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Systemic inflammation is implicated in the onset and progression of several chronic diseases. Periodontitis is a potential trigger of systemic inflammation.To comprehensively appraise all the evidence on the effects of the treatment of periodontitis on systemic inflammation assessed by serum C-reactive protein (CRP) levels.Six electronic databases were searched up to 10 February 2022 to identify and select articles in English language only.Twenty-six randomized controlled clinical trials reporting changes amongst 2579 participants about CRP levels at 6 months or more after treatment.Two reviewers independently extracted data and rated the quality of studies. Meta-analyses were performed using random and fixed effect models.Risk of bias (RoB 2.0 tool) and quality of evidence (GRADEpro GDT tool) analyses were completed.Treatment of periodontitis reduced CRP levels by 0.69 mg/L (95% confidence interval: -0.97 to -0.40) after 6 months, but limited evidence was retrieved from studies with longer follow-ups. Similar findings were observed in participants with other co-morbidities in addition to periodontitis. Greatest reductions were observed in participants with concentrations of CRP3 mg/L at baseline.High level of heterogeneity.Treatment of periodontitis reduces serum CRP levels (up to 6 months follow-up) to a degree equivalent to that observed after traditional lifestyle or drug interventions. This evidence supports a causal association between periodontitis and systemic inflammation.

BACKGROUND Reduced access to dental care may increase cardiovascular risk; however, socioeconomic factors are believed to confound the associations. We hypothesized that the relation persists despite economic wellness and high education, with reduced access to dental care affecting cardiovascular risk at least in part through its effect on blood pressure (BP), possibly mediated by systemic inflammation. METHODS We first assessed the sociodemographic and clinical characteristics related to last dental visit timing (≤ or >6 months; self-reported) using national representative cross-sectional data. Then, the association of last dental visit timing with clinic BP was selectively investigated in highly educated, high income participants, further matched for residual demographic and clinical confounders using propensity score matching (PSM). The mediating effect of systemic inflammation was formally tested. Machine learning was implemented to investigate the added value of dental visits in predicting high BP over the variables included in the Framingham Hypertension Risk Score among individuals without an established diagnosis of hypertension. RESULTS Of 27,725 participants included in the population analysis, 46% attended a dental visit ≤6 months. In the PSM cohort (n = 2,350), last dental visit attendance >6 months was consistently associated with 2 mmHg higher systolic BP (p = 0.001) and with 23 to 35% higher odds of high/uncontrolled BP compared with attendance ≤6 months. Inflammation mildly mediated the association. Access to dental care improved the prediction of high BP by 2%. CONCLUSIONS Dental care utilization impacts on BP profiles independent of socioeconomic confounders, possibly through systemic inflammation. Regular dental visits may contribute to preventive medicine. This article is protected by copyright. All rights reserved.

PurposePeriodontitis is the sixth most prevalent disease worldwide and periodontal bone loss (PBL) detection is crucial for its early recognition and establishment of the correct diagnosis and prognosis. Current radiographic assessment by clinicians exhibits substantial interobserver variation. Computer-assisted radiographic assessment can calculate bone loss objectively and aid in early bone loss detection. Understanding the rate of disease progression can guide the choice of treatment and lead to early initiation of periodontal therapy.MethodologyWe propose an end-to-end system that includes a deep neural network with hourglass architecture to predict dental landmarks in single, double and triple rooted teeth using periapical radiographs. We then estimate the PBL and disease severity stage using the predicted landmarks. We also introduce a novel adaptation of MixUp data augmentation that improves the landmark localisation.ResultsWe evaluate the proposed system using cross-validation on 340 radiographs from 63 patient cases containing 463, 115 and 56 single, double and triple rooted teeth. The landmark localisation achieved Percentage Correct Keypoints (PCK) of 88.9%, 73.9% and 74.4%, respectively, and a combined PCK of 83.3% across all root morphologies, outperforming the next best architecture by 1.7%. When compared to clinicians’ visual evaluations of full radiographs, the average PBL error was 10.69%, with a severity stage accuracy of 58%. This simulates current interobserver variation, implying that diverse data could improve accuracy.ConclusionsThe system showed a promising capability to localise landmarks and estimate periodontal bone loss on periapical radiographs. An agreement was found with other literature that non-CEJ (Cemento-Enamel Junction) landmarks are the hardest to localise. Honing the system’s clinical pipeline will allow for its use in intervention applications.

Recent evidence suggests hypertension and periodontitis are closely linked but limited data is available on the nature of the association. We aimed to investigate the relationship between periodontitis and mean arterial blood pressure in a sample of otherwise systemically healthy individuals. A case-control study including 250 cases (participants with periodontitis) and 250 controls (without periodontitis) was designed from a register of clinical trials conducted between 2000 and 2018 in a university setting. Cases were age, sex, and body mass index balanced with controls. Linear, logistic regression, and mediation models were planned to test the association between various periodontal measures and arterial blood pressure. We further investigated the role of systemic inflammation assessed by hs-CRP (high-sensitivity C-reactive protein) and white cell counts. Cases presented with 3.36 mm Hg (95% CI, 0.91–5.82, P =0.007) higher mean systolic blood pressure and 2.16 mm Hg (95% CI, 0.24–4.08, P =0.027) higher diastolic blood pressure than controls. Diagnosis of periodontitis was associated with mean systolic blood pressure (β=3.46±1.25, P =0.005) and greater odds of systolic blood pressure ≥140 mm Hg (odds ratio, 2.3 [95% CI, 1.15–4.60], P =0.018) independent of common cardiovascular risk factors. Similar findings were observed when continuous measures of periodontal status were modeled against systolic blood pressure. Measures of systemic inflammation although elevated in periodontitis were not found to be mediators of the association between periodontitis and arterial blood pressure values. Periodontitis is linked to higher systolic blood pressure in otherwise healthy individuals. Promotion of periodontal and systemic health strategies in the dental and medical setting could help reduce the burden of hypertension and its complications.

