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.

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.

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.

Healthy individuals who were either smokers or non-smokers, chronic periodontitis patients who were either smokers or non-smokers older than 30 years old and younger than 50 years old were enrolled. The age was specifically chosen because aging changes periodontal and gingival tissues independently of other variables. Any possible factor which might alter connective tissue metabolism were excluded.