Journal of periodontal research最新文献

{"title":"Periodontitis and Diabetes: Mechanistic Evidence of a Circular Relationship.","authors":"Philip M Preshaw, Ren Jie Jacob Chew, Charlene Enhui Goh, Ali A Abdulkareem, Dana T Graves","doi":"10.1111/jre.70131","DOIUrl":"https://doi.org/10.1111/jre.70131","url":null,"abstract":"<p><p>The circular relationship between periodontitis and diabetes mellitus is one of the most established oral-systemic links. Uncontrolled diabetes contributes to an increased susceptibility and severity of periodontitis, while periodontitis contributes to poorer glycaemic control and greater insulin resistance. This reciprocal interaction is mediated by a network of interconnected mechanisms that extends beyond the traditional paradigm of bacteraemia and the hepatic acute phase response triggered by the systemic cytokine spillover from affected periodontal tissues. Experimental and clinical evidence indicate that dissemination of periodontal pathogens and virulence factors can directly affect the pancreas and liver, which are key organs in the pathogenesis of diabetes. Periodontal microbes and their virulence factors have been detected in the pancreas, eliciting β-cell dysfunction and apoptosis, compensatory alpha cell expansion and disruption of insulin-glucagon homeostasis. In addition to haematogenous spread, swallowed oral biofilm can promote oral-gut translocation, altering gut microbial ecology and contributing to entero-hepatic metabolic perturbations that exacerbate insulin resistance. The detection of periodontal pathogens by Toll-like receptors in peripheral tissues, including adipose tissue and the kidney, links periodontitis to adipose inflammation, dysregulated lipid metabolism and diabetic nephropathy. Similarly, other than eliciting the acute phase response, the systemic inflammatory spillover from periodontitis also dysregulates hepatic metabolism, increasing gluconeogenesis and impairing glycogenesis, thus contributing to hyperglycaemia. Beyond metabolic tissues, periodontal inflammation, mediated by pro-inflammatory mediators such as interleukin-6, can promote maladaptive myelopoiesis and the generation of hyperresponsive neutrophils and monocytes. In uncontrolled diabetes, chronic hyperglycaemia induces a similar trained, pro-inflammatory myeloid phenotype and the convergence of these processes may synergistically increase systemic inflammatory burden. The resulting pool of primed circulating innate immune cells can exacerbate periodontal tissue destruction and contribute to inflammatory injury in distant organs, thereby worsening diabetic complications. Overall, this review considers the complex mechanistic framework in which microbial dissemination, immune amplification and metabolic reprogramming collectively connect periodontitis and diabetes. While focused on the periodontitis-diabetes axis, this review also underscores the broader systemic relevance of periodontal inflammation in chronic metabolic disease and supports the inclusion of periodontal care as part of chronic disease management.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Health, Periodontitis, and Respiratory Diseases: Biological Pathways.","authors":"Raluca P Vacaru, Andreea C Didilescu, Frank A Scannapieco","doi":"10.1111/jre.70126","DOIUrl":"https://doi.org/10.1111/jre.70126","url":null,"abstract":"<p><p>Poor oral hygiene and periodontitis influence lung diseases such as pneumonia, chronic obstructive pulmonary disease (COPD), COVID-19, and asthma. The normal lung is not sterile, with a distinct microbial ecosystem that is spatially varied along the respiratory tract. The biogeography of the lung microbiome is balanced between microbial microaspiration from the oral-pharynx and clearance. The mouth is an important reservoir for respiratory pathogens including Streptococcus pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa, and Staphylococcus aureus, as well as oral microbes (Porphyromonas, Prevotella, Fusobacterium, etc.). Poor oral hygiene and periodontitis increase the bacterial load that can be aspirated, and the host produces pro-inflammatory components that enhance microbial virulence and compromize epithelial integrity. Both poor oral hygiene and periodontitis have been associated with pneumonia, particularly in hospitals and nursing home settings. Periodontitis may also facilitate viral pneumonia (including COVID-19) by altering receptor expression and immune function. Periodontitis correlates with COPD severity and exacerbation frequency through pathways involving matrix metalloproteinases and cytokines. Periodontitis also is associated with asthma and acute exacerbations. Inflammation shapes the lung microbiome by impacting microbial nutrient availability through vascular leakage, inducing changes to epithelial cells which facilitate bacterial adherence, and inducing the production of cytokines, leading to mucus overproduction, inhibition of phagocytosis, and enhancement of microbial pathogen virulence. Multiple biological pathways have been examined in vitro that suggest how \"the oral-lung axis\" influences pneumonia, COPD, and asthma. Periodontal treatment and effective oral hygiene should be well integrated into medical care to prevent and manage respiratory diseases.