The role of the IL-33-ST2 axis in the pathogenesis of periodontitis

Abstract

INTRODUCTION: Periodontitis is a chronic inflammatory disease that arises from an interaction of local dysbiosis in the subgingival biofilm and the host immune response. The disease triggers an inflammatory process that can cause periodontal tissue breakdown. In addition, the production of inflammatory mediators can negatively affect other areas of the body and influence the development and/or severity of associated disorders, including asthma, diabetes and cardiovascular diseases. OBJECTIVE: Conduct a literature review to comprehensively investigate the role of ST2 and IL-33 and the contribution of the IL-33 / ST2 axis in the pathogenesis of periodontitis. METHODS: It is a narrative literature review, which used the databases Pubmed and Academic Google a total of 114 results. RESULTS: A range of immunological markers has been shown to be relevant in the immunopathogenesis of periodontitis, cytokines of the interleukin 1 (IL-1) family, such as IL-1β and IL-33. IL-33, through its ST2 receptor, appears to be involved in the development of periodontitis, acting as a molecule that signals tissue damage from infection and also emits an endogenous signal that activates the immune response and / or worsens bone resorption by activating osteoclastogenesis, either through increases in RANK-L and reduced OPG, or regardless of that pathway. CONCLUSION: The diversity of information contained in the methodologies of these studies hampers attempts to standardize and make correlations between published data, in this sense, the IL-33 / ST2 axis remains a relevant topic in investigations focused on the diagnosis and treatment of periodontal disease.

Single nucleotide variants in the IL33 and IL1RL1 (ST2) genes are associated with periodontitis and with Aggregatibacter actinomycetemcomitans in the dental plaque biofilm: A putative role in understanding the host immune response in periodontitis

“…In this context, individuals diagnosed with periodontitis may present with different disease expressions and progression as a result of differences in each individual host genetics. To contribute to the understanding of this topic, this study focused on the investigation of SNVs in the IL33 gene and the ST2 gene since they have been implicated in the host’s immune response in periodontitis [ 37 , 38 ].…”

“…Thus, reinforcing the hypothesis that these SNVs could have a relevant role in the pathogenesis of periodontitis, through the alteration of the IL-33/ST2 axis. In other words, the alteration in circulating ST2 levels in an individual diagnosed with periodontitis could lead to an increase in available IL-33 and, consequently, it could favor bone resorption and contribute to an increase in the severity of periodontitis [ 38 , 39 ].…”

“…study focused on the investigation of SNVs in the IL33 gene and the ST2 gene since they have been implicated in the host's immune response in periodontitis [37,38].…”