Patients who are medically compromised may be at an increased risk of complications and treatment errors following periodontal therapy. A review of the evidence on the topic is presented, in relation to the type of complication reported, of periodontal treatment, and of patients' medical status. Further, a framework for risk assessment and appropriate treatment modifications is introduced, with the aim of facilitating the management of patients with existing comorbidities and reducing the incidence of treatment complications.

Context Periodontitis confers an increased risk of developing type 2 diabetes and, in patients with obesity, it might interfere with the incretin axis. The effect of periodontal treatment on glucoregulatory hormones remains unknown. Objective To evaluate the effect of periodontal treatment on incretin axis in obese and lean nondiabetic individuals. Setting King’s College Dental Hospital and Institute, London, UK. Participants and Methods The metabolic profile of obese and normal-body-mass-index individuals affected by periodontitis was studied at baseline, 2, and 6 months after intensive periodontal treatment, by measuring plasma insulin, glucagon, glucagon-like peptide-1(GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) and markers of systemic inflammation and oxidative stress. Main Outcome Measure(s) Circulating levels of incretins and inflammatory markers. Results At baseline, periodontal parameters were worse for obese than nonobese; this was accompanied by higher levels of circulating high-sensitivity C-reactive protein (hs-CRP), insulin, and GLP-1. The response to periodontal treatment was less favorable in the obese group, without significant variations of hs-CRP or malondialdehyde. Glucoregulatory hormones changed differently after treatment: while insulin and glucagon did not vary at 2 and 6 months, GLP-1 and GIP significantly increased at 6 months in both groups. In particular, GLP-1 increased more rapidly in obese participants, while the increase of GIP followed similar trends across visits in both groups. Conclusions Nonsurgical treatment of periodontitis is associated with increased GLP-1 and GIP levels in nonobese and obese patients; changes in GLP-1 were more rapid in obese participants. This might have positive implications for the metabolic risk of these individuals.

Background Several lines of evidence suggest a bi-directional association between Rheumatoid Arthritis (RA) and Periodontitis (PD). Our aim was to systematically appraise the evidence on the association between RA and PD in terms of clinical and laboratory outcomes. Methods An electronic search of several databases (PubMed, EMBASE, MEDLINE, LILACS, CINHL, Scopus, Web of Science, The Cochrane Library, OpenGrey and Google Scholar) was conducted up to March 2019 (PROSPERO CRD42018107817) by two independent reviewers. Observational studies included in the review were quality-appraised using the Newcastle-Ottawa Scale (NOS) tool. Random effects models were used for quantitative analyses. Results A total of 8 case-control studies were identified after the final search of 1491 titles. Following quality assessment, 2 studies were excluded due to the high risk of bias, while the remaining 6 were further analysed. Meta-analyses revealed no substantial effect of RA on the Probing Pocket Depth (PPD) and Clinical Attachment Level (CAL) of patients with PD when compared to controls but high degree of study heterogeneity was found. To the contrary, PD was associated with substantially worse RA disease activity as assessed by an increase in the DAS28 score of 0.74 (0.25–1.24, 95%CI, p Conclusion There is consistent evidence suggesting that PD is associated with worse RA clinical activity as assessed by DAS28 scores whereas, RA patients do not have worsen PD clinical outcomes.

Background: In Europe cardiovascular disease (CVD) is responsible for 3.9 million deaths (45% of deaths), being ischaemic heart disease, stroke, hypertension (leading to heart failure) the major cause of these CVD related deaths. Periodontitis is also a chronic non-communicable disease (NCD) with a high prevalence, being severe periodontitis, affecting 11.2% of the world's population, the sixth most common human disease. Material and Methods: There is now a significant body of evidence to support independent associations between severe periodontitis and several NCDs, in particular CVD. In 2012 a joint workshop was held between the European Federation of Periodontology (EFP) and the American Academy of Periodontology to review the literature relating periodontitis and systemic diseases, including CVD. In the last five years important new scientific information has emerged providing important emerging evidence to support these associations. Results and Conclusions: The present review reports the proceedings of the workshop jointly organised by the EFP and the World Heart Federation (WHF), which has updated the existing epidemiological evidence for significant associations between periodontitis and CVD, the mechanistic links and the impact of periodontal therapy on cardiovascular and surrogate outcomes. This review has also focused on the potential risk and complications of periodontal therapy in patients on anti thrombotic therapy and has made recommendations for dentists, physicians and for patients visiting both the dental and medical practices.

