Pub Date : 2026-04-01Epub Date: 2026-01-19DOI: 10.1111/jcpe.70087
Mario Aimetti, Federica Romano, Luigi Costanzo, Mario De Caroli, Andrea Di Venanzio, Giulia Maria Mariani, Giacomo Baima
Aim: To describe the efficacy of steps I-II-III of periodontal therapy performed in a specialist university setting following EFP S3 treatment guideline and to assess factors associated with the achievement of endpoints of therapy (EoT).
Methods: Records of 131 stage III-IV periodontitis patients were collected retrospectively. Residual pockets (probing pocket depth [PPD] 5 mm with bleeding on probing [BoP] or PPD ≥ 6 mm) after steps I-II (T1) received repeated subgingival instrumentation (RSI) or surgery and were re-evaluated after 1 year (T2). EoT (no PPD ≥ 5 mm BoP+ and no PPD ≥ 6 mm) rate at T1 and T2 was computed, and predictors explored through multilevel analyses.
Results: At T1, EoT was 67.8%, with step III yielding an additional 90.0% of EoT in PPD = 5 mm BoP+ and 85.3% in PPD ≥ 6 mm. Factors negatively associated with EoT were: posterior teeth, furcation involvement (degree II-III), initial PPD, interproximal location and plaque. When considering only pockets ≥ 6 mm, factors were PPD at T1, type of intervention (resective surgery over RSI) and plaque at T2. Overall, 55.7% of patients reached EoT, 16.1% achieved 'stable periodontitis' (PPD ≤ 4 mm, no PPD = 4 mm BoP+, BoP < 10%).
Conclusions: Guideline-based periodontal therapy achieved EoT targets in 93.3% of sites and 50% of patients with Stage III-IV periodontitis.
目的：描述在专业大学环境下遵循EFP S3治疗指南进行牙周治疗的步骤I-II-III的疗效，并评估与实现治疗终点（EoT）相关的因素。方法：对131例iii ~ iv期牙周炎患者的临床资料进行回顾性分析。步骤I-II （T1）后的残余口袋（探查口袋深度[PPD] 5mm，探查时出血[BoP]或PPD≥6mm）接受反复龈下检查（RSI）或手术，并在1年后重新评估（T2）。计算T1和T2的EoT（无PPD≥5 mm BoP+和无PPD≥6 mm）率，并通过多水平分析探讨预测因素。结果：T1时EoT率为67.8%，其中PPD = 5 mm BoP+的EoT率为90.0%，PPD≥6 mm的EoT率为85.3%。与EoT负相关的因素有：后牙、分叉受累程度（II-III度）、初始PPD、近端间位置和牙菌斑。当仅考虑≥6mm囊袋时，T1时的影响因素是PPD，干预类型（RSI切除手术）和T2时的斑块。总体而言，55.7%的患者达到了EoT， 16.1%的患者达到了“稳定牙周炎”（PPD≤4 mm，无PPD = 4 mm BoP+, BoP）。结论：基于指南的牙周治疗在93.3%的部位和50%的III-IV期牙周炎患者达到了EoT目标。
{"title":"Outcomes of Active Periodontal Therapy in a Specialist University Setting Following EFP S3 Treatment Guideline in Stage III-IV Periodontitis Patients.","authors":"Mario Aimetti, Federica Romano, Luigi Costanzo, Mario De Caroli, Andrea Di Venanzio, Giulia Maria Mariani, Giacomo Baima","doi":"10.1111/jcpe.70087","DOIUrl":"10.1111/jcpe.70087","url":null,"abstract":"<p><strong>Aim: </strong>To describe the efficacy of steps I-II-III of periodontal therapy performed in a specialist university setting following EFP S3 treatment guideline and to assess factors associated with the achievement of endpoints of therapy (EoT).</p><p><strong>Methods: </strong>Records of 131 stage III-IV periodontitis patients were collected retrospectively. Residual pockets (probing pocket depth [PPD] 5 mm with bleeding on probing [BoP] or PPD ≥ 6 mm) after steps I-II (T1) received repeated subgingival instrumentation (RSI) or surgery and were re-evaluated after 1 year (T2). EoT (no PPD ≥ 5 mm BoP+ and no PPD ≥ 6 mm) rate at T1 and T2 was computed, and predictors explored through multilevel analyses.</p><p><strong>Results: </strong>At T1, EoT was 67.8%, with step III yielding an additional 90.0% of EoT in PPD = 5 mm BoP+ and 85.3% in PPD ≥ 6 mm. Factors negatively associated with EoT were: posterior teeth, furcation involvement (degree II-III), initial PPD, interproximal location and plaque. When considering only pockets ≥ 6 mm, factors were PPD at T1, type of intervention (resective surgery over RSI) and plaque at T2. Overall, 55.7% of patients reached EoT, 16.1% achieved 'stable periodontitis' (PPD ≤ 4 mm, no PPD = 4 mm BoP+, BoP < 10%).</p><p><strong>Conclusions: </strong>Guideline-based periodontal therapy achieved EoT targets in 93.3% of sites and 50% of patients with Stage III-IV periodontitis.</p>","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":" ","pages":"562-571"},"PeriodicalIF":6.