Effect of Oral Care on Endothelial Dysfunction in Patients with Acute Coronary Syndrome.

Periodontitis is a common chronic infection and is associated with cardiovascular disease. This study evaluated whether basic oral care for periodontal disease could improve endothelial function in patients with acute coronary syndrome (ACS).This study enrolled 54 patients with acute coronary syndrome admitted to Kagoshima City Hospital and who had undergone percutaneous coronary intervention. Flow-mediated endothelium-dependent dilatation (FMD) was measured before discharge (initial FMD) and at 8 months after percutaneous coronary intervention (follow-up FMD). The following periodontal characteristics were measured: periodontal pocket depth (PPD, mm), plaque control record (%), and bleeding on probing (%). All patients received basic oral care instructions from dentists. The oral health condition was generally poor in the participants and there were 24 patients (44.4%) who had severe PPD. Despite the intervention of basic oral care, the periodontal characteristics did not improve during the study period; initial FMD and follow-up FMD did not significantly differ (4.38 ± 2.74% versus 4.56 ± 2.51%, P = 0.562). However, the follow-up FMD was significantly lower in patients with severe PPD (≥ 6.0 mm, n = 24) than in patients without severe PPD (≤ 5.0 mm, n = 30) (FMD: 3.58 ± 1.91% versus 5.37 ± 2.67%, P = 0.007). FMD tended to be worse in patients with severe PPD than in patients without severe PPD (ΔFMD: -0.55 ± 2.12 versus 0.81 ± 2.77 %, P = 0.055). In conclusion, during the use of basic oral care, endothelial function improved in patients without severe PPD, while it worsened in patients with severe PPD.

No genetic causal association between periodontitis and ankylosing spondylitis: a bidirectional two-sample mendelian randomization analysis.

BACKGROUND: Observational studies that reveal an association between periodontitis (PD) and ankylosing spondylitis (AS) exist. However, observational research is prone to reverse causality and confounding factors, which make it challenging to infer cause-and-effect relationships. We conducted a two-sample Mendelian randomization (MR) study to examine the causal relationship between the genetic prediction of PD and AS. METHODS: In our study, single-nucleotide polymorphisms (SNPs) were defined as instrumental variables (IVs). The genetic association with PD came from the Gene-Lifestyle Interactions and Dental Endpoints (GLIDE) consortium, wherein 17353 cases of European ancestry and 28210 controls of European ancestry were included in this study. The genetic association with AS from the Neale Laboratory Consortium included 337,159 individuals from the United Kingdom, with 968 cases and 336,191 controls. MR analysis was mainly performed using the inverse-variance weighted (IVW) method. In addition, the robustness of the study findings was assessed using sensitivity, pleiotropy, and heterogeneity analyses. RESULTS: Eighteen independent SNPs with P-values significantly smaller than 1 × 10- 5 were used as IV SNPs for PD, while 39 independent SNPs with P-values significantly smaller than 1 × 10- 5 were used as IV SNPs for AS. The results of the IVW method revealed no causal association between PD and AS (odds ratio = 1.00, 95% confidence interval: 0.99953 to 1.00067, P = 0.72). The MR-Egger method did not support the causal association between PD and AS. It is unlikely that horizontal pleiotropy distorts causal estimates based on sensitivity analysis. No significant heterogeneity was observed in the Q test. The ''leave-one-out'' analysis demonstrated that the robustness of our results was unaffected by eliminating any of the IVs. Likewise, no significant causative effect for AS on PD was observed in the inverse MR analysis. CONCLUSIONS: The study results do not support shared heritability or a causal association between PD and AS.

The association between halitosis and periodontitis: a systematic review and meta-analysis.

OBJECTIVES: The purpose of this systemic review and meta-analysis was to explore the association between halitosis and periodontitis in observational studies. MATERIALS AND METHODS: A systematic search covered PubMed, Web of Science, Embase, Scopus, and Cochrane Library until August 18, 2023. Nine observational studies (585 cases, 1591 controls) were analyzed using Stata 17, with odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup analyses considered halitosis assessment methods. RESULTS: The review found a positive association between halitosis and periodontitis. Significant differences were observed with organoleptic test (OR = 4.05, 95% CI: 1.76, 9.30, p < 0.01) and volatile sulfur compound readings (OR = 4.52, 95% CI: 1.89, 10.83, p < 0.01). CONCLUSIONS: A positive association was observed between halitosis and periodontitis, supported by significant differences in both organoleptic and volatile sulfur compound readings. However, conclusive findings are limited by statistical heterogeneity, emphasizing the need for additional research. CLINICAL RELEVANCE: Understanding the halitosis and periodontitis association is clinically significant, informing potential interventions for improved oral health. Further research is vital to refine understanding and guide effective clinical strategies, acknowledging the limitations in current findings.

