Author(s): Apatzidou DA, Riggio MP, Kinane DF
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Abstract OBJECTIVES: The aim of the current study was to assess the impact of smoking on the clinical indices, the humoral immune response and the detection frequency of putative periodontal pathogens in patients with periodontitis cross-sectionally and following therapy. MATERIAL AND METHODS: Clinical measurements, subgingival plaque samples, gingival crevicular fluid (GCF) and sera were collected from 40 untreated patients with moderate-to-advanced chronic periodontitis before and after treatment over a period of 6 months. The treatment consisted of the initial therapy of scaling and root planing. Smoking status was self-reported and was confirmed by cotinine enzyme inhibition assay (CEIA). Whole-mouth clinical measurements were recorded with a manual periodontal probe at baseline (BAS) and at 6 months (RAS). Selected-site analyses were performed on the deepest site in each quadrant before and after therapy and clinical indices were recorded with an electronic pressure-sensitive probe. GCF sample volume was quantified using the Periotron 6000. Polymerase chain reaction (PCR) was utilized to determine the presence of Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, Treponema denticola and Tanerella forsythensis in subgingival plaque. Enzyme-linked immunosorbent assay examined the systemic antibody titres to these bacteria, and thiocyanate disassociation determined the antibody avidity to these organisms. RESULTS: At baseline, smokers showed significantly less gingival inflammation and lower GCF volume compared with non-smokers. After treatment, a compromised clinical outcome was noted for smokers in terms of pocket depth reduction and gain in attachment levels. No significant differences in the detection of putative periodontal pathogens in subgingival plaque existed between smokers and non-smokers. A consistent trend was noted in that smokers had lower sera immunoglobulin G antibody titres to these organisms before and after treatment (statistically significant for A. actinomycetemcomitans). This pattern was less clear when antibody avidities were considered, revealing only small differences, if any, between the two groups of patients. CONCLUSION: Current data indicate that smokers with periodontal disease have a suppressed inflammatory response, a significantly less favourable clinical outcome and seem to have an altered host antibody response to antigenic challenge than non-smokers. In contrast, the subgingival microflora of smokers appears similar to that of non-smokers.
This article was published in J Clin Periodontol
and referenced in Dentistry