Journal of periodontal research最新文献

{"title":"Pharmacological Modulation of Nrf2 Signaling Regulates Oxidative Stress, Inflammation, and Alveolar Bone Loss in Experimental Periodontitis.","authors":"Vitória Bonan Costa, Mariely Araújo de Godoi, Angelo Constantino Camilli, Isabela Rinaldi Gomes Nogueira, Veronica Canela Estevam Dos Santos, Lucas Nogueira Ramos, Juliana Silva Siqueira, Camila Renata Corrêa Camacho, Morgana Rodrigues Guimarães Stabili","doi":"10.1111/jre.70158","DOIUrl":"https://doi.org/10.1111/jre.70158","url":null,"abstract":"<p><strong>Aim: </strong>To investigate whether pharmacological modulation of Nrf2 signaling influences oxidative stress, inflammatory responses, and periodontal tissue destruction in experimental ligature-induced periodontitis.</p><p><strong>Methods: </strong>Ligature-induced experimental periodontitis was established in rats treated with dimethyl fumarate (DMF), an Nrf2 activator, and/or ML385, a selective Nrf2 inhibitor. Alveolar bone loss, oxidative stress markers, inflammatory mediators, and histopathological changes were evaluated.</p><p><strong>Results: </strong>Nrf2 activation attenuated alveolar bone loss, reduced oxidative stress, and decreased inflammatory mediators, accompanied by improved periodontal tissue organization. In contrast, Nrf2 inhibition exacerbated inflammation and increased periodontal tissue destruction.</p><p><strong>Conclusion: </strong>Nrf2 signaling plays a regulatory role in periodontal inflammation and tissue breakdown. Pharmacological activation of Nrf2 exerts protective effects, whereas its inhibition aggravates disease severity.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673906","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-Associated Clock Signaling Impairs Primary Cilia to Promote Periodontal Stem Cell Senescence.","authors":"Xiaoxuan Zhang, Yinci Zhu, Minjie Ying, Pengxiao Hu, Jun Ma, Yuanyuan Chen, Xiaochen Zhang, Mengyun Chen, Yue Dai, Huining Wang, Xia Fan, Yubo Hou","doi":"10.1111/jre.70162","DOIUrl":"https://doi.org/10.1111/jre.70162","url":null,"abstract":"<p><strong>Aim: </strong>To explore circadian involvement in periodontitis and provide insight into mechanisms.</p><p><strong>Methods: </strong>Clinical samples from patients with periodontitis and a ligature-induced periodontitis mouse model were used in the present research. The rhythmic pattern of cortisol, the core circadian rhythm proteins BMAL1 and CLOCK, the expression of senescence markers (p16, p21, and p53), and the percentage and length of primary cilia were detected in hPDLSCs (human periodontal ligament stem cells) exposed to cortisol as an in vitro model of cortisol-associated circadian disruption. BMAL1 expression was manipulated by siRNA transfection to knock down BMAL1 expression, and SR8278 treatment was used to modulate BMAL1-related circadian regulation. Moreover, the effects of SR8278 on the progression of periodontitis were evaluated by micro-CT, mouse behavior tests, the number of primary cilia, and senescence assays.</p><p><strong>Results: </strong>Patients with periodontitis and ligature-induced periodontitis mice exhibited elevated cortisol levels, reduced BMAL1 expression, increased senescence-associated markers, and decreased primary cilia abundance. Elevated cortisol was associated with circadian disruption, accompanied by reduced BMAL1 expression and impaired ciliary homeostasis. BMAL1 regulated ARL13B expression, a key regulator of ciliogenesis. BMAL1 knockdown impaired Hedgehog signaling and induced hPDLSC senescence. SR8278 partially recovered BMAL1-related circadian alterations and primary cilia abundance while attenuating cellular senescence in both periodontitis model mice and cortisol-treated hPDLSCs.</p><p><strong>Conclusions: </strong>Collectively, these findings support the involvement of the cortisol-BMAL1-ARL13B pathway in periodontitis-associated primary cilium dysfunction and hPDLSC senescence. Modulation of BMAL1 partially restored primary cilium homeostasis and attenuated periodontal tissue damage, supporting its potential as a therapeutic target for periodontitis.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678835","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":"Phloridzin Mitigates Aging-Associated Periodontitis by Restraining Inflammatory Cell Death.","authors":"Da Eun Lee, Eun-Nam Kim, Gil-Saeng Jeong","doi":"10.1111/jre.70154","DOIUrl":"https://doi.org/10.1111/jre.70154","url":null,"abstract":"<p><strong>Aim: </strong>Aging is increasingly recognized as an important modifier of periodontitis progression. However, the direct impact of aging-related cellular processes on periodontal tissue degeneration remains insufficiently understood. This study aimed to investigate the protective effects of phloridzin on aging-associated experimental periodontitis and to elucidate its potential role in modulating aging-related alveolar bone loss.