Qiqi Wang, Hongyan Li, Huan Yu, Tianyu Zhou, Jingdan Zhang, Rongkaixuan Fang, Yue Sun, L. A., Wenzhou Xu
In obesity, the pathological remodeling of adipose tissue characterized by hyperplasia and hypertrophy serves as a critical hub driving chronic inflammation. This process triggers adipose microenvironment disruption, manifesting as reduced angiogenesis, excessive extracellular matrix deposition, dysregulated adipokine secretion, and enhanced immune cell infiltration, ultimately leading to a systemic low-grade inflammatory state. Functioning as an active inflammatory organ, dysfunctional adipose tissue specifically exacerbates periodontitis progression through multiple mechanisms: including glucose/lipid metabolic imbalance, dysregulated bone metabolism with imbalanced osteoclast-osteoblast activity, immunometabolic disturbances, microcirculatory impairment, degradation of periodontal extracellular matrix and dysfunction of epithelial barrier and gut microbiota dysbiosis. This review systematically elucidates the interactive mechanisms between adipose tissue-derived inflammatory signaling and periodontal pathology, emphasizing its central role in obesity-associated periodontal diseases. Based on these mechanisms, we propose targeted intervention strategies: modulating adipokine secretion, suppressing immune cell infiltration in adipose tissue or restoring adipose tissue metabolic homeostasis may emerge as novel approaches to disrupt the obesity-periodontitis vicious cycle. Future studies might enhance the clinical translation of multi-organ treatment approaches that target the adipose tissue-periodontium axis while continuing to explore the regulatory effects of immune pathways specific to adipose tissue on the periodontal microenvironment.