Inflammation is a key driver of common noncommunicable diseases. Among common triggers of inflammation, chronic gingival inflammation (periodontitis) triggers a consistent humoral host inflammatory response, but little is known on its impact on circulating inflammatory cell profiles. We aimed to systematically appraise all the evidence linking periodontitis and its treatment to circulating inflammatory cell profiles. From 6 databases, 157 studies were eligible for qualitative synthesis and 29 studies for meta-analysis. Our meta-analysis showed that participants with periodontitis exhibited a significant mean increase in circulating CD4+, CD4+CD45RO+, IFNγ-expressing CD4+ and CD8+ T cells, CD19+CD27+ and CD5+ B cells, CD14+CD16+ monocytes, and CD16+ neutrophils but decrease in CD8+ T and CD14++CD16− monocytes. Our qualitative synthesis revealed that peripheral blood neutrophils of patients with periodontitis consistently showed elevated production of reactive oxygen species (ROS) when compared with those of healthy controls. Some evidence suggested that the treatment of periodontitis reversed the exaggerated ROS production, but limited and inconclusive data were found on several circulating inflammatory cell profiling. We conclude that periodontitis and its treatment are associated with minor but consistent alterations in circulating inflammatory cell profiles. These changes could represent key mechanisms explaining the association of periodontitis with other comorbidities such as cardiovascular disease, diabetes, and rheumatoid arthritis.

The aim of this cross-sectional study was to investigate the association between carotid intima-media thickness (c-IMT) values and periodontal and peri-implant diseases in a sample of patients with hypertension.A total of 151 participants with presence of at least one dental implant in function for 5 years were recruited. Anthropometric measurements, 24-h ambulatory blood pressure monitoring, ultrasound assessment of carotid arteries (c-IMT and presence of plaque) were recorded and venous blood samples obtained. An oral examination was performed by calibrated examiners to ascertain prevalence and severity of periodontal and peri-implant diseases. Binomial logistic regression was performed to investigate the potential association between various measures of exposure of dental diseases and predictors of cardiovascular risk (c-IMT 0.9 mm and presence of plaque or their combination).Diagnosis of periodontitis (OR 6.71, 95% CI: 2.68-16.76, P 0.001), cumulative mucosal/gingival inflammation (Periodontal Screening and Recording score) (OR 1.25, 95% CI:1.12-1.41, P 0.001), and mucositis (OR 3.34, 95% CI:1.13-9.85, P 0.05) were associated with c-IMT 0.9 mm and/or plaque presence independent of age, sex, smoking, 24 h systolic blood pressure and body mass index differences. No statistically significant results were noted for peri-implantitis. Linear regression models confirmed a positive association of cumulative mucosal/gingival inflammation (β = 0.011, SE 0.002, P 0.001), diagnosis of periodontitis (β = 0.114, SE 0.020, P 0.001), and peri-implant diseases (β = 0.011, SE 0.002, P 0.001) with increased c-IMT values.This study confirms a positive association between mucosal/gingival inflammation and subclinical atherosclerosis assessed by c-IMT values and the presence of carotid plaque in patients with hypertension, independent of traditional cardiovascular risk factors. Future studies are needed to further characterize this relationship.

Increased cardiovascular disease risk underlies elevated rates of mortality in individuals with periodontitis. A key characteristic of those with increased cardiovascular risk is endothelial dysfunction, a phenomenon synonymous with deficiencies of bioavailable nitric oxide (NO), and prominently expressed in patients with periodontitis. Also, inorganic nitrate can be reduced to NO in vivo to restore NO levels, leading us to hypothesise that it may be beneficial in reducing periodontitis-associated endothelial dysfunction. Herein we sought to determine whether inorganic nitrate improves endothelial function in the setting of periodontitis and if so to determine the mechanisms underpinning any responses seen.Periodontitis was induced in mice by placement of a ligature for 14 days around the second molar. Treatment in vivo with potassium nitrate, either prior to or following establishment of experimental periodontitis, attenuated endothelial dysfunction, as determined by assessment of acetylcholine-induced relaxation of aortic rings, compared to control (potassium chloride treatment). These beneficial effects were associated with a suppression of vascular wall inflammatory pathways (assessed by quantitative-PCR), increases in the anti-inflammatory cytokine interleukin (IL)-10 and reduced tissue oxidative stress due to attenuation of xanthine oxidoreductase-dependent superoxide generation. In patients with periodontitis, plasma nitrite levels were not associated with endothelial function indicating dysfunction.Our results suggest that inorganic nitrate protects against, and can partially reverse pre-existing, periodontitis-induced endothelial dysfunction through restoration of nitrite and thus NO levels. This research highlights the potential of dietary nitrate as adjunct therapy to target the associated negative cardiovascular outcomes in patients with periodontitis.

