Periodontitis: a complication of type 2 diabetes in Sri Lankans.
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Biomedical subjects
Publications and source records attributed to Peter A Heasman.
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OBJECTIVES: To monitor the efficacy of periodontal maintenance whether conducted in a specialist periodontology clinic or in the practice of the referring general dentist. MATERIALS AND METHODS: Thirty-five subjects with a diagnosis of moderate-severe chronic periodontitis who were referred to the specialist clinic received periodontal non-surgical therapy. Following a 6-month healing phase, subjects were randomly allocated to one of two groups: A (n=18, periodontal maintenance provided within the specialist clinic) or B (n=17, periodontal maintenance provided by the referring general dentist in accordance with written instructions provided by the specialist). All subjects were examined at months 0 (corresponding to 6 months post-completion of non-surgical therapy), 6 and 12. Full-mouth plaque index (PI), % bleeding on probing (%BOP) and probing depth (PD) measurements were recorded. PDs were also recorded at eight test sites which, prior to non-surgical therapy, exhibited PD 5-8 mm, BOP and radiographic alveolar bone loss. Standardized radiographs were exposed at test sites at months 0 and 12, and bone changes assessed using digital subtraction radiography (DSR). RESULTS: As a result of the non-surgical therapy, statistically significant improvements in all clinical parameters were recorded. In the maintenance period, mean PI increased significantly from months 0 to 12 (p<0.05), but this increase did not differ significantly between groups A and B (p>0.05). No other clinical parameters changed significantly in the maintenance phase of the study. Reductions in %BOP, mouth mean PD and mean test sites PD achieved by the non-surgical therapy were maintained and did not differ significantly whether subjects were allocated to group A or group B (p>0.05). Current smokers had significantly deeper PD than non-smokers and former smokers at all time points (p<0.05), although otherwise, smoking status did not affect the outcomes of the study. DSR analysis identified statistically non-significant, slight, alveolar bone loss in both groups between months 0 and 12. CONCLUSION: In the short term, periodontal maintenance can be provided in general dental practice with the same expected outcomes compared with maintenance that is provided in a specialist clinic, providing that general dentists are given specific instructions regarding the maintenance regimen. A strong emphasis on effective plaque control is necessary.
Periodontal research over the last 40 years has been remarkably prolific. We now understand that severe periodontitis affects approximately 10-15% of the population (representing a large number of individuals in the UK) and gingivitis and mild periodontitis affect a majority of people. Microbiological research has identified some of the key pathogens that are implicated in periodontal disease. Plaque bacteria exist in biofilms, which have evolved to protect individual organisms within the subgingival bacterial community. For this reason, root surface instrumentation (RSI) remains the cornerstone of periodontal treatment, and is necessary to disrupt the subgingival biofilm mechanically and reduce the bacterial bioburden. Although bacteria are necessary for periodontal disease to occur, a susceptible host is also required. The immune-inflammatory response that develops in the gingival and periodontal tissues in response to the chronic presence of plaque bacteria results in destruction of structural components of the periodontium leading, ultimately, to the clinical signs of periodontitis. The nature of the host response is determined primarily by genetic factors and environmental and acquired factors such as smoking. The host response is essentially protective in nature, but both under-activity (hypo-responsiveness) and over-activity (hyper-responsiveness) of aspects of the host response can result in enhanced tissue destruction. The purpose of this paper is to review current thinking in periodontics with special reference to periodontal epidemiology, microbiology, and pathogenesis.
