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The aim of this study was to investigate patient- and tooth-level factors that may predict tooth loss and periodontitis progression in patients who have undergone at least 5 years of periodontal maintenance.In this retrospective cohort study, 135 patients were examined after active periodontal therapy (APT) and periodontal maintenance for 5.09-8.65 years (mean 6.16 ± 0.74 years). Regression models were applied to identify risk factors associated with tooth loss and disease progression.Stage IV periodontitis (incidence rate ratio [IRR] = 4.61; 95% confidence interval, CI [2.97-7.18], p .001), the presence of ≥5 sites with probing pocket depth (PPD) ≥5 mm at the end of APT (IRR = 2.04; 95% CI [1.32-3.20], p .01), and residual PPD ≥7 mm at the end of APT (odds ratio [OR] = 3.01; 95% CI [1.14-7.94], p .05) were risk factors for tooth loss. Residual PPDs of 5 mm (OR = 2.02; 95% CI [1.20-3.40], p .01) and 6 mm (OR = 2.41; 95% CI [1.22-4.76], p .05) at the end of APT were risk factors for disease progression. Above 3 mm, each 1 mm increase in maximum PPD/clinical attachment loss was associated with an increased risk of tooth loss and disease progression.Stage IV periodontitis is associated with an increased risk of tooth loss. Teeth with PPD ≥5 mm at the end of APT are at risk of periodontitis progression or tooth loss.

To discover and validate differential protein biomarker expression in saliva and gingival crevicular fluid (GCF) to discriminate objectively between periodontal health and plaque-induced periodontal disease states.One-hundred and ninety participants were recruited from two centres (Birmingham and Newcastle upon Tyne, UK) comprising healthy, gingivitis, periodontitis, and edentulous donors. Samples from the Birmingham cohort were analysed by quantitative mass spectrometry proteomics for biomarker discovery. Shortlisted candidate proteins were then verified by enzyme-linked immunosorbent assay in both cohorts. Leave-one-out cross validation logistic regression analysis was used to identify the best performing biomarker panels.Ninety-five proteins were identified in both GCF and saliva samples, and 15 candidate proteins were selected based upon differences discovered between the donor groups. The best performing panels to distinguish between: health or gingivitis and periodontitis contained matrix metalloproteinase-9 (MMP9), S100A8, alpha-1-acid glycoprotein (A1AGP), pyruvate kinase, and age (area under the curve [AUC] 0.970); health and gingivitis contained MMP9, S100A8, A1AGP, and pyruvate kinase, but not age (AUC 0.768); and mild to moderate and advanced periodontitis contained MMP9, S100A8, A1AGP, pyruvate kinase, and age (AUC 0.789).Biomarker panels containing four proteins with and without age as a further parameter can distinguish between periodontal health and disease states.

AIM To evaluate the efficacy of adjunctive therapies in reducing gingivitis and plaque by means of a systematic review of randomized clinical trials (RCTs). MATERIAL AND METHODS A search protocol was designed to identify 6-month RCTs that investigated the efficacy of adjuncts to mechanical plaque control on gingivitis and plaque. Following screening, relevant information was extracted, and quality and potential risk of bias were estimated. Mean treatment differences were calculated to obtain standardized mean differences and weighted mean differences (SMD and WMD) as appropriate. RESULTS Meta-analyses included 70 studies of adjunctive antiseptics. Compared with mechanical plaque control alone, adjuncts yielded statistically significant reductions in gingival index (n = 72; SMD = -1.268; 95% CI [-1.489; -1.047]; p

Aims: To assess the impact of periodontal treatment on systemic inflammation in type 2 diabetes.\ud \ud Materials and methods: Adults with type 2 diabetes (n = 83) and without diabetes (controls, n = 75) were recruited, and participants with periodontitis received periodontal treatment and 12 months' follow-up. Biomarkers for periodontal inflammation (gingival crevicular fluid interleukin-6, tumour necrosis factor-α, interleukin-1β, interferon-γ, matrix metalloproteinase-8, matrix metalloproteinase-9, adiponectin) and serum markers of inflammation and diabetes control (glycated haemoglobin, high sensitivity C-reactive protein, interleukin-6, tumour necrosis factor-α, interleukin-1β, interferon-γ, leptin, adiponectin) were measured. Structural equation modelling was used to evaluate periodontal treatment effects on oral and systemic inflammation.\ud \ud Results: Periodontal treatment resulted in significant improvements in clinical status and reductions in gingival crevicular fluid biomarkers from baseline to month 12. Structural equation modelling identified that, at baseline, individuals with diabetes and periodontitis had significantly higher systemic inflammation than non-diabetic controls with periodontitis (Δ = 0.20, p = .002), with no significant differences between groups for oral inflammation. There was a greater reduction in systemic inflammation following periodontal treatment in individuals with diabetes and periodontitis compared to those with periodontitis but not diabetes (Δ = -0.25, p = .01).\ud \ud Conclusions: Diabetes and periodontitis together appear to increase systemic inflammation, with evidence of reductions following periodontal treatment.

