Necroptosis and its role in the pathogenesis and treatment of temporomandibular joint osteoarthritis: A narrative review

Objective: This review aimed to explore the role of necroptosis in the pathogenesis and treatment of temporomandibular joint osteoarthritisjoints. We sought to elucidate the mechanisms by which necroptosis contributes to arthritis development and identify potential therapeutic targets within the necroptosis pathway. Design: An electronic literature search was conducted in PubMed, Scopus, EBSCO, ProQuest, ScienceDirect, and Springer for studies on necroptosis, arthritis, and temporomandibular joint osteoarthritis published between 2004 and 2024. Results: Necroptosis, a programmed cell death pathway characterized by the activation of receptor-interacting protein kinase 1/3, leads to cell membrane rupture and the release of damage-associated molecular patterns, which are instrumental in promoting inflammation. This review highlights the involvement of necroptosis in the progression of multiple types of arthritis, especially temporomandibular joint osteoarthritis. These findings highlight the potential of necroptosis inhibitors as therapeutic agents, with several small-molecule inhibitors demonstrating efficacy in preclinical models of arthritis. Conclusions: Necroptosis is a significant factor in the pathogenesis of arthritis, particularly temporomandibular joint osteoarthritis, and represents a promising therapeutic target. Targeting the necroptosis pathway may offer a novel approach for managing joint damage and osteochondral inflammation. Further research is necessary to fully understand the mechanisms of necroptosis in temporomandibular joint osteoarthritis and to develop targeted therapies for clinical application.