Tatiana-Maria Chiuariu, Dorin Ioan Cocoș, Mariana Ilie, Ada Stefanescu, Petru Trifautanu, Dobri Viviana Sorina, Ilie Mihai Luca, Dobri Roberto-Adrian, Buga Vladimir, Vaschevici Ludmila, Alina-Ramona Dimofte, Kamel Earar
ABSTRACT
Periodontitis is a prevalent chronic inflammatory disease characterized by progressive destruction of the tooth-supporting structures, often leading to tooth loss. While the role of dysbiotic oral microbiota in initiating periodontal inflammation is well established, recent studies highlight the critical involvement of host metabolic pathways, particularly the tricarboxylic acid (TCA) cycle, in disease progression. Among TCA cycle intermediates, succinate has emerged as a potent signaling molecule that accumulates in periodontal tissues and biological fluids during inflammation. Succinate exerts its effects through activation of the succinate receptor 1 (SUCNR1), a G-protein-coupled receptor expressed on immune and stromal cells. Activation of SUCNR1 amplifies pro-inflammatory cytokine production, enhances osteoclast differentiation, and promotes alveolar bone loss. Experimental models demonstrate that genetic deletion or pharmacological inhibition of SUCNR1 effectively reduces periodontal inflammation and bone resorption without compromising systemic immunity. These findings position SUCNR1 as a promising therapeutic target for modulating the host response in periodontitis. Additionally, elevated succinate levels in saliva or gingival crevicular fluid show potential as non-invasive biomarkers for disease monitoring. This review summarizes the current knowledge on the role of succinate and SUCNR1 in periodontitis and discusses the therapeutic perspectives of targeting this pathway.
Loading...
Reload document 
Open in new tab