Effect of Smoking and Periodontal Therapy on Salivary and Gingival Crevicular IL-17 and IL-35

Evaluation of the Effect of Non-surgical Periodontal Treatment on Salivary and Gingival Crevicular Fluid Levels of IL-17 and IL-35 in Periodontitis Patients as Smoker and Non-smoker

Periodontal diseases are among the major causes of tooth loss. Smoking may play a role as a contributing factor in the development of periodontitis by reducing the immune response. The role of cytokines in the pathogenesis of periodontal disease is clearly indicated in the literature; it has been shown that microorganisms that cause periodontal disease cause cytokine increase in saliva, gingival tissue and gingival crevicular fluid. Among these cytokines, interleukin (IL) -17 is proinflammatory and IL-35 is antiinflammatory and has been associated with periodontal disease.

Periodontal diseases are among the complex inflammatory diseases that are considered among the leading causes of tooth loss, mostly observed with multiple etiological factors. The complexity of periodontal disease is due to the presence of the biofilm and the accompanying host response together. Smoking, which is considered as one of the risk factors in terms of periodontitis, is one of the most preventable risk factors that affect the periodonium with many different mechanisms. Smoking plays a role in the etiopathogenesis of periodontitis, with its physiological changes in gingival tissue and its effects on host response and is considered to be an established risk factor. Although the effects of smoking on host response and its role in increasing the risk of periodontal disease are still being investigated, its effects on natural and acquired immune response cells have been studied separately. Consequently, components of cigarette suppress the immune system's defense responses; however, it has been reported to exacerbate pathological reactions. The process of progression from periodontal health to periodontitis is formed by biofilm pathogens and host immune responses activated by these microorganisms. Intercellular communication is crucial during the progression of chronic inflammatory diseases, such as periodontitis. Cytokines, one of these ways of communication, are soluble proteins produced by various types of cells, such as structural and inflammatory cells, responsible for maintaining a complex network of communication between homotypic and heterotypic cell groups. Interleukin-17 (IL-17) is a pro-inflammatory cytokine mostly stimulated from Th17 cells, stimulating inflammatory processes with many different mechanisms. IL-35 inhibits the differentiation of Th17 cells and suppresses IL-17 production and therefore plays a protective role in Th17-related diseases. There are many studies evaluating the effect of non-surgical periodontal treatment on individuals with smokers with periodontitis. However, the obtained results do not allow a clear data to be revealed. To exemplify, when the studies which investigates the evaluation of non-surgical periodontal treatment on IL-17 levels were evaluated, contradictory results were determined. In addition, as a result of our research, no studies evaluating the effects of non-surgical periodontal treatment on IL-35 levels in smokers with periodontitis have not been found.

A total of 55 subjects will be grouped as: 18 non-smoker patients with periodontitis (Group 1), 19 smoker patients with periodontitis (Group 2), 18 non-smoker and periodontally healthy individuals who will refer to our department. Spitting method will be used for collecting saliva samples. The paper strip method will be used for gingival crevicular fluid (GCF) sample collection. Samples will be taken from the mesial and distal surfaces of the teeth (healthy or have greater than or equal to 5mm pocket depth) after isolation from the saliva. Paper strips will be transferred to polypropylene tubes and stored at -30 ° C until inspection. After collecting samples, non-surgical periodontal treatment will be performed to all individuals which are classified as Group 1 and Group 2. Collection of saliva and GCF samples will be repeated at the 1st month after the end of treatment. ELISA kits will be used for the detection of saliva and GCF's IL-17 and IL-35.

Non-surgical periodontal treatment includes periodontal prophylaxis and root planning. No other methods or any of drugs will be used.

by using Williams periodontal probe; Scores from 0 to 3, 0 is no visible plaque, 3 is visible plaque or dental calculus.

by using Williams periodontal probe; Scores from 0 to 3, 0 is healthy gingiva, 3 is diseased gingiva with spontaneous bleeding.

by using Williams periodontal probe; BOP is registered with + or - according to the presence of bleeding on probing.

Inclusion Criteria: To be volunteer to participate in the study To be over 18 Being systemically healthy Having greater than or equal to 15 teeth out of 3rd molar teeth To have localized or generalized periodontitis for the experimental group (clinical attachment loss in at least 6 surrounding areas and presence of greater than or equal to 5 mm periodontal pocket) For Smoking group; more than 10 cigarettes a day for more than 5 years For non-smokers; have not smoked for at least 3 years. Exclusion Criteria: Have any systemic disease affecting periodontal condition To receive periodontal treatment in the last 6 months Use any medication that may affect the inflammatory process in the last 3 months Use local or systemic antibiotics in the last 3 months Pregnancy or lactation for female patients Regular use of mouthwash

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