[Differential therapy of osteoporosis--an overview based on recent findings regarding the pathogenesis].

Osteoporosis had long been considered as an unavoidable consequence of aging for which no prevention was possible, whereas it has recently been recognized as a disease that can be prevented and treated. It is of outstanding importance to choose a therapy tailored to the individual patient based on new findings on the pathogenesis of the different types of osteoporosis and the differential diagnosis related to these. During phases of rapid bone loss, usually at the beginning of postmenopause, but sometimes also in older patients, it is useful to use therapeutic drugs to slow down the high bone turnover to a physiological level when osteoporosis is imminent or manifest. The ideal therapy of established osteoporosis should stimulate bone formation and increase bone mass as well as correct changes in the architecture so that the incidence of new fractures will be reduced or even prevented. In case of an increased fragility, it is especially advantageous to increase the cortical bone mass and to stimulate periosteal bone formation in particular. Therapies increasing cortical porosity such as the administration of fluoride in large doses weaken the bones. Therapies reducing bone remodeling in the long term can inhibit bone reparation and compensatory periosteal bone formation, however. Future prospects for the therapy of osteoporosis using drugs are, on the one hand, an improved exploitation of present strategies by means of new galenical types of application, changes in the daily dosage, the introduction of interval therapies, and synergistic effects due to suitable combinations. On the other hand, new developments achieved by varying chemical structures, e.g., the structures of bisphosphonates and vitamin D metabolites and, above all, new strategies leading to increased bone mass while maintaining or even improving bone structure are urgently required. In addition to the vitamin D metabolites, mainly the parathyroid hormone fragments and growth hormones seem to be promising to achieve this aim. The direct use of cytokines (IGF-1, IGF-2, TGF-beta, etc.) is not yet possible because there is no suitable "drug targeting". An increase in bone mass that has been clinically documented does not necessarily indicate an increased mechanical stability. Bone quality results from a complex relationship between bone mass, bone structure, and the strength of the individual structure elements. Its quantitative measurement and influencing by therapies will be a great challenge to future osteoporosis research.