The Adjunctive Use of Melatonin Therapy in the Treatment of Obese Periodontitis Patients (Clinical and Immunological Study).

Periodontitis defined as destruction of periodontal tissue caused by specific microorganisms resulting of pocket formation, recession and mobility.Obesity known to increase the host tolerance by influencing the immune and inflammatory mechanisms in a way that inflammatory tissue destruction is predisposed and leave a person at high risk of developing periodontitis.the relationship between periodontitis and obesity has been reported in several epidemiological and experimental studies.

Obesity can be a higher trigger of chronic stress , stress and how a person copes with stress has been shown to increase the risk of periodontitis.several studied have shown that preserving of normal weight by maintaining regular physical exercise is linked with a lower incidence of periodontitis.

As a matter of truth , overweight and obese individuals are more than twice as likely to have periodontitis compared to normal healthy persons. It has been suggested that obesity decreased the blood flow to periodontal tissue, enabling the development of periodontal disorders. The blood vessels of obese subjects demonstrate a thickening in the inner wall of arteries that reduce the flow of blood into periodontium. The adipocytes produce various active molecules called adipokines involving (TNF- α, IL-6, leptin, adiponectin and others). These compound secrete various molecules of reactive oxygen species (ROS) that lowered antioxidant enzymes activity like (superoxide dismutase, catalase, glutathione and others). Thus modulating the effect of adipokines can lower the pathogenicity of periodontitis by reducing the effect of oxidative stress.

Oxidative stress appear to be the main link between obesity and periodontitis and can aggravates pro-inflammatory pathways frequent in both pathologies. Regarding the significance of oxidative stress in pathologies of both periodontitis and obesity, several antioxidants play an amazing role as a preventive and therapeutic measures for both diseases. Multiple studies had a greater evidence toward melatonin which have an active antioxidant properties , which is an indolamine produced mainly by pinealocytes. It has been documented that salivary melatonin were significantly decreased in patients with periodontal disease, indicated that melatonin may act as a biomarker for periodontal diagnosis and can be used as a possible therapeutic agent in various periodontal diseases.

It is indicated that adjunctive use of melatonin in combination with non-surgical scaling and root planning for 3 weeks can lead to improvement of clinical periodontal parameters in diabetic patients. It was demonstrated that daily dietary supplementation with 3mg melatonin tablet for 4 weeks along with scaling and root planning significantly reduced the oxidative stress in periodontitis patients.

similarly , significant reduction in gingival inflammation when melatonin administrated locally as adjunctive measure to standard periodontal therapy. Melatonin promote bone formation by activating type 1 collagen fibers in osteoblast and enhancing the genetic expression of bone sialoprotein , alkhaline phosphates, osteopontien and osteocalcine and downregulate the RANKL mediated osteoclast formation and activation.

It had been reported that circulatory serum level of melatonin significantly reduced in obesity .Supplementation of antioxidants in conjunction with other treatment modalities such as dietary changes, behavioral changes, and drug therapy might be beneficial in treatment of obesity and associated inflammatory states ., as melatonin participated in homeostasis and metabolism of energy through activation of brown adipose tissue and enhance energy expenditure. furthermore, significant reduction in body weight along with adipose tissue deposit when melatonin were administrated in obese subjects was reported in. Multiple studies reported that melatonin significantly increase HDL level and decrease TG and HDL level in addition to increased cholesterol catabolism.