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aim To clarify the molecular mechanisms of occlusal trauma in bone loss through periodontal tissue transcriptome analysis in mice with periodontitis and traumatic occlusion. Materials and Methods Ligature‐induced periodontitis (Li) and composite resin‐induced traumatic occlusion (Tra) mouse models were established (control [Co], Li, Tra and LiTra). Bone resorption was evaluated using micro‐computed tomography (micro‐CT). RNA‐sequencing was conducted on gingiva, bone and periodontal ligament from all groups 3 days post induction. For long‐term evaluation, the Co and Tra groups were maintained for 8 weeks and then analysed using micro‐CT and qRT‐PCR. Results Traumatic occlusion alone, sustained for 8 weeks, did not directly induce bone resorption; however, it significantly exacerbated bone resorption in mice with periodontitis. Cytokine–cytokine receptor interactions and Toll‐like receptor signalling pathways were up‐regulated in LiTra bone tissue. Il11, Il1rl1 and Mmp3 , associated with inflammation and bone metabolism, were more highly expressed in the LiTra group than in the Li group. TNF‐α signalling via NFκB and inflammatory response gene sets were enriched in the bone tissue of LiTra group. Conclusions Traumatic occlusion accelerates bone resorption in ligature‐induced periodontitis but does not independently cause significant bone loss. Occlusal trauma enhances the expression of inflammation‐related genes, especially in bone with periodontitis.
{"title":"Traumatic Occlusion Exacerbates Bone Resorption by Modifying Gene Expression in the Bone Tissue of Ligature‐Induced Periodontitis in Mice","authors":"Yosuke Tsuchiya, Yujin Ohsugi, Tomomitsu Hirota, Yohei Hayashi, Peiya Lin, Yuta Tsukahara, Takanori Iwata, Sayaka Katagiri","doi":"10.1111/jcpe.70112","DOIUrl":"https://doi.org/10.1111/jcpe.70112","url":null,"abstract":"Aim To clarify the molecular mechanisms of occlusal trauma in bone loss through periodontal tissue transcriptome analysis in mice with periodontitis and traumatic occlusion. Materials and Methods Ligature‐induced periodontitis (Li) and composite resin‐induced traumatic occlusion (Tra) mouse models were established (control [Co], Li, Tra and LiTra). Bone resorption was evaluated using micro‐computed tomography (micro‐CT). RNA‐sequencing was conducted on gingiva, bone and periodontal ligament from all groups 3 days post induction. For long‐term evaluation, the Co and Tra groups were maintained for 8 weeks and then analysed using micro‐CT and qRT‐PCR. Results Traumatic occlusion alone, sustained for 8 weeks, did not directly induce bone resorption; however, it significantly exacerbated bone resorption in mice with periodontitis. Cytokine–cytokine receptor interactions and Toll‐like receptor signalling pathways were up‐regulated in LiTra bone tissue. <jats:italic>Il11, Il1rl1</jats:italic> and <jats:italic>Mmp3</jats:italic> , associated with inflammation and bone metabolism, were more highly expressed in the LiTra group than in the Li group. TNF‐α signalling via NFκB and inflammatory response gene sets were enriched in the bone tissue of LiTra group. Conclusions Traumatic occlusion accelerates bone resorption in ligature‐induced periodontitis but does not independently cause significant bone loss. Occlusal trauma enhances the expression of inflammation‐related genes, especially in bone with periodontitis.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"90 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147507925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eduardo Montero,Nerea Sánchez,Evangelia P Zampa,Bettina Alonso,Marion Arce,Phoebus Madianos
AIMTo evaluate the efficacy of interventions for treating necrotising periodontal diseases (NPDs), including the management of the acute condition and subsequent therapies targeting sequelae and/or predisposing factors.METHODSFollowing PRISMA guidelines, electronic and manual searches were conducted up to April 2025. Randomised controlled trials (RCTs), controlled clinical trials (CCTs) and case series assessing any therapeutic intervention for NPDs (separating them for acute disease resolution and treatment of the preexisting condition and/or management of sequelae) were included.RESULTSThirty-five studies were included (18 RCTs, 2 CCTs, 15 case series). Mechanical debridement combined with antiseptic rinses (e.g., chlorhexidine or hydrogen peroxide) constitutes the primary therapeutic approach. Systemic antimicrobials, mainly metronidazole, have also frequently been evaluated and used as adjuncts or monotherapy. Reduced pain, bleeding and ulcer resolution within days were the common findings for all tested interventions. Recent trials explored photodynamic therapy (PDT) as adjuncts, showing short-term clinical and microbiological benefits. Evidence was heterogeneous and of high risk of bias. Only five studies addressed post-acute management, with none of them investigating reconstructive approaches or long-term recurrence prevention.CONCLUSIONSManagement of NPDs relies primarily on mechanical debridement and antiseptics, with systemic antimicrobials reserved for cases with systemic involvement. Adjunctive modalities such as PDT have shown promising results but require further validation. Evidence on reconstructive approaches and recurrence prevention is lacking.
