Inflammatory diseases can impair proper bone homeostasis by decreasing osteoblast activity and/or increasing osteoclast activity, thereby favoring bone mass loss as well as structural and functional damage. Periodontal disease (PD) is an inflammatory disorder affecting the tissues surrounding and supporting the teeth that can lead to alveolar bone resorption resulting in loss of teeth, and associated comorbidities, such as hypertension, can significantly enhance the progression of periodontitis. Several mechanisms are related to inflammatory-induced alveolar bone loss, and our previous studies demonstrated the role of the renin-angiotensin system in regulating bone loss observed in hypertensive rats via the modulation of inflammatory mediators and bone-related gene expression. MicroRNAs (miRNAs) are epigenetic regulators that suppress the expression of different target mRNAs and they have been drawing attention as an important mechanism in physiological and pathological processes. We intend to evaluate miRNA signature expression profiles in the mandible of Wistar (normotensive) and spontaneously hypertensive rats with periodontal disease by microarray analysis. For the present study, we aim to investigate the function and mechanisms of differentially expressed miRNAs identified from the microarray study by determining their effects on in vitro differentiation of human and rat skeletal progenitor cells toward the osteoblast or osteoclast lineage.
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