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

Smoking Clinical Trial

Official title:

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

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT05281848
• Other study ID #: 21071282-050.99
• Status: Completed
• Phase: N/A
• Start date: January 1, 2018
• Est. completion date: March 7, 2022

Study information

• Verified date: March 2022
• Source: Gazi University
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 55
• Est. completion date: March 7, 2022
• Est. primary completion date: June 1, 2019
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: All
• Age group: 18 Years to 70 Years

Eligibility

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

Related Conditions & MeSH terms

• Periodontal Diseases
• Periodontitis
• Smoking
• Smoking, Tobacco

Intervention

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

Locations

Country	Name	City	State
Turkey	Gazi University Faculty of Dentistry	Ankara
Turkey	Gazi University Faculty of Medicine Immunology Department	Ankara

Sponsors (1)

Lead Sponsor	Collaborator
Gazi University

Country where clinical trial is conducted

Turkey, 

References & Publications (12)

Cua DJ, Tato CM. Innate IL-17-producing cells: the sentinels of the immune system. Nat Rev Immunol. 2010 Jul;10(7):479-89. doi: 10.1038/nri2800. Epub 2010 Jun 18. Review. Erratum in: Nat Rev Immunol. 2010 Aug;10(8):611. Nat Rev Immunol. 2010 Jul;10(7):fol — View Citation

Eshghipour B, Tofighi H, Nehal F, Vohra F, Javed F, Akram Z. Effect of scaling and root planing on gingival crevicular fluid cytokine/chemokine levels in smokers with chronic periodontitis: A systematic review. J Investig Clin Dent. 2018 Aug;9(3):e12327. — View Citation

Kinane DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nat Rev Dis Primers. 2017 Jun 22;3:17038. doi: 10.1038/nrdp.2017.38. Review. — View Citation

Okada H, Murakami S. Cytokine expression in periodontal health and disease. Crit Rev Oral Biol Med. 1998;9(3):248-66. Review. — View Citation

Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997 Jun;14:9-11. — View Citation

Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest. 1976 Mar;34(3):235-49. Review. — View Citation

Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH, Flemmig TF, Garcia R, Giannobile WV, Graziani F, Greenwell H, Herrera D, Kao RT, Kebschull M, Kinane DF, Kirkwood KL, Kocher T, Kornman KS, Kumar PS, Loos BG, Machtei E, Meng H, Mombelli A, Needleman I, Offenbacher S, Seymour GJ, Teles R, Tonetti MS. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018 Jun;89 Suppl 1:S173-S182. doi: 10.1002/JPER.17-0721. — View Citation

Preshaw PM. Host modulation therapy with anti-inflammatory agents. Periodontol 2000. 2018 Feb;76(1):131-149. doi: 10.1111/prd.12148. Epub 2017 Nov 29. Review. — View Citation

Qiu F, Liang CL, Liu H, Zeng YQ, Hou S, Huang S, Lai X, Dai Z. Impacts of cigarette smoking on immune responsiveness: Up and down or upside down? Oncotarget. 2017 Jan 3;8(1):268-284. doi: 10.18632/oncotarget.13613. Review. — View Citation

Vignali DA, Kuchroo VK. IL-12 family cytokines: immunological playmakers. Nat Immunol. 2012 Jul 19;13(8):722-8. doi: 10.1038/ni.2366. Review. — View Citation

Yao Z, Painter SL, Fanslow WC, Ulrich D, Macduff BM, Spriggs MK, Armitage RJ. Human IL-17: a novel cytokine derived from T cells. J Immunol. 1995 Dec 15;155(12):5483-6. — View Citation

Zhang JM, An J. Cytokines, inflammation, and pain. Int Anesthesiol Clin. 2007 Spring;45(2):27-37. Review. — View Citation

* Note: There are 12 references in all — Click here to view all references

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	IL-17 levels in gingival crevicular fluid	by ELISA method	Change from baseline to 1st month after non-surgical periodontal treatment
Primary	IL-17 levels in saliva	by ELISA method	Change from baseline to 1st month after non-surgical periodontal treatment
Primary	IL-35 levels in gingival crevicular fluid	by ELISA method	Change from baseline to 1st month after non-surgical periodontal treatment
Primary	IL-35 levels in saliva	by ELISA method	Change from baseline to 1st month after non-surgical periodontal treatment
Secondary	Plaque Index (PI)	by using Williams periodontal probe; Scores from 0 to 3, 0 is no visible plaque, 3 is visible plaque or dental calculus.	Change from baseline to 1st month after non-surgical periodontal treatment
Secondary	Gingival Index (GI)	by using Williams periodontal probe; Scores from 0 to 3, 0 is healthy gingiva, 3 is diseased gingiva with spontaneous bleeding.	Change from baseline to 1st month after non-surgical periodontal treatment
Secondary	Pocket Depth (PD)	by using Williams periodontal probe with milimeter signs; Pocket Depth is registered by milimeters.	Change from baseline to 1st month after non-surgical periodontal treatment
Secondary	Bleeding in Probing Index (BOP)	by using Williams periodontal probe; BOP is registered with + or - according to the presence of bleeding on probing.	Change from baseline to 1st month after non-surgical periodontal treatment
Secondary	Clinical Attachment Loss (CAL)	by using Williams periodontal probe with milimeter signs; CAL is registered by milimeters.	Change from baseline to 1st month after non-surgical periodontal treatment