{"title":"Management of Necrotising Periodontal Diseases: A Systematic Review.","authors":"Eduardo Montero,Nerea Sánchez,Evangelia P Zampa,Bettina Alonso,Marion Arce,Phoebus Madianos","doi":"10.1111/jcpe.70118","DOIUrl":"https://doi.org/10.1111/jcpe.70118","url":null,"abstract":"AIMTo evaluate the efficacy of interventions for treating necrotising periodontal diseases (NPDs), including the management of the acute condition and subsequent therapies targeting sequelae and/or predisposing factors.METHODSFollowing PRISMA guidelines, electronic and manual searches were conducted up to April 2025. Randomised controlled trials (RCTs), controlled clinical trials (CCTs) and case series assessing any therapeutic intervention for NPDs (separating them for acute disease resolution and treatment of the preexisting condition and/or management of sequelae) were included.RESULTSThirty-five studies were included (18 RCTs, 2 CCTs, 15 case series). Mechanical debridement combined with antiseptic rinses (e.g., chlorhexidine or hydrogen peroxide) constitutes the primary therapeutic approach. Systemic antimicrobials, mainly metronidazole, have also frequently been evaluated and used as adjuncts or monotherapy. Reduced pain, bleeding and ulcer resolution within days were the common findings for all tested interventions. Recent trials explored photodynamic therapy (PDT) as adjuncts, showing short-term clinical and microbiological benefits. Evidence was heterogeneous and of high risk of bias. Only five studies addressed post-acute management, with none of them investigating reconstructive approaches or long-term recurrence prevention.CONCLUSIONSManagement of NPDs relies primarily on mechanical debridement and antiseptics, with systemic antimicrobials reserved for cases with systemic involvement. Adjunctive modalities such as PDT have shown promising results but require further validation. Evidence on reconstructive approaches and recurrence prevention is lacking.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"11 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147483235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Giusy Rita Maria La Rosa,Lakshman Perera Samaranayake,Egija Zaura,Ang Sun,Virginia Fuochi,Pio Maria Furneri,Jan Kowalski,Karol Myszel,Iain Chapple,Riccardo Polosa
AIMTo examine whether the oral microbiota of e-cigarette users differs from that of never smokers and current smokers.MATERIALS AND METHODSPubMed, Scopus and Web of Science were searched on 27 August 2025. Human studies using molecular methods to compare oral microbiota in saliva, subgingival plaque and oral mucosal swabs among e-cigarette users, never smokers and current smokers were included. Primary outcomes were alpha diversity, beta diversity and differential taxonomic abundance. Risk of bias was assessed using JBI tools and certainty of evidence using GRADE.RESULTSTwelve studies were included; most were cross-sectional and heterogeneous in design, exposure and samples. Alpha diversity findings were inconsistent across samples, whereas beta diversity more consistently indicated distinct microbial communities in e-cigarette users compared with never smokers and current smokers. Taxonomic differences were heterogeneous and sample-dependent, with some enrichment of genera such as Veillonella, Leptotrichia, and Fusobacterium compared with never smokers.CONCLUSIONSElectronic cigarette use is associated with sample-specific oral microbiota differences that partly overlap with, but differ from, those observed in never smokers and current smokers. However, the certainty of evidence is very low due to predominantly cross-sectional designs and methodological limitations, underscoring the need for longitudinal studies with standardised exposure and protocols.