BACKGROUND AND AIMS: The scope of this working group was to review: (1) the effect of professional mechanical plaque removal (PMPR) on secondary prevention of periodontitis; (2) the occurrence of gingival recessions and non-carious cervical lesions (NCCL) secondary to traumatic tooth brushing; (3) the management of hypersensitivity, through professionally and self administered agents and (4) the management of oral malodour, through mechanical and/or chemical agents. RESULTS AND CONCLUSIONS: Patients undergoing supportive periodontal therapy including PMPR showed mean tooth loss rates of 0.15 ± 0.14 teeth/year for 5-year follow-up and 0.09 ± 0.08 teeth/year (corresponding to a mean number of teeth lost ranging between 1.1 and 1.3) for 12-14 year follow-up. There is no direct evidence to confirm tooth brushing as the sole factor causing gingival recession or NCCLs. Similarly, there is no conclusive evidence from intervention studies regarding the impact of manual versus powered toothbrushes on development of gingival recession or NCCLs, or on the treatment of gingival recessions. Local and patient-related factors can be highly relevant in the development and progression of these lesions. Two modes of action are used in the treatment of dentine hypersensitivity: dentine tubule occlusion and/or modification or blocking of pulpal nerve response. Dentifrices containing arginine, calcium sodium phosphosilicate, stannous fluoride and strontium have shown an effect on pain reduction. Similarly, professionally applied prophylaxis pastes containing arginine and calcium sodium phosphosilicate have shown efficacy. There is currently evidence from short-term studies that tongue cleaning has an effect in reducing intra-oral halitosis caused by tongue coating. Similarly, mouthrinses and dentifrices with active ingredients based on Chlorhexidine, Cetylpyridinium chloride and Zinc combinations have a significant beneficial effect. ispartof: Journal of Clinical Periodontology vol:42 issue:S16 pages:S214-S220 ispartof: location:SPAIN status: published

Aim To identify the best available evidence for the effect of toothbrushing on the initiation and progression of gingival recession and non-carious cervical lesions (NCCLs). Methods A protocol was developed for the questions: Does traumatic toothbrushing, compared to normal toothbrushing, lead to an increased prevalence of non-inflammatory gingival recession? [FQ1] and NCCLs? [FQ2]. The search covered four electronic databases. Bibliographies of review articles, relevant texts, World and European Workshops were screened. Hand searches were performed of the Journals of Clinical Periodontology, Periodontology, Periodontal Research and IADR abstracts. Results A meta-analysis included 159 subjects and showed that subjects who used MTBs (manual toothbrush) had greater gingival recession after 12 months when compared with those using PTBs (powered toothbrush). Thirteen cross-sectional studies identified the most frequent toothbrushing factors associated with gingival recession as being toothbrushing frequency, a horizontal or scrub toothbrushing method, bristle hardness, toothbrushing duration and the frequency of changing a toothbrush. The principal toothbrushing factors associated with NCCLs were toothbrushing method and frequency. Conclusion The data to support or refute the association between toothbrushing and gingival recession and NCCLs remain largely inconclusive.

Aim To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. Methods A systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was undertaken. Results Seventy-three articles were included (43 for periodontitis, 30 for caries). Study results were found to be generally heterogeneous. Regarding periodontitis, human studies suggest evidence for altered neutrophil function and increased production of pro-inflammatory mediators (e.g. interleukin-1β, interleukin-6 and prostaglandin E2) in older compared to younger subjects, and animal experiments suggest increased expression of genes that contribute to a pro-inflammatory state in older compared to younger animals. Regarding dental caries, research relating to changes in immune functioning and the impact of ageing is in its infancy. A small number of studies have reported components of innate and adaptive immunity that affect the composition of saliva and dental biofilms with possible impacts on caries progression. Conclusion There is evidence that immune functioning related to periodontitis and (less investigated) dental caries alters with increasing age. In both conditions, age-associated mechanistic changes in immune functioning are complex and incompletely understood and it is not clear how these relate to disease susceptibility.

