The literature examining the association between obesity and bony properties has predominantly focused on bone mineral density (BMD) and bone mineral content (BMC). Compared with normal-weight people, overweight individuals (BMI > 26) have higher BMD and BMC at both weight-bearing (e.g., femur) and non-weight-bearing (e.g., radius) sites (30). Nevertheless, the association between obesity, defined as an increased BMI, and BMD/BMC is not this simplistic and is dependent on several other factors, including body composition. Abdominal obesity, body weight, and muscle strength have emerged as strong correlates of BMD in older persons (31).
Although certain parameters of body composition, such as abdominal obesity, are strongly associated with BMD, gender is arguably the strongest factor that mediates the obesity-BMD relationship. In both men and women, decreased BMD occurs after the age of 50 (32), although women demonstrate greater variability than men. In particular, lean body mass and total fat mass are significant determinants of BMD among postmenopausal women (33). In premenopausal women, lean mass, but not total fat mass, is a significant determinant of BMD. These findings infer that whereas lean body mass is associated with BMD across the female lifespan, adiposity is most strongly associated with BMD after menopause. This may be partly attributable to the interdependence of the increased mechanical forces that occur across the obese skeleton, as well as the metabolic changes, such as the adipose-derived estrogen, that occurs after menopause. Whatever the mechanism, a positive outcome of postmenopausal obesity is its protective role against the onset and progression of osteoporosis, which is characterized by reduced BMD.
Although the association between an increased BMI and BMD/BMC is important in the pathogenesis of osteoporosis, it is likely that other properties of bone are associated with OA. Osteophytosis in the thoracic and lumbar spine is associated with increased BMI (34). Likewise, longitudinal work has demonstrated that women in the top tertile of obesity (BMI > 26.4) have a significantly increased risk of radiographic knee osteophytes (11). Twin studies have demonstrated that for each kilogram increase in body weight, the likelihood of developing osteophytes is greatly increased at the tibiofemoral, patellofemoral, and carpometacarpal joints (35). Nevertheless, few studies have examined the link between measures of body composition and the bony features of OA. Of the limited studies, it does not appear that fat distribution is as strongly associated with the bony features of OA as it is for osteoporosis (26-29).
Some studies have suggested that bone size alters in response to increasing BMI. Studies using DEXA, have reported a positive correlation between BMI and bone area in the tibia and femoral diaphyses in boys and girls (36,37). Whereas one study found that BMI was not significantly correlated with tibial plateau area measured on radiographs (38), another found that both medial and lateral tibial bone area increased significantly with increasing BMI (24). Given such contrasting results, the association between BMI and bone size is equivocal, and whether a greater BMI can induce sub-chondral bone growth is unclear. Future work is required to examine such issues, as well as determining whether the features of body composition, such as adiposity and lean body mass, are associated with bony properties. Such work will have important ramifications for the prevention and management of joint diseases, most prominently OA. In particular, if cartilage volume reduces with the passage of time, and bone size is increased, then theoretically the combined result of these two events may result in the exposure of highly innervated articular bone surfaces and the presentation or progression of symptomatic and radiological OA.
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