Rafael Scaf de Molon, Sotirios Tetradis, Rolando Vernal, Fabio Renato Manzolli Leite, Thomas E. Van Dyke
{"title":"Periodontitis as a Model for Inflammatory Uncoupling of Bone Remodeling","authors":"Rafael Scaf de Molon, Sotirios Tetradis, Rolando Vernal, Fabio Renato Manzolli Leite, Thomas E. Van Dyke","doi":"10.1111/jre.70148","DOIUrl":"10.1111/jre.70148","url":null,"abstract":"<p>Periodontitis is traditionally regarded as an oral biofilm-driven inflammatory disease that leads to progressive loss of the tooth-supporting alveolar bone. However, accumulating evidence indicates that periodontal bone loss is more accurately understood as a state of pathological uncoupling of bone remodeling, in which exaggerated bone resorption coexists with inadequate bone formation response. In this review, we reposition periodontitis within the broader context of inflammatory skeletal diseases and synthesize current mechanistic insights from osteoimmunology, bone biology, and mechanobiology. We discuss how excessive osteoclastogenesis in periodontitis is sustained by receptor activator of nuclear factor kappa-B ligand (RANKL) dominance derived from osteocytes, osteoblast-lineage cells, stromal cells, monocytes/macrophages, B and T lymphocytes, and neutrophils within a cytokine-rich microenvironment characterized by tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-17A signaling. Persistent activation of nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways further enhance osteoclast differentiation, survival, and resorptive activity. At the same time, inflammatory mediators actively suppress osteoblast-lineage commitment by inhibiting Runx2 and Osterix, antagonizing canonical Wnt/β-catenin signaling through the upregulation of sclerostin and Dickkopf-1 (DKK1), and impairing bone matrix production and mineralization. We further examine how disruption of key osteoclast–osteoblast coupling mechanisms, including ephrinB2/EphB4 and semaphorin signaling, prevents the effective transition from resorption to formation, while osteocyte dysfunction amplifies the uncoupled phenotype by integrating inflammatory and mechanical signals. Comparisons with rheumatoid arthritis, inflammatory bowel disease-associated bone loss, and peri-implantitis reveal shared immune-driven mechanisms of remodeling imbalance, whereas the unique features of alveolar bone, including high turnover, continuous mechanical loading, and chronic microbial exposure, make it particularly susceptible to inflammatory uncoupling. Together, these concepts support a therapeutic shift toward restoring physiological coupling instead of solely inhibiting resorption and position periodontitis as a clinically accessible model for understanding and targeting inflammatory bone loss across skeletal diseases.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"61 6","pages":"662-694"},"PeriodicalIF":5.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jre.70148","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148391186","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}
{"title":"Anti-Proliferative Effects of Resveratrol on Gingival Fibroblasts Derived From Amlodipine-Induced Gingival Overgrowth","authors":"Bilkan Kara, Nuriye Işıl Saygun, Cansel Köse Özkan, Melis Özgül Slezovic, Muhittin Abdulkadir Serdar, Mualla Pınar Elçi, Alpdoğan Kantarci","doi":"10.1111/jre.70112","DOIUrl":"10.1111/jre.70112","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>This study aimed to investigate the anti-proliferative effects of resveratrol on gingival fibroblasts derived from amlodipine-induced gingival overgrowths and its impact on the levels of transforming growth factor-<i>β</i>1 (TGF-<i>β</i>1), connective tissue growth factor (CTGF), collagen type I (COL-1), interleukin-6 (IL-6), transglutaminase-2 (TGM-2), and superoxide dismutase (SOD), which play critical roles in collagen and extracellular matrix metabolism in gingival enlargement.