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Objective: To use a discourse analysis approach to identify salient features in the lived experiences of dental professionals in relation to explaining periodontal (gum) disease to patients. Methods: Interview data from 13 UK-trained and three internationally-trained dental professionals was examined using thematic discourse analysis. The first stage (discourse analysis) focused on the identification of language patterns in the interview data. This stage forms the focus of this paper. Findings: Six discourse categories (Clinician, Collaborator, Educator, Rapport Builder, Mentor and Professional) were identified that related to the participants’ perceived professional roles. The categories were associated with differing worldviews and language use patterns, but with some overlap. All interviewees used a variety of discourse categories in their accounts, but a few relied predominantly on one category, e.g., Clinician or Mentor. Conclusions: The local discourse categories identified in this study reflect broader discourses in healthcare relating to the roles of providers and patients, which have evolved through time. Practice implications: Practising dental professionals are faced with a diverse range of patients who have different communication preferences. A suite of discourse categories can act as a ‘toolbox’ that dental professionals can flexibly draw on when needing to adopt a role that could predispose a particular patient to positive oral health behaviour change.

Objectives The association of periodontal disease in people diagnosed with RA is emerging as an important driver of the RA autoimmune response. Screening for and treating periodontal disease might benefit people with RA. We performed a systematic literature review to investigate the effect of periodontal treatment on RA disease activity. Methods Medline/PubMed, Embase and Cochrane databases were searched. Studies investigating the effect of periodontal treatment on various RA disease activity measures were included. The quality of included studies was assessed. Data were grouped and analysed according to RA disease outcome measures, and a narrative synthesis was performed. Results We identified a total of 21 studies, of which 11 were of non-randomized experimental design trials and 10 were randomized controlled trials. The quality of the studies ranged from low to serious/critical levels of bias. RA DAS-28 was the primary outcome for most studies. A total of 9 out of 17 studies reported a significant intra-group change in DAS-28. Three studies demonstrated a significant intra-group improvement in ACPA level after non-surgical periodontal treatment. Other RA biomarkers showed high levels of variability at baseline and after periodontal treatment. Conclusion There is some evidence to suggest that periodontal treatment improves RA disease activity in the short term, as measured by DAS-28. Further high-quality studies with longer durations of follow-up are needed. The selection of the study population, periodontal interventions, biomarkers and outcome measures should all be considered when designing future studies. There is a need for well-balanced subject groups with prespecified disease characteristics.

According to Dental Protection, 'good dentists are good communicators, it's that simple!' Unfortunately, dental communication is an under-researched field, so it is not yet clear exactly what good communication in this context entails. The dominant method of researching dental communication to date has followed a 'process approach' where the focus has been on evaluating the communicative competence of the clinician using a checklist of communicative functions; for example, 'the clinician explains the condition'. Conversation analysis, discourse analysis and linguistic analysis are discursive approaches that bring precision by analysing the actual language/discourses being used by patients and providers in interactions. These discursive approaches can be used to capture exactly how, for example, patient engagement is maintained in routine dental consultations, patient reassurance is achieved during invasive procedures and which communication strategies are the most likely to result in enhanced treatment outcomes in paediatric dentistry. In addition to shedding new light on the unique nature of dental communication, discursive approaches provide targeted new tools for developing needs-based training packages for dental professionals.

