Resorption, of bone

In normal bone, resorption and bone formation occur continuously, although to a lesser degree in the mature than in the immature skeleton. It is the coupling of bone resorption to bone formation that controls the volume of bone present at any particular time; if bone resorption exceeds bone formation, a net loss of bone volume occurs. Synthesis and resorption of bone are mediated by the action of humoral agents; parathyroid hormone, calcitonin and vitamin D are among the compounds that influence bone resorption directly or indirectly.

Bone modelling and remodelling also require closely coordinated processes of resorption and apposition.

In patients with primary or secondary hyperparathyroidism, bone resorption is evident on histological and radiological examination, especially in the hands in the early stages of the disease. The resorption can be categorized into various types. Subperiosteal resorption of cortical bone is virtually diagnostic of hyperparathyroid bone disease. In this form, a lacelike appearance of the phalangeal bone may progress to a spiculated contour and, eventually, to complete resorption of the entire cortex. Other sites of subperiosteal resorption include the phalangeal tufts; medial aspect of the proximal ends of the tibia, humerus and femur; superior and inferior margins of the ribs; and lamina dura. Subperiosteal resorption of bone may also be apparent at the margins of certain joints, especially those in the hand, wrist and foot. Sometimes the erosions simulate the appearance of rheumatoid arthritis. Intracortical resorption by osteoclasts within cortical haversian canals can produce radiographically detectable intracortical linear striations; these are best observed in the cortex of the second metacarpal bone. Endosteal resorption, particularly in the hands, may be observed on radiographs as localized defects along the inner margin of the cortex, reminiscent of abnormalities occurring in multiple myeloma. Subchondral resorption, a common manifestation of hyperparathyroidism, is most frequent in the sacroiliac, sternoclavicular and acromioclavicular joints, symphysis pubis and discovertebral junctions. Subphyseal resorption may occur in children with primary or secondary hyperparathyroidism. Irregular radiolucent areas may appear in the metaphysis adjacent to the growth plate, reminiscent of the abnormalities accompanying rickets. Trabecular resorption within medullary bone occurs throughout the skeleton in hyperparathyroidism. Subligamentous and subtendinous resorption is sometimes seen at sites of tendon and ligament attachment to bone, especially in hyperparathyroidism. This occurs particularly frequently at the femoral trochanters, ischial and humeral tuberosities, elbow, inferior surface of the calcaneus, and inferior aspect of the distal end of the clavicle.

Resorption of bone also occurs in numerous other pathologic conditions, including rheumatoid arthritis, scleroderma, acromegaly and Gauchers disease. Phalangeal tufts may undergo resorption in frostbite, mixed connective tissue disease, renal osteodystrophy, systemic lupus erythematosus and psoriatic arthritis.

Bone mineral analysis makes use of numerous methods for measuring the extent of bone loss from resorption.

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