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Primary gingival fibroblasts were isolated from patients with amlodipine-induced gingival overgrowth (GO group) and from healthy gingival tissues (H group). Each group was divided into untreated and resveratrol-treated subgroups. Cell proliferation and viability at 24 and 48 h were assessed by MTT assay. The levels of TGF-<i>β</i>1, CTGF, COL-1, IL-6, TGM-2, and SOD were quantified using ELISA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>MTT values were significantly higher in the GO group than in the H group at both 24 and 48 h (<i>p</i> = 0.01). Resveratrol treatment significantly decreased proliferation in the GO group at both time points (<i>p</i> < 0.001). In the GO group, resveratrol reduced TGF-<i>β</i>1 (<i>p</i> = 0.0090), CTGF (<i>p</i> = 0.0090), TGM-2 (<i>p</i> = 0.0088), COL-1 (<i>p</i> = 0.0139), and IL-6 (<i>p</i> = 0.050) levels at 24 h and significantly increased SOD levels (<i>p</i> = 0.0143).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Resveratrol suppressed cellular proliferation without exerting cytotoxic effects in amlodipine-induced GO, while downregulating fibrosis markers (TGF-<i>β</i>1, CTGF, COL-1, IL-6, and TGM-2) and restoring diminished SOD synthesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registiration</h3>\u0000 \u0000 <p>This study did not involve a clinical trial and therefore registration was not required</p>\u0000 </section>\u0000 </div>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"61 6","pages":"716-729"},"PeriodicalIF":5.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jre.70112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147654425","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}
Yao-Wen Zhang, Yu-Hua Hu, Yi-Hui Pan, Rong-Hui Xia, Xiang-Zhen Yan
{"title":"Histopathological Characterization of Granulation Tissue Suggests Three Distinct Types of Periodontal Intrabony Defects","authors":"Yao-Wen Zhang, Yu-Hua Hu, Yi-Hui Pan, Rong-Hui Xia, Xiang-Zhen Yan","doi":"10.1111/jre.70093","DOIUrl":"10.1111/jre.70093","url":null,"abstract":"<p>Three distinct types of pathological appearances of soft tissues obtained from intrabony defects were identified. Consequently, our findings serve to alert the heterogeneity of soft tissues retrieved from periodontal intrabony defects and emphasize the requisite caution when interpreting related histopathological findings.\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 6","pages":"730-732"},"PeriodicalIF":5.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146180293","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}
Larysa Saboya Cavalotti Perdonsini, Rafael Scaf de Molon, Søren Jepsen, Iain Chapple, Joao Paulo Steffens
{"title":"Diagnosing and Treating Periodontitis and Multimorbidity Altogether: The Case Example of the Physical Exercise Hormone Irisin","authors":"Larysa Saboya Cavalotti Perdonsini, Rafael Scaf de Molon, Søren Jepsen, Iain Chapple, Joao Paulo Steffens","doi":"10.1111/jre.70081","DOIUrl":"10.1111/jre.70081","url":null,"abstract":"<p>Irisin is an extracellular peptide stimulated by exercise and could act as both a biomarker and mediate the positive impact of exercise. This scoping review synthesizes human evidence on irisin variations in non-communicable diseases, showing an increase of irisin in saliva and gingival tissues in periodontitis, potentially reflecting reparative or immunomodulatory activity.\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 6","pages":"733-735"},"PeriodicalIF":5.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jre.70081","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377957","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}
Antonin Tichy, Nils Werner, Helena Dujic, Charlotte Wetzel, Vinay Pitchika, Caspar Victor Bumm, Matthias Folwaczny, Falk Schwendicke
{"title":"Artificial Intelligence in Periodontology: A Systematic Review","authors":"Antonin Tichy, Nils Werner, Helena Dujic, Charlotte Wetzel, Vinay Pitchika, Caspar Victor Bumm, Matthias Folwaczny, Falk Schwendicke","doi":"10.1111/jre.70107","DOIUrl":"10.1111/jre.70107","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>To provide a comprehensive review of artificial intelligence (AI) applications in periodontology, focusing (1) on deep learning for image-based diagnosis of periodontitis and (2) on non-image-based AI applications across periodontal care.