Summary Medical procedures can disperse infectious agents and spread disease. Particularly, dental procedures may pose a high risk of disease transmission as they use high-powered instruments operating within the oral cavity that may contain infectious microbiota or viruses. Here we assess the ability of powered dental devices in removing the biofluid films and identified mechanical, hydrodynamic, and aerodynamic forces as the main underlying mechanisms of removal and dispersal processes. Our results indicate that potentially infectious agents can be removed and dispersed immediately after dental instrument engagement with the adherent biofluid film, while the degree of their dispersal is rapidly depleted owing to the removal of the source and dilution by the coolant water. We found that droplets created by high-speed drill interactions typically travel ballistically, while aerosol-laden air tends to flow as a current over surfaces. Our mechanistic investigation offers plausible routes for reducing the spread of infection during invasive medical procedures., Graphical abstract, Highlights • Mechanical, hydrodynamic, and aerodynamic forces drive removal/dispersal processes • The air-rotor has the highest ability to remove and disperse infectious agents • The aerosol cloud flows as a current and continuously settles • Manipulating rheological properties of the fluids can suppress aerosol generation, Dentistry; Therapeutic procedure; Applied physics

Complement plays a key role in immunosurveillance and homeostasis. When dysregulated or overactivated, complement can become a pathological effector, as seen in several inflammatory disorders, including periodontal disease. Recently, clinical correlative studies and preclinical mechanistic investigations have collectively demonstrated that complement is hyperactivated during periodontitis and that targeting its central component (C3) provides therapeutic benefit in nonhuman primates (NHPs). The preclinical efficacy of a C3-targeted drug candidate combined with excellent safety and pharmacokinetic profiles supported its use in a recent Phase IIa clinical study in which C3 inhibition resolved gingival inflammation in patients with periodontal disease. We posit that C3-targeted intervention might represent a novel and transformative host-modulation therapy meriting further investigation in Phase III clinical trials for the treatment of periodontitis.

AIM To investigate the effect of treatment of periodontitis on systemic health outcomes, pregnancy complications, and associated quality of life. MATERIALS AND METHODS Systematic electronic searches were conducted to identify randomized controlled trials with minimum 6-month follow-up and reporting on the outcomes of interest. Qualitative and quantitative analyses were performed as deemed suitable. RESULTS Meta-analyses confirmed reductions of high-sensitivity C-reactive protein (hs-CRP) [0.56 mg/L, 95% confidence interval (CI) (-0.88, -0.25), p

Objective: Inflammation, oxidative stress, and endothelial dysfunction are known to contribute to ischemia-reperfusion injury. Remote ischemic preconditioning (RIPC) protects from endothelial dysfunction and the damage induced by ischemia-reperfusion. Using intensive periodontal treatment (IPT), an established human model of acute systemic inflammation, we investigated whether RIPC prevents endothelial dysfunction and modulates systemic levels of inflammation and oxidative stress. Approach and Results: Forty-nine participants with periodontitis were randomly allocated to receive either 3 cycles of ischemia-reperfusion on the upper limb (N=24, RIPC) or a sham procedure (N=25, control) before IPT. Endothelial function assessed by flow-mediated dilatation of the brachial artery, inflammatory cytokines, markers of vascular injury, and oxidative stress were evaluated at baseline, day 1, and day 7 after IPT. Twenty-four hours post-IPT, the RIPC group had lower levels of IL-10 (interleukin-10) and IL-12 (interleukin-12) compared with the control group ( P P for interaction P for interaction P =0.011). After 7 days from IPT, most of the inflammatory markers, endothelial-dependent and -independent vasodilation, were similar between groups. Conclusions: RIPC prevented acute endothelial dysfunction by modulation of inflammation and oxidation processes in patients with periodontitis following exposure to an acute inflammatory stimulus. Registration: URL: https://clinicaltrials.gov/ct2/show/NCT03072342 ; Unique identifier: NCT03072342.

This systematic review and meta-analysis evaluated the association between periodontitis (PD) and systemic lupus erythematosus (SLE). A systematic search was conducted through the following electronic databases: Cochrane Library, MEDLINE, EMBASE, Scopus, LILACS, CINAHL and SIGLE (System for Information on Grey Literature in Europe) for relevant publications up to September 2020 with no language restriction. The association between PD and SLE was assessed by the prevalence of PD in SLE patients (both sex and females only) as the primary outcome. Secondary outcomes included differences in common gingival parameters including probing pocket depth (PPD), clinical attachment level (CAL), disease activity index (SLEDAI) scores of SLE patients with or without PD. A total of 1183 citations and 22 full text articles were screened. Eighteen articles were included in the qualitative synthesis, and 13 in the quantitative analysis. SLE diagnosis was associated with greater odds of PD (OR = 1.33, 95% Confidence Interval [CI]: 1.20-1.48), but these were non-significant when examined in females (OR = 3.20, 95%CI: 0.85-12.02). Patients with SLE exhibited no differences in PPD (SMD: -0.09 mm, 95%CI: -0.45-0.27) and CAL (SMD: 0.05 mm, 95%CI: -0.30-0.40) when compared with systemically healthy controls. PD diagnosis was, however, associated with higher SLEDAI scores in patients suffering from SLE (SMD: 0.68, 95% CI: 0.03-1.32). PD and SLE are both inflammatory diseases and their association could be bi-directional. This review suggested that the patients with SLE have greater odds of suffering with PD. Further investigations are required to assess the association between PD and SLE.