</p><p><strong>Methods: </strong>HPDLCs were exposed to H₂O₂ to induce oxidative stress-induced premature senescence, after which the effects of phloridzin on cellular senescence, inflammatory responses, and osteogenic differentiation capacity were evaluated. In addition, an aging-associated experimental periodontitis model was established in Wistar rats through D-galactose administration combined with ligature placement. Phloridzin was concurrently administered, and alveolar bone loss, periodontal tissue morphology, and systemic aging-and inflammation-related markers were analyzed to assess the in vivo effects of phloridzin.</p><p><strong>Results: </strong>Phloridzin attenuated oxidative stress-induced senescence-associated changes, suppressed aging-associated inflammatory responses in HPDLCs, and preserved osteogenic differentiation capacity. In vivo, phloridzin administration significantly reduced alveolar bone loss and alleviated periodontal tissue damage in the aging-associated experimental periodontitis model. The protective effects observed in both cellular and animal models suggest that regulation of excessive inflammatory responses during aging is important for maintaining periodontal tissue integrity.</p><p><strong>Conclusion: </strong>These findings indicate that phloridzin alleviates aging-associated alveolar bone loss by modulating aging-related inflammatory processes. Collectively, the results suggest that phloridzin may contribute to the improvement of periodontal tissue function under aging-related conditions.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630937","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":"Heat-Modified Platelet-Rich Fibrin (H-PRF) Enhances Bone Regeneration Through Improved Structural Stability.","authors":"Jihua Chai, Yiqian Yu, Detian Miao, Richard J Miron, Nima Farshidfar, Qihang Fan, Yufeng Zhang","doi":"10.1111/jre.70144","DOIUrl":"https://doi.org/10.1111/jre.70144","url":null,"abstract":"<p><strong>Aim: </strong>Platelet-rich fibrin (PRF) has been widely utilized in oral and craniofacial tissue regeneration owing to its autologous origin and favorable biological properties. However, the limited structural stability of conventional PRF restricts its space-maintaining capacity and osteogenic performance in guided bone regeneration (GBR). To address these shortcomings, a novel heat-modified PRF (Heat-H-PRF) was developed to improve the structural stability and osteogenic performance of PRF.</p><p><strong>Methods: </strong>Human PRF was subjected to brief thermal treatment to generate Heat-H-PRF. Material microstructure was examined by scanning electron microscopy. In vitro biocompatibility and osteogenic potential were assessed using MC3T3-E1 preosteoblasts through analyses of cell adhesion, proliferation, alkaline phosphatase activity, matrix mineralization, and osteogenic marker expression in comparison to a commercially available collagen membrane. Bone regeneration was also evaluated in vivo using a murine critical-size calvarial defect model, with micro-computed tomography, histological staining, and immunohistochemical analysis performed at 4 weeks post-implantation.</p><p><strong>Results: </strong>Heat-H-PRF demonstrated excellent cytocompatibility and significantly enhanced osteoblast-lineage cell proliferation, spreading, osteogenic differentiation, and mineralized matrix formation in vitro compared with collagen membrane. In a murine calvarial defect model, Heat-H-PRF resulted in significantly greater new bone volume, bone surface, and collagen deposition, accompanied by stronger expression of osteogenic markers Runx2, Osterix, osteocalcin, and collagen 1. Furthermore, the improved structural integrity of Heat-H-PRF suggests enhanced handling stability and potential space-maintaining properties, which may contribute to improved bone regeneration.</p><p><strong>Conclusion: </strong>Heat-modified PRF represents a simple and autologous biomaterial with improved handling properties and enhanced osteogenic potential. These findings suggest that Heat-H-PRF may serve as a promising adjunctive membrane-like scaffold for guided bone regeneration.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620495","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":"Porphyromonas gingivalis Translocation Along the Oral-Atrial Axis: A Microbial Contributor to Atrial Fibrosis and Atrial Fibrillation.","authors":"Chenxi Li, Yan Chen","doi":"10.1111/jre.70157","DOIUrl":"https://doi.org/10.1111/jre.70157","url":null,"abstract":"<p><p>This Perspective aimed to synthesize evidence of Porphyromonas gingivalis hematogenous translocation from periodontal lesions to the left atrium, outline GAL3/TGF-β1-mediated atrial fibrotic remodeling pathways, evaluate critical limitations of current preclinical and human data, and propose translatable upstream periodontal interventions for atrial fibrillation risk reduction.