Jiang Shuai, Liang Chen, Jing Jing, Wang Mengmeng, Sun Hao, Zuo Bingli
Qingdao Stomatological Hospital Affiliated to Qingdao University, Qingdao, 266001, China.
Outpatient Department, Qingdao Municipal Hospital, University of Health and Rehabilitation Sciences, Qingdao, 266011, China.
BMC Oral Health. 2025 Jul 2;25(1):1015. doi: 10.1186/s12903-025-06362-y.
Obesity is a well-established risk factor for periodontitis, a chronic inflammatory disease with systemic implications. While diabetes has been proposed as a potential mediator in this relationship, its clinical heterogeneity limits its utility in causal modeling. Insulin resistance, quantified by the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), offers a more mechanistically grounded alternative.
This study aimed to investigate the associations between obesity, insulin resistance, and periodontitis, with a specific focus on the mediating role of HOMA-IR.
Data from the National Health and Nutrition Examination Survey (NHANES, 2009-2012) including 8,473 participants were analyzed. Obesity was assessed using body mass index (BMI) and waist circumference (WC), and insulin resistance was measured using HOMA-IR. Periodontitis was evaluated using clinical attachment loss and probing depth. Multivariable logistic regression, restricted cubic splines, and mediation analyses were conducted.
Both BMI and WC were significantly associated with an increased risk of periodontitis (P < 0.05). HOMA-IR was positively associated with periodontitis risk (P < 0.01). Mediation analysis revealed that HOMA-IR mediated 63.44% of the association between BMI and periodontitis and 36.77% of that between WC and periodontitis. Nonlinear analyses showed no significant nonlinear trends.
Insulin resistance, as reflected by HOMA-IR, plays a significant mediating role in the relationship between obesity and periodontitis. These findings underscore the importance of early metabolic regulation in mitigating obesity-related periodontal risk and provide mechanistic insight into the interplay between systemic and oral health.
肥胖是牙周炎这一具有全身影响的慢性炎症性疾病的既定风险因素。虽然糖尿病被认为是这种关系中的潜在中介因素，但其临床异质性限制了其在因果模型中的效用。通过胰岛素抵抗稳态模型评估（HOMA-IR）量化的胰岛素抵抗提供了一种更具机制基础的替代方法。
本研究旨在调查肥胖、胰岛素抵抗和牙周炎之间的关联，特别关注HOMA-IR的中介作用。
分析了来自国家健康与营养检查调查（NHANES，2009 - 2012年）的8473名参与者的数据。使用体重指数（BMI）和腰围（WC）评估肥胖，使用HOMA-IR测量胰岛素抵抗。使用临床附着丧失和探诊深度评估牙周炎。进行了多变量逻辑回归、受限立方样条分析和中介分析。
BMI和WC均与牙周炎风险增加显著相关（P < 0.05）。HOMA-IR与牙周炎风险呈正相关（P < 0.01）。中介分析显示，HOMA-IR介导了BMI与牙周炎之间63.44%的关联以及WC与牙周炎之间36.77%的关联。非线性分析未显示显著的非线性趋势。
HOMA-IR所反映的胰岛素抵抗在肥胖与牙周炎的关系中起显著的中介作用。这些发现强调了早期代谢调节在减轻肥胖相关牙周风险方面的重要性，并为全身健康与口腔健康之间的相互作用提供了机制性见解。