The role of periodontitis in the development of atherosclerotic cardiovascular disease in participants with the components of metabolic syndrome: a systematic review and meta-analysis.

OBJECTIVES: Prevention of atherosclerotic cardiovascular disease (ASCVD) is important in individuals with metabolic syndrome components (MetS), and periodontitis may play an important role in this process. This study aims to evaluate the association between periodontitis and ASCVD in participants with the components of MetS, including obesity, dysglycemia, hypertension, and dyslipidemia. MATERIALS AND METHODS: This study conducted followed the MOOSE reporting guidelines and the PRISMA 2020 guidelines. EMBASE, MEDLINE, Web of Science, Cochrane Library, PubMed and OpenGrey were searched for observational studies about the linkage of periodontitis to ASCVD in people with MetS components up to April 9, 2023. Cohort, case-control and cross-sectional studies were included after study selection. Quality evaluation was carried out using the original and modified Newcastle-Ottawa Scale as appropriate. Random-effects model was employed for meta-analysis. RESULTS: Nineteen studies were finally included in the quality analysis, and all of them were assessed as moderate to high quality. Meta-analyses among fifteen studies revealed that the participants with periodontitis were more likely to develop ASCVD in those who have dysglycemia (RR = 1.25, 95% CI = 1.13-1.37; p < 0.05), obesity (RR = 1.13, 95% CI = 1.02-1.24; p < 0.05), dyslipidemia (RR = 1.36, 95% CI = 1.13-1.65; p < 0.05), or hypertension (1.20, 95% CI = 1.05-1.36; p < 0.05). CONCLUSIONS: Periodontitis promotes the development of ASCVD in participants with one MetS component (obesity, dysglycemia, hypertension or dyslipidemia). CLINICAL RELEVANCE: In people with MetS components, periodontitis may contribute to the ASCVD incidence.

Periodontitis and the risk of oral cancer: a meta-analysis of case-control studies.

OBJECTIVE: The current studies have yielded inconclusive findings regarding the connection between periodontitis  and oral cancer (OC). Therefore, our goal is to elucidate this relationship. MATERIALS AND METHODS: We conducted a thorough search of electronic databases (EMBASE, PubMed, Web of Science, and Cochrane Library) up to September 2023. The Newcastle-Ottawa Scale (NOS) was applied to assess study quality. To evaluate potential publication bias, both a funnel plot and Egger's test were employed. Additionally, a sensitivity analysis was conducted to explore the source of heterogeneity when the I2 statistic exceeded 50%. RESULTS: This systematic review encompassed 16 studies, involving a total of 6,032 OC patients and 7,432 healthy controls. Our meta-analysis, incorporating data from nine studies, revealed a significant correlation between periodontitis and the risk of OC (OR [odds ratio] = 2.94, 95% CI [confidence interval] (2.13, 4.07); five studies, 6,927 participants; low certainty of evidence). Findings also suggested that individuals with more than 15 missing teeth may have a heightened risk of OC (OR = 1.91, 95% CI (1.01, 3.62)). Furthermore, clinical attachment loss (CAL) and decayed, missing, and filled teeth (DMFT) in OC patients were more pronounced compared to the control group (CAL, SMD = 1.94, 95% CI (0.22, 3.66); DMFT, SMD = 0.65, 95% CI (0.12, 1.18)). CONCLUSION: Periodontitis may serve as a potential risk factor for OC. However, caution is warranted in interpreting these findings due to the substantial level of heterogeneity.

Association between weight-adjusted-waist index and periodontitis risk: A cross-sectional study.