Current regenerative strategies for alveolar bone and periodontal tissues are effective and well adopted. These are mainly based on the use of a combination of synthetic/natural scaffolds and bioactive agents, obviating the incorporation of cells. However, there are some inherent limitations associated with traditional techniques, and we hypothesized that the use of cell-based therapies as part of comprehensive regenerative protocols may help overcome these hurdles to enhance clinical outcomes. We conducted a systematic review of human controlled clinical trials investigating the clinical and/or histological effect of the use of cell-based therapies for alveolar bone and periodontal regeneration and explored the translational potential of the different cell-based strategies identified in the included trials. A total of 16 studies (11 randomized controlled trials, 5 controlled clinical trials) were included for data synthesis and qualitative analysis with meta-analyses performed when appropriate. The results suggest a clinical benefit from the use of cell therapy. Improved outcomes were shown for alveolar ridge preservation, lateral ridge augmentation, and periodontal regeneration. However, there was insufficient evidence to identify best-performing treatment modalities amongst the different cell-based techniques. In light of the clinical and histological outcomes, we identify extraction socket and challenging lateral and vertical bone defects requiring bone block grafts as strong candidates for the adjuvant application of mesenchymal stem cells. Given the complexity, invasiveness, and costs associated with techniques that include “substantial manipulation” of tissues and cells, their additional clinical benefit when compared with “minimal manipulation” must be elucidated in future trials. Stem Cells Translational Medicine 2019;8:1286&1295

Recent evidence suggests a link between periodontitis (PD) and hypertension, but the nature of this association remains unclear. The overall aim of this review was to critically appraise the evidence linking these two common disorders. Systematic search was conducted for studies published up to December 2018. Prevalence of hypertension in patients with PD (moderate/severe groups) vs. those without PD (non-PD) was the primary outcome. Additional outcomes included adjusted mean difference in systolic (SBP) and diastolic (DBP) blood pressure (BP) levels in PD vs. non-PD, assessment of biomarkers in PD and hypertension, and BP changes after periodontal therapy. From 81 studies selected, 40 were included in quantitative meta-analyses. Diagnoses of moderate-severe PD [odds ratio (OR) = 1.22; 95% confidence interval (CI): 1.10–1.35] and severe PD (OR = 1.49; 95% CI: 1.09–2.05) were associated with hypertension. Prospective studies confirmed PD diagnosis increased likelihood of hypertension occurrence (OR = 1.68; 95% CI: 0.85–3.35). Patients with PD exhibited higher mean SBP [weighted mean difference (WMD) of 4.49 mmHg; 95% CI: 2.88–6.11] and DBP (2.03 mmHg; 95% CI: 1.25–2.81) when compared with non-PD. Lastly, only 5 out of 12 interventional studies confirmed a reduction in BP following periodontal therapy, ranging from 3 to 12.5 mmHg of SBP and from 0 to 10 mmHg of DBP. PD is associated with increased odds of hypertension (SORT C) and higher SBP/DBP levels. The evidence suggesting that PD therapy could reduce BP is inconclusive. Although additional research is warranted on this association, these results suggest that oral health assessment and management of PD could not only improve oral/overall health and quality of life but also be of relevance in the management of patients with hypertension.

Introduction Ce cycle de conferences se propose d’explorer, a la lumiere aussi de quelques recherches nouvelles en cours, un territoire des etudes consacrees au Moyen Âge grec qui ne parait pas avoir encore ete analyse comme il meriterait de l’etre : celui des textes, des manuscrits et des types d’ecriture des regions orientales byzantines (ou ex-byzantines), consideres sous le double point de vue des formes typiques d’une expression locale et des attestations de contacts multiples avec les d...

Aim To evaluate the superiority of coronally advanced flaps (CAFs) when used in combination with a xenogeneic collagen matrix (CMX) for root coverage of multiple adjacent gingival recessions. Materials and methods Participants with at least 2 upper adjacent teeth exhibiting gingival recession depth ≥2 mm were recruited and randomized to CAF with (test) or without (control) CMX, respectively. Mean and complete root coverage, amount of keratinized tissue (KTw), gingival thickness (GThick) and patient-reported outcomes (PROMs) were recorded at baseline, 3, 6 and 12 months. Results Twenty-four patients providing 61 gingival recessions were analysed. After 1 year, gingival recession depth decreased from 2.3 ± 0.7 to 0.3 ± 0.4 mm in the CAF + CMX group (2.0 ± 0.8 mm meanRC) and from 2.6 ± 1.0 to 0.6 ± 0.3 mm in the control group (2.0 ± 1.1 mm meanRC). No difference was observed between the two groups (p = 0.2023). Nineteen (63%) of the test and 16 (52%) of control defects showed complete root coverage (p = 0.4919). GThick greatly increased in the test group (0.5 mm; 0.2-0.8 mm, 95% CI; p = 0.0057). No difference between the two groups was observed for KTw (p = 0.5668) and PROMs. Conclusion At 1 year, CAF + CMX provided similar root coverage to CAF alone, but a significant increase in gingival thickness.