目的探讨电子烟使用者的口腔微生物群是否与从不吸烟者和当前吸烟者不同。材料与方法于2025年8月27日检索spubmed、Scopus和Web of Science。使用分子方法比较唾液、龈下菌斑和口腔粘膜拭子中的口腔微生物群的人类研究包括电子烟使用者、从不吸烟者和当前吸烟者。主要结果为α多样性、β多样性和差异分类丰度。使用JBI工具评估偏倚风险，使用GRADE评估证据的确定性。结果共纳入12项研究；大多数是横断面的，在设计、暴露和样本上都是异质的。不同样本的α多样性结果不一致，而β多样性更一致地表明，与从不吸烟者和当前吸烟者相比，电子烟使用者中存在不同的微生物群落。分类差异具有异质性和样本依赖性，与不吸烟者相比，微孔菌属、细毛菌属和梭杆菌属的数量有所增加。结论：电子烟的使用与样本特异性口腔微生物群差异有关，这些差异与从不吸烟者和当前吸烟者观察到的差异部分重叠，但又不同。然而，由于主要是横断面设计和方法学的限制，证据的确定性非常低，强调了对标准化暴露和方案的纵向研究的需要。
{"title":"Impact of Electronic Cigarette Use on the Oral Microbiota: A Systematic Review.","authors":"Giusy Rita Maria La Rosa,Lakshman Perera Samaranayake,Egija Zaura,Ang Sun,Virginia Fuochi,Pio Maria Furneri,Jan Kowalski,Karol Myszel,Iain Chapple,Riccardo Polosa","doi":"10.1111/jcpe.70111","DOIUrl":"https://doi.org/10.1111/jcpe.70111","url":null,"abstract":"AIMTo examine whether the oral microbiota of e-cigarette users differs from that of never smokers and current smokers.MATERIALS AND METHODSPubMed, Scopus and Web of Science were searched on 27 August 2025. Human studies using molecular methods to compare oral microbiota in saliva, subgingival plaque and oral mucosal swabs among e-cigarette users, never smokers and current smokers were included. Primary outcomes were alpha diversity, beta diversity and differential taxonomic abundance. Risk of bias was assessed using JBI tools and certainty of evidence using GRADE.RESULTSTwelve studies were included; most were cross-sectional and heterogeneous in design, exposure and samples. Alpha diversity findings were inconsistent across samples, whereas beta diversity more consistently indicated distinct microbial communities in e-cigarette users compared with never smokers and current smokers. Taxonomic differences were heterogeneous and sample-dependent, with some enrichment of genera such as Veillonella, Leptotrichia, and Fusobacterium compared with never smokers.CONCLUSIONSElectronic cigarette use is associated with sample-specific oral microbiota differences that partly overlap with, but differ from, those observed in never smokers and current smokers. However, the certainty of evidence is very low due to predominantly cross-sectional designs and methodological limitations, underscoring the need for longitudinal studies with standardised exposure and protocols.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"57 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147483700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AIMTo investigate the association between baseline periodontitis and uncontrolled hypertension across two cohort waves.MATERIALS AND METHODSPeriodontitis severity was assessed using a categorical variable (non-severe, localised severe and generalised severe) and continuous measures, including mean probing depth (PD) and clinical attachment level (CAL). The primary outcome was uncontrolled hypertension, defined as systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg. Secondary outcomes were uncontrolled SBP and DBP analysed separately. Mixed-effects logistic regression was applied to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between periodontitis and blood pressure outcomes, with adjustment for potential confounders.RESULTSThe study included 417 treated hypertensive participants, aged 53-73 years. Individuals with localised or generalised severe periodontitis were more likely to have uncontrolled hypertension than those with non-severe disease (OR 1.56, 95% CI: 1.01-2.41 and OR 1.74, 95% CI: 1.13-2.69, respectively). When SBP and DBP were examined separately, severe periodontitis was significantly associated with uncontrolled SBP but not DBP. Similar findings were observed for mean PD and CAL.CONCLUSIONSSevere periodontitis was associated with poorer blood pressure control in treated hypertensive individuals, particularly through an increased likelihood of uncontrolled SBP.
