Obesity and skeletal fragility: revisiting an old paradigm

Obesity has traditionally been considered protective against osteoporosis because of its association with higher bone mineral density (BMD). However, emerging evidence demonstrates that individuals with obesity remain at increased risk of peripheral fractures despite preserved BMD. This review summarizes current evidence on the complex relationship between obesity and skeletal health, including underlying mechanisms, fracture patterns, assessment strategies, and management considerations.

Studies indicate that fracture risk in obesity is site-specific, with a greater propensity for peripheral fractures. Visceral adiposity, bone marrow adipose tissue, chronic low-grade inflammation, altered adipokine signaling, gut microbiota dysbiosis, and obesity-related comorbidities contribute to impaired bone quality and skeletal fragility. Conventional Dual Energy X-ray Absorptiometry (DXA) may underestimate skeletal risk in obesity, while newer tools such as trabecular bone score (TBS) version 4.0, peripheral quantitative computerized tomography (pQCT) may improve risk assessment. Weight-loss interventions, including lifestyle modification, Glucagon-like peptide-1 receptor agonists (GLP-1RA), and bariatric surgery, provide substantial metabolic benefits but may increase fracture risk if skeletal health is not adequately addressed.

Obesity should no longer be regarded as protective for bone health. Although BMD is often normal or elevated, obesity is associated with alterations in bone quality and increased fracture susceptibility. Comprehensive skeletal assessment, incorporation of lifestyle measures to preserve bone health, and appropriate osteoporosis therapy are essential. Future research should focus on obesity-specific fracture prediction tools, advanced imaging modalities, and dedicated clinical guidelines for the prevention, diagnosis, and management of osteoporosis in individuals with obesity.