ObjectivesTo adapt the supranational European Federation for Periodontology (EFP) S3-Level Clinical Practice Guideline for treatment of periodontitis (stage I-III) to a UK healthcare environment, taking into account the views of a broad range of stakeholders, and patients.SourcesThis UK version is based on the supranational EFP guideline (Sanz et al., 2020) published in the Journal of Clinical Periodontology. The source guideline was developed using the S3-level methodology, which combined the assessment of formal evidence from 15 systematic reviews with a moderated consensus process of a representative group of stakeholders, and accounts for health equality, environmental factors and clinical effectiveness. It encompasses 62 clinical recommendations for the treatment of stage I–III periodontitis, based on a step-wise process mapped to the 2017 classification system.MethodologyThe UK version was developed from the source guideline using a formal process called the GRADE ADOLOPMENT framework. This framework allows for the adoption (unmodified acceptance), adaptation (acceptance with modifications) and the de novo development of clinical recommendations. Using this framework and following the S3-process, the underlying systematic reviews were updated and a representative guideline group of 75 delegates from 17 stakeholder organisations was assembled into three working groups. Following the formal S3-process, all clinical recommendations were formally assessed for their applicability to the UK and adoloped accordingly.Results and conclusionUsing the ADOLOPMENT protocol, a UK version of the EFP S3-level clinical practice guideline was developed. This guideline delivers evidence- and consensus-based clinical recommendations of direct relevance to the dental community in the UK.Clinical significanceThe aim of S3-level guidelines is to combine the evaluation of formal evidence, grading and synthesis with the clinical expertise of a broad range of stakeholders to form clinical recommendations. Herein, the first major international S3-level guideline in dentistry, the EFP guideline, was implemented for direct clinical applicability in the UK healthcare system.

This synthesis addresses the issue of devotional practices, traditions of worship and forms of prayer – especially in private devotion – in Greek-speaking Italy of the Byzantine and post-Byzantine periods. In general, even from this point of view the Italo-Greek world displays a remarkable uniformity with the other areas of the Byzantine oecumene, if one disregards some small local peculiarities or emphases on particular aspects. The specific features are few in number and seem on the one hand to be a matter of close contacts, from the early Middle Ages on, with regions of the Eastern Mediterranean (Syria and Palestine) – contacts that leave important and lasting traces particularly in the liturgy – and on the other hand seem to be due to the influence of the traditions of liturgy, devotion and worship of the Latin West.

An accumulating body of evidence supports an independent association between high blood pressure (BP) and periodontitis, possibly mediated by low-grade inflammation. This joint report by the Italian Society of Hypertension (SIIA) and the Italian Society of Periodontology and Implantology (SIdP) working group on Hypertension and Periodontitis (Hy-Per Group) provides a review of the evidence on this topic encompassing epidemiology, biological plausibility, relevance, magnitude, and treatment management. Consensus recommendations are provided for health professionals on how to manage BP in individuals showing signs of poor oral health. In summary, (1) large epidemiological studies highlight that individuals with periodontal diseases have increased risk for high/uncontrolled BP independent of confounders; (2) mechanistically, low-grade inflammation might have a causal role in the association; (3) BP profile and control might benefit from periodontal treatment in pre-hypertensive and hypertensive individuals; (4) oral health status should be evaluated as a potential risk factor for high/uncontrolled BP, and effective oral care should be included as an adjunct lifestyle measure during hypertension management. Further research is needed to optimize BP management in individuals with poor oral health.

Aim: Quantitative comparison of the effects of intensive (IPT) or conventional (CPT) periodontal treatment on arterial blood pressure, endothelial function and inflammatory/metabolic biomarkers. Materials and methods: A systematic search was conducted to identify randomized controlled trials (RCT) of IPT (supra and subgingival instrumentation). Eight RCTs were included in the meta-analysis. Difference in change of systolic blood pressure (SBP) and diastolic blood pressure (DBP) before and after IPT or CPT were the primary outcomes. The secondary outcomes included: endothelial function and selected inflammatory/anti-inflammatory (CRP, IL-6, IL-10, IFN-γ) and metabolic biomarkers (HDL, LDL, TGs). Results: The overall effect estimates (pooled Weighted Mean Difference (WMD)) of the primary outcome for SBP and DBP was −4.3 mmHg [95%CI: −9.10–0.48], p = 0.08 and −3.16 mmHg [95%CI: −6.51–0.19], p = 0.06 respectively. These studies were characterized by high heterogeneity. Therefore, random effects model for meta-analysis was performed. Sub-group analyses confirmed statistically significant reduction in SBP [WMD = −11.41 mmHg (95%CI: −13.66, −9.15) P < 0.00001] and DBP [WMD = −8.43 mmHg (95%CI: −10.96,−5.91)P < 0.00001] after IPT vs CPT among prehypertensive/hypertensive patients, while this was not observed in normotensive individuals. The meta-analyses showed significant reductions in CRP and improvement of endothelial function following IPT at all analysed timepoints. Conclusions: IPT leads to improvement of the cardiovascular health in hypertensive and prehypertensive individuals.

