Similarly, MSCs from inflammatory periodontal ligament in earlier research shown a reduced ability for development of nodules of mineralization in relation to those derived from gingival tissue that were healthy.[23] It was postulated that excessive pro-inflammatory cytokine production during periodontitis may influence the process of osteoblastic delineation of MSCs through a variety of regulatoryprocesses, including suppression of nuclear factor-kappa B biomarker by means of catenin signaling, which suppresses miR-21 biomarker , and/or RUNX2 biomarker inhibition. The gene discussed is RUNX2; the disease is periodontitis.