Introduction.Oral tissues are generally homeostatic despite exposure to many potential inflammatory agents including the resident microbiota. This requires the balancing of inflammation by regulatory mechanisms and/or anti-inflammatory commensal bacteria. Thus, the levels of anti-inflammatory commensal bacteria in resident populations may be critical in maintaining this homeostatic balance.Hypothesis/Gap Statement.The incidence of immunosuppressive streptococci in the oral cavity is not well established. Determining the proportion of these organisms and the mechanisms involved may help to understand host-microbe homeostasis and inform development of probiotics or prebiotics in the maintenance of oral health.Aim.To determine the incidence and potential modes of action of immunosuppressive capacity in resident oral streptococci.Methodology.Supragingival plaque was collected from five healthy participants and supragingival and subgingival plaque from five with gingivitis. Twenty streptococci from each sample were co-cultured with epithelial cells±flagellin or LL-37. CXCL8 secretion was detected by ELISA, induction of cytotoxicity in human epithelial cells by lactate dehydrogenase release and NFκB-activation using a reporter cell line. Bacterial identification was achieved through partial 16S rRNA gene sequencing and next-generation sequencing.Results.CXCL8 secretion was inhibited by 94/300 isolates. Immunosuppressive isolates were detected in supragingival plaque from healthy (4/5) and gingivitis (4/5) samples, and in 2/5 subgingival (gingivitis) plaque samples. Most wereStreptococcus mitis/oralis. Seventeen representative immunosuppressive isolates all inhibited NFκB activation. The immunosuppressive mechanism was strain specific, often mediated by ultra-violet light-labile factors, whilst bacterial viability was essential in certain species.Conclusion.Many streptococci isolated from plaque suppressed epithelial cell CXCL8 secretion, via inhibition of NFκB. This phenomenon may play an important role in oral host-microbe homeostasis.

ObjectivesAn increased prevalence of periodontitis and perturbation of the oral microbiome has been identified in patients with rheumatoid arthritis (RA). The periodontal pathogen Porphyromonas gingivalis may cause local citrullination of proteins, potentially triggering anti-citrullinated protein antibody production. However, it is not known if oral dysbiosis precedes the onset of clinical arthritis. This study comprehensively characterised the oral microbiome in anti-cyclic citrullinated peptide (anti-CCP) positive at-risk individuals without clinical synovitis (CCP+at risk).MethodsSubgingival plaque was collected from periodontally healthy and diseased sites in 48 CCP+at risk, 26 early RA and 32 asymptomatic healthy control (HC) individuals. DNA libraries were sequenced on the Illumina HiSeq 3000 platform. Taxonomic profile and functional capability of the subgingival microbiome were compared between groups.ResultsAt periodontally healthy sites, CCP+at risk individuals had significantly lower microbial richness compared with HC and early RA groups (p=0.004 and 0.021). Microbial community alterations were found at phylum, genus and species levels. A large proportion of the community differed significantly in membership (523 species; 35.6%) and structure (575 species; 39.1%) comparing CCP+at risk and HC groups. Certain core species, including P. gingivalis, had higher relative abundance in the CCP+at risk group. Seventeen clusters of orthologous gene functional units were significantly over-represented in the CCP+at risk group compared with HC (adjusted p value ConclusionAnti-CCP positive at-risk individuals have dysbiotic subgingival microbiomes and increased abundance of P. gingivalis compared with controls. This supports the hypothesis that the oral microbiome and specifically P. gingivalis are important in RA initiation.

Diabetes and periodontal disease are non-communicable chronic diseases that have a bi-directional relationship. The European Federation of Periodontology and International Diabetes Federation recommend patients with diabetes should be screened for periodontal disease and referred to a dental professional where appropriate. This study investigated the awareness among Paediatric Diabetes Care Teams across England and Wales of diabetes as a risk factor for periodontal disease. The study enquired to the practices, training, and confidence of health care professionals in relation to periodontal disease. A semi-structured online questionnaire was sent to all health care professionals working within Paediatric Diabetes Care Teams across England and Wales. Findings showed that 76.2% of participants were aware that periodontitis is a possible complication of diabetes. Only 5.2% screened for periodontal issues, while 27% of respondents stated that oral advice is not typically given to patients at their clinics and 92.3% said that there is no access to a periodontal service within their clinics. There were 76.4% participants who stated that patients are rarely or never referred to an external dental service for their periodontal health. Only 4.8% of respondents said they have received training for recognizing patients who require dental care for their periodontal health, while 23.2% feel confident identifying children who require referral and 85.4% of participants feel they would benefit from further training in periodontal health. In conclusion, patients are not routinely being informed of the risk of periodontitis or being screened or referred for it. Further training would be perceived as beneficial.

