Galectin-3, Possible Role in Pathogenesis of Periodontal Diseases and Potential Therapeutic Target

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.

Next-Generation Sequencing Analysis of Root Canal Microbiota Associated with a Severe Endodontic-Periodontal Lesion

“…Despite the bacterial etiology, tissue damage and inflammation are sustained and enhanced by the inflammatory host response with inflammatory mediators such as Galectin-3 (Gal-3), the Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and Interleukine-1. In particular, Gal-3 is implicated in the regulation of inflammation, as demonstrated in similar disease models [6][7][8].…”

“…In bacterial infections, tissue damage and progression of endo-periodontal disease can be determined and sustained by host-released inflammatory mediators. In particular, Gal-3 [6] is implicated in pro-inflammatory In the palatal canal, there was not a predominant taxon. Several anaerobic taxa were identified, such as F. nucleatum (8%), and two species belonging to Porphyromonas spp.…”

“…In bacterial infections, tissue damage and progression of endo-periodontal disease can be determined and sustained by host-released inflammatory mediators. In particular, Gal-3 [6] is implicated in pro-inflammatory stimuli in innate immune cells [27], such as neutrophils [28]. A significant higher expression of Gal-3 is reported in inflammatory diseases such as periapical granulomas, radicular cysts, osteonecrosis of the jaw associated with bisphosphonates and periodontal diseases [29].…”

Galectin-3 Inhibition Ameliorates Streptozotocin-Induced Diabetic Cardiomyopathy in Mice

“…Galectin-3 (Gal-3), which is a 30-kDa lectin secreted mainly by macrophages, contains a carbohydrate-recognition binding domain that binds to β-galactoside ( 16 ). Gal-3 plays an important disease-exacerbating role in autoimmune/inflammatory and malignant diseases ( 17 – 19 ).…”

Gal3 Plays a Deleterious Role in a Mouse Model of Endotoxemia

“…Gal3 has many physiological functions, including adhesion, apoptosis, cell cycle regulation, and cell-to-cell interactions within the extracellular matrix [8][9][10][11]. Moreover, Gal3 has been associated with several diseases, such as cancer, liver diseases, cardiovascular diseases, periodontal diseases, and fibrotic diseases and has even been proposed as a biomarker in several conditions [12][13][14][15][16]. Indeed, we have recently suggested that Gal3 is an attractive molecule to consider in the regulation of the macrophage-related hyperinflammation phase associated withsevere COVID-19 patients [17].…”