BACKGROUND: There may be an association between obesity and periodontitis, yet no studies have investigated the correlation between the new obesity indicator, the weight-adjusted-waist Index (WWI), and periodontitis. OBJECTIVE: This study aims to investigate the association between the novel obesity index, weight-adjusted-waist index, and periodontitis. SUBJECTS AND METHODS: WWI was utilized to assess obesity, through measuring waist circumference (WC) and body weight. We analyzed cross-sectional NHANES data from 2009 to 2014 (1) using multivariate logistic regression to explore WWI's association with moderate/severe periodontitis; (2) conducting subgroup analyses and interaction tests; and (3) fitting smoothed curves to the age-stratified logistic regression model. RESULTS: The study involved 11,256 individuals, with 48.55% having moderate/severe periodontitis. Upon adjusting for all relevant variables, a significant correlation between WWI and moderate/severe periodontitis was observed (OR = 1.08, 95% CI: 1.01-1.17). Compared to the lowest quartile of WWI, there was a significant increase in the likelihood of moderate/severe periodontitis in Quartile 2 (OR = 1.21, 95% CI: 1.06-1.39) and Quartile 3 (OR = 1.23, 95% CI: 1.07-1.42). Subgroup analyses for gender, age, education, smoking, and diabetes highlighted a positive association between WWI and moderate/severe periodontitis in all subgroups, except for the diabetic population and individuals aged 65 years and older. CONCLUSION: The analysis revealed a positive correlation between WWI, a novel obesity index, and moderate/severe periodontitis prevalence through diverse modeling approaches.

No genetic causal associations between periodontitis and brain atrophy or cognitive impairment: evidence from a comprehensive bidirectional Mendelian randomization study.

BACKGROUND: Observational studies have explored the relationships of periodontitis with brain atrophy and cognitive impairment, but these findings are limited by reverse causation, confounders and have reported conflicting results. Our study aimed to investigate the causal associations of periodontitis with brain atrophy and cognitive impairment through a comprehensive bidirectional Mendelian randomization (MR) research. METHODS: We incorporated two distinct genome-wide association study (GWAS) summary datasets as an exploration cohort and a replication cohort for periodontitis. Four and eight metrics were selected for the insightful evaluation of brain atrophy and cognitive impairment, respectively. The former involved cortical thickness and surface area, left and right hippocampal volumes, with the latter covering assessments of cognitive performance, fluid intelligence scores, prospective memory, and reaction time for mild cognitive impairment to Alzheimer's disease (AD), Lewy body dementia, vascular dementia and frontotemporal dementia for severe situations. Furthermore, supplementary analyses were conducted to examine the associations between the longitudinal rates of change in brain atrophy and cognitive function metrics with periodontitis. The main analysis utilized the inverse variance weighting (IVW) method and evaluated the robustness of the results through a series of sensitivity analyses. For multiple tests, associations with p-values < 0.0021 were considered statistically significant, while p-values ≥ 0.0021 and < 0.05 were regarded as suggestive of significance. RESULTS: In the exploration cohort, forward and reverse MR results revealed no causal associations between periodontitis and brain atrophy or cognitive impairment, and only a potential causal association was found between AD and periodontitis (IVW: OR = 0.917, 95% CI from 0.845 to 0.995, P = 0.038). Results from the replication cohort similarly corroborated the absence of a causal relationship. In the supplementary analyses, the longitudinal rates of change in brain atrophy and cognitive function were also not found to have causal relationships with periodontitis. CONCLUSIONS: The MR analyses indicated a lack of substantial evidence for a causal connection between periodontitis and both brain atrophy and cognitive impairment.

Systematic Review of Prognosis Models in Predicting Tooth Loss in Periodontitis.

