Bone Abstracts

For many years obesity has been considered to be protective against fragility fractures, since low BMI contributes to fracture risk. However, recent studies indicate that obese women represent a subset of patients with low-trauma fractures. In fact, obesity increases the risk of fracture at specific sites such as ankle, upper and lower leg and predictably, proximal humerus. By contrast, wrist, hip and pelvis fracture rates are lower in obese women. Interestingly, the majority of fractures occur in spite of a very low rate of osteoporosis by DXA measurements, although obese women who sustain fractures usually have lower BMD than those without fractures. The increased risk of falling, the different patterns of falls and the higher impact of the fall due to the high body weight may be related to this site-dependent increased fracture risk. Conversely, greater soft tissue padding may reduce skeletal trauma protecting against fractures in well-padded central body sites. The effects of fat on bone may differ according to its distribution. Thus, high visceral adipose tissue is detrimental to bone, unlike subcutaneous fat, reasonably because of lower levels of leptin and higher levels of adiponectine and pro-inflammatory cytokines. In addition, visceral fat is associated with decreased GH and testosterone in males, with deleterious effects on microarchitecture. Decreased levels of vitamin D and high levels of PTH contribute to the picture of bone disease in obesity.

Bariatric surgery, which includes restrictive, malabsorptive and combined procedures, is the most effective route to weight loss in morbid obesity. Bariatric surgery has been linked to a reduction of BMD, without a significant effect on fracture risk for the first few years after surgery. Of interest, frequent nutritional and metabolic deficiencies have been observed, particularly in malabsorptive procedures, including calcium and vitamin D deficiency.