Importance The prevalence of periodontitis is increased in patients with rheumatoid arthritis (RA) and periodontopathic bacteria can citrullinate proteins. Periodontitis may, therefore, be an initiator of RA and a target for prevention. Periodontal disease and periodontal bacteria have not been investigated in at-risk individuals with RA autoimmunity but no arthritis. Objective To examine periodontal disease and periodontopathic bacteria in anti–cyclic citrullinated protein (anti-CCP) antibody–positive at-risk individuals without arthritis. Design, Setting, and Participants This cross-sectional study took place at a teaching hospital from April 27, 2015, to May 8, 2017. Forty-eight anti-CCP–positive individuals without arthritis (CCP+ at-risk) were recruited nationally. Twenty-six patients with early RA (ERA) and 32 healthy control individuals were recruited locally. Data were analyzed between June 1, 2017, and December 1, 2017. Interventions Periodontal assessment and examination of joints using ultrasonography. Main Outcomes and Measures Prevalence of diseased periodontal sites, clinical periodontitis, and periodontal inflamed surface area in CCP+ at-risk individuals compared with patients with ERA and healthy individuals matched for age and smoking. Paired-end sequencing of DNA from subgingival plaque from diseased and healthy periodontal sites was performed and DNA was profiled and analyzed. Results A total of 48 CCP+ at-risk individuals (mean [SD] age, 51.9 [11.4] years; 31 [65%] female), 26 patients with ERA (mean [SD] age, 54.4 [16.7] years; 14 [54%] female), and 32 healthy individuals (mean [SD] age, 49.4 [15.3] years; 19 [59%] female) were recruited. Of 48 CCP+ at-risk individuals, 46 had no joint inflammation on ultrasonography. Thirty-five CCP+ at-risk individuals (73%), 12 healthy individuals (38%), and 14 patients with ERA (54%) had clinical periodontitis. The median (interquartile range) percentage of periodontal sites with disease was greater in CCP+ at-risk individuals compared with healthy individuals (3.3% [0%-11.3%] vs 0% [0%-0.7%]) and similar to patients with ERA (1.1% [0%-13.1%]). Median (interquartile range) periodontal inflamed surface area was higher in CCP+ at-risk individuals compared with healthy individuals (221 mm2[81-504 mm2] vs 40 mm2[12-205 mm2]). Patients with CCP+ at-risk had increased relative abundance ofPorphyromonas gingivalis(but notAggregatibacter actinomycetemcomitans) at healthy periodontal sites compared with healthy individuals (effect size, 3.00; 95% CI, 1.71-4.29) and patients with ERA (effect size, 2.14; 95% CI, 0.77-3.52). Conclusions and Relevance This study found increased prevalence of periodontitis andP gingivalisin CCP+ at-risk individuals. This suggests periodontitis andP gingivalisare associated with disease initiation and could be targets for preventive interventions in RA.

