ReviewThe role of microRNA in periodontal tissue: A review of the literature

- Bone remodeling and inflammatory mediators orchestrate periodontal tissue pathogenesis.
- MicroRNAs modulate RANKL and inflammatory mediator in periodontal resident cells such as gingival fibroblast and periodontal ligament cells.
- MicroRNA profiling on diseased periodontal tissue demonstrates consistent identification of miR-223 indicating its potency to be further investigated in periodontitis-related processes.

MicroRNAs (miRNAs) bind at the 3′UTR of their target mRNA to induce gene silencing. Through this mechanism, number of biological pathways implicated in developmental, physiological, and pathological processes, have been frequently found to involve miRNA functions. MiRNA functions in bone metabolism have also been reported, especially in association with receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastogenesis. Expression of RANKL has been related to several inflammatory mediators, and thus some miRNAs may be implicated in the regulatory mechanism of inflammatory-induced RANKL expression as shown in periodontal resident cells such as gingival fibroblasts or periodontal ligament cells. This review aims to review the current miRNA research relating periodontal tissue and its relevance in periodontal inflammation. In miRNA profiling studies of tissues isolated from individuals with periodontal disease, miR-223 has been consistently identified as a potential candidate miRNA to be further investigated in periodontitis-related processes. Although these studies point to an important role of miRNA-mediated epigenetic changes in tissue inflammation and alveolar bone loss, further investigation is still required to determine the function of miRNAs in the complex processes of periodontal tissue homeostasis and pathogenesis. Knowledge gained from future studies will be beneficial in developing alternative therapeutic approaches, especially ones that use miRNA delivery systems to treat periodontal disease.