MicroRNAs and Periodontal Disease: Helpful Therapeutic Targets?

Periodontal disease is the most common oral disease. This disease can be considered as an inflammatory disease. The immune response to bacteria accumulated in the gum line plays a key role in the pathogenesis of periodontal disease. In addition to immune cells, periodontal ligament cells and gingival epithelial cells are also involved in the pathogenesis of this disease. miRNAs which are small RNA molecules with around 22 nucleotides have a considerable relationship with the immune system affecting a wide range of immunological events. These small molecules are also in relation with periodontium tissues especially periodontal ligament cells. Extensive studies have been performed in recent years on the role of miRNAs in the pathogenesis of periodontal disease. In this review paper, we have reviewed the results of these studies and discussed the role of miRNAs in the immunopathogenesis of periodontal disease comprehensively. miRNAs play an important role in the pathogenesis of periodontal disease and maybe helpful therapeutic targets for the treatment of periodontal disease

Effects of atrovastatin on concentrations of 3-hydroxy-3-methylglutaryl-coenzyme A- reductase (HMG-CoA-R), proprotein convertase subtilisin/kexin type 9 (PCSK9) and sortilin in patients with type 2 diabetes mellitus and pre-diabetics

Introduction: Atorvastatin hinders cardiovascular disease by reducing cholesterol levels. Proprotein convertase subtilisin/kexin type 9 (PCSK9) enhances the secretion of insulin by binding to LDL receptor. Sortilin is committed in the transfer of intracellular proteins through the plasma membrane. Objectives: The purpose of this research was to determine the effect of atorvastatin consumption on alterations in the levels of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA-R), PCSK9 and sortilin in diabetic patients and pre-diabetics. Patients and Methods: This study was carried out on 80 individuals including normal subjects, diabetic patients and pre-diabetics. The participated individuals were divided as control group (i) (healthy individuals without diabetes mellitus), diabetic group receiving statin (ii), diabetic group not receiving statin (iii), pre-diabetic group receiving statin (iv) and pre-diabetic group not receiving statin (v). Levels of HMG-COA-R, PCSK9 and sortilin were determined by ELISA method. Results: In diabetics and pre-diabetics taking atorvastatin, the level of HMG-COA-R was not altered significantly compared to diabetics and pre-diabetics not taking atorvastatin, respectively (P> 0.05). The serum PCSK9 level in diabetics and pre-diabetics was significantly higher than the healthy individuals (P= 0.001). Additionally, the serum PCSK9 level in diabetics and pre-diabetics receiving atorvastatin was significantly higher than diabetics and pre-diabetics not receiving atorvastatin, respectively (P=0.001). The serum sortilin level in diabetics and pre-diabetics was significantly higher than the healthy individuals (P=0.001). In addition, the serum sortilin level in pre-diabetics receiving atorvastatin was significantly higher than pre-diabetics not receiving atorvastatin (P=0.001). Conclusion: Atorvastatin improved insulin secretion and sensitivity by increasing serum sortilin and PCSK9 levels. Thereby, it prevented the development of diabetes in diabetics and the progression of pre-diabetes to diabetes in pre-diabetics