OBJECTIVES: We set out to monitor gingival crevicular fluid prostaglandin E2 (GCF-PGE2) concentrations longitudinally in a cohort of subjects with chronic periodontitis, given that we had noted an unexplained trend for GCF-PGE2 concentrations to gradually increase in control groups and placebo populations in previously published clinical trials. MATERIAL AND METHODS: 41 adults with moderate-severe chronic periodontitis were recruited. GCF samples were collected from 8 test sites (with 5-8 mm probing depths and attachment loss) every 30 days for 150 days, and assayed for PGE2. Clinical measurements (probing depths, attachment levels, bleeding on probing) were recorded at days 0 and 150. RESULTS: A gradual and statistically significant increase in GCF-PGE2 concentrations was observed over the course of the study, from 40.3 ng/ml to 83.1 ng/ml (p<0.001). When data were expressed as absolute PGE2 content, a similar statistically significant increase from baseline to day 150 was observed (p<0.001). GCF volumes did not vary significantly during the study (p>0.05). Over the same time period, no statistically significant changes in clinical parameters were recorded, with the exception of mean probing depths, which decreased slightly from 5.73 mm to 5.51 mm (p<0.05). CONCLUSION: A trend for gradually increasing GCF-PGE2 concentrations in the absence of any clinical signs of disease progression was noted in a group of patients monitored longitudinally. We suggest that this phenomenon is to be expected in longitudinal clinical trials, and propose a new model for the role of PGE2 in the pathogenesis of periodontal destruction. We feel that if GCF mediators are to be monitored in clinical studies, then both concentrations and absolute mediator content should be calculated, and a standardised sampling protocol should be employed.
BACKGROUND: The programme of supportive periodontal care (SPC) is essential to the long-term stability of patients with chronic periodontitis. The clinical strategy for SPC is often determined according to 'clinical needs' of the patient and is thus determined by clinical observation and individual decision-making rather than being based on the best available clinical evidence. OBJECTIVE: To evaluate the effectiveness of supragingival prophylaxis vs. sub-gingival debridement for SPC following the treatment of chronic periodontitis. SEARCH STRATEGY: Computerized for Medline and the Cochrane Oral Health Group Specialty Trials Register. Hand searching of the Journals of Clinical Periodontology, Periodontal Research and Periodontology. Reference lists from relevant articles were scanned and the authors of eligible studies were contacted to obtain additional information. SELECTION CRITERIA: Studies were selected if they were designed as a prospective clinical trial in which patients with chronic periodontitis had followed a programme of SPC, which included at least one of the regimens of interest in part of the mouth, for a minimum of 12 months. DATA COLLECTION AND ANALYSIS: Information regarding methods, patients, interventions (SPC), outcome measures and results were extracted independently, in duplicate, by two reviewers (P.A.H., G.McC.). Absent data were recorded as such and incomplete data were sought from the researchers wherever possible. RESULTS: In all, 28 papers were identified by the manual and electronic searches; 11 papers were eligible for inclusion. Only one study reported a direct comparison of the two SPCs of interest. The data were reported as mean changes in probing depth and attachment level between baseline and the 12-month follow-up point. For coronal scaling DeltaPD = 0.59 mm [0.13], DeltaAL = -0.13 mm [0.19]. For subgingival debridement DeltaPD = 0.37 mm [0.15], DeltaAL = -0.14 mm [0.18]. There were no significant differences between the SPC regimens. The weighted mean DeltaPD [95% confidence intervals] for the five additional studies that reported supragingival prophylaxis as the SPC regimen was 1.15 mm [-0.17, 2.38]. The weighted mean DeltaPD [95% confidence intervals] for the four studies that reported subgingival debridement as the SPC regimen was 0.56 mm [0.37, 1.47]. The difference between the SPC treatments for the mean DeltaPD is therefore 0.23 mm. The confidence interval for the combined studies was very wide [0.37, 1.47] and very little additional information is gained unless some strong assumptions are made about the comparability of the populations from which the samples are drawn. Such an assumption was not considered appropriate. The weighted mean DeltaAL [95% confidence intervals] for the six additional studies that reported supragingival prophylaxis as the SPC regimen was 0.18 mm [-0.38, 0.74]. The weighted mean DeltaAL [95% confidence intervals] for the six additional studies that reported supragingival prophylaxis as the SPC regimen was 0.50 mm [0.11, 0.89]. The difference between the SPC treatments for mean DeltaAL is 0.32 mm. The confidence interval [-0.36, 1.00] is very wide and the data from the additional studies provide little extra information than that reported in the one study that compared the treatments directly. CONCLUSION: It is not possible to make any firm recommendations regarding clinical practice based on the crude meta-analysis and the review of these 11 studies. The best available evidence indicates that SPC regimens of supragingival prophylaxis and subgingival debridement are comparable with respect to the clinical outcomes of probing depth and attachment levels at 12 months post non-surgical treatment.