Effect of Smoking and Periodontal Therapy on Salivary and Gingival Crevicular IL-17 and IL-35
Condition: Periodontitis; Periodontal Diseases; Smoking; Smoking, Tobacco
MeSH terms: Periodontitis; Periodontal Diseases
Study type: Interventional

Summary: 
      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.
    

Detailed description: 
      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.
    

Intervention name(s): Non-surgical periodontal treatment
Intervention type(s): Procedure
Intervention description(s): Non-surgical periodontal treatment includes periodontal prophylaxis and root planning. No other methods or any of drugs will be used.
Allocation: Randomized
Intervention model: Parallel Assignment
Intervention model description: 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.
Masking: None (Open Label)
Primary purpose: Treatment
Keywords: periodontitis; non-surgical periodontal treatment; IL-17; IL-35; saliva; gingival crevicular fluid