Abstract
During the last few decades, it has been established that messenger ribonucleic acid (mRNA) transcription does not inevitably lead to protein translation, but there are numerous processes involved in post-transcriptional regulation, which is a continuously developing field of research. MicroRNAs (miRNAs) are a group of small non-coding RNAs, which negatively regulate protein expression and are implicated in several physiological and pathological mechanisms. Aberrant expression of miRNAs triggers dysregulation of multiple cellular processes involved in innate and adaptive immune responses. For many years, it was thought that miRNAs acted only within the cell in which they were synthesised, but, recently, they have been found outside cells bound to lipids and proteins, or enclosed in extracellular vesicles, namely exosomes. They can circulate throughout the body, transferring information between cells and altering gene expression in the recipient cells, as they can fuse with and be internalised by the recipient cells. Numerous studies on miRNAs have been conducted in order to identify possible biomarkers that can be used in the diagnosis of periodontal disease. However, as therapeutic agents, single miRNAs can target several genes and influence multiple regulatory networks. The aim of this review was to examine the molecular role of miRNAs and exosomes in the pathophysiology of periodontal disease and to evaluate possible clinical and future implications for a personalised therapeutical approach.
Highlights
For many years, it was simplistically assumed that biological information was transferred from DNA to messenger RNA and proteins in a linear and sequential manner
The aim of this review is to examine the role of exosomes and miRNA in periodontitis pathophysiology, and assessments of their clinical potential are discussed in detail
The study indicated a significant increase in miRNA-223 expression associated with a significant positive correlation with TNF-α and clinical parameters in the chronic periodontitis groups with and without diabetes compared to healthy controls, associating miRNA-223 with inflammation, neutrophil recruitment and the pathogenesis of chronic periodontitis [71]
Summary
It was simplistically assumed that biological information was transferred from DNA to messenger RNA (mRNA) and proteins in a linear and sequential manner. Epigenetic including miRNAs, polymorphisms canresponse alter innate adaptive immune system responses, inducingthat variations in individual duces an immune oforthe periodontium [23] It is known bacterial expoof clinical expression inflammation different therapeutic sure is essential responses, to initiatemodulation periodontal disease, but theofhost responseand determines the disresponses. Dividual responses, modulation ofbeen clinical expression of inflammation and(P.different It has described how Porphyromonas gingivalis gingivalis),thera key pathogen in periodontal disease, manages to evade both innate and adaptive immune apeutic responses. When its expression levels are normal, it targets vascular endothelial growth factor alpha (VEGFA), inhibiting angiogenesis [8] These findings would suggest a protective role of miR-203 in chronic periodontitis and its potential to be used as a healing-promoting therapeutic target. These miRNAdependent effects may complement other forms of deception exerted by P. gingivalis to attempt to subvert the host’s innate and adaptive immune responses [13]
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