Taehoon Park, Kyungwon Seo, Ki Hyun Kim, Yoonhong Kim, Bukyung Kim
Patients with obesity demonstrated site-specific reductions in trabecular bone quality, particularly in the lower lumbar spine compared with non-obese people. IR was independently and inversely associated with TBS, suggesting that metabolic dysfunction, not mechanical loading, influences bone fragility in obesity. TBS represents a valuable adjunct to BMD for assessing skeletal health in metabolically impaired obese populations.
BACKGROUND: Obesity has been considered protective against osteoporosis due to its association with higher bone mineral density (BMD). However, metabolic dysfunction, particularly insulin resistance (IR), may compromise bone quality even with BMD preserved.
METHODS: This retrospective cross-sectional study (n=254) included 153 individuals with severe obesity undergoing bariatric metabolic surgery and 101 age- and sex-matched non-obese controls. BMD and trabecular bone score (TBS) were measured using dualenergy X-ray absorptiometry. A subgroup of participants with obesity was further analyzed to examine associations between IR, assessed using the homeostasis model assessment of insulin resistance (HOMA-IR), and bone parameters.
RESULTS: BMD was significantly higher in the obese group, indicating preserved bone mass in obesity. But the proportions of spine-hip Z-score discordance was significant higher in the obese group (P=0.001). TBS displayed sitespecific findings: TBS at L1 was significantly higher in the obese group (P=0.002), whereas no significant differences were observed at L2-L4. Partially degraded or degraded TBS were higher in the obese group (P=0.021). Among participants with obesity, TBS decreased progressively across HOMA-IR quartiles (P=0.043), whereas BMD remained stable. In multivariable regression, higher HOMA-IR was independently associated with lower TBS (β=-0.0025; 95% confidence interval, -0.0043 to -0.0006; P=0.015), although this association was attenuated by hemoglobin A1c adjustment.
CONCLUSION: Patients with obesity demonstrated site-specific reductions in trabecular bone quality, particularly in the lower lumbar spine compared with non-obese people. IR was independently and inversely associated with TBS, suggesting that metabolic dysfunction, not mechanical loading, influences bone fragility in obesity. TBS represents a valuable adjunct to BMD for assessing skeletal health in metabolically impaired obese populations.