Outline of Veterinary Skeletal Pathology

contents Ch 2, p 4 Chapter 2, Page 5 Ch 2, p 6 

Outline of Veterinary Skeletal Pathology

Chapter 2 - Bone, Pathologic Conditions

D. Bone Disease of Unknown Cause
1. Hypertrophic (Pulmonary) Osteoarthropathy (Marie's disease).
This is a rare disease but may affect all domestic animals. Characteristic lesions are chronic proliferation of new bone that results in marked thickening and deformity of the limbs.
a. Clinical features. There is considerable pain on movement and in advanced cases on palpation.
(1) association with pulmonary disease.
(a) cough, dyspnea, or other pulmonary disturbances often precede the disease by a few months.
(b) usually there are extensive lesions in the lungs, most often pulmonary abscess or a thoracic neoplasm such as lymphoma or metastatic osteosarcoma (figs. Ib4-1, Ib4-2).
(c) the occurrence of hypertrophic osteoarthropathy does not depend so much on the nature of the disease causing the pulmonary lesion as it does on its location and duration.
(2) cases without lung lesions
(a) the disease is occasionally seen with nonpulmonary neoplasms, and
(b) the location of the tumors seems to follow the distribution of the vagus and glossopharyngeal nerves.
(c) urinary bladder or esophageal neoplasms may occasionally be the cause.
(d) animals with chronic heart disease or insufficiency rarely develop hypertrophic osteoarthropathy.
(e) the disease is associated with lesions outside the thorax, including liver disease, colitis, and gastrointestinal tumors.
(f) the condition has been reported in single bones following infection of local vascular grafts.
(3) pathogenesis
(a) postulated mechanisms causing bone formation.
(i) longstanding hypoxia,
(ii) failure to inactivate a vasodilator and
(iii) bone-remodeling substance normally present in the systemic venous circulation, and
(iv) increased peripheral blood flow to the bone.
(b) it has been demonstrated that in cases of osteoarthropathy caused by pulmonary neoplasia, severing the vagus nerve quickly cures the disorder.
(c) vagotomy results in a prompt fall in blood flow to the limbs, and this supports the hypothesis that increased peripheral blood flow is responsible for the bony growths.
(d) it has been hypothesized that inappropriate stimulation of the vagus or glossopharyngeal nerve leads to excess fluid and dilated vessels in all four limbs as a secondary effect that is possibly mediated via a cerebral sodium homeostatic mechanism.
b. Pathology
(1) subperiosteal proliferation of bone is found in the appendicular skeleton but not in the axial skeleton.
(2) trabeculae of reactive, woven bone form perpendicular to the surface of the cortex and push the periosteum outward.
(3) the osteophytic growths
(a) are irregular,
(b) sometime bulbous, and
(c) have intervening vascular channels and adventitial spaces, and
(d) cause the diaphyseal surface to be extremely rough (fig. Ib4-3).
(4) occasionally, a bone may attain twice its normal diameter.
(5) the bones usually affected are those of all four limbs (fig. Ib4-4), but the bones of the upper limbs and phalanges may be partially spared (fig. Ib4-5).
(6) although periarticular tissue may be affected, the joint surfaces are not involved (fig. Ib4-6).

