Abstract
The effects of preterm birth and perinatal events on bone health in later life remain largely unknown. Bone mineral density (BMD) and osteoporosis risk may be programmed by early life factors. We summarise the existing literature relating to the effects of prematurity on adult BMD and the Developmental Origins of Health and Disease hypothesis and programming of bone growth. Metabolic bone disease of prematurity and the influence of epigenetics on bone metabolism are discussed and current evidence regarding the effects of breastfeeding and aluminium exposure on bone metabolism is summarised. This review highlights the need for further research into modifiable early life factors and their effect on long-term bone health after preterm birth.
Highlights
Preterm birth accounts for 5–10% of births in the UK
We present a review of the current literature regarding early life factors and the impact of nutrition on bone mineral density and bone health after preterm birth, in order to inform further research and highlight current challenges facing the clinicians responsible for this cohort
Metabolic bone disease of prematurity is often asymptomatic and self-limiting [9], concern remains that under-mineralisation during such a critical period could increase the risk of childhood fracture and cause reduced peak bone mass [26] and an increased risk of future osteoporosis
Summary
Preterm birth accounts for 5–10% of births in the UK. Worldwide almost 10% of babies are born preterm, representing more than 15 million births every year [1]. More than 50% of babies born at 24 weeks gestation regularly survive long term with improved nutrition being one potential factor contributing to these improvements As this cohort of survivors reaches middle age the impact of preterm birth on long-term metabolic outcomes such as bone mineral density will become increasingly important. A retrospective study involving term infants demonstrated independent effects of birth weight and weight at one year on bone size and strength during the sixth and seventh decades after adjustment for confounding lifestyle factors [12] These associations may reflect the intrauterine programming of skeletal development [13] and its subsequent tracking throughout the lifecourse. It is proposed that this remaining variation results from the programming of systems controlling skeletal growth trajectory during critical growth periods [13]
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