This study reviews and appraises the methodological and reporting quality of prediction models for tooth loss in periodontitis patients, including the use of regression and machine learning models. Studies involving prediction modeling for tooth loss in periodontitis patients were screened. A search was performed in MEDLINE via PubMed, Embase, and CENTRAL up to 12 February 2022, with citation chasing. Studies exploring model development or external validation studies for models assessing tooth loss in periodontitis patients for clinical use at any time point, with all prediction horizons in English, were considered. Studies were excluded if models were not developed for use in periodontitis patients, were not developed or validated on any data set, predicted outcomes other than tooth loss, or were prognostic factor studies. The CHARMS checklist was used for data extraction, TRIPOD to assess reporting quality, and PROBAST to assess the risk of bias. In total, 4,661 records were screened, and 45 studies were included. Only 26 studies reported any kind of performance measure. The median C-statistic reported was 0.671 (range, 0.57-0.97). All studies were at a high risk of bias due to inappropriate handling of missing data (96%), inappropriate evaluation of model performance (92%), and lack of accounting for model overfitting in evaluating model performance (68%). Many models predicting tooth loss in periodontitis are available, but studies evaluating these models are at a high risk of bias. Model performance measures are likely to be overly optimistic and might not be replicated in clinical use. While this review is unable to recommend any model for clinical practice, it has collated the existing models and their model performance at external validation and their associated sample sizes, which would be helpful to identify promising models for future external validation studies.

Impact of periodontitis on type 2 diabetes: a bioinformatic analysis.

BACKGROUND: Periodontitis is strongly associated with type 2 diabetes (T2D) that results in serious complications and mortality. However, the pathogenic role of periodontitis in the development of T2D and the underlain mechanism have not been fully elucidated. METHODS: A Mendelian randomization (MR) was performed to estimate the causality between two diseases. Bioinformatics tools, including gene ontology and pathway enrichment analyses, were employed to analyze the common differentially expressed genes (DEGs) in periodontitis and T2D. MR and colocalization analyses were then utilized to investigate the causal associations between potential pathogenic gene expression and the risk of T2D. Single cell-type expression analysis was further performed to detect the cellular localization of these genes. RESULTS: Genetically predicted periodontitis was associated with a higher risk of T2D (OR, 1.469; 95% CI, 1.117-1.930; P = 0.006) and insulin resistance (OR 1.034; 95%CI 1.001-1.068; P = 0.041). 79 common DEGs associated with periodontitis and T2D were then identified and demonstrated enrichment mainly in CXC receptor chemokine receptor binding and interleutin-17 signaling pathway. The integration of GWAS with the expression quantitative trait locis of these genes from the peripheral blood genetically prioritized 6 candidate genes, including 2 risk genes (RAP2A, MCUR1) and 4 protective genes (WNK1, NFIX, FOS, PANX1) in periodontitis-related T2D. Enriched in natural killer cells, RAP2A (OR 4.909; 95% CI 1.849-13.039; P = 0.001) demonstrated high risk influence on T2D, and exhibited strong genetic evidence of colocalization (coloc.abf-PPH4 = 0.632). CONCLUSIONS: This study used a multi-omics integration method to explore causality between periodontitis and T2D, and revealed molecular mechanisms using bioinformatics tools. Periodontitis was associated with a higher risk of T2D. MCUR1, RAP2A, FOS, PANX1, NFIX and WNK1 may play important roles in the pathogenesis of periodontitis-related T2D, shedding light on the development of potential drug targets.

The impact of systemic administration of polyphenols on periodontitis associated with diabetes mellitus: a systematic review.

OBJECTIVE: The aim of this work was to explore the potential of polyphenol supplement consumption in enhancing the treatment of periodontitis and diabetes mellitus in both diabetic animals and humans. MATERIALS AND METHODS: A comprehensive search across eight databases (MEDLINE, EBSCO, Taylor & Francis, PRIMO, Web of Science, Wiley Online Library, ScienceDirect, and SAGE Journals) and two registers (ClinicalTrials.gov and Cochrane Library Trials) was conducted. Methodological quality assessment employed the Cochrane Collaboration Risk of Bias Assessment Tool for randomised controlled trials and the Systematic Review Centre for Laboratory Animal Experimentation Risk of Bias Tool for experimental animal studies. RESULTS: Ten articles meeting inclusion criteria were identified. Three clinical studies demonstrated significant reductions in probing depth (PD) and clinical attachment loss (CAL). Ginger supplementation showed a decrease in CAL (-0.57 ± 0.50 vs. -0.14 ± 0.35, p = 0.003) and PD (-0.52 ± 0.51 vs. -0.19 ± 0.51, p = 0.04), while resveratrol supplementation exhibited a reduction in PD (-1.1 ± 0.58 vs. -0.6 ± 0.47, p < 0.001). Additionally, cranberry juice supplementation led to a decrease in PD (-0.56 ± 0.03, p < 0.001). However, there was no significant improvement in inflammation status. Although polyphenol supplementation did not impact fasting blood glucose levels, it did result in improved insulin resistance (3.66 ± 0.97 vs. 4.49 ± 1.56, p = 0.045). In diabetic animals, six studies reported a significant reduction (p < 0.05) in bone loss along with marked improvements in inflammation status. CONCLUSIONS: Despite the promising results observed in the included studies, the overall evidence supporting the positive effects of polyphenols on periodontal and diabetes mellitus status, along with their anti-inflammatory properties, remains inadequate.