Background:The prevalence of periodontal disease and the citrullinating bacteriumPorphyromonas gingivalisare increased in anti-CCP positive individuals at-risk of rheumatoid arthritis (RA) (1). This suggests periodontal inflammation may have an important role in the initiation and development of RA. Despite significant interest in the role of the periodontium and other mucosal sites in the initiation of RA-related autoimmunity, the influence of mucosal inflammation on progression to inflammatory arthritis (IA) in at-risk individuals remains unclear.Objectives:To investigate the association between periodontitis and progression to inflammatory arthritis in anti-CCP+ at-risk individuals without synovitis.Methods:Anti-CCP positive individuals with musculoskeletal symptoms but no clinical synovitis (CCP+ at-risk) were recruited as part of a national prospective cohort study. Comprehensive periodontal examination was performed at baseline by a dentist; six sites per tooth were assessed for clinical attachment level (CAL), pocket depth (PD) and bleeding on probing (BOP). Periodontal disease sites (PDD) were defined as CAL ≥2mm and PD ≥4mm. The distribution of PDD was classified in line with recent guidelines (2). The severity i.e. total burden of periodontal inflammation, was quantified at patient level using the periodontal inflamed surface area (PISA) index(3). CCP+ at-risk were monitored for progression to IA. Multivariable Cox regression was used to assess the effect of PDD distribution and PISA on progression to IA.Results:126 CCP+ at-risk underwent full periodontal examination and were followed up for median 23.4 months (range 0.6 – 56.8 months). Mean age was 49 years, 86 (68%) were females. At baseline, 42(33%) subjects had no PDD, 51(40%) had localised PDD (2. 31 subjects (25%) progressed to IA after median of 12.6 months (range 0.6 – 49.5 months). Progression to IA was significantly higher in subjects with localised PDD compared with those without PDD (33% vs 16%, HR (95% CI) 2.45 (1.02, 5.94) p=0.02), figure 1. Interestingly, this association was not seen in subjects with generalised PDD (19% progression, HR 0.68 (0.20, 2.32). In addition, severity (i.e. total burden) of periodontal inflammation (PISA) was not significantly predictive of progression to IA alone (HR 1.001 (0.999-1.002), p=0.08). However, when adjusting for distribution of PDD, PISA was significantly associated with progression to IA (HR 1.0016 (1.0003- 1.003), p=0.00163).Conclusion:Periodontal inflammation predicts progression to IA in CCP+ at-risk individuals without clinical synovitis. The severity (i.e. total burden) of periodontitis appears to be particularly predictive of progression to IA in patients with localised periodontitis. These data suggest periodontitis may be an important factor in the development of RA and provide rationale for periodontal intervention with the aim of arthritis prevention in at-risk individuals.References:[1] Mankia K et al, JAMA Network Open(2019)[2] Caton J et al, J Clin Periodontol(2018)[3] Nesse W et al, J Clin Periodontol(2008)Disclosure of Interests :Kulveer Mankia: None declared, Zhain Mustufvi: None declared, Jing Kang: None declared, Aradhna Tugnait: None declared, Robert Letton: None declared, Laurence Duquenne: None declared, Alastair Speirs: None declared, Val Clerehugh: None declared, Deirdre Devine: None declared, Paul Emery Grant/research support from: AbbVie, Bristol-Myers Squibb, Merck Sharp & Dohme, Pfizer, Roche (all paid to employer), Consultant of: AbbVie (consultant, clinical trials, advisor), Bristol-Myers Squibb (consultant, clinical trials, advisor), Lilly (clinical trials, advisor), Merck Sharp & Dohme (consultant, clinical trials, advisor), Novartis (consultant, clinical trials, advisor), Pfizer (consultant, clinical trials, advisor), Roche (consultant, clinical trials, advisor), Samsung (clinical trials, advisor), Sandoz (clinical trials, advisor), UCB (consultant, clinical trials, advisor)

