Outline of Veterinary Skeletal Pathology

contents Ch 5, p 2 Chapter 6, Page 1 contents 

Outline of Veterinary Skeletal Pathology

Chapter 6 - Joints, Specific Diseases

A. Horse
1. Osteoarthritis.
a. Exostoses. Equines are subject to formation of excessive exostoses of the limbs.
(1) Ringbone, Sidebone. Exostoses arise on the second or, less commonly, on the first phalanx of ungulates where periarticular osteophyte formation tends to encircle the bone (figs. IIc-1, IIc-2). Sidebone is the ossification of the lateral cartilages of the third phalanx.
(2) splints. Inflammation along the interosseous ligament produces exostoses of the shafts and at the ends of the second and fourth metacarpal (rarely metatarsal) bones. Because they do not impinge on joints or cause pain, they usually do not cause lameness.
(3) spavin. Exostoses frequently form on the medial portions of the distal bones of the tarsus. Though small, They are a serious and stubborn cause of lameness.
b. Navicular disease is a degenerative disease involving the equine distal sesamoid (navicular) bone, and there is inflammation of the associated podotrochlear bursa (fig. IIc-3).
(1) incidence. The condition is very common and has an insidious onset.
(2) clinical features. The condition causes intermittent, shifting-leg lameness and occurs almost exclusively in the forefeet. If only one foot is involved or if the condition is more severe in one limb, the horse points with the more severely affected limb. In some cases, there are no clinical signs.
(3) pathology.
(a) macroscopic appearance. Lesions are not always apparent in clinically lame animals. Sometimes small osteophytes and bone pseudocysts are seen (fig. IIc-4).
(b) microscopic appearance. Important changes include degenerative changes and adhesions between the fibrocartilaginous surface of the navicular bone and the deep flexor tendon. Osteophyte formation, focal subchondral osteolysis (subchondral pseudocysts), and mild villus hypertrophy of the synovium of the podotrochlear bursa are also common (fig. IIc-5). Degenerative changes in the fibrocartilaginous surfaces, the development of osteophytes, and pseudocysts appear to be age-related.

2. Pyosepticemia neonatorum, "Joint-ill" Fibrinous or purulent arthritis is common in foals. The outcome of arthritis is dependent, to a large degree, on the extent of the destruction of cartilage. In fibrinous arthritis, cartilage destruction occurs if the condition is of long duration. In contrast, with purulent arthritis cartilage necrosis and chondrolysis are seen in the early stages.

B. Cow.
1. Mycoplasma arthritis.
a. Mycoplasma bovis causes disease outbreaks in feedlots where the condition is preceded by management stress.
b. Usually 15% of animals may show signs of lameness and severe swelling around the stifle, shoulder, elbow or hock (fig. IIc-6).
c. Severe arthritis is frequently limited to one limb.
d. The joint is distended with opaque white/yellow fluid that contains clumps or strands of fibrin (fig. IIc-7).
e. The synovial membrane is swollen and congested.
f. Microscopic alterations include hyperplasia of the synovial membrane with increased number of villi.
g. The synovial membrane contains a dense infiltrate of lymphocytes, plasma cells and macrophages.
h. Synovial fluid may contain numerous neutrophils.

2. Osteoarthritis.
a. This is probably common in older cattle; but because old cows are uncommon, the disease in not often seen.
b. Cystic bone lesions may be seen with ossification of tendons, joint capsule and menisci (figs. IIc-8, IIc-9).

C. Goat.
1. Caprine arthritis-encephalitis virus infection.
a. Incidence. Goats infected with the Caprine Arthritis-Encephalitis Virus sometimes develop a disease in which chronic arthritis is the principal manifestation. Up to thirty percent of some herds may show clinical signs.
b. Clinical features. In addition to lameness, animals may have carpal hygromas, and there may be a dramatic reduction in milk production (figs. IIc-10, IIc-11).
c. Mechanism of arthritis.
(1) development of arthritis is dependent on persistence of virus infection.
(2) the virus remains latent in macrophages.
(3) specific cytokines direct virus-infected macrophages from the blood stream to synovial membrane where they interact with lymphocytes to produce an inflammatory cascade.
(4) this results in further production of cytokines, and immune complexes between virus and immunoglobulins lead to further enhancement of pathologic changes.
d. Pathology.
(1) macroscopic appearance. The joint capsule is distended, and the synovial membrane is thickened with marked villus hypertrophy. Fibrin mixed with red cells may be attached to the synovial surface and appears as blood clots (fig. IIc-12) , or serosanguineous joint fluid may contain small, hard, white grains of inspissated fibrin (so-called rice grains).
(2) microscopic appearance. There is thickening of the joint capsules of the atlanto-occipital, carpal, stifle, and hock joints (fig. IIc-13). The synovial membrane contains a heavy inflammatory cell infiltrate composed principally of lymphocytes and plasma cells; the connective tissue of the joint capsule is sometimes mineralized (fig. IIc-14). In severe cases, fibrillation and erosion of articular cartilage is seen as well as cartilage destruction by pannus that rarely leads to joint fusion. Lesions are also found in brain, lung, and mammary gland.