Association between periodontitis and dental caries: a systematic review and meta-analysis.

OBJECTIVES: Recent evidence suggested a link between periodontitis (PD) and dental caries, but the trends and nature of this association remained unclear. The overall aim of this study was to critically assess the correlation of two disorders. METHODS: A comprehensive search was conducted within the PUBMED and EMBASE databases including grey literatures up to July 5th, 2023. The Newcastle-Ottawa scale was used to qualitatively evaluate the risk of bias. RESULTS: Overall, 18 studies were included. In terms of caries risk in PD patients, the prevalence of caries was increased by PD (OR = 1.57, 95%CI:1.20-2.07), both in crown (OR = 1.03, 95%CI:1.01-1.05) and root caries (OR = 2.10, 95%CI:1.03-4.29). Odds of caries were also raised by PD severity (OR moderate = 1.38, 95%CI:1.15-1.66; OR severe = 2.14, 95%CI:1.74-2.64). Besides, patients with PD exhibited a higher mean number of decayed, missing and filled teeth (DMFT) and decayed and filled root teeth (DFR) [weighted mean difference (WMD)DMFT = 0.87, 95%CI: -0.03-1.76; WMDDFR = 1.13, 95%CI: 0.48-1.78]. Likewise, patients with caries had an elevated risk of PD (OR = 1.79, 95%CI:1.36-2.35). However, Streptococcus mutans, one of the main pathogens of caries, was negatively correlated with several main pathogens of periodontitis. CONCLUSIONS: This study indicated a positive correlation between dental caries and periodontitis clinically, while the two disease-associated pathogens were antagonistic. CLINICAL RELEVANCE: Further research, including clinical cohort studies and mechanisms of pathogens interaction is needed on this link for better prevention and treatment of PD and caries. In addition, innovative prevention strategies need to be developed and incorporated in dental practices to prevent these two highly prevalent oral diseases.

Association of specific nutritional intake with periodontitis.

BACKGROUND: The present study aimed to evaluate nutritional intake among a group of male patients in the dental clinic with and without periodontal disease to search for associations between nutritional profile and periodontal health. METHODS: To this purpose, nutritional intake of macronutrients, fiber, vitamins, and minerals were compared evaluating both clinical parameters and periodontal status. Non periodontitis patients were compared with stage III and IV periodontitis and its extension according to the 2017 classification. RESULTS: After multivariate analysis, statistically significant associations were found between the dietary intake of energy, total fat, cholesterol, calcium, saturated fat, monounsaturated fat and folic acid and iodine and periodontitis status. This study reports an inverse association between cholesterol and iodine and periodontitis and a direct association with saturated fat, monounsaturated fat, and folic acid. CONCLUSIONS: Maintaining an adequate intake of fat, iodine, calcium, and cholesterol and avoiding an excessive intake of energy, saturated fat, monounsaturated fat, and folic acid could be important to controlling periodontitis.

Linking periodontitis with 20 cancers, emphasis on oropharyngeal cancer: a Mendelian randomization analysis.

