Outline of Veterinary Skeletal Pathology

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



Outline of Veterinary Skeletal Pathology

Chapter 5 - Joints, Pathologic Conditions

A. Abnormalities of Joint Development. Joint formation does not depend upon functional demand or extrinsic stimulation, but the maintenance of joints does. The mesenchyme of a presumptive joint region of a fetus can be cultured in vitro and will differentiate into a morphologically normal joint with articular cartilage. Either prolonged in vitro cultivation, transplantation of joint tissue to an ectopic site, or neurologic paralysis of the limb in vivo causes fusion of tissues across preexisting joints and fusion of joints with other connective or skeletal tissues.
1. Arthrogryposis.
a. Definition. Congenital arthrogryposis is persistent flexure or contracture of a joint.
(1) Causes. Failure to develop the joint space results in persistent joint fixation. Arthrogryposis also develops because of neurologic disturbances or failure for flexors and extensors to be innervated properly in fetal life. This results in denervation atrophy of muscle, lack of balance between the opposing flexors and extensors and thus a lack of proper fetal movement. This can cause distortion of the limb and articular surfaces. Ingestion of alkaloids from burley or wild tree tobacco (Nicotiana), lupines (Lupinus) or poison hemlock (Cicuts douglassi) cause sustained uterine contraction that again interferes with the ability of the fetus to move in utero. Intrauterine infections with akabane or blue-tongue viruses in cattle and sheep cause arthrogryposis.

2. Joint luxation and subluxation. Joint laxity may lead to subluxation or luxation of the joint.
a. Cause. Laxity of the joint may be caused by hypoplasia of the epiphysis, defective synthesis of type I collagen or delayed motor nerve development in support muscles that may be transitory.
b. Examples:
(1) hypoplasia of the epiphysis. Hypoplasia of long bone epiphyses (epiphyseal dysplasia) may cause abnormal bone length and shape and lead to joint contracture (see contracted tendon). When it affects the humeral head, joint laxity leads to subluxation and hip dysplasia. Hypoplasia of epiphyses of vertebral bodies represent malformations that arise from abnormal interactions between mesoderm, notochord and spinal cord. Subluxation leads to abnormal curvature of the spine.
(2) atlantoaxial luxation. Luxation of the atlantoaxial joint occurs in toy-breed dogs less than one year of age and is caused by luxation of an intact dens, luxation due to congenital malformation of the dens, or fracture of the dens due to rupture of the transverse ligament of the atlas. Clinical signs begin with cervical pain, may progress to tetraplegia, and are due to compression of the spinal cord by dorsal displacement of the axis.

3. Joint Dysplasia.
a. Cause. Abnormal development of the joint leads to incongruity between opposing articular surfaces and causes secondary osteoarthritis and lameness. Joint dysplasia may result from those causes capable of inducing pathologic change during the intrauterine (fetal) period, the perinatal period, or later during the animal's growth.
b. Types:
(1) elbow dysplasia. Elbow dysplasia develops when there is joint incongruity and has several causes including ununited anconeal process (fig. IIb-1), fragmented coronoid process, patella cubiti (ectopic sesamoid bone of the elbow), osteochondrosis of the medial condyle and ununited medial epicondyle.
(2) hip dysplasia occurs most frequently in large breed dogs; occasionally it is observed in cats; and it is rarely seen in farm animals (see specific diseases).

4. Abnormal spinal curvature. In addition to malformation of vertebral bodies causing abnormal spinal curvature (see epiphyseal hypoplasia), abnormal neuromuscular function may also cause vertebral maldevelopment. This is the result of failure to innervate all abaxial muscles with the result there is a lack of balance between flexors and extensors and/or left and right flexors. The continued muscle stress on one side of the vertebral column results in distorted vertebral growth.
a. Scoliosis is abnormal curvature of the spine with lateral displacement.
b. Lordosis is ventral displacement of spine ("hump back").
c. Kyphosis occurs when the curvature has a dorsal prominence ("sway back").

5. Contracted tendon. "Contracted foals" have congenital contraction of the axial or appendicular skeleton. The contracted condition arises during early pregnancy and probably results because muscles attempt to stabilize joints that are deformed by hypoplasia of metacarpal or metatarsal epiphyses.