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"'The Simpsons' Did It Again! Periodontitis and Tooth Loss Predict Mortality in Springfield: A Retrospective Cohort Study.","authors":"Praveen Sharma, Thomas Dietrich","doi":"10.1111/jre.70138","DOIUrl":"10.1111/jre.70138","url":null,"abstract":"<p><p>The IMPOSTERS study analysed 150 recurring 'human' Simpsons characters and found that periodontitis or tooth loss was associated with a 23-fold higher hazard of all-cause mortality. This was reported in the Simpsons universe, with the death of 'Bleeding Gums' Murphy, 3 years before the first such reports in our universe. Fictional universe, very real methodological lessons to learn.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis and Adverse Pregnancy Outcomes: Mechanistic Evidence.","authors":"Gregory C Valentine, Yiorgos A Bobetsis, Benjamin C Shayo, Peter Milgrom, Phoebus N Madianos","doi":"10.1111/jre.70134","DOIUrl":"https://doi.org/10.1111/jre.70134","url":null,"abstract":"<p><p>Periodontal diseases, including both gingivitis and periodontitis, occur commonly among pregnant individuals. Both gingivitis and periodontitis are associated with adverse pregnancy outcomes (APOs) such as early pregnancy loss, preterm birth, preeclampsia, low birth weight, and stillbirth. This review highlights that the strongest mechanistic evidence linking periodontal diseases with APOs involves the domains of systemic inflammation, including increased pro-inflammatory cytokines and activation of matrix metalloproteases associated with preterm labor, and microbial translocation involving hematogenous dissemination of periodontopathic bacteria to the fetoplacental unit. Yet, other mechanistic domains remain underexplored, including maladaptive myelopoiesis with alterations of neutrophil activity, immune player trafficking with autoantibody development, masticatory dysfunction-diet interactions that may further increase risk of critical vitamin and nutritional deficiencies related to both periodontitis and APOs, and functional dysregulation of the oral microbiome including generation of nitric oxide that could impact pregnancy outcomes. Additionally, specific underlying vulnerabilities unique to pregnancy such as increased hormone production such as progesterone and cortisol likely impact the risk of periodontal diseases in pregnancy. By delving into these critical mechanistic domains, this review reveals both current understanding and critical areas for future research to overcome deficits in knowledge pertaining to how periodontal diseases in pregnancy lead to APOs. Elucidating these novel insights can promote scientific advancement, facilitate the development of novel interventions that prevent and/or treat periodontal diseases in pregnancy, and concurrently improve the lives and well-being of pregnant individuals and their children worldwide.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Minimally Invasive (MINST) Versus Conventional Non-Surgical Therapy for Residual Pockets in Patients With Periodontitis: A Randomized Clinical Trial.","authors":"Gaetano Isola, Alessandro Polizzi, Paolo Pesce, Angela Alibrandi, Giuseppe Pizzo","doi":"10.1111/jre.70083","DOIUrl":"https://doi.org/10.1111/jre.70083","url":null,"abstract":"<p><p>MINST treatment was more effective in reducing median periodontal outcomes at 12-month follow-up than the conventional approach. Across 12-months follow-up, the overall PPD reduction was significantly influenced by a high number of cigarettes/day, erratic/non-compliance supportive treatment, high no. pockets ≥ 4 mm BoP+, number of pockets 4-5 mm, number of pockets ≥ 6 mm, and by high FMBS.