Aim The aim was to assess the potential trends in Periodontology and Periodontics in Europe that might be anticipated by the year 2025, using the Delphi method. Material and Methods The expert opinion of 120 experts was sought through the use of an open-ended questionnaire, developed by an advisory group, containing 40 questions concerning the various trends in periodontology. Results The experts (113 responders) expect a stabilization of the prevalence of periodontitis, both for the chronic as well as the aggressive cases, but an increase in implant-related diseases up to the year 2025. Concurrently, the importance of implants is seen to be increasing. They foresee an increased demand for postgraduate periodontology and implantology training. This is mirrored in an increase in publications for implant dentistry and increase in demand and need for training. Concerning the patients, better-informed individuals seeking more routine check-ups are expected. Conclusion A continued need for specialized periodontists, but also well trained dental practitioners is foreseen for next decade in Europe. Apart from periodontology they will be increasingly exposed to and trained in implant dentistry.

Background: Major challenges in periodontology include understanding the pathophysiology, the interplay between various components of the host response, parallels with other diseases and identifying biomarkers of the disease. Objectives: Four reviews were compiled with the aim of better understanding: (1) the role of polymorphic nuclear leucocytes (PMNs), i.e. neutrophils; (2) the function of cytokine networks in the host response; (3) whether parallels exist with rheumatoid arthritis (RA); and (4) whether useful biomarkers currently exist to help in the management of periodontal disease. Material and Methods: Based on the focused questions, electronic and manual searches were conducted for human, animal and cellular studies on the above topics. Results: Papers fulfilling the inclusion criteria were selected and reviews were written and reviewed and corrected before the academy meeting to produce consensus statements. Conclusion: The following consensus statements were produced. PMNs are important in the pathophysiology of periodontal disease but there is limited evidence on their much quoted destructive potential. Cytokine networks are enormously complex and we are really at the beginning of understanding their role in the disease process. RA has both similarities and marked differences to periodontal disease although the existing utilization of anticytokine therapies and other molecules in its treatment may have importance in periodontal disease therapy. Biomarkers for periodontal disease have yet to be completely defined but the ratio of receptor activator of NF-kB ligand to osteoprotegerin appears to be a biomarker test with utility for detecting bone destruction.

Preshaw PM, Taylor JJ. How has research into cytokine interactions and their role in driving immune responses impacted our understanding of periodontitis? J Clin Periodontol 2011; 38 (Suppl. 11): 60–84. doi: 10.1111/j.1600-051X.2010.01671.x. Abstract Objective: To review current knowledge on cytokine interactions and the cytokine-mediated links between innate and adaptive immunity that are relevant to the pathophysiology of periodontitis. Materials and Methods: A structured review of the literature was undertaken to identify relevant research publications using a Medline search from 1950 to September 2010. The focus of the search was on the functional role of cytokines, i.e. their actions and responses relevant to the pathogenesis of periodontal disease rather than more descriptive studies of their expression in tissues and body fluids. It was not possible to conduct a traditional systematic review with a focussed question due to the heterogeneity of published research. Results: There is enormous heterogeneity in the periodontal literature in terms of experimental approaches. We have the deepest understanding of the role of the pro-inflammatory cytokines [e.g. interleukin (IL)-1β, tumour necrosis factor-α, IL-6] with accumulating data on T-cell regulatory cytokines (e.g. IL-12, IL-18), chemokines and cytokines which mediate bone cell development and function (e.g. receptor activator of NF-κB ligand, osteoprotegerin). It is clear that there are multiple, overlapping and complex functional links between cytokines with regulatory control exerted at a number of levels and involving numerous cell types (both immune cells and resident cells in the periodontium). Conclusion: Cytokines appear to interact functionally in networks in the periodontium and integrate aspects of innate and adaptive immunity. However, our understanding is far from complete, particularly how molecular and cellular pathways relate to disease pathogenesis. We should adopt consistent experimental approaches to gain better insight into the totality of cytokine networks and how they drive immune responses in the periodontium.

