Bone Abstracts

The epidemiological evidence is clear that higher body weight is protective against most fractures in adults. However, the same may not be true in children. Understanding the mechanisms of interaction of fat and bone may give useful insights into underlying physiology for prevention of fracture.

In general, higher body weight in adults is associated with higher bone mineral density and is protective against fracture, but may be associated with an increased risk of some fractures. Possible mechanisms for higher bone density include mechanostat response to increased loading and increased oestrogen production by adipocyte aromatase. Increased soft tissue padding may also contribute to reduced fracture risk, particularly at the hip.

In children, obesity may be associated with impaired bone accrual and obese children with fracture have a bone mass deficit relative to their body size and lean mass.

It has been increasingly recognised that bone interacts with other organs and tissues (such as fat, the gastrointestinal tract and the CNS), and also that fat is not just a passive energy reservoir but an endocrine organ with regulatory functions. Fat may have effects on bone through the central and peripheral actions of leptin and other adipokines.

Higher body weight may result from more muscle mass or more fat mass. For a given body weight, greater adiposity may be associated with lower bone density. Subcutaneous and visceral fat may have differing effects on bone; visceral fat produces inflammatory cytokines which may have pro-resorptive effects on bone, and higher visceral fat mass has been associated with increased bone turnover and lower bone density.

These results suggest that the relationship between fat and bone may be more complex than first thought.