Abstract
The aim of this study was to evaluate the levels of prostaglandin E2 (PGE2) on the gingival crevicular fluid (GCF) of smokers (light and heavy) and non-smokers with gingivitis (G) and chronic periodontal disease (CPD). Forty-five patients were selected: 15 heavy smokers whose daily tobacco consumption was more than 10 cigarettes/day (HS), 15 light smokers whose daily tobacco consumption was fewer than 10 cigarettes/day (LS), and 15 non-smokers who had never smoked tobacco (NS). Clinical periodontal parameters (plaque index (PI), bleeding on probing (BOP), probing depth (PD), gingival recession (GR), and clinical attachment level (CAL)) were recorded for all groups. Each group was separated in both sites: G and CPD, and GCF samples were collected, and analyzed for PGE2 content by enzyme-linked immunosorbent assay. The results indicated that the non-smoking group had higher PI (88.53±17.08%) and BOP (82.80±17.14%) scores than the two smoking groups. PD, GR and CAL scores did not differ significantly among the three groups. Statistically significance differences in GCF-PGE2 were found among G versus CPD sites (P≤0.05) for the three groups. This study confirms that heavy and light smokers have less BOP and GCF-PGE2 levels than non-smokers and that the GCF-PGE2 was higher to CPD sites when compared with G sites. Key words: Periodontal disease, gingival crevicular fluid, smoker, prostaglandin E2.
Highlights
Periodontal disease is a local inflammation in the tissues that support the teeth, which leads to progressive loss of periodontal ligament tissue and bone
The objective of this study was to evaluate the levels of prostaglandin E2 (GCF-Prostaglandin E2 (PGE2)) in the gingival crevicular fluid (GCF) of each group heavy, light and non-smokers according to gingivitis and periodontitis sites
In the gingival crevicular fluid of heavy, light and nonsmokers according to G and chronic periodontal disease (CPD) sites
Summary
Periodontal disease is a local inflammation in the tissues that support the teeth, which leads to progressive loss of periodontal ligament tissue and bone. There is evidence that nicotine may distort the clinical signs and symptoms of periodontal inflammation (e.g. periodontal bleeding, erythema and edema), indicating a suppressive influence of smoking on inflammatory responses (Bernzweig et al, 1998; Boström et al, 1998; Bergström et al, 2000). Other factors, such as the type of tobacco product, amount consumed and duration of exposure to tobacco, can exacerbate the periodontal destructive effects of tobacco (Schuller and Holst, 2001)
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