Endocrine Abstracts

Introduction: The interaction between obesity and bone metabolism is complex and not fully understood. Historically, higher body weight was considered to be protective against osteoporosis. This association has affected clinical practice: body mass index (BMI) is one of the variables included in Fracture Risk Assessment Tool (FRAX), where a higher BMI leads to a lower fracture risk. Despite this association between bone mineral density (BMD) and body weight, it is not clear whether it prevails for higher BMI values, or which components of body composition are responsible for this correlation. The aim of our study was to evaluate the impact of BMI and body composition on BMD in patients with obesity.

Methods: Cross-sectional study including patients with obesity from a tertiary hospital. To assess BMD, T-score value was used for postmenopausal women or men aged 50 or over; Z-score value for the remaining patients. Body composition was assessed by bioimpedance and DEXA.

Results: A total of 30 patients were included, 80% female, mean age of 45±11 years. Mean BMI was 42.1±5.9 kg/m² (70% in class III obesity). Mean fat mass percentage was 51.9±10.6% and 47.8±5.9%, as measured through bioimpedance and DEXA, respectively. There was no significant correlation between BMI and BMD (P=0.251). There was a negative correlation between total body BMD and body fat mass percentage assessed by bioimpedance (r=-0.423; P=0.040) and by DEXA (r=-0.730; P=0.003). Femoral neck BMD was negative and weakly correlated with body fat mass percentage assessed by DEXA (r=-0.455; P=0.022). Although there was no significant correlation between visceral adipose tissue and total body BMD (P=0.097), there was a negative and weak correlation between visceral adipose tissue index and femoral neck BMD (r=-0.448; P=0.025).

Conclusions: Our study challenges the belief that obesity is protective against osteoporosis, suggesting that increased fat mass should act as a red flag for the development of osteoporosis. The exact mechanism for the effects of obesity on bone health remains unclear. Several mechanisms have been proposed: accelerated senescence in stromal stem cells; increased inflammation (especially visceral adiposity, due to associated low-grade chronic systemic inflammation); replacement of osteoblasts by adipocytes in bone marrow; mutations in the obesity-associated genes leading to bone fragility. In our study, fat mass had a negative impact on femoral neck BMD, suggesting that body fat may selectively affect cortical rather than trabecular bone. The effects of fat mass on skeletal strength might be site dependent.