2. Osteochondrosis
a. Definition. This is a focal disorder of endochondral ossification, including both chondrogenesis and osteogenesis, that occurs in a site of bone growth that was previously normal. Osteochondrosis is more commonly seen in long bones, but many other bones of the skeleton may be affected.
b. Incidence.
(1) osteochondrosis is a common disease in pigs, dogs and horses.
(2) it is less common in cattle, uncommon in sheep and rarely seen in goats and cats.
c. Clinical features.
(1)animals begin showing clinical signs at 4-8 months of age. These include:
(a) joint stiffness,
(b) unwillingness to stand,
(c) non-weight bearing lameness or shortened stride.
d. Pathology.
(1) lesion sites. The lesions of osteochondrosis fundamentally involve three areas of abnormal endochondral ossification:
(a) non-articular surface of the epiphysis.
(i) lesions occur principally at sites of attachment of tendons and ligaments.
(ii) excessive traction at tendon or ligamentous insertions can cause fracture or avulsion of cartilage at the point of attachment (See epiphysiolysis below and ununited anconeal process [fig. IIb-1]).
(b) articular cartilage of the epiphysis. Early lesions in subarticular cartilage of young animals often are characterized by chondrocyte necrosis, which leads to osteochondritis dissecans (dissection of cartilage, formation of a cartilage flap, and development of free joint bodies) (fig. Ib4-7).
(c) physis. In contrast to lesions in articular cartilage, there is often no evidence of cartilage necrosis, but there is focal failure for hypertrophic cartilage cells to mineralize.
(i) this mineralization failure causes a focal rachitic-like lesion characterized by persistence of hypertrophic cartilage cells, which result in disorganization of the cartilage pattern of the physeal plate (fig. Ib4-8).
(ii) other lesions include metaphyseal trabecular fractures, abrupt displacement lines in the physeal plate, cartilage matrix degeneration, and disorientation of cartilage cells similar to those observed following cartilage creep.
e. Macroscopic appearance.
(1) early lesions in dogs appear as a white circular area on the articular surface of the humeral head (fig. Ib4-9).
(2) the predilection site is at the apex of the caudocentral contour of the articular surface.
(3) later, the cartilage surface becomes ruffled and develops tears as the cartilage separates from mineralized cartilage and subchondral bone.
(4) the affected cartilage may dissect completely from the bone and become a free body (joint mouse)(fig. IIa-10).
(5) afterwards, the defect attempts to heal by deposition of fibrocartilage (figs. Ib4-10, Ib4-11).
(6) with early lesions in swine, longitudinal sections of bone show triangular areas of articular cartilage that protrude into subchondral bone or triangular areas of physeal cartilage that protrude into the spongiosa (fig. Ib4-12).
(7) below the thickened articular cartilage, the bone of the epiphysis appears unusually dense.
(8) epiphysiolysis is separation of the epiphysis from the metaphyseal bone probably as a consequence of osteochondrosis (fig. Ib4-13).
f. Microscopic appearance.
(1) there is a failure to mineralize areas of hypertrophic cartilage that leads to abnormal endochondral ossification at foci in non-articular cartilage, articular cartilage, or the physis (fig. Ib4-14).
(2) usually, the lesion is characterized by thickened cartilage.
(3) the microscopic appearance differs depending upon the species, anatomic location, and duration of the lesion.
g. Pathogenesis. Some consider focal dyschondroplasia to be the primary lesion in osteochondrosis. However, it is difficult to determine whether deformation of the growth cartilage is a primary event or an adaptive response.
(1) failure to mineralize matrix in the hypertrophic cartilage zone is a fundamental lesion that disturbs endochondral ossification.
(2) lack of mineralization may be brought about by several different pathogenetic mechanisms and may be due to different causes.
(3) one mechanism affecting the articular cartilage of swine, and possibly dogs and horses, is vascular injury that leads to chondrocyte necrosis and matrix degradation, and results in focal disturbance in endochondral ossification (figs. Ib4-15, Ib4-16).
(4) differences in the vascularity of growth cartilage at different ages of maturity between large and small breed animals may be responsible for the reduced incidence of osteochondrosis in smaller animals.
(5) normal physical activity may induce injury if the material properties of articular cartilage or subchondral bone are abnormal or if the animal is of a young age such that the osteochondral interface has not fully matured.
h. Cause and significance.
(1) theories concerning the cause of osteochondrosis involve ischemia, trauma, and a constitutional disease.
(2) the causes are not necessarily mutually exclusive, and all may play a pathogenetic role in individual cases.
(3) the finding of multiple bone involvement and bilateral symmetry is strong circumstantial evidence that there is a constitutional component.
(4) it is likely that biomechanical forces represent a fundamental cause, and physical stress initiates subsequent changes.

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