Background: Inflammation is a key driver of common non-communicable diseases. Among common triggers of inflammation, chronic gingival inflammation (periodontitis) triggers a consistent humoral host inflammatory response but little is known on its impact on the circulating peripheral cell profiles. Our aim was to critically appraise the whole existing evidence linking periodontitis and its treatment to circulating inflammatory cell profiles. Methods: In this systematic review and meta-analysis, we searched Cochrane CENTRAL, MEDLINE, Embase, Web of science, Scopus, and CINAHL databases for studies published in English up to 1 March 2021. Case-control, non-randomised and randomised controlled trials that reported the impact of periodontitis and its treatment on circulating inflammatory cell populations and functions were included. Qualitative and quantitative (meta-analysis) syntheses were performed. Weighted mean difference (WMD) with 95% CI of percentage of cell populations values between periodontitis patients and healthy controls were calculated in random effects models. Risk of Bias, including publication and heterogeneity were considered. Findings: Of 12687 studies identified, 157 were eligible for qualitative synthesis and 29 for meta-analysis. Participants with periodontitis exhibited a mean increase in circulating CD4+ (WMD of 0∙04, 95% CI 0∙01 to 0∙07, p=0·0144) and decrease in CD8+ lymphocytes (WMD of -0∙02, 95% CI -0∙04 to -0∙01, p=0∙0075). Peripheral blood neutrophils of patients with periodontitis consistently showed an elevated production of reactive oxygen species (ROS) when compared to those of healthy controls. Some evidence suggested that the treatment of periodontitis reversed the exaggerated ROS production but limited and inconclusive data was found on several circulating inflammatory cell profiling. Peripheral naive cytotoxic T (CD8+CCR7+CD45RA+), T helper (CD4+CCR7+CD45RA+), and effector T helper (CD4+CD45RA+) lymphocytes increased, whereas myeloid dendritic (CD1C+CCR6+), Th17 (CD4+IL-17+Foxp3+/-), CD8+ effector memory, and B (CD19+) lymphocytes decreased after periodontal treatment. Interpretation: Periodontitis and its treatment cause minor but consistent alterations in circulating inflammatory cell profiles. These changes could represent key mechanisms explaining the association of periodontitis with other co-morbidities such as cardiovascular diseases, diabetes, and rheumatoid arthritis. FundingNIHR-BRC at UCL/UCLH and Indonesia Endowment Fund for Education Registration Information: This study was registered with PROSPERO, CRD42020199995. Funding Information: NIHR-BRC at UCL/UCLH and Indonesia Endowment Fund for Education. Declaration of Interests: We declare no competing interests.

Periodontitis is a chronic inflammatory disease with local and systemic implications. Evidence suggests consistent hematologic changes associated with periodontitis. Our aim was to critically appraise the available evidence on hemogram, leukogram, and thrombogram alterations in otherwise healthy patients suffering from periodontitis when compared with controls. For this systematic review (SR), we searched MEDLINE, Web of Science, EMBASE, and the Cochrane Library (CENTRAL) for studies published up to June 2020. Both observational and interventional studies with baseline standard hematologic levels were included. Outcomes of interest were baseline hemogram, leukogram, and thrombogram values and the impact of periodontitis treatment on these outcomes. Upon risk of bias assessment, data extraction and both qualitative and quantitative (standardized mean differences) analyses were performed. Random-effects meta-analyses were performed to provide pooled estimates. The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines were followed (PROSPERO Reg. No. CRD42020164531). A total of 45 studies, eight intervention and 37 case–control studies, were identified after the final search of 3,012 titles. Following quality assessment, 43 articles were deemed to have low risk of bias, and two articles moderate risk. Meta-analyses confirmed that periodontitis was associated with both white and red cell lineages. Severe chronic periodontitis was associated with greater white blood cell counts (mean difference [MD] = 0.53, 95% confidence interval [CI]: 0.26–0.79) when compared with controls. Periodontitis was associated with a larger number of neutrophils (MD = 7.16%, 95% CI: 5.96–8.37) and lower mean platelet volume (MD = 0.30 fL, 95% CI: 0.49 to −0.10) compared with healthy participants. Nonsurgical periodontal treatment was associated with a decrease in white blood cell (WBC) levels (MD = 0.28 109/L, 95% CI: −0.47 to −0.08) in patients with chronic periodontitis. Periodontitis is associated with hematologic changes (Strength of Recommendation Taxonomy [SORT] A recommendation). Higher WBC levels, higher neutrophil levels, higher erythrocyte sedimentation rate, and lower mean platelet volumes are the most common blood count findings. The association between periodontitis and WBC could be causal in nature. Further assessment to determine whether periodontitis causes changes in circulating blood cells and to identify the molecular mechanisms underlying these associations is warranted.

Cardiovascular diseases are the worldwide leading cause of mortality. Cardiovascular diseases are noncommunicable conditions with a complex pathogenesis, and their clinical manifestations include major cardiovascular events such as myocardial infarction and stroke. Epidemiologic evidence suggests a consistent association between periodontitis and increased risk of cardiovascular diseases. Some evidence supports a beneficial effect of the treatment of periodontitis on both surrogate and hard cardiovascular outcomes. This narrative review has been conducted as an update of the most recent evidence on the effects of periodontitis treatment on cardiovascular outcomes since the last commissioned review of the European Federation of Periodontology-American Academy of Periodontology World Workshop in 2012. Newer evidence originating from published randomized controlled trials confirms a positive effect of periodontal treatment on surrogate measures of cardiovascular diseases, whereas there have been no randomized controlled trials investigating the effect of periodontal treatment on the incidence of cardiovascular disease events such as myocardial infarction and stroke. In conclusion, there is sufficient evidence from observational and experimental studies on surrogate cardiovascular measures to justify the design and conduct of appropriately powered randomized controlled trials investigating the effect of effective periodontal interventions on cardiovascular disease outcomes (ie, myocardial infarction and stroke) with adequate control of traditional cardiovascular risk factors.

