ABSTRACT: Periodontal disease (PD) is characterized by inflammation affecting the tissue surrounding the teeth, primarily affecting the soft tissues, like the gingiva. However, without proper treatment, the condition exacerbates and progresses to impact the deeper structures, as the alveolar bone. The periodontal inflammation leads to the alveolar bone resorption, that eventually results in the complete loss of tooth support. Given its potential consequences, periodontal disease is a significant public health concern, as one of the primary causes of tooth loss, contributing to issues such as impaired mastication, speech difficulties, low self-esteem, and quality of life. Notably, comorbidities, like hypertension, can exacerbate the progression and severity of periodontal disease. In addition, the coexistence of periodontal disease and hypertension is highly likely to occur due to sharing of several risk factors. A better understanding of the underling molecular mechanisms associated to the severity of periodontal disease in the context of hypertension would greatly contribute to the advancement of translational research in the field of periodontics. MicroRNAs, a class of small non-coding RNA molecules, have an important role in regulating gene expression at the post-transcriptional level. These molecules can regulate multiple mRNA targets through complementary base pairing between the miRNA 5' seed sequence and the mRNA 3' untranslated region (UTR). Therefore, microRNAs can potentially modulate a wide variety of cellular processes, in both normal and pathological contexts. Presently, most of the studies in the field concentrate on the periodontium soft tissues, while our understanding of microRNA modulation in the alveolar bone remains comparatively limited. We used microarray analysis to evaluate the expression profiles of microRNAs in the mandibles of Wistar and SHR rats with periodontal disease, compared to their respective control groups. Our aim was to identify microRNAs of interest that could possibly be associated to the periodontal disease-induced alveolar bone loss.