B. Crystal Deposition Disease is characterized by the deposition of certain types of crystals in periarticular tissues, joints, bursae, or tendon sheaths. The crystals induce inflammation that cause pain.
1. Types:
(a) Gout. Deposition of monosodium urate crystals in human beings causes gout that results in white foci (tophi) of granulomatous inflammation. Gout is not seen in domestic animals because they have the enzyme uricase that oxidizes uric acid to allantoin. It is seen in birds or reptiles (figs. IIb-2, IIb-3, IIb-4) that synthesize uric acid as their principal end product of nitrogen metabolism (uricotelic).
(b) Calcium phosphate deposition disease (calcium gout, pseudogout, or calcinosis). Various forms of calcium phosphate may be deposited in articular tissue such as joint capsule, articular cartilage and menisci and may cause arthritis. The deposition of calcium pyrophosphate dihydrate in the synovial lining or periarticular connective tissue is called pseudogout. Basic calcium phosphate is the most commonly deposited mineral phase found in domestic animals. Articular calcification is separable from other types of metastatic mineralization because the viscera frequently are not involved. Calcium phosphate deposition may affect single joints or may be inherited and represent a metabolic disease (fig. IIb-5).

C. Degenerative Joint Disease, osteoarthritis (osteoarthropathy, hypertrophic arthritis, degenerative arthropathy, degenerative arthritis). In the United States, it is generally called osteoarthritis, and it is the most common form of articular disease affecting diarthrodial joints. Although inflammation may not be an outstanding feature or the primary cause of the condition, the name osteoarthritis emphasizes the role inflammation plays in the early stage of the disease processes.
1. Types:
a. Primary osteoarthritis. An intrinsic alteration in the articular cartilage causes the initial lesion.
b. Secondary osteoarthritis. This is a consequence of some other joint disturbance such as traumatic injury, joint dysplasia, or osteochondrosis.

2. Macroscopic appearance.
a. Primary alteration. Osteoarthritis may be recognized in its early stages by articular cartilage losing its normal hyaline appearance and becoming dull white or light yellow (fig. IIb-6). This is followed by the formation of pits, depressions and linear grooves (fig. IIb-7), and portions may break free to produce loose bodies (joint mice).
b. Secondary alterations. Another lesion that occurs later is the development of marginal osteophytes (figs. IIb-8, IIb-9, IIb-10) that may be seen at the articular rim or as enthesiophytes that occur at sites of muscular insertions. In advanced cases, constant friction results in eburnation (fig. IIb-10), polishing of the subchondral bone in contact areas where the articular cartilage has been eroded away and in grooving of the subchondral bone. Eburnation and continued formation of perichondral cartilage, which usually undergoes endochondral ossification to form osteophytes, alter the contour of the articular surface and produce the irregular margins (lipping)(fig. IIb-11) that are easily seen radiographically. In the late stages, subchondral pseudocysts are produced (see chapter 4).

3. Microscopic appearance. The initial lesion is a loss of cartilage proteoglycans. This loss causes the articular cartilage to appear less hyalin, and the fibrillary substratum of the cartilage becomes more apparent microscopically. The articular surface undergoes fibrillation by developing deep clefts that separate strands of matrix (figs. IIa-8, IIa-9). The remaining chondrocytes divide and develop clones or daughter cells (chondrones) that appear as clusters of chondrocytes arranged in rows. As the articular cartilage is lost or worn away in some locations, there is a progressive increase in the thickness of cartilage at other sites, and this may undergo endochondral ossification, which adds bone to the surface. The synovial membrane may show synoviocyte hyperplasia, villus formation and chondroid or osseous metaplasia.


4. Spondylosis deformans is a degenerative arthropathy of joints between vertebral bodies (amphiarthroses, intervertebral disks) and is characterized by osteophytes that grow toward each other and ultimately bridge the intervertebral space (figs. IIb-12, IIb-13).
a. Incidence. It commonly occurs in dogs, cats, cattle, and swine and is relatively rare in other domestic animals. It has been described as an occupational hazard of stud bulls.
b. Cause. Not completely known. Protrusion of the intervertebral disk ventrally leads to spondylosis deformans if it is accompanied by avulsion of the fibers of the annulus fibrosus from its attachment site at the margin of the vertebral body. Severe spondylosis of cervical vertebrae in cats is usually due to hypervitaminosis A.
c. Pathogenesis. The process of osteophytes' development at the attachment of the ventral longitudinal ligament to the vertebral body is similar to that of an enthesiophyte in osteoarthritis. Intervertebral disk degeneration may gradually lead to ventral protrusion of disk material. The outer fibers of the annulus are fused with the ventral longitudinal ligament and are firmly attached to the ventral margin of the vertebral body. When the disk ruptures, there is break-down in the attachment of the annulus fibrosus to the vertebral rim; the disk protrudes ventrally and displaces the ventral longitudinal ligament. This causes traction on the periosteal attachment site of the ligament at the margin of the vertebral body and provokes subperiosteal new bone production. Formation of an exostosis progresses, and well-developed buttresses of bone from opposing vertebrae grow toward each other and may eventually fuse. Usually they are joined by fibrocartilage rather than bone. Spinal osteophytes are also associated with other vertebral diseases such as diffuse idiopathic skeletal hyperostosis or ankylosing spondylitis.

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