Background The prevalence of periodontal disease is increased in RA, and periodontitis is associated with the bacterium Porphyromonas gingivalis (Pg), which can citrullinate arginine residues.1 These observations suggest periodontitis may be a key initiator of RA-related autoimmunity. Importantly, clinical periodontal disease, and the relative abundance of periodontal bacteria have not been described in seropositive individuals at risk of developing RA who do not have synovitis. Objectives To investigate the prevalence of periodontal disease and the relative abundance of key periodontal bacteria in anti-CCP positive at-risk individuals without synovitis. Methods Anti-CCP positive individuals with musculoskeletal symptoms but no clinical synovitis (CCP+), early RA (RA) patients and healthy controls (HC) were recruited. CCP +underwent a 38 joint ultrasound (US) assessment. Periodontal examination was performed by a dentist; six sites per tooth were assessed for clinical attachment level (CAL), pocket depth (PD) and bleeding on probing (BOP). Periodontal disease sites (PDD) were defined as CAL≥2 mm and PD ≥4 mm. A clinical consensus was agreed for each case by three dentists. DNA, isolated from subgingival plaque from diseased and healthy periodontal sites, was pair-end sequenced (Illumina HiSeq3000). Taxonomic and functional profiles were obtained from MG-Rast and differences between groups studied using DESeq2. Mann-Whitney U tests were used to compare groups and Spearman Rho used for correlations. For metagenomic data, Wald test was used to compare relative abundance. Results 48 CCP+, 26 RA and 32 HC were recruited. Groups were balanced for age, sex and smoking. All but 2 (96%) CCP +had no US synovitis (greyscale ≥1 and power Doppler≥1). Dentists classified 73% CCP+, 38% HC (p=0.02) and 54% RA as having clinical periodontitis. The percentage of periodontal sites with CAL ≥2 mm, PD ≥4 mm, BOP, PDD and active PDD (PDD +BOP) were all greater in CCP +compared to HC (p Conclusions We report an increased prevalence of periodontal disease, Pg and Aa in anti-CCP positive at-risk individuals without synovitis. Interestingly, relative abundance of Pg, but not Aa, was associated with periodontitis, suggesting potential mechanistic differences that require further exploration. These data support the concept that periodontal inflammation and periodontopathic bacteria may both be important in the initiation of RA-related autoimmunity. Reference [1] Lundberg K. Nat Rev Rheumatol2010. Disclosure of Interest None declared

Background: The studies of the distribution of Actinomyces spp. on carious and non-carious root surfaces have not been able to confirm the association of these bacteria with root caries, although they were extensively implicated as a prime suspect in root caries.Objective: The aim of this study was to observe the gene expression of Actinomyces spp. in the microbiota of root surfaces with and without caries.Design: The oral biofilms from exposed sound root surface (SRS; n=10) and active root caries (RC; n=30) samples were collected. The total bacterial RNA was extracted, and the mRNA was isolated. Samples with low RNA concentration were pooled, yielding a final sample size of SRS=10 and RC=9. Complementary DNA (cDNA) libraries were prepared and sequenced on an Illumina® HiSeq 2500 system. Sequence reads were mapped to eight Actinomyces genomes. Count data were normalized using DESeq2 to analyse differential gene expression applying the Benjamini-Hochberg correction (false discovery rate [FDR]0.05), except for Actinomyces OT178 (p=0.001) and Actinomyces gerencseriae (p=0.004), which had higher read counts in the SRS. Genes that code for stress proteins (clp, dnaK, and groEL), enzymes of glycolysis pathways (including enolase and phosphoenolpyruvate carboxykinase), adhesion (Type-2 fimbrial and collagen-binding protein), and cell growth (EF-Tu) were highly – but not differentially (p>0.001) – expressed in both groups. Genes with the most significant upregulation in RC were those coding for hypothetical proteins and uracil DNA glycosylase (p=2.61E-17). The gene with the most significant upregulation in SRS was a peptide ABC transporter substrate-binding protein (log2FC=−6.00, FDR=2.37E-05).Conclusion: There were similar levels of Actinomyces gene expression in both sound and carious root biofilms. These bacteria can be commensal in root surface sites but may be cariogenic due to survival mechanisms that allow them to exist in acid environments and to metabolize sugars, saving energy.Keywords: RNA-seq; Actinomyces spp.; root caries; transcriptome; differential expression(Published: 16 September 2016)Citation: Journal of Oral Microbiology 2016, 8: 32383 - http://dx.doi.org/10.3402/jom.v8.32383

Background/Aim: The aim of study was to conduct a meta-analysis to investigate whether or not there was a temporal trend in the treatment efficacy reported in the randomized-controlled trials (RCTs) on guided tissue regeneration (GTR) or enamel matrix protein derivatives (EMD) in the treatment of infrabony defects. Material and Methods: The treatment outcomes were changes in probing pocket depth (PPD) and clinical attachment level (CAL). Weighted multilevel and ordinary regression analyses were performed to test the temporal relationship between treatment effect difference or treatment effectiveness and publication years. Results: For PPD reduction, non-significant positive relationships were found in the treatment effect difference or treatment effect of both GTR and flap operation. For CAL gain, a small positive relationship was found in the treatment effect difference, but a significant positive trend in the treatment effect of flap operation was found. No significant temporal trend was found in the treatment effect difference for EMD. Conclusions: There was no evidence to support or refute a temporal trend in the treatment effect of regenerative procedures, but a positive trend was observed in the control group. These results suggest that only RCTs should be included in the meta-analysis, as the treatment effect of the control group may not be constant.