Background: Smoking has been identified as a significant risk factor for periodontal diseases and is regarded as being responsible for incomplete or delayed healing in patients following treatment. Aim and Method: The aim of this conventional review was to review, collate and tabulate the relative effectiveness of treatments of chronic periodontitis in smokers, non-smokers and ex-smokers. Observations: The majority of clinical trials show significantly greater reductions in probing depths and bleeding on probing, and significantly greater gain of clinical attachment following non-surgical and surgical treatments in non-smokers compared with smokers. This benefit is also seen at class I and II furcation sites and in patients prescribed systemic or local antimicrobial treatments. Conclusions: Data from epidemiological, cross-sectional and case–control studies strongly suggest that quitting smoking is beneficial to patients following periodontal treatments. The periodontal status of ex-smokers following treatment suggests that quitting the habit is beneficial although there are only limited data from long-term longitudinal clinical trials to demonstrate unequivocally the periodontal benefit of quitting smoking.

Aim: The purpose of this study was to determine if a 9-month regimen of sub-antimicrobial doxycycline (20 mg, bid) had an effect on either the intestinal or the vaginal microflora. Material and Methods: A total of 69 periodontally diseased subjects were randomized to receive drug or placebo control for a 9-month period. Stool specimens and vaginal swabs were collected at baseline and after 3 and 9 months of therapy. Samples were examined for total anaerobic counts, opportunistic pathogens, and doxycycline-resistant (4 μg/ml) bacteria. All isolates that survived sub-culture were identified and their susceptibilities determined to six antibiotics. Analyses were performed to determine if treatment differences were present. Results: The only statistically significant differences (p

Objectives: To evaluate the crossover clinical trial design to assess plaque removal efficacy of the Sonicare Elite. Material and Methods: A single-cohort, 12-week, two-treatment, single-blind, crossover clinical trial recruited 45 subjects. Plaque was recorded using the modified Quigley and Hein index plaque index (PI). After screening, subjects used the toothbrush for 2 weeks and were reminded to abstain from tooth cleaning 12–18 h prior to appointments. At visit two, subjects were randomized to 2 or 2½ min. brushing time. PIs was recorded pre- and post-brushing. Subjects brushed for the allocated time for a further 2 weeks. At visit 3, PIs were recorded pre- and post-brushing. Two weeks later, at visit 4, the subjects crossed over and the protocol was repeated. Results: There was no evidence of a learning effect within each arm of the crossover. A significant period effect was detected; however, no significant treatment by period effect was found. 2½ min. brushing removed more plaque at full mouth (p=0.037), smooth (p=0.012) and lingual (p=0.002) sites compared with 2 min. Conclusion: The crossover design is a valid model for assessing plaque removal efficacy in tooth-brushing studies where no carry-over effect is clinically plausible.

Preshaw PM, Heasman L, Stacey F, Steen N, McCracken GI, Heasman PA. The effectof quitting smoking on chronic periodontitis. J Clin Periodontol 2005; 32: 869–879.doi: 10.1111/j.1600-051X.2005.00779.x. r Blackwell Munksgaard 2005.AbstractObjectives: To evaluate longitudinally the effect of smoking cessation on clinical andradiographic outcomes following non-surgical treatment in smokers with chronicperiodontitis.Material and Methods: Forty-nine smokers with chronic periodontitis who wished toquit smoking were recruited. Full-mouth probing depths, bleeding and plaque datawere recorded at baseline, 3, 6 and 12 months. Clinical attachment levels wererecorded at target sites and subtraction radiography was used to assess bone densitychanges. Patients received non-surgical periodontal therapy during the first 3 monthsand supportive periodontal care over the remainder of the study. Smoking cessationcounselling was provided according to individual need.Results: After 12 months, of patients with complete data, 10 had continuously quitsmoking (20% of the original population), 10 continued smoking and six wereoscillators (those patients who quit and then relapsed). There were no differencesbetween the groups following treatment with respect to mean clinical or radiographicparameters. Analysis of probing depth reductions between baseline and month 12,however, and comparing quitters with the other two groups combined, demonstrated asignificant difference in favour of quitters (po0.05). Furthermore, quitters weresignificantly more likely to demonstrate probing depth reductions X2 and X3mmthan non-quitters and oscillators (po0.05).Conclusion: Quitting smoking has an additional beneficial effect in reducing probingdepths following non-surgical treatment over a 12-month period.

