Role of RvD1 on Osteogenic Factors Involved in the Inflammatory and Resolution Processes in Periodontal Periapical Lesions
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Introduction: Inflammation is a protective body response against invading traumatic or microbial injury. However, persistent or unresolved acute inflammation can result in a chronic injury to local tissues that may lead to long term complications. Periodontal diseases (e.g. marginal and apical periodontitis) are examples of chronic inflammation affecting the periodontal tissues. Persistence of these conditions may lead to permanent tooth loss. Recent evidences suggest that Resolvins derived from ω-3 PUFAs play an important role in resolution of inflammation. Knowledge about the effects of Resolvin D1 on periodontitis is limited. Yet, it is postulated that RvD1 therapy demonstrates a great efficacy in reducing the inflammatory process without the side effects of chronic antibiotic usage. Aims: to investigate the effect of different doses of RvD1 in the regulation of tissue destruction and resolution of inflammation in periodontal lesion models and to evaluate its potential in therapy of these conditions. Methods: An in vitro study was performed in which periodontal ligament fibroblasts from three different donors were used. Cells were cultured in DMEM and further treated with different doses of RvD1 (1ng/ml, 10ng/ml and 100ng/ml) in the presence and absence of TNF-α (1ng/ml). Cell proliferation was observed using MTT cell proliferation assay in three different time points (1, 3 and 7 days). Cells were also cultured in osteoinductive medium (OM) and then treated with different doses of RvD1 (10ng/ml and 100ng/ml) in the presence and absence of TNF-α (1ng/ml). Expression of bone marker genes (ALP, Col-1 and OC) was assessed using RT-PCR. An in vivo pilot study then followed, in which nine mice were used. Pulp exposure (in the mandibular first molar) was performed for six mice and then they were divided into two groups (three mice each). One group received RvD1 injection and the other group received normal saline injection. A third control group was also included (neither pulp exposure nor treatment). At the end of the experiment jaws were dissected and both TRAP staining and micro-CT were performed to assess the osteoclastic activity and the bone volume respectively. Results: RvD1 induced the proliferation of PDL fibroblasts after three and seven days. Expression of ALP and Col-1 genes was increased when cells were treated with RvD1 (10ng/ml). RvD1 treated mice had lesser number of osteoclasts although no difference in the bone volume measurements observed between the groups. Conclusion: Treatment of PDL fibroblasts with RvD1 leads to cellular proliferation which can lead to improvement of the healing process. It can also lead to reduction of inflammation and stimulate bone formation. Further investigations on the effects of RvD1 on inflammation and wound healing are needed.