Maintaining the life-long vitality and integrity of skeletal tissue

Abstract

Although decreased bone strength and a consequent increase in fragility fractures has been regarded as an inevitable consequence of aging, there is great variability in this process. Moreover there are new findings concerning the mechanisms by which the skeleton maintains it vitality and integrity that should change this view. There are four basic mechanisms that can lead to decreased bone mass and strength and an increase in fragility fractures. 1) Genetic and lifestyle factors that impair the ability to achieve optimal peak bone mass and strength during childhood and adolescence. 2) Loss of bone mass and microarchitectural deterioration due to increased bone resorption, for which estrogen deficiency is probably the most important cause. 3) Inadequate bone formation during remodeling, which appears to be age related but for which the specific causes are not known. 4) Increased propensity to fall and decreased mobility that may be associated both with age related impairment in neuromuscular function and the use of drugs that impair balance. Substantial advances have been made in our understanding of the bone remodeling cycle, particularly the interaction of osteoblasts and osteoclasts that initiates resorption. Inflammatory cytokines may be involved in this process, but their specific role in human osteoporosis has not been resolved. New information on the roles of osteocytes and the Wnt signaling pathway in the regulation of bone formation indicate that these may be critical in the regulation of skeleton vitality and integrity. Hence new interventions that affect regulators of bone growth and remodeling may be developed that can maintain skeletal tissue and prevent the development of osteoporosis and fragility fractures.