References: Les maladies cardio-vasculaires representent un groupe tres heterogene de conditions qui ont une mortalite et une morbidite importantes. Ces maladies variees et leurs traitements peuvent avoir un impact sur le parodonte et sur le traitement parodontal But: Dans cet article, nous considerons trois aspects principaux et explorons leurs relations avec le parodontiste et l'etablissement du traitement parodontal. Methode: Les aspects qui ont ete passe en revue comprennent: les effets des medicaments cardio-vasculaires sur le parodonte, et la gestion des patients presentant des maladies parodontales; le risque de survenue d'endocardite infectieuse d'origine iatrogene parodontale ; les interrelations entre une maladie parodontale et une maladie des arteres coronaires. Resultats et conclusions: Les bloqueurs des canaux de calcium et du beta adrenocepteur entrainent respectivement une hyperplasie gingivale et une demineralisation dentaire. Des preuves montrent que l'arret des anti-coagulants avant un traitement parodontal entraine plus un risque accru de desordres thrombo-emboliques qu'un risque hemorragique. La relation entre la dentisterie et l'endocardite infectieuse demeure un probleme sujet a controverse. Il apparaitrait que la bacteriemie survenant lors des manoeuvres d'hygiene orale du patient sont plus a meme de provoquer une endocardite qu'une unique intervention parodontale. L'efficacite de la prophylaxie aux antibiotiques est incertaine (et peu susceptible d'etre demontree) et le risque mortel du a la penicilline apparait etre plus important que le risque mortel inherent a l'endocardite infectieuse. Finalement, l'association entre maladie parodontale et maladie des arteres coronaires a ete recherchee et il semble qu'il y ait beaucoup de probleme concemant l'interpretation de la manipulation des donnees. Plusieurs mecanismes putatifs ont ete avances, mais cela souligne cependant la necessite d'etudes d'intervention.

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 0.05). 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

The handpiece of a Florida sleeve probe was modified to create a flange with the capability to detect the cemento-enamel junction (CEJ). This new instrument (the Pressure-controlled, Automated, Standardised Handpiece or Florida PASHA probe) was used to determine whether (a) the CEJ could be reproducibly detected in dried, human skulls and (b) clinical attachment levels could be reliably measured in human subjects. When using the Florida PASHA probe to detect the CEJ at 157 different sites in four dried, human skulls, there were no statistically significant (p > or = 0.15) differences in mean CEJ detection measurements for any of the three participating examiners; either when the CEJ was visualised or obscured. The mean differences between first and second replicates ranged from 0.00 to 0.08 mm. Intraclass correlation coefficients (ICCs) of repeated measures in both conditions ranged from 0.70 to 0.83 for tactile CEJ detection (CEJ obscured), and from 0.95 to 0.96 for visual detection (CEJ visible). In human studies, the Florida PASHA probe was used by two examiners to determine clinical attachment levels (CAL) at 660 sites in 5 human subjects undergoing supportive periodontal therapy. Intra-examiner agreement of replicate measurements recorded by the probe, as measured by calculating ICCs, ranged from 0.79 to 0.85 for the 2 examiners, respectively. A statistically significant inter-examiner difference in mean CAL measurements when using the Florida PASHA probe was found (p

The aim of this cross-sectional study was to determine concentrations of prostaglandin E2 (PGE2) in gingival crevicular fluid (GCF) in a cohort of periodontal disease-resistant (PDR) adults with chronic gingivitis but with minimal evidence of bone loss, and to compare these data with GCF-PGE2 levels in patients with untreated chronic adult periodontal disease (CAPD). 20 PDR and 35 CAPD subjects with mean (+/-se) ages 52.4 (+/-2.9) and 43.7 (+/-1.2) years respectively, were recruited. GCF was sampled from 6 sites in each PDR subject and 4 sites in each CAPD subject. The GCF-PGE2 concentrations were determined by enzyme immunoassay (Assay Designs). Whole mouth medians of site-specific GCF-PGE2 concentrations were calculated for each subject. The means of the median GCF-PGE2 concentrations were: PDR 54.94+/-4.06 ng/ml; CAPD 41.57+/-2.91 ng/ml (p=0.009). We hypothesise that the higher concentrations of PGE2 in the PDR group may be associated with the proliferating pocket epithelia of the chronic gingivitis. In the CAPD cohort, there were no differences in GCF-PGE2 concentrations between subgroups of smokers (n=13), ex-smokers (n=11) and non smokers (n=11). In the PDR cohort, 19/20 subjects were non-smokers.