While associations between periodontitis and an elevated risk of cancer have been suggested, the results of existing observational studies have been inconsistent, also leaving room for further investigation into the underlying mechanisms. This study was designed to delve into the possible causal link between periodontitis and 20 standard cancers while concurrently identifying potential mediators. We initiated a Mendelian randomization analysis that drew from either publicly accessible or personally obtained genome-wide association study (GWAS) datasets. The inverse variance weighting (IVW) method served as our primary tool for analysis. To ensure the strength and consistency of our results, we implemented additional strategies, including weighted median, weighted mode, MR-Egger regression, and MR pleiotropy residual sum and outlier (MR-PRESSO), bolstered by funnel plots. Our analysis unveiled an elevated risk of head and neck cancer concomitant with periodontitis (p = 0.041, OR 0.999, 95% CI 0.999-1.000), specifically a heightened risk of oropharyngeal cancer (p = 0.022, OR 0.999, 95% CI 0.999-1.000). As a result of probing into potential mediators, Fusobacterium nucleatum emerged as a likely intermediary in the promoting effect of periodontitis on oropharyngeal cancer (p = 0.021, OR 0.999, 95% CI 0.998-1.000). Inversely, basal cell carcinoma and endometrial cancer demonstrated an association with an increased incidence of periodontitis (basal cell carcinoma: p = 0.020, OR 0.987, 95% CI 0.976-0.998; endometrial cancer: p = 0.027, OR 0.984, 95% CI 0.970-0.998). However, periodontitis exerted no significant causal impact on the 19 other common cancers or the three subtypes of head and neck cancer. To conclude, our results support the theory that periodontitis contributes to an enhanced risk of head and neck cancer, particularly oropharyngeal cancer, with Fusobacterium nucleatum functioning as a potential intermediary.

P. gingivalis in oral-prostate axis exacerbates benign prostatic hyperplasia via IL-6/IL-6R pathway.

BACKGROUND: Benign prostatic hyperplasia (BPH) is the most common disease in elderly men. There is increasing evidence that periodontitis increases the risk of BPH, but the specific mechanism remains unclear. This study aimed to explore the role and mechanism of the key periodontal pathogen Porphyromonas gingivalis (P. gingivalis) in the development of BPH. METHODS: The subgingival plaque (Sp) and prostatic fluid (Pf) of patients with BPH concurrent periodontitis were extracted and cultured for 16S rDNA sequencing. Ligature-induced periodontitis, testosterone-induced BPH and the composite models in rats were established. The P. gingivalis and its toxic factor P. gingivalis lipopolysaccharide (P.g-LPS) were injected into the ventral lobe of prostate in rats to simulate its colonization of prostate. P.g-LPS was used to construct the prostate cell infection model for mechanism exploration. RESULTS: P. gingivalis, Streptococcus oralis, Capnocytophaga ochracea and other oral pathogens were simultaneously detected in the Pf and Sp of patients with BPH concurrent periodontitis, and the average relative abundance of P. gingivalis was found to be the highest. P. gingivalis was detected in both Pf and Sp in 62.5% of patients. Simultaneous periodontitis and BPH synergistically aggravated prostate histological changes. P. gingivalis and P.g-LPS infection could induce obvious hyperplasia of the prostate epithelium and stroma (epithelial thickness was 2.97- and 3.08-fold that of control group, respectively), and increase of collagen fibrosis (3.81- and 5.02-fold that of control group, respectively). P. gingivalis infection promoted prostate cell proliferation, inhibited apoptosis, and upregulated the expression of inflammatory cytokines interleukin-6 (IL-6; 4.47-fold), interleukin-6 receptor-α (IL-6Rα; 5.74-fold) and glycoprotein 130 (gp130; 4.47-fold) in prostatic tissue. P.g-LPS could significantly inhibit cell apoptosis, promote mitosis and proliferation of cells. P.g-LPS activates the Akt pathway through IL-6/IL-6Rα/gp130 complex, which destroys the imbalance between proliferation and apoptosis of prostate cells, induces BPH. CONCLUSION: P. gingivalis was abundant in the Pf of patients with BPH concurrent periodontitis. P. gingivalis infection can promote BPH, which may affect the progression of BPH via inflammation and the Akt signaling pathway.

The prevention of adverse pregnancy outcomes by periodontal treatment during pregnancy (PROBE) intervention study-A controlled intervention study: Protocol paper.

