Abstract
Osteoporotic fracture has a major impact upon health, both in terms of acute and long term disability and economic cost. Peak bone mass, achieved in early adulthood, is a major determinant of osteoporosis risk in later life. Poor early growth predicts reduced bone mass, and so risk of fracture in later life. Maternal lifestyle, body build and 25(OH) vitamin D status predict offspring bone mass. Recent work has suggested epigenetic mechanisms as key to these observations. This review will explore the role of the early environment in determining later osteoporotic fracture risk.
Highlights
Medical Research Council Epidemiology Resource Centre, University of Southampton School of Medicine, Southampton General Hospital, Southampton SO16 6YD, UK; Tel.: +44-23-8077-7624; Fax: +44-23-8070-4021
Osteoporosis is a skeletal disorder characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility [1]
Optimization of peak bone mass may be more amenable to public health strategies and has been shown in mathematical models to be a powerful predictor of age of onset of osteoporosis [6,10]. This crucial characteristic is partly inherited, the currently identified genetic markers only explain a small amount of the variation in individual peak bone mass and fracture risk [11]
Summary
Osteoporosis is a skeletal disorder characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility [1]. Bone mass appears to track through childhood and adolescence to reach a peak in early adulthood, more through an increase of bone size than true volumetric density [7] It declines in older age, through loss of bone tissue (thinning of trabeculae and cortex), with an accelerated rate of decline at the menopause. Optimization of peak bone mass may be more amenable to public health strategies and has been shown in mathematical models to be a powerful predictor of age of onset of osteoporosis [6,10] This crucial characteristic is partly inherited, the currently identified genetic markers only explain a small amount of the variation in individual peak bone mass and fracture risk [11]. Evidence is accruing that environmental factors may act early in development (in utero and early postnatal life), interacting with the genome to produce a persisting influence on postnatal skeletal development
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