{"title":"Periodontitis Is Associated With Poor Blood Pressure Control in Treated Hypertensive Individuals.","authors":"Kitti Torrungruang,Prin Vathesatogkit,Piyamitr Sritara","doi":"10.1111/jcpe.70119","DOIUrl":"https://doi.org/10.1111/jcpe.70119","url":null,"abstract":"AIMTo investigate the association between baseline periodontitis and uncontrolled hypertension across two cohort waves.MATERIALS AND METHODSPeriodontitis severity was assessed using a categorical variable (non-severe, localised severe and generalised severe) and continuous measures, including mean probing depth (PD) and clinical attachment level (CAL). The primary outcome was uncontrolled hypertension, defined as systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg. Secondary outcomes were uncontrolled SBP and DBP analysed separately. Mixed-effects logistic regression was applied to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between periodontitis and blood pressure outcomes, with adjustment for potential confounders.RESULTSThe study included 417 treated hypertensive participants, aged 53-73 years. Individuals with localised or generalised severe periodontitis were more likely to have uncontrolled hypertension than those with non-severe disease (OR 1.56, 95% CI: 1.01-2.41 and OR 1.74, 95% CI: 1.13-2.69, respectively). When SBP and DBP were examined separately, severe periodontitis was significantly associated with uncontrolled SBP but not DBP. Similar findings were observed for mean PD and CAL.CONCLUSIONSSevere periodontitis was associated with poorer blood pressure control in treated hypertensive individuals, particularly through an increased likelihood of uncontrolled SBP.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"11 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147483699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ziqi Chen, Gagandeep Kaur, Nadia Kaunein, Claireta Handoko, Marco A. Peres, Melissa Russell, Ankur Singh
Aims This systematic review aims to examine the causal effect of tobacco smoking on tooth loss. Further, the impact of different frequencies, intensities and lifetime exposures to tobacco smoking on tooth loss and whether the relationship differs by socioeconomic status (SES) are reviewed in the sub‐group analysis. Methods An electronic search was conducted in Embase (Ovid), Ovid MEDLINE and Web of Science for studies published up to May 2025. No limits on publication dates were applied. This review included case–control and cohort studies that reported the effect of tobacco smoking on tooth loss. Risk of Bias of included studies was assessed by ROBINS‐E assessment tool. Results A total of 30 studies were included in this systematic review. The meta‐analysis from five studies indicated that current smokers have 1.41 times higher risk of tooth loss (RR 1.41, 95% CI: 1.24–1.60) than nonsmokers (sample size range: 273–34,975, n = 5). Past smoking also increases the risk of having tooth loss (RR 1.21, 95% CI: 1.07–1.37) (sample size range: 547–34,975, n = 2). None of the studies examined the effect of smoking on tooth loss by different SES. Conclusions This systematic review highlights the importance and urgency of quitting smoking for better oral health.
