Outline of Veterinary Skeletal Pathology

contents Ch 2, p 2 Chapter 2, Page 3 Ch 2, p 4 



Outline of Veterinary Skeletal Pathology

Chapter 2 - Bone, Pathologic Conditions

metabolic bone diseases

b. osteomalacia
(1) definition. Disease of bone in adults where there is defective bone mineralization. The condition is characterized by excessively wide seams of osteoid on bone forming surfaces.
(2) macroscopic appearance.
(a) the long bones may show irregular, diffuse thickening along the length of their diaphyses; but the bone is soft, easy to cut or saw, and may become permanently deformed.
(b) since the physes are "closed" and there is no bone growth, metaphyseal changes are absent or minimal.
(c) enlargement at the carpal and tarsal regions occurs in equines. The flat bones of the head and pelvis are prominently thickened and distorted, and due to the stress of weight-bearing, the pelvis is markedly deformed (fig. Ib2-7).
(3) microscopic appearance. There are unusually wide seams of osteoid, which may persist on quiescent bone surfaces (figs. Ib2-8, Ib2-9, Ib2-10).
(4) causes and significance. Much the same as given under rickets. Phosphorus deficiency is a common cause of reduced bone mass (osteopenia) and improper bone mineralization (osteomalacia) in cattle.
(5) pathogenesis.
(a) during normal activation of the remodeling cycle, osteoclasts remove bone, and osteoblasts deposit osteoid and are active in the mineralization process.
(b) in osteomalacia, there is a decrease in the rate of calcification (calcification rate) and
(c) an increase in the time between osteoid deposition and the onset of mineralization (increased mineralization lag time) that leads to:
(i) an increase in the width of unmineralized osteoid (wide osteoid seams) and
(ii) an increase in the area of bone surfaces covered with osteoid (hyperosteoidosis).
c. Fibrous Osteodystrophy (osteitis fibrosa cystica, osteodystrophia fibrosa)
(1) definition. Marked bone resorption, fibrous replacement, and increased activation of bone remodeling that is the direct result of continuous and excessive action of parathyroid hormone on bone.
(2) macroscopic appearance.
(a) the bones in general, and especially the ones with higher turnover, such as the mandible and maxilla, gradually soften and become flexible and deformed (fig. Ib2-11).
(b) at the same time, long bones are easily fractured and are painful when bearing weight.
(c) radiologic examination shows widespread areas of rarefaction, sometimes with cystic spaces (figs. Ib2-12, Ib2-13).
(3) microscopic appearance. Severely affected bones show a marked disappearance of osseous tissue, which occurs because activation of remodeling leads to bone resorption and an increase in the number of resorption cavities (fig. Ib2-14).
(a) hyperparathyroidism can be recognized early as an increase in eroded trabecular surfaces (figs. Ib2-15, Ib2-16).
(b) numerous osteoclasts, each in a Howship's lacuna, are seen on trabecular surfaces, and marrow fibrosis begins close to bone trabeculae, initially in regions of resorption (fig. Ib2-15).
(c) as the condition progresses, dissection osteoclasia becomes a pathognomonic feature as groups of osteoclasts can be seen as if boring into the center of bone trabeculae (fig. Ib2-16).
(d) in more severe cases, cortical bone is characterized by enlarged Haversian canal centers, leading to loss of bone substance (fig. Ib2-17).
(e) the remodeling space formerly occupied by calcified bone is filled by fibrous connective tissue.
(f) in some places, osteoclasts line the surfaces of receding bone; and in others, osteoblasts attempt to replace lost bone (fig. Ib2-18).
(g) as the disease becomes chronic, large portions of cortical bone are replaced by trabeculae of woven bone, many of which remain unmineralized (figs. Ib2-19, Ib2-20).
(h) a distinctive feature is the irregular pattern of mineralization of the osteoid (fig. Ib2-21).
(i) the fibrous tissue may undergo cystic degeneration in places, probably because of insufficient blood supply.
(4) causes.
(a) hyperparathyroidism can be seen in several different animal conditions:
(1) primary hyperparathyroidism, usually the result of a functioning parathyroid adenoma, is uncommon in animals.
(2) secondary hyperparathyroidism is without question the commonest cause of fibrous osteodystrophy in animals.
(i) in animals, secondary hyperparathyroidism occurs in nutritional deficiencies (nutritional secondary hyperparathyroidism) and in chronic renal disease.
(ii) the lesions are similar to those of primary hyperparathyroidism but with the added features of osteomalacia.
(5) hypocalcemia, regardless of cause, is the stimulus for increased activity of the parathyroid glands.
(6) pathogenesis.
(a) the condition is the result of hyperparathyroidism (fig. Ib2-22), which is responsible for a marked increase in activation of bone remodeling sites (fig. Ib2-23).
(b) since many more osteons are in the remodeling process during any one period of time, the remodeling space formerly occupied by osseous tissue is increased.
(c) at this stage, the bone disease is reversible (fig. Ib2-24).