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620533","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":"Diagnostic Biomarkers of Periodontitis and Peri-Implantitis: The Past, the Present, the Future.","authors":"Denis F Kinane, Başak Bıyıkoğlu","doi":"10.1111/jre.70140","DOIUrl":"https://doi.org/10.1111/jre.70140","url":null,"abstract":"<p><p>In this narrative review we present our perspective on the past, present and future of periodontal and peri-implantitis diagnostic biomarkers. This topic parallels aetio-pathogenic research in that our understanding of the pathogenic, biological and biochemical mechanisms of these diseases is deeply entwined in the search for potential biomarkers of utility to diagnose them. Germane to this point is the marked success of bone-related molecules in saliva compared to cytokines and metalloproteinases in differentiating soft and hard tissue destruction. Despite these advances, translation into routine practice remains limited. Methodological heterogeneity, lack of standardised sampling protocols, biological variability, and insufficient longitudinal validation continue to impede progress. The roadmap ahead requires harmonised protocols, robust multicentre studies, clinically validated thresholds, and technologies that are rapid, affordable, and easily integrated into daily workflows. Biomarkers combined with other factors and interpreted by AI tools may be utilised in future to disclose current disease, predict future disease and aid in monitoring treated conditions: they may provide prognostic tools and have potential in epidemiological screening, particularly if readily available and easily accessible sample matrices such as saliva are used. Ultimately, the future of periodontal and peri-implant diagnostics lies in biologically informed, multi-modal assessment frameworks that complement traditional examination rather than replace it. As molecular technologies mature and AI-assisted personalised models evolve, biomarker-based diagnostics have the potential to transform early detection, risk prediction, and treatment monitoring-bringing us closer to precision periodontology and implantology. The salivary sample matrix is feasible for home use with utility for population screening, whereas the gingival and peri-implant crevicular fluid and the simple periodontal probe will continue to be invaluable in the analysis of localised disease.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520431","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":"Biologically-Oriented Alveolar Ridge Preservation (BARP) in Intact and Compromised Extraction Sockets.","authors":"Mattia Pramstraller, Roberto Farina, Anina Nives Zuercher, Ronald Ernst Jung, Mike Barbeck, Marco Fracasso, Alberto Sclip, Leonardo Trombelli","doi":"10.1111/jre.70153","DOIUrl":"https://doi.org/10.1111/jre.70153","url":null,"abstract":"<p><p>Alveolar ridge preservation (ARP) remains challenging in extraction sockets, particularly in the presence of buccal bone dehiscence, where post-extraction remodeling predominantly affects the coronal ridge. The Biologically-oriented Alveolar Ridge Preservation (BARP) concept and its modified application for compromised sockets (mBARP) were developed as innovative biologically driven protocols based on selective compartmentalized grafting. Instead of completely filling the socket, these approaches preserve spontaneous healing in the apical compartment while reinforcing the coronal portion, where dimensional changes are greatest. The protocols combine a collagen sponge in the apical part of the socket with xenograft particles and a collagen sponge sealing the coronal compartment. In compromised sockets, an additional collagen sponge is positioned between the residual buccal or lingual wall and the mucoperiosteal flap to enhance graft containment and soft tissue support. Thirty extraction sites were treated using this approach. After 4-6 months, ridge dimensions were effectively preserved, with a slight vertical loss (+0.3 mm), limited horizontal reduction (0.7-1.0 mm), controlled buccal soft tissue contraction (2.0-2.2 mm), and substantial new bone formation (38%-40%), while residual graft particles remained mainly confined to the coronal compartment. Within the limitations of this study, the BARP concept and its modified application demonstrated favorable clinical, radiographic, and histological outcomes, supporting selective coronal grafting as an innovative strategy to preserve ridge dimensions while maintaining physiological healing in the deeper portion of the extraction socket.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497772","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":"Durumamide A Inhibits NLRP3 Assembly, Limiting Pro-Inflammatory Signaling in Human Gingival Fibroblasts","authors":"Jiyeon Park,&nbsp;Munseon Lee,&nbsp;In Hyun Hwang,&nbsp;Wonwoong Lee,&nbsp;Juhee Lim","doi":"10.1111/jre.70084","DOIUrl":"10.1111/jre.70084","url":null,"abstract":"<p>This study elucidates a potential mechanistic pathway by which DAA attenuates IL-1β secretion in HGF-1 cells, through the disruption of NLRP3 inflammasome assembly, thereby highlighting a novel anti-inflammatory property of DAA at the molecular level.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"61 5","pages":"624-626"},"PeriodicalIF":5.4,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146040960","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":"Tooth Movement Modulation and Root Protection via Piezo1-Mediated Production of Superoxide Dismutase 3","authors":"Xiaomeng Dong,&nbsp;Yujie Zhu,&nbsp;Bin Li,&nbsp;Jie Feng,&nbsp;Fan Yang,&nbsp;Wanxi Chen,&nbsp;Yongwen Guo,&nbsp;Ding Bai,&nbsp;Hui Xu","doi":"10.1111/jre.70056","DOIUrl":"10.1111/jre.70056","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This study investigated the role of superoxide dismutase 3 (SOD3) in alveolar bone remodeling and cementum repair under orthodontic loading.