Interleukin-1β–Mediated Orofacial Bone Defects and Alveolar Bone Loss in Periodontal Disease: A Scoping Review

Abstract : Orofacial bone defects, particularly alveolar bone loss, are hallmark features of periodontal disease and represent a significant clinical challenge affecting oral function and quality of life. Interleukin-1β (IL-1β) has emerged as a key pro-inflammatory cytokine mediating the link between periodontal inflammation and osteoclastic bone resorption. This scoping review using keywords related to orofacial bone defects, alveolar bone loss, and IL-1β, published between 2016 and 2026. The studies included experimental models, animal studies, and clinical observations. Results consistently indicate that ligature induced periodontitis and microbial dysbiosis upregulate IL-1β expression, correlating with enhanced alveolar bone resorption. Interventions such as desipramine, epigallocatechin-3-gallate (EGCG), curcumin, and four-day fermented milk kefir demonstrated reductions in IL-1β levels alongside attenuated alveolar bone loss, highlighting the functional role of IL-1β in periodontal bone destruction. Immune modulation studies, including TLR-activated B10 cell transfer and Ifi204-deficient mouse models, further suggest that IL-1β–mediated osteoclast activity contributes directly to alveolar bone resorption independently of certain bone marrow–derived immune cell responses. Mechanistically, IL-1β promotes osteoclastogenesis via upregulation of RANKL and matrix metalloproteinases while downregulating tissue inhibitors of metalloproteinases. Collectively, the findings underscore IL-1β as a pivotal mediator in periodontitis-related bone loss and as a promising therapeutic target. Understanding these IL-1β mediated pathways informs the development of novel anti-inflammatory and regenerative strategies to improve oral and dental health outcomes.