The aim of this study was to gain information of the cellular and molecular events which occur during the development of experimental gingivitis and to determine whether such changes occur in the presence or absence of alveolar bone resorption. Clinical, radiographic, biochemical and immunological variables were monitored in a 3-week, single-centre, experimental gingivitis study of 10 healthy volunteers. Following screening and professional prophylaxis to achieve visibly healthy gingival status, subjects abstained from all oral hygiene practises in one maxillary (test) quadrant for a period of 21 days. At days 0 and 21, in test and (contralateral) control quadrants, % bleeding on controlled pressure probing (% BOP) was calculated, and radiographic alveolar bone status was assessed using bilateral standardised vertical bite-wing radiographs and digital subtraction radiography (DSR) analysis. In test quadrants, gingival crevicular fluid (GCF) was sampled from 4 sites per subject with Periopaper strips, and prostaglandin E2 (PGE2) levels measured using an enzyme immunoassay (EIA) kit. At days 0, 7 and 21, one interdental papilla was surgically excised from the test quadrant, and the expression of T cell receptor B variable (TCRBV) genes was investigated using a reverse transcription-polymerase chain reaction (RT-PCR) procedure. At days 0, 7 and 21, peripheral blood lymphocytes (PBL) were isolated and additionally investigated for TCRBV gene expression. Following 21 days of plaque accumulation in test quadrants, a statistically significant increase in % BOP scores confirmed the presence of gingival inflammation (p0.001). DSR analysis revealed that there were no significant alveolar bone changes in either the test or control quadrants between days 0 and 21 (p0.05). EIA analysis of GCF samples identified a significant decrease in mean GCF PGE2 concentrations from day 0 to day 21 (p0.05). RT-PCR analysis indicated that genes from all 3 TCRBV families studied (TCRBV-2, -6, -8) were expressed in the PBL samples at all time points and in healthy gingival tissues at day 0. A restriction in the expression pattern of TCRBV genes similar to those which have previously been reported in chronic periodontitis was noted at gingivitis sites. It is possible that such an event may identify susceptibility to periodontal disease independently of other positive predictive markers such as GCF-PGE2.

Major challenges in periodontology include understanding the pathophysiology, the interplay between various components of the host response, parallels with other diseases and identifying biomarkers of the disease.Four reviews were compiled with the aim of better understanding: (1) the role of polymorphic nuclear leucocytes (PMNs), i.e. neutrophils; (2) the function of cytokine networks in the host response; (3) whether parallels exist with rheumatoid arthritis (RA); and (4) whether useful biomarkers currently exist to help in the management of periodontal disease.Based on the focused questions, electronic and manual searches were conducted for human, animal and cellular studies on the above topics.Papers fulfilling the inclusion criteria were selected and reviews were written and reviewed and corrected before the academy meeting to produce consensus statements.The following consensus statements were produced. PMNs are important in the pathophysiology of periodontal disease but there is limited evidence on their much quoted destructive potential. Cytokine networks are enormously complex and we are really at the beginning of understanding their role in the disease process. RA has both similarities and marked differences to periodontal disease although the existing utilization of anti-cytokine therapies and other molecules in its treatment may have importance in periodontal disease therapy. Biomarkers for periodontal disease have yet to be completely defined but the ratio of receptor activator of NF-κB ligand to osteoprotegerin appears to be a biomarker test with utility for detecting bone destruction.

To review current knowledge on cytokine interactions and the cytokine-mediated links between innate and adaptive immunity that are relevant to the pathophysiology of periodontitis.A structured review of the literature was undertaken to identify relevant research publications using a Medline search from 1950 to September 2010. The focus of the search was on the functional role of cytokines, i.e. their actions and responses relevant to the pathogenesis of periodontal disease rather than more descriptive studies of their expression in tissues and body fluids. It was not possible to conduct a traditional systematic review with a focussed question due to the heterogeneity of published research.There is enormous heterogeneity in the periodontal literature in terms of experimental approaches. We have the deepest understanding of the role of the pro-inflammatory cytokines [e.g. interleukin (IL)-1β, tumour necrosis factor-α, IL-6] with accumulating data on T-cell regulatory cytokines (e.g. IL-12, IL-18), chemokines and cytokines which mediate bone cell development and function (e.g. receptor activator of NF-κB ligand, osteoprotegerin). It is clear that there are multiple, overlapping and complex functional links between cytokines with regulatory control exerted at a number of levels and involving numerous cell types (both immune cells and resident cells in the periodontium).Cytokines appear to interact functionally in networks in the periodontium and integrate aspects of innate and adaptive immunity. However, our understanding is far from complete, particularly how molecular and cellular pathways relate to disease pathogenesis. We should adopt consistent experimental approaches to gain better insight into the totality of cytokine networks and how they drive immune responses in the periodontium.