D. Sheep.
1. Chlamydial arthritis.
a. Incidence. Nonfatal disease of major importance in the sheep industry. It is a regional disease in the West United States. It affects feedlot and nursing lambs of all breeds.
b. Clinical signs. Lambs with polyarthritis have fever, lameness, serositis, and conjunctivitis. All joints are affected, particularly those of the limbs, and animals are stiff and have painful movement. Animals may become emaciated.
c. Pathology.
(1) macroscopic appearance. There is distension of the joint capsule and an increased volume of synovial fluid that has an amber color. The joints, including the atlanto-occipital, tendon sheaths, eyes, and lungs are involved. The joint fluid contains fibrin flakes and plaques. The synovium is edematous and hyperemic, and may have petechiae.
(2) microscopic appearance. Synovial fluid contains increased numbers of mononuclear cells. The synovial membranes contain granulomas and perivascular accumulation of mononuclear cells. Inclusion bodies are found within the synoviocytes.

E. Pig.
1. Erysipelas arthritis. Erysipelothrix rhusiopathiae may cause acute, subacute or chronic disease. Most severe arthritis is seen in the chronic disease and has an immunologic mechanism.
a. Incidence. It is fairly common in swine-raising areas. Greatest economic loss comes from the chronic form.
b. Clinical signs. Various degrees of stiffness and joint enlargement are observed. The condition does not affect growth rate, but the major economic loss comes from condemnation of prime pork cuts.
c. Pathology.
(1) macroscopic appearance. There is enlargement of one or more joints (hock, carpus). The joint capsule is thickened by edema. Synovial fluid is serosanguineous, is increased in volume, and may be slightly cloudy. Hyperemia and proliferation of the synovial membrane occurs (fig. IIc-15), and pannus (fig. IIa-6) may extend across the surface of the articular cartilage. Diskospondylitis, infection of the intervertebral disk that spreads to the contiguous vertebra, also is seen (fig. IIc-16).
(2) microscopic appearance. Changes in the synovial membrane may vary in severity. Typical lesions show pronounced hyperplasia of synoviocytes, vascularization, and accumulation of lymphoid cells in subsynovial connective tissue (figs. IIc-17, IIc-18). Changes in the synovial membrane include fibrin deposits that may become organized. Other changes are villus hyperplasia, proliferation of periarticular fibrous connective tissue, erosion of the articular cartilage, and periostitis.

F. Dog.
1. Canine hip dysplasia. In the dog, hip dysplasia is a phenomenon of gradual deformation of the joint that occurs postnatally. Subluxation of the femoral head, perhaps due to inadequate muscle strength, is followed by a sequence of events that results in acetabular dysplasia and degenerative joint disease.
a. Structural alterations.
(1) primary structural alterations probably occur during the neonatal period when the animal's growth is most pronounced.
(2) gentle mechanical forces, if persistently applied, may lead to a gradual progressive deformation of normal bone structure.
(3) such deformation occurs much more readily during periods of excessively rapid growth.
b. Mechanical Forces. Because the largest loads placed on the hips are from muscular contractions, abnormal muscle activity influences the cartilage modeling process of the acetabulum.
(1) the mechanical forces that hold the femoral head firmly in the acetabulum are a result of pull by muscles vertically or medially on the hip.
(2) it has been shown that, if the rear limb is held in extension or adduction, there is a tendency to dislocate the hip.
(3) the alterations that cause hip dysplasia tend to concentrate the mechanical loads on the craniodorsal aspect of the acetabular rim, and this excessive force retards cartilage modeling and causes the bone to become abnormally shaped.
(4) these structural changes lead to subluxation of the femoral head.
c. Pathology.
(1) besides retarded development of the craniodorsal acetabular rim and lag in its ossification, other early changes are tearing of fibers in the teres ligament and stretching of the joint capsule. Subluxation and bending of the greater trochanter occur later.
(2) joint incongruity leads to secondary osteoarthritis (fig. IIb-8).
(3) because progressive reconstruction of the femoral head (fig. IIb-9), formation of marginal osteophytes, osseous filling of the acetabular fossa and changes in the contour of the acetabular rim, radiographic changes become more noticeable after six months of age.
(4) hip dysplasia could be caused by an intrinsic defect in bone structure or to a lack of strength of supporting ligaments, tendons and connective tissue that results in joint laxity.
(5) because the condition develops after birth, it is more likely to be due to a lack of balance in the muscles pulling medially and pulling vertically on the hip. Such differences could be related to muscle strength or to defect in neuromuscular function such as partial denervation atrophy.

