Last update:
27-Apr-2016

The belief that obesity protects against fractures was prevalent until recently, when researchers began questioning its possible protective action and exploring its complex effects on bone mass and strength. Adipose tissue and bone are associated by many pathways, which involve leptin, adiponectin, adipocyte estrogen and the insulin/amylin interaction, which ultimately serve the function of providing an adequate backbone for the mass of adipose tissue which it supports. Excess body fat, however, and especially abdominal fat, produces inflammatory cytokines that can stimulate bone resorption and reduce thus bone strength. Obesity is associated with increased risk of a number of chronic diseases, including diabetes mellitus, osteoarthritis, chronic obstructive pulmonary disease (COPD) and cardiovascular disease. The main cause of obesity in children and adults is considered to be an increase in energy intake relative to energy expenditure. The risk of fracture is associated with obesity via osteoporosis, which is an important fracture risk factor. Risk factors can be assessed using the algorithm FRAX, which has been developed by WHO based on relevant studies to provide an overall risk estimate. Obesity leads to osteoporosis both through the resistance to leptin and by deficiency of vitamin D. Many studies demonstrate the correlation between obesity and increased risk of fracture, particularly through osteoporosis, but positive benefits of obesity in patients with osteoporosis have also been documented. There is a need for further investigation of the role of obesity in fracture risk, linking the role of genes and hormones and daily physical activity with the occurrence of fracture.

Key words: Bone metabolism, Diabetes mellitus, Fracture risk, Obesity, Osteoporosis.