Evaluation of apoptosis and hypoxia‐related factors in gingival tissues of smoker and non‐smoker periodontitis patients

Abstract Objective Smoking causes pathological changes in all tissues, including gingiva and alveolar bone. The aim of present study was to evaluate apoptotic tissue alterations and tissue destruction in smoker and non‐smoker periodontitis patients and healthy individuals. Methods Gingival biopsy samples from 15 systemically and orally healthy individuals (Group 1), 15 systemically healthy periodontitis patients (Group 2), 15 systemically and orally healthy smokers (Group 3), and 15 systemically healthy smoker periodontitis patients (Group 4) were enrolled in the present study. Clinical periodontal measurements as plaque index (PI), gingival index (GI), and clinical attachment levels (CAL) were recorded, and gingival biopsies were obtained. Biopsy samples were fixed in formalin solution and embedded in paraffin. Fibroblast and inflammatory cell counts were determined via histomorphometrically. Hypoxia‐inducible factor alpha (HIF‐1α), vascular endothelial growth factor(VEGF), tissue inhibitor of matrix metalloproteinase‐1(TIMP‐1), matrix metalloproteinases‐8(MMP‐8) expressions, Bax, Bcl‐2, and caspase‐3 expressions were evaluated via immunohistochemistry. Results Demographic data of the study groups were similar. Smoking levels of the smokers were also similar. The highest fibroblast cell counts were observed in healthy controls and the counts were similar in other groups. The highest inflammatory cell counts were found in smoker periodontitis group, and the lowest counts were found in healthy control groups. The differences were statistically significant. HIF‐1α and Bax expressions were elevated and Bcl‐2 decreased in smoker periodontitis patients compared with healthy individuals. However, there were no differences in VEGF, MMP‐8, and TIMP‐1 expressions. Conclusion Within limits of present study, it can be suggested that both smoking and periodontitis caused similar decrease in fibroblast counts while causing a dramatic increase in inflammatory cell counts. Increased apoptosis and hypoxia also accompanied to the increased inflammation.