Aim: To determine the prevalence of periodontitis in an urban population of Sri Lankans with type 2 diabetes (T2DM) and to compare the data with those from a population of adults without diabetes. Methods: Demographic data and a diabetes profile were recorded for a population of urban Sri Lankan adults with T2DM including duration of diabetes, blood pressure; percentage glycosylated haemoglobin, fasting blood glucose level, total cholesterol; triglycerides, low- and high-density lipoproteins. The clinical examination comprised an oral soft tissue examination, full-mouth probing depths (PD), gingival recession (GR), clinical attachment levels and bleeding on probing (BoP). Results: Two hundred and eighty-five individuals with T2DM and 72 controls were examined. 33.3% of T2DM patients were diagnosed with chronic periodontitis compared with 21.7% of controls (p50.077). Subjects with T2DM had significantly more sites with PDX4 and X5mm (po0.01), and higher mean GR and BoP scores (po0.01). Conclusion: This urban Sri Lankan population of subjects with T2DM demonstrated a compromised periodontal status compared with non-diabetic controls.

O'Dowd LK, Durham J, McCracken GI, Preshaw PM. Patients' experiences of the impact of periodontal disease. J Clin Periodontol 2010; 37: 334–339. doi: 10.1111/j.1600-051X.2010.01545.x. Abstract Aim: To examine critically patients' experiences of the impact of periodontal disease on their daily lives. Material and Methods: Semi-structured interviews of a purposive sample of patients with periodontal conditions were conducted using a flexible evolving topic guide. Data collection and analysis were an inductive, iterative process that occurred concurrently. The data were organized in a framework and recurrent themes identified. Interviews occurred until it was felt that no new themes or ideas were being expressed by respondents (n=14). Results: Effects of periodontal disease on patients' daily lives included impairment, functional limitation, discomfort and disability (including physical, psychosocial and social disability). A large number of the emergent themes from the analysis were relevant to the domains of Locker's conceptual model of oral health. The domain within Locker's model that had no data relevant to it in the context of periodontal disease was death. Two additional themes emerged that appeared unrelated to Locker's model, these were stigma and retrospective regret. Conclusion: Periodontal disease reportedly affects patients' lives in a negative manner in a variety of ways. This is of relevance in the management of patients with periodontitis.

Aim: To explore the possibility of using plaque weight rather than plaque index as a more objective, clinical outcome measure in periodontal clinical trials. Materials and methods: The study initially recruited 12 healthy volunteers who abstained from tooth cleaning for 24 h on each of the three occasions and then for 48 h on each of a further three occasions to accumulate plaque. On a further three visits, the subjects abstained from tooth cleaning for 24 h and then brushed with a powered toothbrush for 2 min. A split-mouth design with target teeth was adopted and plaque was first scored separately on each side of the mouth using the Turesky modification of the Quigley and Hein plaque index. Post-brushing residual plaque was also scored after tooth cleaning. Inter-proximal plaque was dried, removed, pooled and weighed: on one side of the mouth from the entire inter-proximal surfaces; and from beneath the contact points on the contra-lateral side. Results: Discriminant validity showed the index to have an advantage over weight in discerning between 24- and 48-h plaque deposits, and between 24-h plaque and post-brushing plaque. Test-retest validity confirmed that for repeated plaque growth, variability within subjects was greater than the variability between subjects. There was an association between plaque weight and plaque index although the regression lines were non-linear. Conclusion: There appears to be no significant advantage in using plaque weight in periodontal clinical trials.

