Published online by Cambridge University Press: 08 August 2009
Introduction
Osteoporosis is a multifactorial skeletal disorder characterised by low bone mass and microarchitectural deterioration of bony tissue, with a consequent increase in the risk of fracture (Jordan and Cooper 2002). The bone mass of an individual in later life depends upon the peak obtained during skeletal growth, and the subsequent rate of bone loss. Preventive strategies against osteoporotic fracture may be aimed at either increasing the peak bone mass attained or reducing the rates of bone loss. As shown in the previous chapter, epidemiological studies have indicated that poor growth during fetal life, infancy and childhood is associated with decreased bone mass in adulthood and an increased risk of fracture (Cooper et al. 1995, 1997, Fall et al. 1998). These relationships appear to be mediated through the programming of metabolic and endocrine systems governing bone growth, by environmental influences acting during critical periods of intrauterine or early postnatal development (Barker 1995, 2000, Barker and Martyn 1997, Godfrey and Barker 2001). In particular, maternal nutrition appears to be important in determining skeletal size at maturity. However, to date, there is little understanding of the cellular and molecular mechanisms whereby environmental modulation in utero could lead to an altered skeletal development among the offspring. This review will examine the benefits and information gained from animal models of intrauterine programming (maternal dietary modulation) with respect to the skeletal development of the young offspring, peak bone mass and bone quality of aged offspring, and will correlate to other animal studies undertaken ex utero and, as appropriate, to the human scenario.
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