BACKGROUND Cardiovascular diseases (CVD) including hypertension, are characterized by underlying systemic inflammation. Periodontitis, which can impact the systemic inflammatory burden has recently been linked to high blood pressure (BP). However, the relationship of gingival bleeding, as an easily accessible marker of periodontal disorder, with hypertension, remains unclear. METHODS Survey-based propensity score matching (PSM) incorporating major confounders shared between hypertension and periodontal diseases was applied to cross-sectional NHANES III data from 5396 adults at least 30 years old who underwent BP measurement and periodontal examination, identifying two matched groups with and without gingival bleeding. The association of bleeding gums with SBP (mmHg) and high/uncontrolled BP was then assessed with generalized additive models incorporating inflammatory markers. Stratification by periodontal status (healthy; gingivitis; stable periodontitis; unstable periodontitis) was performed. Variables importance was estimated using machine learning. RESULTS Gingival bleeding (gingivitis; unstable periodontitis) was independently associated with +2.6 mmHg (P

Objective: The primary objective was to investigate the relationship between periodontitis and hypertension in two independent large surveys. The secondary objective was to ascertain whether systemic inflammation had a mediation effect in the association. Methods: This cross-sectional study analysed representative samples of the US (n = 3460; NHANES 2009/10) and Korean (n = 4539; 2015 KNHANES VI-3) populations. The association between periodontitis (exposure), hypertension (outcome) and inflammatory markers [C-reactive protein (CRP) and white blood cell counts (WBC)] (mediators) was assessed using multivariate linear and logistic regression models and mediation analysis. Results: Participants with periodontitis were more likely to have hypertension (NHANES: OR = 1.3, 95% CI: 1.0–1.6, P = 0.025; KNHANES: OR = 1.2, 95% CI: 1.0–1.4, P = 0.041) and actual systolic blood pressure ≥ 140 mmHg (NHANES: OR = 1.6, 95% CI: 1.1–2.3, P < 0.001; KNHANES: OR = 1.3, 95% CI :1.0–1.6, P < 0.031) than those without the disease. These associations were independent of age, gender, BMI, education level, smoking, alcohol consumption, creatinine, physical activity, presence of other comorbidities and confirmed in participants not taking antihypertensive medications. Diagnosis of periodontitis was directly associated with WBC (in both surveys: NHANES: β ± SE = 0.3 ± 0.1, P < 0.004; KNHANES: β ± SE = 0.3 ± 0.1, P < 0.001) and with CRP levels (in one survey: NHANES: β ± SE = 0.1 ± 0.03, P < 0.007; KNHANES: β ± SE = 0.1 ± 0.04, P > 0.213). Mediation analyses confirmed that CRP acted as a mediator in the association between periodontitis and hypertension in both populations (mediated effect: NHANES: β ± SE = 0.010 ± 0.003, P < 0.001; KNHANES: β ± SE = 0.003 ± 0.001, P = 0.015). WBC acted as a mediator in the KNHANES (mediated effect: β ± SE = 0.004 ± 0.001, P = 0.004) whilst in the NHANES, its effect was dependent of CRP inclusion in the model (mediated effect WBC + CRP: β ± SE = 0.002 ± 0.001, P = 0.001). Conclusions: These findings suggest that periodontitis is closely linked to hypertension and systemic inflammation is, in part, a mediator of this association. info:eu-repo/semantics/publishedVersion

Objective To evaluate the effect of periodontitis (PD) on glucoregulatory hormones in obesity, never explored so far, a cross-sectional study was conducted in 110 severely obese, non-diabetic individuals. Methods We collected clinical periodontal parameters, including probing pocket depth (PPD), bleeding on probing (BOP), clinical attachment level (CAL). Insulin, glucagon, GLP-1 and GIP were measured after 3 days of standardized diet. Results Forty-seven subjects had periodontitis (PD+) and 63 did not (PD−). PD+ showed 30.3% of gingival sites with PPD > 4 mm, 55.2% of BOP sites and a mean CAL loss of 4.1 mm. Compared with PD−, PD+ had higher glucagon (26.60 [25.22] vs 3.93 [7.50] ng/l, p

The purpose of this paper was to identify and summarize current evidence describing periodontal complications associated with obesity. Electronic searches supplemented with manual searches were carried out to identify relevant systematic reviews. Identification, screening, eligibility, and inclusion of studies were performed independently by two reviewers. A MeaSurement Tool to Assess systematic Reviews (AMSTAR) was used to assess the quality and risk of bias of the included reviews. From 430 titles and abstracts screened, 14 systematic reviews were considered as eligible for inclusion in this meta-review. Eight reviews reported on cross-sectional studies investigating the association of obesity and periodontal diseases, 4 included longitudinal studies, 5 addressed response to periodontal therapy, 5 reported on studies investigating biomarkers, and only 2 were related to pediatric population samples. Systematic review summaries in the various study design domains (cross-sectional, longitudinal and experimental) report that obese individuals are more likely to have periodontal diseases, with more severe periodontal conditions, than nonobese individuals, with cross-sectional evidence congruent with longitudinal studies showing that obesity or weight gain increases the risk of periodontitis onset and progression. Published research on the effect of obesity on responses to periodontal therapy, or systemic or local biomarkers of inflammation, is variable and therefore inconclusive based on the evidence currently available, which suggests that overweight/obesity contributes to periodontal complications independently of other risk factors, such as age, gender, smoking, or ethnicity. This evidence supports the need for risk assessments for individual patients to facilitate personalized approaches in order to prevent and treat periodontal diseases.