Objectives: Previous studies have demonstrated the clinical benefits of sub-antimicrobial dose doxycycline (SDD) in the treatment of chronic periodontitis (CP). The aim of this study was to retrospectively evaluate the role of SDD as an adjunct to scaling and root planing (SRP) in the treatment of smokers and non-smokers with CP. Material and Methods: A meta-analysis of two previously reported clinical studies was undertaken. Both were 9-month, double-blind, randomized, placebo-controlled, multi-centre clinical trials that investigated the efficacy of SDD (20 mg doxycycline twice daily) in combination with SRP in subjects with moderate–severe CP. 36.9% of the combined study population were smokers. Three hundred and ninety-two subjects were included in the meta-analysis, which evaluated per-subject mean changes in clinical attachment level (CAL) and probing depth (PD) from baseline and the total number of sites with attachment gains and PD reductions 2 and 3 mm from baseline in four subgroups: smokers/SDD; smokers/placebo; non-smokers/SDD; non-smokers/placebo. Results: A hierarchical treatment response was observed, with non-smokers who received SDD demonstrating the greatest CAL gains and PD reductions. Smokers who received placebo demonstrated the smallest clinical improvements following treatment. Smokers who received SDD demonstrated an intermediate treatment response that was broadly equivalent to that seen in non-smokers who received placebo. In sites with baseline PD 4–6 mm, month 9 CAL gains were 19–45% better in non-smokers who received SDD compared with all other subgroups (p

Objective: To compare the Sonicare Elite with the Sonicare Advance in terms of the reduction in supragingival plaque in the posterior, hard-to-reach areas of the mouth. Method: This was a single-cohort, 6-week, two-treatment, single-blind, cross-over clinical trial that recruited 45 subjects. Plaque scores were recorded throughout the study using a modification of the Quigley and Hein plaque index (PI). All subjects had a minimum pre-brushing PI of 1.8 at screening following 24 h abstention from tooth cleaning. Subjects then used a Sonicare Advance powered toothbrush at home for 4 weeks for familiarisation purposes. At the next visit (2), subjects were given either the Sonicare Elite or the Sonicare Advance powered toothbrush for a further 2 weeks of home use. Twenty-four hours prior to visit 3, subjects abstained again from tooth cleaning. At visit 3, the PI was recorded pre- and post-tooth brushing and then all remaining “mature” plaque was removed professionally with a dental prophylaxis. After a further period of 24 h (to accumulate new plaque) without tooth brushing the subjects returned for visit 4 at which PIs were again recorded pre- and post-tooth brushing. The subjects were then given the second toothbrush in the cross-over sequence and attended for visits 5 and 6 at which the protocol for visits 3 and 4 was repeated. Results: The Sonicare Elite powered toothbrush was more effective than the Sonicare Advance model in removing both mature and newly formed plaque. The magnitude of the differences between the toothbrushes for all posterior sites, interproximal and smooth surfaces, respectively, was 0.35 U (p

Background: Subantimicrobial dose doxycycline (SDD – 20 mg doxycycline twice daily) is indicated as an adjunctive treatment for periodontitis. Doxycycline downregulates the activity of matrix metalloproteinases (MMPs), key destructive enzymes in periodontal disease. Current understanding of periodontal pathogenesis suggests that MMPs play a major role in the destruction of periodontal tissues, leading to the clinical signs of periodontitis. Research supports that downregulation of MMPs by SDD confers benefit to patients with periodontitis. Method: We review the clinical, microbiological and safety data relating to the use of SDD in patients with periodontitis, and consider the historical events that led to the development of adjunctive SDD as a treatment for periodontitis. Results: Studies have shown that SDD, when prescribed as an adjunct to scaling and root planing (SRP), results in statistically and clinically significant gains in clinical attachment levels and reductions in probing depths over and above those that are achieved by SRP alone. SRP must be thorough and performed to the highest standard to maximise the benefits of adjunctive SDD. SDD does not result in antibacterial effects, or lead to the development of resistant strains or the acquisition of multiantibiotic resistance. The frequency of adverse events is low, and does not differ significantly from placebo. Conclusions: Adjunctive SDD confers clinical benefit to patients with periodontitis. A comprehensive treatment strategy is suggested, involving patient education and motivation, reduction of the bacterial burden by SRP, host response modulation with SDD, and periodontal risk factor modification.

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.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.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 (p0.001). When data were expressed as absolute PGE2 content, a similar statistically significant increase from baseline to day 150 was observed (p0.001). GCF volumes did not vary significantly during the study (p0.05). 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 (p0.05).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.