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148271926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontal Diseases as a Public Health Challenge: Rationale, Prevention, Equity, and Sustainable Care-A Global Call for Action.","authors":"Marco A Peres, Lijian Jin, Gustavo G Nascimento, Philip M Preshaw, Eero Juhani Raittio, Dian Yi Chow, John Rong Hao Tay","doi":"10.1111/jre.70133","DOIUrl":"https://doi.org/10.1111/jre.70133","url":null,"abstract":"<p><p>Periodontal diseases are among the most prevalent noncommunicable diseases (NCDs) worldwide, with advanced stage contributing to disability, impaired nutrition, frailty, and reduced quality of life. Despite this burden, periodontal care remains weakly integrated into global NCD strategies, limiting public health advocacy and healthy aging. We conducted a conceptual and policy-oriented analysis to identify opportunities for repositioning periodontal care as a public health function. Key domains examined included (a) preventive healthcare through the common risk factor approach; (b) case identification and diagnosis designed to serve both clinical care and population surveillance; (c) de-implementation of care with limited incremental benefit at scale, including the role of payment incentives in shaping utilization. To evaluate long-term affordability, projected global periodontal healthcare expenditure through 2050 was modeled using a cohort-based Monte Carlo simulation, comparing current utilization patterns, expansion to 80% population coverage, and an alternative capitation-informed scenario. Reorienting periodontal care toward proactive, cost-effective prevention and integrating case identification within primary care and NCD platforms offer greater potential for equitable population health gains than simply expanding procedure-intensive treatments. Risk-stratified care pathways based on patient-important outcomes, combined with de-implementation of low-value practices, can preserve oral function while reducing avoidable service volume and costs. Expenditure modeling indicates that achieving high coverage under prevailing fee-for-service delivery would substantially increase global financial burden, whereas a capitation-informed scenario reduced projected expenditure by 30% at the same coverage level, suggesting alternative incentives could expand access with less cost escalation, including in low- and middle-income settings worldwide. Aligning periodontal care with public health principles-prioritizing prevention, value, and equity over treatment volume-is a paradigm shift essential for achieving sustainable improvements in population health, healthy aging, and long-term health-system affordability.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148271970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis and Rheumatoid Arthritis-Mechanistic Evidence.","authors":"Mark Bartold, Chia Wei Cheah, Rathna Devi Vaithilingam","doi":"10.1111/jre.70132","DOIUrl":"10.1111/jre.70132","url":null,"abstract":"<p><p>Current evidence strongly supports an association between periodontitis and rheumatoid arthritis (RA) in a subset of susceptible individuals. The relationship between these conditions is underpinned by a complex interplay between chronic inflammation and subgingival bacterial infection. Several hypotheses have been proposed to explain the mechanistic basis of this association. Among these, the \"two-hit\" model is particularly compelling, as it suggests that inflammation, infection, or a combination of both may contribute to the initiation and progression of RA in predisposed individuals. According to this model, the progression of gingivitis and periodontitis, together with associated microbial dysbiosis, may promote protein citrullination, carbamylation, and the formation of malondialdehyde-acetaldehyde (MAA) adducts. These post-translational modifications may subsequently induce the production of autoantibodies before the clinical onset of joint inflammation and RA. Once synovial inflammation develops, additional citrullination, carbamylation, and MAA adduct formation may occur within the joint microenvironment, further amplifying autoantibody production. In previously sensitized individuals, such as those with chronic gingivitis or periodontitis, this secondary immune response may be substantially enhanced, resulting in increased joint inflammation and tissue destruction. Subgingival bacteria may also contribute directly, or indirectly, to the periodontitis/RA axis through translocation to distant tissues, induction of protein citrullination and other protein post-translational modifications, stimulation of autoantibody production, and exacerbation of inflammatory responses. Central to the role bacteria play in the periodontitis/RA axis is the emergence of functional alterations in the microbiome. Dysbiosis in the subgingival microenvironment, and the emergence and proliferation of recognized periodontal pathobionts, underpins these key elements. This, along with bacterial-induced inflammation and direct influence on immune player trafficking, results in a complex synergy within the mechanistic processes involved in the relationship between periodontitis and RA. In this narrative review, we critically examine the inflammatory and microbial mechanisms implicated in the interaction between periodontitis and RA and propose an updated framework integrating inflammation, dysbiosis, and autoimmunity.