(d) fibrosis of the marrow cavity that is closely applied to the surfaces of bone trabeculae occurs early.
(e) eventually, there is significant loss of cortical bone, which is replaced by trabeculae of poorly mineralized woven bone. Thus, there is marked osteopenia.
d. Osteoporosis
(1) definition. An atrophic disorder in which the mass of the bone is below normal (osteopenia) for the age, sex and species, but the bone is adequately mineralized. Bones are brittle and porous and are less resistant to cutting and sawing.
(2) macroscopic appearance.
(a) cortical bone is reduced in thickness,
(b) porosity is increased, and
(c) the medullary cavity of long bones may be increased in diameter (fig. Ib2-25).
(d) the amount of cancellous bone is also reduced with the trabeculae becoming thin, less numerous and more widely separated (fig. Ib2-26).
(e) the bones have increased fragility, and pathologic fracture is common.
(f) abnormally bent bones with thin cortices and increased bone diameter may indicate that osteoporosis occurred as an aftermath of previous nutritional osteodystrophy (fig. Ib2-26).
(3) microscopic appearance.
(a) the cortices of bone are thin and porous.
(b) bony trabeculae of the spongiosa are thin, reduced in number, and
(c) the connections between adjacent trabeculae are reduced (figs. Ib2-27, Ib2-28).
(d) the surfaces of bone usually are quiescent, indicating that the events that led to bone loss occurred previously or operated slowly (figs. Ib2-29, Ib2-30).
(e) in special cases where there is high bone turnover (see pathogenesis), biopsy may show active remodeling sites.
(f) in all cases, the trabeculae appear adequately mineralized, but increased bone fragility may result in bone fracture.
(g) increased bone fragility can not be accounted for solely on the basis of reduction in bone mass.
(h) osteoporosis affects mainly the endosteal envelope.
(i) during normal aging, negative bone balance is responsible for continuous erosion and trabeculation of the cortex on the endosteal surface (i.e. replacement of compact bone by trabecular bone) and thinning and loss of trabeculae of the spongiosa in the center of the medullary cavity. This process is accelerated in osteoporosis.
(4) causes:
(a) nutritional. Inanition or malnutrition due to deficiencies in calcium, phosphorus, copper, vitamin C or protein.
(b) metabolic. Chronic acidosis.
(c) endocrine. Excess of corticosteroids, parathyroid hormone, and thyroid hormones or reduced secretion of estrogens or androgens.
(d) age-related. Senile osteoporosis.
(e) disuse. Sudden withdrawal of mechanical loading, weight bearing, or physical exertion against gravity leads to disuse osteoporosis (fig. Ib2-31).
(5) pathogenesis.
(a) growth-modeling dependent.
(i) longitudinal and transverse growth is ultimately responsible for the final amount of bone present at maturity.
(ii) during growth, bone modeling expands the outer and inner diameters of the cortex at different rates.
(iii) too rapid an expansion of the marrow cavity, as in nutritional deficiencies, can lead to thin cortices.
(b) remodeling-dependent.
(i) the amount of spongiosa that is retained is dependent on its turnover and the degree of imbalance between resorptive and formative processes.
(ii) slow bone loss occurs when there is negative bone balance (fig. Ib2-24 C).
(iii) the resorption phase of the basic multicellular unit may be of normal or reduced size, but these are incompletely filled by osteoblasts.
(iv) additional bone loss can occur because excessive depth of osteoclastic resorption of thin trabeculae leads to perforation and discontinuity of bone trabeculae.
(c) reversible osteopenias or high turnover osteopenias arise when the remodeling space is increased because osteoclastic resorption is activated or because the remodeling period is prolonged.
(i) in the osteopenia of thyrotoxicosis or hyperparathyroidism, there is increased activation of remodeling sites and initiation of bone resorption (fig. Ib2-24 B).
(ii) drugs such as bisphosphonates that depress activation of new remodeling sites can prevent reversible osteopenias.
(d) irreversible osteopenia or low-turnover osteopenia is the result of absolute bone volume deficits that usually arise on the trabecular and endocortical surfaces.
(i) during aging, the amount of bone removed during remodeling declines, but the amount of bone that refills the space formed during the resorption phase of the basic multicellular unit declines even more.
(ii) therefore, there is accelerated bone loss even though there is decreased bone resorption.
(iii) conditions that enhance the deficit cause an irreversible osteopenia (fig. Ib2-24 C and D).
(e) disuse osteoporosis.
(i) mechanical usage normally retards remodeling activity.
(ii) acute disuse releases that inhibition, and the number of remodeling sites increases.
(iii) increased remodeling of the cortex increases its porosity.
(iv) disuse may also create a more negative balance between the amount of bone resorbed and formed.
(1) these two activities lead to accelerated loss of spongiosa and increased volume of the marrow cavity (fig. Ib2-31).

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