{"title":"The Effect of Tobacco Smoking on Tooth Loss: A Systematic Review and Meta‐Analysis","authors":"Ziqi Chen, Gagandeep Kaur, Nadia Kaunein, Claireta Handoko, Marco A. Peres, Melissa Russell, Ankur Singh","doi":"10.1111/jcpe.70110","DOIUrl":"https://doi.org/10.1111/jcpe.70110","url":null,"abstract":"Aims This systematic review aims to examine the causal effect of tobacco smoking on tooth loss. Further, the impact of different frequencies, intensities and lifetime exposures to tobacco smoking on tooth loss and whether the relationship differs by socioeconomic status (SES) are reviewed in the sub‐group analysis. Methods An electronic search was conducted in Embase (Ovid), Ovid MEDLINE and Web of Science for studies published up to May 2025. No limits on publication dates were applied. This review included case–control and cohort studies that reported the effect of tobacco smoking on tooth loss. Risk of Bias of included studies was assessed by ROBINS‐E assessment tool. Results A total of 30 studies were included in this systematic review. The meta‐analysis from five studies indicated that current smokers have 1.41 times higher risk of tooth loss (RR 1.41, 95% CI: 1.24–1.60) than nonsmokers (sample size range: 273–34,975, <jats:italic>n</jats:italic> = 5). Past smoking also increases the risk of having tooth loss (RR 1.21, 95% CI: 1.07–1.37) (sample size range: 547–34,975, <jats:italic>n</jats:italic> = 2). None of the studies examined the effect of smoking on tooth loss by different SES. Conclusions This systematic review highlights the importance and urgency of quitting smoking for better oral health.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"49 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147465373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aim To evaluate the real‐world comparative effectiveness of various adjunctive systemic antibiotic regimens in combination with scaling and root planing (SRP) using a large, multi‐centre retrospective cohort. Materials and Methods Electronic health records were used retrospectively to categorise periodontitis patients into ‘SRP Only’ or ‘SRP + Antibiotic’ groups based on prescriptions within 7 days of therapy. Primary outcomes included changes in probing depth (PD), clinical attachment level (CAL), percentage of sites with PD ≥ 4 mm and bleeding on probing (BOP). Secondary outcomes assessed tooth‐level worsening in mobility or furcation status. Results Among 3125 patients, the amoxicillin + metronidazole combination was found to be statistically superior to SRP alone for reducing PD, BOP and residual disease burden. It significantly reduced the odds of worsening tooth mobility by 63% and furcation involvement by 50%. While azithromycin and doxycycline improved CAL, the benefits of the amoxicillin + metronidazole combination were most pronounced in Stage III/IV (severe) periodontitis (−11.4% residual burden reduction, OR 4.55 for clinical success), compared to a modest effect in Stage I/II disease (−3.8%, p = 0.030). Conclusion Adjunctive systemic antibiotics, particularly the amoxicillin + metronidazole combination, significantly enhance clinical outcomes in non‐surgical periodontitis treatment compared to SRP alone, with the greatest benefits seen in severe disease.
{"title":"The Effect of Adjunctive Systemic Antibiotics on the Outcomes of Non‐Surgical Periodontal Therapy: A Retrospective Cohort Study","authors":"Georgios S. Chatzopoulos, Larry F. Wolff","doi":"10.1111/jcpe.70117","DOIUrl":"https://doi.org/10.1111/jcpe.70117","url":null,"abstract":"Aim To evaluate the real‐world comparative effectiveness of various adjunctive systemic antibiotic regimens in combination with scaling and root planing (SRP) using a large, multi‐centre retrospective cohort. Materials and Methods Electronic health records were used retrospectively to categorise periodontitis patients into ‘SRP Only’ or ‘SRP + Antibiotic’ groups based on prescriptions within 7 days of therapy. Primary outcomes included changes in probing depth (PD), clinical attachment level (CAL), percentage of sites with PD ≥ 4 mm and bleeding on probing (BOP). Secondary outcomes assessed tooth‐level worsening in mobility or furcation status. Results Among 3125 patients, the amoxicillin + metronidazole combination was found to be statistically superior to SRP alone for reducing PD, BOP and residual disease burden. It significantly reduced the odds of worsening tooth mobility by 63% and furcation involvement by 50%. While azithromycin and doxycycline improved CAL, the benefits of the amoxicillin + metronidazole combination were most pronounced in Stage III/IV (severe) periodontitis (−11.4% residual burden reduction, OR 4.55 for clinical success), compared to a modest effect in Stage I/II disease (−3.8%, <jats:italic>p</jats:italic> = 0.030). Conclusion Adjunctive systemic antibiotics, particularly the amoxicillin + metronidazole combination, significantly enhance clinical outcomes in non‐surgical periodontitis treatment compared to SRP alone, with the greatest benefits seen in severe disease.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"20 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147465372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wenjie Zhou,Ausra Ramanauskaite,Clemens Raabe,Emilio A Cafferata,Neelam Lingwal,Frank Schwarz
AIMTo explore the treatment outcome of surgical peri-implantitis protocols in a university-based setting.MATERIALS AND METHODSFour-hundred and six implants in 223 patients were surgically treated by four trained surgeons using open-flap debridement (OFD, 37 implants), implantoplasty (Impl, 39 implants), reconstructive surgery (Rec, 241 implants) or a combined approach (Comb, 89 implants). Treatment success after 1 year (maximum probing depth (max PD) ≤ 5 mm, bleeding on probing (BOP) at ≤ 1 site and no suppuration) was the primary outcome. Logistic regression was used to explore associations between patient-/implant-related factors, treatment modalities and treatment success, implant loss and surgical retreatment.RESULTSTreatment was successful in 54.7% of implants after 1 year: OFD 62.5%, Impl 58.3%, Rec 55.4%, Comb 48.3%, with no significant group differences. Over a mean follow-up of 30.80 ± 19.62 months, 40 implants (9.9%) were lost and 38 (9.4%) required surgical retreatment. In exploratory multivariable analyses, systemic antibiotic use (pre-operative: OR = 3.54, p = 0.04; pre- and post-operative: OR = 4.49, p = 0.02) and surgeon experience (OR = 0.12, p = 0.003) showed associations with treatment success. Molar site (OR = 3.21, p = 0.03), antibiotic (pre- and post-operative: OR = 3.13, p = 0.02) and baseline suppuration (OR = 4.51, p = 0.002) were associated with implant loss. Surgical retreatment was associated with overdenture (OR = 3.59, p = 0.003) and max PD at baseline (OR = 1.30, p = 0.001).CONCLUSIONSSurgical peri-implantitis outcome was associated with systemic antibiotic, surgeon, molar site, overdenture, baseline suppuration and PD.
目的探讨以大学为基础的种植体周围炎手术治疗方案的效果。材料与方法223例患者的246个种植体由4名训练有素的外科医生进行手术治疗，包括开瓣清创（OFD， 37个种植体）、种植体成形术（Impl， 39个种植体）、重建手术（Rec， 241个种植体）或联合入路（Comb， 89个种植体）。1年后治疗成功(最大穿刺深度（max PD)≤5mm，穿刺出血(BOP)≤1个部位，无化脓）是主要结局。采用Logistic回归探讨患者/种植体相关因素、治疗方式和治疗成功、种植体丢失和手术再治疗之间的关系。结果1年后种植体治疗成功率为54.7%，其中OFD为62.5%，Impl为58.3%，Rec为55.4%，Comb为48.3%，组间差异无统计学意义。在平均30.80±19.62个月的随访中，40个种植体（9.9%）丢失，38个（9.4%）需要手术治疗。在探索性多变量分析中，全系统抗生素使用（术前：OR = 3.54, p = 0.04；术前和术后：OR = 4.49, p = 0.02）和外科医生经验（OR = 0.12, p = 0.003）与治疗成功相关。磨牙位置（OR = 3.21, p = 0.03）、抗生素（术前和术后：OR = 3.13, p = 0.02）和基线化脓（OR = 4.51, p = 0.002）与种植体丢失相关。手术再治疗与覆盖义齿（OR = 3.59, p = 0.003）和基线时最大PD （OR = 1.30, p = 0.001）相关。结论手术种植周炎的预后与全身抗生素、外科医生、臼齿部位、覆盖义齿、基线化脓和PD有关。
