SYSTEMIC LUPUS ERYTHEMATOSUS AND PERIODONTITIS: A NARRATIVE REVIEW OF PHYSIOPATHOLOGICAL MECHANISMS AND POTENTIAL SHARED THERAPEUTIC BENEFITS

Abstract

The present article explored the immunopathogenic interface between Systemic Lupus Erythematosus (SLE) and Periodontitis, highlighting the sharing of inflammatory pathways and the implications of this interaction for clinical practice. This is a narrative literature review, with studies selected from the PubMed and Virtual Health Library (VHL) databases, following eligibility criteria and synthesizing information through descriptive and integrative analysis. The results show that SLE, as an inflammatory condition mediated by the immune system, shares pathophysiological mechanisms with periodontitis, including exacerbated activation of both innate and adaptive immunity. In addition, immune imbalance promotes chronic inflammation and autoimmunity, with increased levels of pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α, and IL-17, which are directly associated with tissue destruction. Both conditions also present common genetic and epigenetic factors, such as polymorphisms in cytokine genes and Toll-like receptors. Oral dysbiosis may intensify the systemic inflammatory response, worsening SLE, while periodontal inflammatory mediators contribute to the exacerbation of the autoimmune disease. It is concluded that there is a bidirectional relationship between SLE and periodontitis, mediated by convergent immunoinflammatory pathways. Recognizing this association is essential for the development of integrated therapeutic strategies aimed at improving systemic health and achieving more effective control of both conditions.