Clin Osteol 2011; 16(2): 38-42

Atypical fractures and long-term antiresorptive therapy of osteoporosisReview articles

J. Štěpán, J. Vaculík, P. Dungl

Skeletal remodelling replacing weak bone with new bone is the key event regulating bone mass and quality. The decrease in osteoblast activity and the rate of involutional bone loss with age in healthy individuals may be negatively influenced by circulating endogenous glucocorticoids. Chronic imbalances in bone remodelling may result in disabling bone diseases such as osteoporosis. Reductions in the number of active remodelling sites by antiresorptive drugs reduce the loss of bone that occurs through remodelling and maintains bo­ ne mineral density (BMD) and architecture. The antiresorptive drugs suppress specifically at the remodelling sites and probably do not have a direct effect on bone formation. The individual antiresorptive drugs vary with respect to magnitude of suppression of me­ tabolic bone turnover by speed of onset and duration of effect. An increased mean tissue age and accumulation of microdamage in bo­ ne was demonstrated after alendronate treatment. However, an increased bone mass in long-term treatment with antiresorptive drugs may, at least for the first five years, compensate for altered bone quality, particularly in most women with postmenopausal osteoporo­ sis. Rarely, long-term treatment of osteoporosis with potent antiresorptive drugs may result in serious side effects where impaired bo­ ne quality is manifested by increased predisposition to poorly healing fractures, particularly of the femoral shaft after minimal trauma at a given BMD. Bone biopsies of these individuals often demonstrate suppressed remodelling. Interestingly, inhibition of osteoblasts by glucocorticoids, the major cause of progressive bone loss, is associated with one-third of these fractures. Also, up to 86% of bis­ phosphonate-treated patients in whom osteonecrosis of the jaw developed were exposed to systemic steroids. In contrast to the effects experienced by patients receiving alendronate, glucocorticoid-treated patients receiving teriparatide experienced accelerated bone re­ modelling and decreased risk of vertebral fractures. In a continuation study, slight but significantly sustained increases in markers of bone formation were observed over 36 months. Currently available data seline, further suppression of osteoblast activity should be avoided.

Keywords: bone quality, fracture, osteoporosis, remodelling

Published: December 11, 2011  Show citation