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Mice were subjected to models of tooth movement with or without adenovirus-SOD3 treatment, and were examined for osteolytic activity, distance of tooth movement, and volume of root resorption. The periodontal ligament cells (PDLCs) were cultured under mechanical loading or unloaded controls, in the presence or absence of piezo-type mechanosensitive ion channel component1 (Piezo1) inhibitor GsMTx4 or Yes-associated protein (YAP) inhibitor Verteporfin, and were examined for SOD3 expressions. The MC3T3-E1, BMSCs, OCCM-30, BMMs, and RAW264.7 cell cultures with or without recombinant mouse SOD3 (rmSOD3) administration were examined for osteogenic or osteoclastogenic markers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Orthodontic loading induced SOD3 expressions in the periodontal ligament (PDL). The mechanical force-induced production of SOD3 in the PDLCs was potentially mediated by Piezo1 and YAP signaling. Exogenous rmSOD3 promoted osteoblastogenesis, boosted cementoblast differentiation and mineralization, and inhibited osteoclastogenesis from osteoclast precursors. Adenovirus-mediated SOD3 overexpression in the PDL suppressed osteoclast differentiation, reduced root resorption, and retarded orthodontic tooth movement.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Piezo1-mediated production of SOD3 from the PDLCs protected the root from resorption and retarded tooth movement by suppressing osteoclastogenesis and promoting osteoblast and cementoblast differentiation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"61 5","pages":"572-585"},"PeriodicalIF":5.4,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146040973","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":"Economic Impact of Periodontitis: Global, Regional and National Estimates of Periodontal Expenditure, With Forecasts to 2050","authors":"Dian Yi Chow,&nbsp;Robin D. Blythe,&nbsp;John Rong Hao Tay,&nbsp;Gustavo G. Nascimento,&nbsp;Mario Romandini","doi":"10.1111/jre.70104","DOIUrl":"10.1111/jre.70104","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>To estimate the global, regional and national economic impact of periodontitis in 2021 (including expenditure on prevention, diagnosis, treatment, maintenance and rehabilitation), and to forecast expenditures through 2050 under two utilisation scenarios: continuation of current treatment coverage trends and an illustrative expanded coverage scenario.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A cohort-based gross-costing Monte Carlo model was developed to estimate global, regional and national expenditure on periodontitis in 2021. Model estimates were validated against known national periodontal spending and aggregate dental expenditure. The model was then applied to generate forecasts for 2025–2050 at five-year intervals under two utilisation scenarios: (i) continuation of current utilisation patterns of periodontal care and (ii) an illustrative expanded coverage scenario in which 80% of the population receives periodontal care by 2030.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In 2021, global expenditure on periodontitis was US$168.1 billion (95% UI: 133.8–202.4), with marked regional disparities; five countries (the United States, China, Germany, Japan and France) accounted for more than two-thirds of global spending. Under current utilisation trends, global expenditure is projected to increase modestly to US$174.9 billion by 2050 (95% UI: 137.4–212.3), despite a projected 44.3% increase in severe periodontitis prevalence. Under the expanded coverage scenario, expenditure would instead increase threefold to US$500.6 billion (95% UI: 389.2–612.1) by 2050, implying an annual financing gap of US$325.7 billion. Global per-capita expenditure was US$21.32 (95% UI: 16.97–25.67) in 2021, projected to decline to US$18.36 (95% UI: 14.43–22.29) in 2050 under current utilisation, but to rise to US$52.56 (95% UI: 40.86–64.26) under the expanded coverage scenario.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Periodontitis imposes a substantial and unequally distributed economic impact worldwide. Under current utilisation patterns, the projected rise in prevalence by 2050 will primarily translate into unmet care needs. Achieving universal coverage under WHO targets would require tripling global periodontal expenditure—a level unlikely to be feasible—highlighting the need to rethink current models of periodontal care delivery.</p>\u0000 </section>\u0000 </div>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"61 5","pages":"518-559"},"PeriodicalIF":5.4,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jre.70104","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147864260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}