Abstract
Periodontal diseases are chronic inflammatory diseases that occur due to the imbalance between microbial communities in the oral cavity and the immune response of the host that lead to destruction of tooth supporting structures and finally to alveolar bone loss. Galectin-3 is a β-galactoside-binding lectin with important roles in numerous biological processes. By direct binding to microbes and modulation of their clearence, Galectin-3 can affect the composition of microbial community in the oral cavity. Galectin-3 also modulates the function of many immune cells in the gingiva and gingival sulcus and thus can affect immune homeostasis. Few clinical studies demonstrated increased expression of Galectin-3 in different forms of periodontal diseases. Therefore, the objective of this mini review is to discuss the possible effects of Galectin-3 on the process of immune homeostasis and the balance between oral microbial community and host response and to provide insights into the potential therapeutic targeting of Gal-3 in periodontal disease.
Highlights
Periodontal diseases include a number of inflammatory conditions that affect the supporting structures of the teeth, gingiva, bone and periodontal ligament (Kinane et al, 2017)
The aim of this review is to, according to results obtained from investigation of Gal-3 impact on maintenance of epithelial cell, microbes, immune cells and its role in development of different inflammatory diseases, give a relevant rationale for a possible role of Gal-3 in pathogenesis of periodontal diseases
In mouse model for primary biliary cholangitis (PBC) induced by infection with Novosphingobium aromaticivorans, that Gal-3 contributes to enhanced activation of NLRP3 inflammasome in the liver, higher production of IL-1β and enhanced Th17 immune response that contributes to greater liver tissue damage (Arsenijevic et al, 2019)
Summary
Periodontal diseases include a number of inflammatory conditions that affect the supporting structures of the teeth, gingiva, bone and periodontal ligament (Kinane et al, 2017). Periodontitis is an inflammatory disease of periodontal tissue characterized by activation of host-derived proteinases that mediate loss of tooth supporting tissue (Tonetti et al, 2018). According to the newest classification, the forms of the disease previously recognized as “chronic” and “aggressive” are grouped under a single category, periodontitis (Chapple et al, 2018; Papapanou et al, 2018). The result of the disturbed homeostasis is a boosted inflammation that causes damage of the periodontal tissue (Graves, 2008), including ressorption of alveolar bone by osteoclasts, degradation of ligaments by matrix metalloproteinases and the formation of granulation tissue (Gemmell and Seymour, 2004; Sorsa et al, 2016).
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