Treatment of osteoporosis: role of bone-forming agents.

Abstract

Osteoporosis is characterized by a decrease in bone mass and a deterioration in skeletal microarchitecture leading to an increased fragility and susceptibility to fractures [1]. In treating established osteoporosis, the objective is to prevent further skeletal deterioration, improve bone mass and/or bone microarchitecture to provide a documented reduction of the risk of vertebral and/or peripheral fractures [2]. Care takers often face complicated situations with women consulting for the first time at later stages of the disease, namely after the diagnosis of osteoporosis has already been made on the basis of random radiographs, densitometry measurements or, even worse, a fracture. Unfortunately, none of the antiresorptive medications has unequivocally demonstrated the ability to prevent fully the occurrence of new vertebral or peripheral osteoporotic fractures once the disease is established. Although promising results have been reported with inhibitors of bone resorption [3–7], patients treated with these drugs usually achieve modest increases in bone mass that translate into a partial reduction of incident fractures when compared with the rate observed in subjects receiving a placebo or treated with calcium alone. Although emerging bisphosphonate drugs [8,9] seem to be more effective and better tolerated, there is little chance their use will restore bone mineral density to normal values and radically prevent the occurrence of new fracture events. Therefore, there is an urgent need for the development of medications that stimulate osteoblast activity to such an extent that bone density can be brought back to values observed in normal subjects. However, for the positive effect of a drug on bone mineral content to translate into a decrease in fracture rate, it is mandatory that pharmacologic intervention does not induce deleterious effects in the biochemical properties of the skeleton [2]. Parathyroid Peptides