Abstract
Short-chain fatty acids (SCFA), bacterial metabolites released from dental biofilm, are supposed to target the oral epithelium. There is, however, no consensus on how SCFA affect the oral epithelial cells. The objective of the present study was to systematically review the available in vitro evidence of the impact of SCFA on human oral epithelial cells in the context of periodontal disease. A comprehensive electronic search using five databases along with a grey literature search was performed. In vitro studies that evaluated the effects of SCFA on human oral epithelial cells were eligible for inclusion. Risk of bias was assessed by the University of Bristol’s tool for assessing risk of bias in cell culture studies. Certainty in cumulative evidence was evaluated using GRADE criteria (grading of recommendations assessment, development, and evaluation). Of 3591 records identified, 10 were eligible for inclusion. A meta-analysis was not possible due to the heterogeneity between the studies. The risk of bias across the studies was considered “serious” due to the presence of methodological biases. Despite these limitations, this review showed that SCFA negatively affect the viability of oral epithelial cells by activating a series of cellular events that includes apoptosis, autophagy, and pyroptosis. SCFA impair the integrity and presumably the transmigration of leucocytes through the epithelial layer by changing junctional and adhesion protein expression, respectively. SCFA also affect the expression of chemokines and cytokines in oral epithelial cells. Future research needs to identify the underlying signaling cascades and to translate the in vitro findings into preclinical models.
Highlights
Periodontitis is characterized by a complex inflammatory response triggered by the presence of a dental biofilm
Butyrate induced cell death in starved and sufficient nutrient conditions. butyrate treatment induced about 10 times higher caspase-3 activity compared to the non-treated cells, butyrate-induced apoptosis accounted for only 29.4 or 12.3% of total cell death induced by butyrate in the starved and fed conditions, respectively.The combined effects of histone H3 acetilatilation, AMPK activation, and light chain 3 (LC3) upregulation during starvation and butyrate exposure resulted in induction of cell autophagy
Butyrate suppressed in a dose-dependent manner the cytokine-induced ICAM1 expression in HSC-2 and primary gingival epithelial cells but not in TR146 cells
Summary
Periodontitis is characterized by a complex inflammatory response triggered by the presence of a dental biofilm. This bacterial biofilm is able to elicit a dysbiosis in the subgingival microbiome leading to the destruction of the periodontal supporting tissues and eventually tooth loss [1]. Metabolites released by periodontopathic bacteria are capable of provoking an immune response inducing the influx of neutrophils and macrophages to the gingival crevice and epithelium [2,3]. An excessive migration of leukocytes facilitates the periodontal breakdown and is often associated with the initiation and progression of periodontal diseases. It can be assumed that the release of secondary metabolites may play a crucial role in periodontal disease [4]. The specific role of these metabolites remains unclear
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