2. Degeneration of the intervertebral disk
a. Incidence. Alterations in the structure of the intervertebral disk occur as an aging change, and the disk becomes progressively more fibrous. In addition to aging fibrosis, certain breeds of dogs have accelerated degeneration of the intervertebral disk.
b. Clinical features. Chondrodystrophoid dog breeds, such as the dachshund, Pekinese, and French bulldog, develop chondroid metaplasia of the nucleus pulposus at an early age, often during the first year of life (fig. IIc-19). Other breeds of dogs, such as the beagle and cocker spaniel, which are probably not chondrodystrophoid, develop similar degenerative changes in the disk. In other nonchondrodystrophoid breeds, the initial degenerative changes occur later in life and consists of degeneration of the annulus fibrosis. Trauma also may cause sudden dorsal protrusion of a nondegenerated disk.
c. Pathogenesis. Degeneration of the disk begins when the notochord cells of the nucleus pulposus are replaced by cartilage cells (fig. IIc-19). Cartilaginous transformation begins in the periphery of the nucleus and progresses from the inner to the outer lamellae of the annulus fibrosus. Degeneration of the nucleus pulposus predisposes the disk to displacement by penetrating the annulus fibrosus. Because of the relative immobility of the thoracic spine and the presence of the conjugal ligament that reinforces the dorsal annulus fibrosus, herniation of disks in the thoracic region is uncommon.
d. Pathology. Protrusion of the intervertebral disk into the epidural space of the vertebral canal may directly compress the spinal cord and cause paralysis (fig. IIc-20). There is an initial inflammatory reaction to the liberated degenerated disk material that involves the periosteum, longitudinal ligament, and dura matter. The inflammatory reaction becomes chronic, and there is marked fibroplasia. The degenerated disk material may calcify, cause a granulomatous reaction, and lead to osseous metaplasia (see spondylosis deformans) (figs. IIb-12, IIb-13) . Compression of the spinal cord causes myelomalacia because of direct cord injury or vascular compromise.

3. Canine rheumatoid arthritis.
a. Difference between human disease. Canine rheumatoid arthritis differs from the counterpart disease in human beings because in the dog, systemic manifestations of the disease are lacking, and usually rheumatoid nodules do not develop. However, the canine disease is more severe in its early stages and progresses more rapidly. The articular pathology and clinical signs are similar to those in human beings, although rheumatoid factor is present in comparatively low titer and in only twenty-five percent of affected dogs.
b. Clinical features. The canine disease is manifested by severe polyarthritis with swollen, painful joints, fever and neutrophilia (in initial stages)(figs. IIc-21, IIc-22). The condition is rare and is seen more commonly in small or toy dog breeds. The joints of the small bones of the appendicular skeleton are more commonly affected, but other joints may be involved.
c. Pathology.
(1) synovial fluid. Changes in synovial fluid indicate synovitis with elevated total cell count and a high population of neutrophils; there may be a variable decrease in mucin.
(2) biopsy. Neutrophils are rarely seen in synovial biopsy specimens, and when they do occur, it is in the early disease phase. There is marked synovial villus hyperplasia, and the synovium is infiltrated with lymphocytes, plasma cells, and macrophages (figs. IIc-23, IIc-24).
(3) macroscopic appearance. Articular cartilage is eroded at the cartilage margins. Granulation tissue from the inflamed synovium may extend across the articular surface to form pannus (see chapter 4).
(4) microscopic appearance. A distinctive lesion is the undermining of cartilage and ingrowth into subchondral bone by pannus that arises from the synovium.