Radiographs are commonly used in the diagnosis of periodontal diseases. They can be used to assess bone loss and the pattern of loss as well as in the identification of other periodontally relevant features, such as overhanging restoration margins, calculus deposits and furcation lesions. Horizontal and vertical bitewings, panoramic radiographs and periapicals can be used for periodontal assessment. Referral (selection) criteria based on clinical signs can assist the decision of the radiographs to use. All exposures must be made in accordance with the Ionizing Radiation (Medical Examination) Regulations 2000 and each exposure justified.Following a clinical examination, optimum selection of radiographs can assist in the assessment of patients with periodontal diseases.

There is limited knowledge of bacterial metabolism in root caries lesions. The aim of this study was to describe the bacterial metatranscriptomes associated with root caries and sound root surfaces using an RNA-seq analysis approach. The biofilms from exposed root surfaces were sampled from caries-free volunteers (n=10), and from the infected dentine of volunteers with root caries (n=30). Total bacterial RNA was extracted; cDNA libraries were prepared and sequenced on the Illumina Hi-Seq2500. The function and composition of the metabolically active microbiota were investigated using: a) MG-RAST, and b) denovo assembly of the read data and mapping to contigs. Differential gene expression analysis was done using the R package DESeq2 (padj

Serum anti-citrullinated protein antibodies (ACPAs), present in 70% of people with rheumatoid arthritis (RA), can be detected ≤10years before the onset of clinical disease. RA and periodontitis are epidemiologically associated and we have reported a high incidence of periodontitis in people who are ACPA+ and at risk of RA. Periodontal bacteria may contribute by multiple routes to the generation of RA-autoantibodies. This study aims to characterise the subgingival microbiomes from periodontitis and health in individuals with/without RA and at risk of RA. Forty-five ACPA+ no RA (RA-at-risk; RAR), 31 healthy controls (HC) and 30 ACPA+ RA patients (RA) underwent a periodontal examination. DNA from subgingival plaque from healthy and deep pocket sites were paired-end sequenced using the Illumina HiSeq3000 and data analysed using MG-RAST + DESeq. Metagenomes in RA samples had high proportions of Actinobacteria; RAR microbiomes contained higher proportions of Bacteroidetes than HC. The relative abundance of P. gingivalis was high in periodontitis and RAR; Aggregatibacter actinomycetemcomitans was detected with similar frequency in each group. Other bacteria implicated in periodontitis and/or autoantibody generation (Filifactor alocis, Prevotella spp, Leptotrichia spp.) were detected. Analyses are on-going to elucidate the diversity and functional potential of the subgingival microbiome associated with RA.

A number of periodontal diseases, some forms of which can be aggressive, can affect children and adolescents. Plaque is the key aetiological agent but local and systemic factors that can modify the response of the periodontal tissues to plaque may be identified from the history and during examination of the child or adolescent. Periodontal screening should be an integral part of the dental examination of younger individuals. It can be used in conjunction with the history and examination to reach a diagnosis, which then forms the basis for future management.

