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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. K E Y W O R D S apoptosis, hypoxia, smoking | 393 KARATAS eT Al.

Aim: Generalized aggressive periodontitis (G-AgP) is the most severe and destructive form of periodontitis.It usually starts under the age of 30 and it is difficult to recover tissue health with sole periodontal treatment. In this case was to evaluate effect of full-mouth ozone treatment on clinical parameters and blood CRP levels in a G-AgP patient. Methodology: A 23 year-old male patient was diagnosed as G-AgP.Clinical attachment levels (CAL), plaque index (PI), gingival index (GI), bleeding on probing (BoP) and blood C-reactive protein (CRP) levels were recorded.Full mouth scaling and root planning and ozone application were performed. Results: Baseline mean full-mouth PI,GI scores and CAL were 3,2 and 5.2mm respectively. 42% of sites showed a CAL of 4-6mm and 26% showed ≥7mm. 72% of the sites exhibited BOP.15 teeth had CAL ≥6mm. After treatments, PI and GI scores were both 1.0.  19% of sites had 4-6mm and 16% of sites were ≥7mm CAL; 12% exhibited BOP. Six teeth had CAL ≥6mm.Baseline CRP was 9 mg/dL and increased to 34 during treatments and decreased to 2 mg/dL after 4 weeks. Conclusion: Within limitations of this case report, it could be suggested that monitoring CRP and subgingival ozone application might be beneficial in treating GAgP.

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Background: Furcation involvement is characterized by periodontal disease invading furcation regions of multi-