4. Calcium phosphate deposition disease in Great Danes.
a. Incidence. Uncommon condition that is possibly familial.
b. Clinical features. Condition characterized by paraplegia and incoordination in very young puppies. Serum calcium concentrations are within normal limits, but serum phosphorus concentrations are decreased.
c. Pathology.
(1) macroscopic appearance. The paraplegia and incoordination is caused by canal stenosis that is the result of dorsal displacement of the seventh cervical vertebra and deformation of the vertebral articular processes (figs. IIc-25, IIc-26). Amorphous calcium phosphate is deposited in the diarthrodial joints of the axial skeleton in weanling puppies, and the appendicular skeleton becomes involved as the dogs mature.
(2) microscopic appearance. Periarticular mineralization of vertebral articulations (figs. IIc-27, IIc-28) and long bones is associated with shorter bones of the appendicular skeleton that had a thin cortex and abnormal bone curvature. Soft tissue mineralization may be also noted.

5. Chondrocalcinosis is an incidental lesion most frequently found in the head of the humerus of Greyhounds. Focal mineralization of articular cartilage appear as circular white deposits (figs. IIc-29, IIc-30).
a. Focal chondrocyte necrosis and matrix degeneration above the tidemark are considered to antedate chondrocalcinosis lesions.
b. Scanning electron microscopy demonstrated mineralized foci contained irregularly fused stone material (fig. IIc-31) and irregular spheroids that formed needle-like crystals of apatite.
c. Some foci appear to rupture at the articular cartilage surface and to empty the contained mineral into the joint space.
d. Chondrocalcinosis is seen in young Greyhounds, and the lesion is unlikely the result of biomechanical stress of racing.

6. Erosive polyarthritis of Greyhounds.
a. Incidence. This disease of unknown cause in young Greyhounds has been described in Australia, Europe, England and the United States. It is thought to have an immunologic mechanism.
b. Pathology.
(1) macroscopic appearance. Significant macroscopic lesions are primarily limited to the stifle, elbow, carpal, and tibiotarsal joints. Fibrinous strands may bridge across articular surfaces that have irregular erosions. In other areas, the cartilage appears thin, grooved, and eroded to varying depths. The synovium contains velvet-like plaques that are yellow-brown and slightly raised. Marginal osteophytes may be present (fig. IIc-32).
(2) microscopic appearance. Full thickness necrosis of articular cartilage may be a distinguishing feature, but the condition is not well studied. Surface articular cartilage is sloughed, sometimes to the subchondral bone. A prominent feature is the necrosis of the hyaline cartilage of the radial and calcified cartilage zones and relative sparing of the surface (fig. IIc-33). The synovium has marked villus hypertrophy and is infiltrated diffusely and focally with lymphocytes and plasma cells, macrophages, and occasional foci of neutrophils (fig. IIc-34). Hemosiderosis may be prominent with hemosiderin occurring in fibroblasts and synoviocytes.

G. Cat
1. Progressive feline polyarthritis.
a. Incidence. This is a specific entity affecting young adult male cats.
b. Pathogenesis. Although the pathogenesis and precise cause is unknown, it is thought to be related to infections with feline-syncytia-forming-virus (FeSFV) and feline-leukemia-virus (FeLV). All affected animals have antibodies to FeSFV, and seventy percent have antibodies to FeLV. The disease cannot be reproduced experimentally, and arthritis is thought to be an uncommon manifestation of retrovirus infection in genetically predisposed individuals.
c. Pathology. The arthritis appears in two forms, an erosive and deforming arthritis and a periosteal proliferative form. The sequential changes are not well documented. The erosive and deforming variant is less common, and macroscopic and microscopic features are similar to canine rheumatoid arthritis. Ingrowth of pannus is seen at the articular margins, and there is joint instability and deformity. The more common periosteal proliferative form is similar to Reiter's arthritis of humans and is associated with extensive new bone formation that surrounds the joint. There is collapse of the joint space, and fibrous ankylosis; but bone deformity does not occur with this variant.

2. Arthritis in Scottish-fold cats. Arthritis is a feature of a bone disease characterized by exostosis, and it occurs in cats homozygous (FdFd) for the ear-fold allele (see chapter 3). A less disabling degenerative arthritis, affecting particularly the carpus, is seen in Scottish-fold cats that do not have typical bone lesions of homozygous animals.

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