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis, Edentulism, and Risk of Metabolic Syndrome, Obesity, and Dyslipidemia: A Systematic Review With Meta-Analyses.","authors":"Luigi Barbato, Maria Di Martino, Walter Castelluzzo, Cosimo Rupe, Folco Spoleti, Michele Nieri, Francesco Cairo","doi":"10.1111/jre.70130","DOIUrl":"10.1111/jre.70130","url":null,"abstract":"<p><strong>Aim: </strong>This systematic review (SR) aimed to investigate the risk of metabolic syndrome (MetS) and its single components in individuals with and without periodontitis/edentulism.</p><p><strong>Methods: </strong>The protocol was registered in the PROSPERO database (CRD420261301248). The focused PECOS question was: \"Is the risk of metabolic syndrome and its single components (obesity and dyslipidemia) increased among individuals with periodontitis/edentulism compared to those without periodontitis/edentulism?\" Results were reported according to the PRISMA statement. Electronic and manual searches were conducted to identify longitudinal studies. Effect estimates expressed as RRs for MetS, obesity, and dyslipidemia were the outcomes of interest. Random-effects meta-analyses were conducted.</p><p><strong>Results: </strong>Ten longitudinal studies were included (584 590 participants), of which four were rated as having a low risk of bias. Follow-up ranged from 1 to 18 years. Newly diagnosed MetS ranged from 10.5% to 23%, obesity from 1.2% to 7.1%, and dyslipidemia from 6.7% to 14.3%. The risk of developing ≥ 1 MetS component was higher in individuals with periodontitis (RR: 1.18 [95% CI 1.04-1.35], p = 0.01; I² = 28%) than in those without periodontitis, whereas the risk of a new MetS diagnosis, defined as ≥ 3 components (RR: 1.17 [95% CI 0.97-1.42], p = 0.10; I² = 46%), did not differ between groups. The RR for severe periodontitis compared with no periodontitis was 1.34 [95% CI 1.10-1.64], p = 0.004; I² = 0%. The risk ratio for obesity was statistically significant (RR: 1.30 [95% CI 1.05-1.62], p = 0.02; I² = 73%), but subgroup analyses did not confirm this significance. The risk ratio for dyslipidemia was not significant (RR: 1.08 [95% CI 0.94-1.24], p = 0.29; I² = 16%). Meta-Analyses for edentulism were not considered appropriate.</p><p><strong>Conclusion: </strong>Within the limits of this SR, periodontitis was associated with the development of ≥ 1 MetS component, but the association was not significant for a new MetS diagnosis defined as ≥ 3 components. The association may be stronger for severe periodontitis. The impact of edentulism remains unclear. Further prospective longitudinal studies using homogeneous definitions of periodontitis, reporting data on dental care exposure, and including ≥ 10 years of follow-up are strongly encouraged to further investigate these associations.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"61 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148094673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontitis and Inflammatory Bowel Diseases: Mechanistic Evidence.","authors":"Ana Paula V Colombo, Adriana M de Oliveira, Nobuhiko Kamada, Sho Kitamoto","doi":"10.1111/jre.70124","DOIUrl":"10.1111/jre.70124","url":null,"abstract":"<p><p>Inflammatory Bowel Disease (IBD) is a multifactorial disorder characterized by chronic intestinal inflammation. Focusing on a single aspect of its pathogenesis is insufficient to capture the complexity of the disease. In this context, systemic inter-organ communication, particularly the periodontitis-IBD axis mediated by host immune cells and commensal microbiota, has recently emerged as an area of increasing importance in IBD research. This review aims to provide an integrative overview of gut seeding of potentially harmful oral bacteria (oral pathobionts) in IBD and its mechanistic insights along with the oral-gut relationship in the context of IBD pathology. We also discuss potential factors that facilitate the gut seeding of oral pathobionts, a pivotal event underlying the oral-gut axis. Elucidating these complex immune-microbial dynamics across distant mucosal sites will deepen our understanding of the shared pathophysiology of oral and intestinal disorders and inform the development of novel therapeutic interventions.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}