INTRODUCTION: Pregnancy increases the risk of periodontitis due to the increase in progesterone and estrogen. Moreover, periodontitis during pregnancy is associated with development of pregnancy and birth related complications. The aim of this study is to determine, whether periodontal treatment during pregnancy can reduce systemic inflammation and lower the risk of adverse pregnancy and birth related outcomes. METHODS AND ANALYSIS: The PROBE study is a non-randomized controlled intervention study conducted among 600 pregnant women with periodontitis. The women will be recruited among all pregnant women at two Danish hospitals in Region Zealand during their nuchal translucency scan and will subsequently be screened for periodontitis. The intervention group includes 300 pregnant women, who will be offered state-of-the-art periodontal treatment during pregnancy. The control group includes additional 300 pregnant women, who will be offered periodontal treatment after giving birth. Outcome measures include periodontal measures, inflammatory, hormonal and glycaemic markers as well as the prevalence of preterm birth risk, low birth weight and risk markers of gestational diabetes mellitus (GDM) and preeclampsia that will be collected from all screened women and further during pregnancy week 20 and pregnancy week 35 for women enrolled in the intervention. ETHICS AND DISSEMINATION: The study's findings will be published in peer reviewed journals and disseminated at national and international conferences and through social media. The PROBE study is designed to provide important new knowledge as to whether periodontal treatment during pregnancy can reduce the prevalence of complications related to pregnancy and birth. CLINICAL TRIALS REGISTRATION: The study was registered on clinicaltrials.gov (NCT06110143).

Systemic benefits of periodontal therapy in patients with obesity and periodontitis: a systematic review.

This systematic review aimed to answer the focused question: "What are the benefits of subgingival periodontal therapy on blood hematological and biochemical index, biomarkers of inflammation and oxidative stress, quality of life, and periodontal pathogen counts in patients with obesity and periodontitis?". A systematic literature search was performed in six databases: PubMed, Embase, LILACS, Web of Science, Cochrane and SCOPUS and other sources, and a manual search was conducted as well. Inclusion criteria were randomized and non-randomized clinical trials, and before-and-after studies on patients with obesity subjected to periodontal therapy. The results were synthesized qualitatively. Risk of bias within studies was assessed using RoB 2 and ROBINS-I tools. The certainty of evidence was evaluated following the GRADE approach. Three randomized controlled trials and 15 before-and-after studies were included. Randomized controlled trials were considered to have a low risk of bias, as compared to before-and-after studies assessed as having low, serious, and critical risks of bias. Non-surgical periodontal therapy plus azithromycin, chlorhexidine, and cetylpyridinium chloride reduced blood pressure and decreased serum levels of HbA1c, hsCRP, IL-1ß, and TNF-α. Salivary resistin level also decreased in patients with obesity and periodontitis after therapy and chlorhexidine mouth rinse. Before-and-after data suggest an improvement in total cholesterol, LDL, triglycerides, insulin resistance, C3, GCF levels of TNF-α, chemerin, vaspin, omentin-1, visfatin, 8-OHdG, and periodontal pathogen counts after therapy.

Successful Regenerative Therapy of Periodontal Defects Associated With Tongue Piercing: A Clinical Report.

Oral piercing habits are associated with various degrees of complications. Tongue piercing increases the risk of gingival recession and infrabony defects, subsequently leading to localized periodontitis. In the case presented, the patient had persistent swelling and suppuration around her mandibular anterior teeth attributed to tongue piercing jewelry that was placed approximately 12 years prior. Intraoral examinations revealed a localized deep pocket, purulent discharge, swelling, plaque accumulation, bleeding on probing, gingival recession, and teeth mobility. The patient was diagnosed with localized stage III, grade C periodontitis. Following full-mouth debridement and the placement of an extracoronal lingual splint, minimally invasive, papillae-sparing incisions were made, and regenerative therapy with bone allograft and collagen membrane was used to manage the infrabony defects. During the 18-month postoperative follow-up, complete soft-tissue healing was observed along with a significant reduction in pocket depth and the absence of bleeding on probing or suppuration. Radiographic evaluation showed evidence of bone fill. The reported case demonstrates how careful diagnosis and treatment planning are crucial for managing different periodontal defects and emphasizes the importance of proficient periodontal management, which can save teeth that would otherwise be extracted and replaced with implant therapy or fixed bridgework.

Association between carotenoid intake and periodontitis in diabetic patients.