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study adhered to PRISMA guidance. Six databases (PubMed, Scopus, Web of Science, Embase/Ovid, IEEE Xplore, and arXiv) were searched. The first review question (PICO 1) focused on applications of deep learning to human imaging data for diagnosing periodontitis, and the systematic review was followed by a modified QUADAS-2 risk-of-bias (RoB) assessment. The second part (PICO 2) scoped AI applications in periodontology using non-imaging data. Because of substantial heterogeneity in tasks, inputs, and outcomes, PICO 2 was synthesized narratively without formal RoB assessment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>PICO 1 included 29 studies, predominantly using panoramic radiographs (<i>n</i> = 21). Binary periodontitis classification achieved accuracies of 81%–99% on panoramic radiographs and 78% on CBCT, whereas staging/severity showed lower performance (accuracy 64%–91% in panoramic radiographs; 83% in intraoral radiographs with AUROC 0.84–0.93). Photograph-based screening achieved AUROC 0.93. RoB was generally low, but applicability concerns were frequent, mainly because of single-center datasets. PICO 2 included 65 studies, covering diagnosis and classification of periodontitis (AUROC 0.77–0.85), risk stratification and screening (AUROC 0.60–0.98), progression, and treatment outcome modeling (AUROC 0.58–0.89), oral-systemic associations, biomarker identification, and clinical data mining using natural language processing, which achieved near-perfect metrics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Generalizability remains the key limitation across applications, driven by limited data diversity, inconsistent tasks/metrics, and scarce external testing. Future studies should prioritize multicenter evaluation, transparent reporting, and prospective assessments of workflow impact and patient-related outcomes.</p>\u0000 \u0000 <p><b>Registration:</b> PROSPERO identification number CRD420251128758.</p>\u0000 </section>\u0000 </div>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":"61 6","pages":"639-661"},"PeriodicalIF":5.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jre.70107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147574648","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}
{"title":"Periodontal Plastic Surgery: The Past, the Present, the Future","authors":"Francesco Cairo, Giovan Paolo Pini Prato","doi":"10.1111/jre.70151","DOIUrl":"10.1111/jre.70151","url":null,"abstract":"<p>Over 40 years of clinical research, Periodontal Plastic Surgery has evolved from a niche topic into an issue of great collective interest in Periodontology.\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 6","pages":"633-638"},"PeriodicalIF":5.4,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jre.70151","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148471514","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}
Mario Aimetti, Giacomo Tonello, Vivek Thumbigere-Math, Davide Giuseppe Ribaldone, Mario Romandini, Federica Romano, Giacomo Baima
{"title":"Periodontitis, Edentulism, and Risk of Inflammatory Bowel Disease (IBD): A Systematic Review With Meta-Analysis.","authors":"Mario Aimetti, Giacomo Tonello, Vivek Thumbigere-Math, Davide Giuseppe Ribaldone, Mario Romandini, Federica Romano, Giacomo Baima","doi":"10.1111/jre.70161","DOIUrl":"https://doi.org/10.1111/jre.70161","url":null,"abstract":"<p><strong>Aim: </strong>To systematically evaluate whether periodontitis and edentulism are associated with the presence or development of inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), and to additionally assess evidence relating periodontitis to IBD activity and severity.</p><p><strong>Methods: </strong>A systematic search of MEDLINE, Embase, Scopus, and Web of Science, supplemented by manual searches, was conducted through February 2026. Cohort and cross-sectional studies assessing periodontitis or edentulism in relation to IBD were included. Risk of bias was evaluated using the Newcastle-Ottawa Scale. Meta-analyzes were performed separately for longitudinal and cross-sectional studies using random-effects models, with subgroup and sensitivity analyzes conducted where appropriate.</p><p><strong>Results: </strong>Twenty-two studies met the eligibility criteria, including 6 cohort studies and 16 cross-sectional studies, comprising 12 627 564 participants. In cohort studies, periodontitis was associated with a trend toward increased incident IBD overall (RR 1.25; 95% CI 0.98-1.58), although statistical significance was not reached, while no significant association was observed for CD (RR 1.05; 95% CI 0.86-1.29). In contrast, a significant association emerged between periodontitis and incident UC (RR 1.18; 95% CI 1.07-1.31). No longitudinal estimates were available for severe periodontitis or edentulism. In cross-sectional studies, periodontitis was significantly associated with prevalent IBD (OR 2.11; 95% CI 1.53-2.93), CD (OR 2.02; 95% CI 1.59-2.55), and UC (OR 2.48; 95% CI 1.71-3.59). Severe periodontitis was also associated with UC in a limited number of studies, whereas evidence regarding edentulism was scarce and inconsistent. Evidence linking periodontitis to IBD activity or severity was more limited and heterogeneous, although several studies suggested associations with markers of disease burden.