Array analysis for T-cell associated cytokines in gingival crevicular fluid: Identifying altered profiles associated with periodontal disease status.

OBJECTIVE: Cytokine networks regulate innate and adaptive immune responses, which in turn are recognised to direct the progression or arrest of periodontal disease. This study aimed to compare the profile of seven cytokines, implicated in regulating T-cell networks, in gingival crevicular fluid (GCF) samples with differing classification of periodontal status. METHODS: GCF samples were collected from patients with strong clinical evidence for chronic periodontitis, aggressive periodontitis, gingivitis or no gingival inflammation. Cytokines IL-6, IFN-É£, IL-4, IL-2, IL-17 A, IL10 and TNFα were measured in each sample using a commercial cytometric bead array assay. Descriptive statistics were used to indicate central tendency, data scatter and analysis of variance for each cytokine concentrations between respective patient groups. Heat maps with dendrograms were produced to visualise hierarchical clustering and trends within the data. RESULTS: Median concentrations for all cytokines analysed were highest for gingivitis samples and lowest for aggressive periodontitis samples. The median concentration of IL-6 in gingivitis samples was observed to be 10.5 fold higher (˜17,300 pg/µl) than IL-6 in aggressive periodontitis samples (˜1600 pg/µl). Median concentrations of IL-10, IL-17 A and TNFα were also 2-2.2 fold higher in gingivitis samples compared to aggressive periodontitis. CONCLUSIONS: Descriptive statistical analysis noted raised concentrations of IL-6, IL-17 A and TNFα associated with gingivitis; pro-inflammatory cytokines usually associated with periodontal tissue destruction, including bone. Our results would suggest that these cytokines can additionally provide protective roles in preventing progression to advanced forms of periodontal disease. Potential for how these cytokines contribute to providing this role is discussed. CLINICAL SIGNIFICANCE: Defining the roles for the many cytokines involved in the pathogenesis of periodontal disease is far from complete. Consequently the results of this study serve to evidence proposals that cytokines can exhibit both pro- and anti-inflammatory effects, which is dependent on the signalling environment within which they exist and the antagonizing or modifying actions of other cytokines. Whilst future research is necessary to explore mechanistic action, our study contributes new knowledge suggesting that IL-6 and IL-17 A can provide roles in stabilising the lesion to limit disease progression, which does not preclude alternative roles in promoting periodontal bone loss in advanced forms of disease progression, which is also documented in the literature.

Prognostic factors in the treatment of generalized aggressive periodontitis: I. Clinical features and initial outcome.

AIMS: The aims of this study were to investigate prognostic factors for initial response to non-surgical periodontal treatment for generalized aggressive periodontitis. METHODS: Seventy-nine patients with generalized aggressive periodontitis were included in this prospective follow-up intervention study. Patients' clinical and demographic parameters were collected at baseline and 10 weeks following a standard course of treatment (four visits of non-surgical root surface debridement together with OHI as required). The relationship between clinical variables and treatment outcome were analysed at site-specific level by chi(2) analysis and for patient-specific variables by logistic regression. RESULTS: In general, there was a good response to the treatment provided. In deep sites the mean pocket depth reduction was 2.11+/-2.01 mm. Site-specific analysis showed that the presence of plaque had a small but significant predictive effect on outcome (odds ratio 1.4). Sites on teeth with grade II/III mobility showed a significantly reduced response to treatment. Twenty-five patients were classified as "non-responders". Current smoking was strongly associated with non-responding patients (odds ratio 3.8) in a logistic regression model; plaque, baseline bleeding and initial pocket depth were not significantly associated with treatment outcomes. CONCLUSIONS: Overall, the results emphasize the importance of smoking as a negative prognostic factor, and suggest that treatment outcomes may be determined by a wide range of different determinants requiring further study.

Prognostic factors in the treatment of generalized aggressive periodontitis: II. Effects of smoking on initial outcome.

AIMS: The aim of this study was to investigate the effects of smoking on the response to non-surgical treatment for aggressive periodontitis. METHODS: Seventy-nine patients with generalized aggressive periodontitis were included in the study; 20 were smokers. All patients received a course of non-surgical periodontal therapy and outcomes assessed 10 weeks post-operatively. Non-responding patients were designated if they had 30% or more non-responding deep sites. RESULTS: At baseline, bleeding scores were lower in smokers. There was no difference in baseline plaque, pocket depth (PD), recession or clinical attachment levels (CALs); when sites were selected by equal levels of CAL, increased recession was seen in smokers. Outcomes were poorer in smokers (mean PD change 1.75+/-0.56 versus 2.23+/-0.87 mm). The odds ratio for 30% of sites not responding in smokers was 2.9; for 40% non-responding it was 5.9. Smoking altered the distribution of site-specific responses to increase specifically the number of non-responding sites. There was no significant difference in responses between ex-smokers and never-smokers. CONCLUSIONS: The results demonstrate that smoking is a major risk factor for poor response to initial treatment and emphasize the importance of smoking cessation in periodontal therapy.