusion.
c. Other forms of dwarfism are seen in calves; most are inherited in an autosomal recessive manner. Calves are born dead or die shortly after birth. There is phenotypic variability, and individual syndromes have not been distinguished.

2. Osteogenesis Imperfecta (see chapter 2) has been reported in Charolais cattle but was most thoroughly studied in Holstein calves (fig. Ic-14). Two different varieties are recognized as an autosomal dominant. The amount of type I collagen is deficient causing joint hypermobility, blue sclera, fragile teeth with defective dentine, and bone osteopenia with fracture and growth arrest lines. No qualitative collagen defects have been identified in calves, but the two clinically identical bovine diseases can be easily distinguished in Holsteins by the osteonectin content of the bone matrix. Osteonectin is a noncollagenous bone matrix macromolecule. The Australian variety of osteopetrosis has a normal complement of osteonectin; whereas, the Texas type has severely depleted osteonectin in bones.


3. Osteopetrosis (see chapter 2) is seen in calves of several breeds. In Aberdeen Angus, it is inherited as an autosomal recessive trait. Prominent clinical features are brachygnathia inferior, sloping forehead, impacted molars, and protruding tongue. Long bones have slight thickening of the metaphysis at the cut-back zone, and the marrow-cavity is filled with unresorbed trabeculae of woven bone that may show zonal density (fig. Ic-15). Skeletal abnormalities are generalized and are especially noticeable in the skull where the membranous bones are dense and thick and compress the brain.


4. Erythropoietic porphyria is a congenital disease with defective heme biosynthesis and is seen in cattle, pigs and cats. The disease is also called osteohemochromatosis or pink tooth because of the red-brown discoloration that occurs when porphyrin pigments are deposited in dentin and bone during mineralization (fig. Ic-16).


5. Hyena disease is a rare condition of cattle that causes premature physeal plate closure. The condition affects bone growth and causes animals to have a hyena-like appearance with sloping hind quarters when viewed in lateral profile (figs. Ic-17, Ic-18). Hyena disease has a world-wide distribution. Its cause is unknown, but similar lesions in calves were produced by feeding toxic levels of vitamin A.


6. Actinomycosis (Actinomyces bovis) is a pyogranulomatous osteomyelitis that may only be apparent in the jaw (lumpy jaw) (fig. Ib5-8). The inflammatory response proliferates and destroys surrounding bone that reacts by a reparative proliferation at the same time that adjoining areas are being resorbed. The result is a pronounced local enlargement that after the soft tissues are removed by maceration has a texture much like that of a honey comb.

7. Neoplasia. Bone neoplasms are infrequent, probably because of the shortened life span of most cattle.
Osteosarcomas occur far more frequently in the head than in any other region.
C. Sheep
1. Spider-lamb chondrodysplasia.
a. Incidence. This is a type of osteochondrodysplasia that develops in sheep predominately of Suffolk breeding and may be very common in this breed in certain locations. The disease has recessive inheritance.
b. Clinical signs. Animals may be affected at birth (fig. Ic-19), or animals that appear almost normal may develop abnormal conformation at 4-6 weeks of age. Animals may not be able to rise and nurse unassisted. Diagnosis is best made by radiographic changes that show multiple irregular islands of ossification that are in most bones, but are most consistently seen in the elbow, sternum, and shoulder.
c. Pathology.
(1) macroscopic appearance. Varied lesions may be seen in the skull, sternum, vertebrae and appendicular skeleton. Bones may have abnormal shapes and contours. There is lateral bowing of the ulna/radius with flaring of the metaphysis. Hind limbs are less distorted than the fore limbs. Excessive amounts of cartilage are seen in the scapula and olecranon (fig. Ic-20).
(2) microscopic appearance. Histologic lesions are confined to growth cartilage throughout the skeleton (fig. Ic-21). There is failure to maintain orderly cartilage development. Cartilage protrusions at different sites appear as nodules or tongues of disorganized cartilage. There is increase in the depth of the proliferative and hypertrophic cartilage zones and an unevenness of the growth cartilage.

2. Neoplasia. The sterno-costal complex is a frequent site for osteosarcoma. The head, skull and jaws are the second most frequent site. Chondrosarcoma occurs most frequently in the sterno-costal complex, followed by the scapula and then the remainder of the foreleg.

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