</p><p><strong>Conclusion: </strong>Longitudinal evidence suggests that periodontitis has a modest association with incident UC, whereas associations with IBD overall and CD appeared weaker and less consistent. At the same time, cross-sectional studies consistently support the coexistence of periodontitis and IBD, possibly reflecting shared susceptibility, bidirectional interactions, or common oral-gut inflammatory pathways. Whether periodontitis contributes to IBD burden or disease expression over time warrants further longitudinal and mechanistic investigation.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706713","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}
Mariana Martins Guerreiro, Amanda Paino Santana, Daniela Moreira Cunha, Gabriel Mulinari-Santos, Marlise Inêz Klein, Edilson Ervolino, Ludovica Parisi, Martin Degen, Maria Eduarda Fiorentino Ferreira de Andrade, Marta Maria Alves Pereira, Stefany Barbosa Alves da Cruz, Leonardo P Faverani, Paula Aboud Barbugli, Rodolfo Debone Piazza, Vitória Marega Marchetti, Rodrigo Isaias Lopes Pereira, Rafael Scaf de Molon, Anton Sculean, Erica Dorigatti de Avila
{"title":"Smart Coatings Integrating Antimicrobial and Tissue-Remodeling Functions for Implant Interfaces.","authors":"Mariana Martins Guerreiro, Amanda Paino Santana, Daniela Moreira Cunha, Gabriel Mulinari-Santos, Marlise Inêz Klein, Edilson Ervolino, Ludovica Parisi, Martin Degen, Maria Eduarda Fiorentino Ferreira de Andrade, Marta Maria Alves Pereira, Stefany Barbosa Alves da Cruz, Leonardo P Faverani, Paula Aboud Barbugli, Rodolfo Debone Piazza, Vitória Marega Marchetti, Rodrigo Isaias Lopes Pereira, Rafael Scaf de Molon, Anton Sculean, Erica Dorigatti de Avila","doi":"10.1111/jre.70156","DOIUrl":"https://doi.org/10.1111/jre.70156","url":null,"abstract":"<p><strong>Aim: </strong>This study aimed to assess the antimicrobial performance and biocompatibility of our drug delivery platform, based on layer-by-layer (LbL) coating incorporating tetracycline (TC) complexed with anionic β-cyclodextrin (TCβCD) and a pH-responsive poly(methacrylic acid) (PMAA) film, applied to titanium (Ti) surfaces representing abutment components.</p><p><strong>Methods: </strong>A rat subcutaneous implant-related infection model was established using a polymicrobial biofilm derived from peri-implantitis patient saliva. Contaminated Ti controls and coated discs were implanted and analyzed after 1 and 7 days through clinical, microbiological, confocal, and histological assessments. In parallel, in vitro experiments using fibroblast cultures were conducted to evaluate the expression of genes associated with collagen synthesis and extracellular matrix remodeling.</p><p><strong>Results: </strong>Coated implants exhibited minimal inflammatory response, whereas control specimens presented with purulent exudate. Microbiological analysis demonstrated sustained antimicrobial activity, with > 3 log<sub>10</sub> reduction in viable bacteria at both time points. Confocal microscopy confirmed strong microbicidal effects, particularly in the PMAA group. Coatings also modulated host responses, decreasing pro-inflammatory cytokines and increasing anti-inflammatory mediators and matrix remodeling markers. Histology revealed enhanced collagen deposition and accelerated connective tissue maturation, especially with LbL/TCβCD/PMAA, consistent with upregulated collagen-related gene expression observed in vitro.</p><p><strong>Conclusion: </strong>The multifunctional coating provides sustained antimicrobial activity alongside immunomodulatory and pro-regenerative effects, supporting its potential to treat implant-related infections while enhancing peri-implant soft tissue remodeling.</p>","PeriodicalId":16715,"journal":{"name":"Journal of periodontal research","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148689206","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":"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}