Notes: 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 ΔPD = 0.59 mm [0.13], ΔAL = −0.13 mm [0.19]. For subgingival debridement ΔPD = 0.37 mm [0.15], ΔAL = −0.14 mm [0.18]. There were no significant differences between the SPC regimens. The weighted mean ΔPD [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 ΔPD [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 ΔPD 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 ΔAL [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 ΔAL [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 ΔAL 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.

Notes: 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.

Notes: 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.

Notes: Background, aims: Early onset periodontal diseases (EOP) are a group of inflammatory disorders characterised by a rapid rate of periodontal tissue destruction, in young individuals who are otherwise healthy. There is now substantial evidence to suggest that genetic factors play a rôle in the pathogenesis of EOP but the precise nature of these factors remains unclear. Polymorphisms in cytokine genes which may underpin inter-individual differences in cytokine synthesis and secretion have been associated with other diseases which have an inflammatory pathogenesis, including chronic adult periodontal disease (CAPD).Method: We therefore investigated the frequency of polymorphisms in the genes encoding interleukin-1β (IL-1β) and its receptor antagonist (IL-1RA) in 70 EOP patients, including a subgroup of 21 localised EOP (L-EOP) patients and 72 periodontally healthy controls. All subjects were of Caucasian heritage and systemically healthy. A single nucleotide polymorphism (SNP) in exon 5 of the IL-1β gene (IL-1β+3953) was analysed by amplifying the polymorphic region using PCR, followed by restriction digestion with Taq1 and gel electrophoresis.Results: The frequency of IL-1β genotypes homozygous for allele 1 (corresponding to the presence of a restriction site) of the IL-1β+3953 SNP was found to be significantly increased in EOP patients (χ2 test, p=0.025). Upon stratification for smoking status a significant difference was found in the IL-1β genotype distribution between EOP smokers compared to control smokers (F-exact test, p=0.02), but not between EOP non-smokers and control non-smokers. The IL-1β 1/1 genotype occurred at a higher frequency in EOP smokers (odds ratio=4.9) compared to control smokers. A variable number tandem repeat polymorphism (VNTR) in intron 2 of the IL-1RA gene was analysed by amplifying the polymorphic region using PCR and fragment size analysis by gel electrophoresis. There was no evidence for an association of an IL-1RA genotype with EOP. However the combination of IL-1β allele 1 and IL-1RA allele 1 (corresponding to 4 repeats) was associated with EOP (Clump, p=0.01).Conclusions: These findings suggest that an IL-1β genotype in combination with smoking, and a combined IL-1β and IL-1RA genotype are risk factors for EOP and support a role for genetic and environmental factors in susceptibility to EOP.