Chronic Periodontitis, Smoking
Conditions
Keywords
smoking, hypoxia, apoptosis, chronic periodontitis
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.
Interventions
None listed
Sponsors
Tokat Gaziosmanpasa University
Study design
Observational model
CASE_CONTROL
Time perspective
CROSS_SECTIONAL
Eligibility
Sex/Gender
ALL
Age
30 Years to 50 Years
Healthy volunteers
Yes
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.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| 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
| Measure | Time frame | Description |
|---|---|---|
| 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. |
Countries
Turkey (Türkiye)
Outcome results
None listed