Background The prevalence of periodontal disease is increased in rheumatoid arthritis (RA) patients (1) but has not been reported in seropositive at risk individuals. Comprehensive periodontal examination requires expert evaluation of six sites per tooth for bleeding on probing (BOP), clinical attachment loss (CAL) and pocket depth (PD). Periodontal disease is associated with Porphyromonas gingivalis , which, through its unique ability to citrullinate arginine residues (2) may trigger RA-related mucosal autoimmunity. Salivary IgA anti-CCP antibodies have been reported in RA patients (3) but their presence in at risk individuals has not been described. Objectives To investigate the prevalence of periodontal disease and to describe evidence of RA-related mucosal autoimmunity in anti-CCP positive subjects at risk of progression to inflammatory arthritis. Methods Anti-CCP positive individuals with no evidence of synovitis (CCP+), healthy controls (HC) and anti-CCP positive RA patients were recruited. All patients underwent periodontal examination by a dentist; six sites per tooth were assessed for BOP (present/absent), CAL (mm) and PD (mm). Dentists later agreed a consensus clinical diagnosis for each case, blinded to patient group. Unstimulated saliva and serum samples were collected. CAL≥2mm and PD≥4mm at the same site signified periodontal disease (PDD). The % of evaluable sites with BOP (%BOP) and % with PDD (%PDD) were calculated per patient. Anti-CCP antibodies (anti-CCP2; immunocap assay, Phadia) were measured in paired saliva & serum samples. IgA anti-CCP titres exceeding the 95th centile in HCs were considered positive. Mann-Whitney U tests were used to compare groups. Spearman rho is reported for associations. Results We recruited 31 CCP+, 20 HC and 12 RA patients. Groups were balanced for sex, smoking and number of missing teeth. Dentists classified 77% of CCP+ and 45% of HC as having clinical periodontal disease. %BOP was higher in CCP+ than HC (CCP+=26.9 [8.6, 46.3], HC=9.8 [3.1, 17.9]; p=0.033) (fig 1a). %PDD was higher in CCP+ compared to HC (CCP+=1.9 [0.0, 15.7], HC=0.3 [0.0, 1.4]; p=0.050) (fig 1b). PDD was recorded at ≥1 site in 65% of CCP+ and 50% of HC. Similar results were obtained for percentage of sites with both PDD and BOP present. 4 patients (CCP+ n=3, RA n=1) had positive saliva IgA anti-CCP results (>6μg/L). 21% of CCP+ (n=6) and 17% of RA (n=2) had positive serum IgA anti-CCP results (>15μg/L); these were not associated with periodontal disease measures. RA patients were slightly older (mean age CCP+=52, HC=50, RA=62) and on disease-modifying treatments; the latter may account for similar %BOP and lower %PDD in this group compared to HC. Age was not associated with %BOP (rho=0.05, p=0.714) or %PDD (rho=0.03, p=0.833). Conclusions We provide preliminary evidence of both an increased prevalence of periodontal disease and the presence of salivary IgA anti-CCP antibodies in anti-CCP positive individuals at risk of arthritis development. These findings support the concept that periodontal inflammation precedes joint inflammation as a potential trigger or early target of RA-related autoimmunity. References A Abou-Raya et al. Scan J Rheum,2005. W McGraw et al. Infect Immun, 1999. A Svard et al. Immunobiology, 2013. Disclosure of Interest K. Mankia: None declared, L. Hunt: None declared, E. Hensor: None declared, J. Nam: None declared, V. Clerehugh: None declared, A. Speirs: None declared, A. Tugnait: None declared, T. Do: None declared, D. Devine: None declared, P. Emery Consultant for: Pfizer, Abbvie, Roche, MSD, BMS, Novartis, Samsung, Lilly, Sandoz, UCB

Many of the periodontal diseases affecting children and adolescents can be successfully managed in general dental practice. The decision to treat the young patient in the practice setting or to refer to a periodontal specialist will depend on the complexity of treatment, patient factors and the expertise of the practitioner. Treatment should be provided in three phases: the initial cause-related phase is aimed at controlling microbial plaque; the corrective phase is intended to restore function and aesthetics; supportive periodontal therapy is aimed at preventing recurrence and progression of periodontal disease. Even in cases requiring specialist referral, the dental team in general practice has a key role in the initial and supportive phases of therapy.