This study aimed to evaluate the association between dietary carotenoid intake and periodontitis in diabetic patients. Data on diabetic patients were collected from the National Health and Nutrition Examination Survey (NHANES) 2009-2014 for this cross-sectional study. Dietary intake of carotenoids was assessed through the first 24-hour dietary recall interview. Full-mouth periodontal examinations were conducted by trained dental examiners. Subgroup analysis was conducted in terms of age, gender, the number of missing teeth, cardiovascular disease, smoking, and anti-diabetic drugs. Totally 1914 diabetic patients were included, with 1281 (66.93%) in the periodontitis group. After adjusting for age, gender, race, education, smoking, dental implants, hepatitis, and the number of missing teeth, α-carotene intake ≥55.82 mcg was associated with lower odds of periodontitis than α-carotene intake <55.82 mcg [OR = 0.70, 95% CI: 0.53-0.91, P = 0.010]; lutein and zeaxanthin intake ≥795.95 mcg was associated with decreased odds of periodontitis than lutein and zeaxanthin intake <795.95 mcg (OR = 0.75, 95%CI: 0.57-0.98, P = 0.039). The association between carotenoid intake and periodontitis varied across different subpopulations. In diabetes, dietary intake of α-carotene and lutein and zeaxanthin was inversely associated with the odds of periodontitis, which may facilitate clinical periodontitis management.

Periodontitis: A Plausible Modifiable Risk Factor for Neurodegenerative Diseases? A Comprehensive Review.

The aim of this comprehensive review is to summarize recent literature on associations between periodontitis and neurodegenerative diseases, explore the bidirectionality and provide insights into the plausible pathogenesis. For this purpose, systematic reviews and meta-analyses from PubMed, Medline and EMBASE were considered. Out of 33 retrieved papers, 6 articles complying with the inclusion criteria were selected and discussed. Additional relevant papers for bidirectionality and pathogenesis were included. Results show an association between periodontitis and Alzheimer's disease, with odds ratios of 3 to 5. A bidirectional relationship is suspected. For Parkinson's disease (PD), current evidence for an association appears to be weak, although poor oral health and PD seem to be correlated. A huge knowledge gap was identified. The plausible mechanistic link for the association between periodontitis and neurodegenerative diseases is the interplay between periodontal inflammation and neuroinflammation. Three pathways are hypothesized in the literature, i.e., humoral, neuronal and cellular, with a clear role of periodontal pathogens, such as Porphyromonas gingivalis. Age, gender, race, smoking, alcohol intake, nutrition, physical activity, socioeconomic status, stress, medical comorbidities and genetics were identified as common risk factors for periodontitis and neurodegenerative diseases. Future research with main emphasis on the collaboration between neurologists and dentists is encouraged.

Periodontitis, Dental Procedures, and Young-Onset Cryptogenic Stroke.

Periodontitis is associated with an increased risk of ischemic stroke, and the risk may be particularly high among young people with unexplained stroke etiology. Thus, we investigated in a case-control study whether periodontitis or recent invasive dental treatments are associated with young-onset cryptogenic ischemic stroke (CIS). We enrolled participants from a multicenter case-control SECRETO study including adults aged 18 to 49 y presenting with an imaging-positive first-ever CIS and stroke-free age- and sex-matched controls. Thorough clinical and radiographic oral examination was performed. Furthermore, we measured serum lipopolysaccharide (LPS) and lipotechoic acid (LTA) levels. Multivariate conditional regression models were adjusted for stroke risk factors, regular dentist visits, and patent foramen ovale (PFO) status. We enrolled 146 case-control pairs (median age 41.9 y; 58.2% males). Periodontitis was diagnosed in 27.5% of CIS patients and 20.1% of controls (P < 0.001). In the fully adjusted models, CIS was associated with high periodontal inflammation burden (odds ratio [OR], 95% confidence interval) with an OR of 10.48 (3.18-34.5) and severe periodontitis with an OR of 7.48 (1.24-44.9). Stroke severity increased with the severity of periodontitis, having an OR of 6.43 (1.87-23.0) in stage III to IV, grade C. Invasive dental treatments performed within 3 mo prestroke were associated with CIS, with an OR of 2.54 (1.01-6.39). Association between CIS and invasive dental treatments was especially strong among those with PFO showing an OR of 6.26 (1.72-40.2). LPS/LTA did not differ between CIS patients and controls but displayed an increasing trend with periodontitis severity. Periodontitis and recent invasive dental procedures were associated with CIS after controlling for multiple confounders. However, the role of bacteremia as a mediator of this risk was not confirmed.