Apoptotic Changes in Gingiva Caused by Smoking

Completed

• Conditions: Smoking; Chronic Periodontitis

• Registration Number: NCT03631498
• Lead Sponsor: Tokat Gaziosmanpasa University

Brief Summary

Smoking is a major environmental risk factor associated with common forms of human chronic periodontitis. The aim of the present study was to evaluate apoptotic tissue alterations and tissue destruction in smoker and non-smoker chronic periodontitis patients and healthy individuals. The investigators of the study suggest that smoking decrease tissue quality and increase inflammation level in gingival tissues in both healthy individuals and periodontitis patients. One possible mechanism for this is suggested to be increased apoptosis.

Detailed Description

Periodontal disease disrupts soft tissue metabolism in the gingiva through a decrease in the production of collagen, the quality, and quantity of the connective tissue. The etiology and pathogenesis of chronic periodontitis are mostly revealed, however, the mechanism of environmental factors such as smoking yet to be clarified. Major consequences of smoking in gingival tissues are suggested to be the reduction in neutrophil and fibroblast function, decreased immunoglobulin G production, increased periodontal pathogen bacteria prevalence, difficulty in eliminating pathogens with mechanical therapy, and reduction in growth factor production. In the present study, markers of tissue destruction, matrix metalloproteinase-8 and tissue inhibitor of matrix metalloproteinase-1, hypoxia markers, vascular endothelial growth factor and hypoxia-inducible factor and apoptotic markers, bax, bcl-2, and caspase-3 were evaluated.

Study Timeline

• Study Start: 2017-01-10
• Primary Completion: 2018-01-10
• Study Completion: 2018-04-10
• Status Verified: 2018-08
• Study First Submitted: 2018-08-13
• Study First Submitted QC: 2018-08-13
• Study First Posted: 2018-08-15
• Last Update Submitted: 2018-08-15
• Last Update Posted: 2018-08-16

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 60

Inclusion Criteria

• Age range from 30 to 45,
• the existence of at least 20 functioning teeth,
• systemical health,
• no antibiotic use within 6 months,
• no periodontal therapy within 6 months,
• no pregnancy or lactation,
• no drug use, in addition; for the smokers existence of the smoking condition for at least five years.

Exclusion Criteria

• Patients younger than 30 older than 50 years old,
• the absence of occlusion,
• drug use,
• pregnancy/lactation,
• previous antibiotic use,
• previous periodontal therapy,
• the existence of any systemical disease.

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
Fibroblast and total inflammatory cell counts	Biopsies were obtained a day after initial examinations, histological analysis were performed 2 weeks after.	Fibroblast and total inflammatory cell counts in the groups were determined in a standardized 1000 micrometer square area with histomorphometric evaluation.

Secondary Outcome Measures

Name	Time	Method
Apoptotic markers	Biopsies were obtained a day after initial examinations, histological analysis were performed 2 weeks after	Apoptotic and anti-apoptotic proteins and enzymes related to apoptosis were evaluated via immunohistochemistry.
Hypoxia and tissue destruction markers	Biopsies were obtained a day after initial examinations, histological analysis were performed 2 weeks after	Vascular endothelial growth factor and hypoxia-inducible factor as hypoxia markers and matrix metalloproteinase and it inhibitor as destruction markers were evaluated via immunohistochemistry.

Trial Locations

Locations (1)

Gaziosmanpasa University Faculty of Dentistry; 🇹🇷 Tokat, Turkey