{"title":"Treatment Outcome of Surgical Protocols for Peri-Implantitis: A Retrospective Cohort Study in a Specialised University Centre.","authors":"Wenjie Zhou,Ausra Ramanauskaite,Clemens Raabe,Emilio A Cafferata,Neelam Lingwal,Frank Schwarz","doi":"10.1111/jcpe.70115","DOIUrl":"https://doi.org/10.1111/jcpe.70115","url":null,"abstract":"AIMTo explore the treatment outcome of surgical peri-implantitis protocols in a university-based setting.MATERIALS AND METHODSFour-hundred and six implants in 223 patients were surgically treated by four trained surgeons using open-flap debridement (OFD, 37 implants), implantoplasty (Impl, 39 implants), reconstructive surgery (Rec, 241 implants) or a combined approach (Comb, 89 implants). Treatment success after 1 year (maximum probing depth (max PD) ≤ 5 mm, bleeding on probing (BOP) at ≤ 1 site and no suppuration) was the primary outcome. Logistic regression was used to explore associations between patient-/implant-related factors, treatment modalities and treatment success, implant loss and surgical retreatment.RESULTSTreatment was successful in 54.7% of implants after 1 year: OFD 62.5%, Impl 58.3%, Rec 55.4%, Comb 48.3%, with no significant group differences. Over a mean follow-up of 30.80 ± 19.62 months, 40 implants (9.9%) were lost and 38 (9.4%) required surgical retreatment. In exploratory multivariable analyses, systemic antibiotic use (pre-operative: OR = 3.54, p = 0.04; pre- and post-operative: OR = 4.49, p = 0.02) and surgeon experience (OR = 0.12, p = 0.003) showed associations with treatment success. Molar site (OR = 3.21, p = 0.03), antibiotic (pre- and post-operative: OR = 3.13, p = 0.02) and baseline suppuration (OR = 4.51, p = 0.002) were associated with implant loss. Surgical retreatment was associated with overdenture (OR = 3.59, p = 0.003) and max PD at baseline (OR = 1.30, p = 0.001).CONCLUSIONSSurgical peri-implantitis outcome was associated with systemic antibiotic, surgeon, molar site, overdenture, baseline suppuration and PD.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"10 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147461773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiancheng Zeng,Yanjun Ge,Jiayun Dong,Jianfeng Liufu,Xiaofeng Shan,Ruifang Lu
AIMTo evaluate peri-implant keratinised mucosa augmentation using free gingival grafts (FGG) versus a combined FGG/xenogeneic collagen matrix (XCM) approach in reconstructed maxillae.MATERIALS AND METHODSThis prospective, non-randomised cohort study included patients with vascularised bone flap reconstructed maxillae. Keratinised mucosa width (KMW) was measured pre-operatively (baseline), immediately after operation and at 1 year. The primary outcome was buccal KMW gain, which was analysed using adjusted mixed-effects models with random intercepts. Exploratory histological evaluation was performed.RESULTSTwenty-five patients (76 implants) were included. Baseline buccal KMW was 0.00 ± 0.00 mm (FGG) and 0.02 ± 0.15 mm (FGG/XCM). At 1 year, it increased to 4.00 ± 1.60 mm (FGG) and 2.51 ± 1.22 mm (FGG/XCM). The adjusted mean difference in buccal KMW gain was 0.84 mm (95% CI: -0.09 to 1.77 mm; p = 0.074); 97% and 93% of implants achieved palatal KMW ≥ 2 mm, respectively (adjusted p = 0.803). Vestibular depth positively predicted buccal KMW gain. Histologically, FGG sites exhibited features of orthokeratinised epithelium, whereas XCM sites resembled parakeratinised epithelium.CONCLUSIONSKMW increased in both approaches. Although buccal KMW gain tended to be greater with the FGG approach, the non-randomised design and potential residual confounding limit definitive comparisons.TRIAL REGISTRATIONChiCTR2000041104.
目的评价游离龈移植物（FGG）与游离龈移植物/异种胶原基质（XCM）联合入路在重建上颌骨种植周角化黏膜的效果。材料与方法本前瞻性、非随机队列研究纳入了血管化骨瓣重建上颌的患者。术前（基线）、术后即刻和术后1年分别测量角化粘膜宽度（KMW）。主要结果是口腔KMW增益，使用随机截距调整的混合效应模型进行分析。进行探索性组织学评价。结果共纳入25例患者（76颗种植体）。颊部KMW基线值为0.00±0.00 mm （FGG）和0.02±0.15 mm （FGG/XCM）。1年时，FGG/XCM分别为4.00±1.60 mm和2.51±1.22 mm。调整后的颊部KMW增益平均差为0.84 mm (95% CI: -0.09 ~ 1.77 mm; p = 0.074)；种植体的腭KMW≥2 mm分别为97%和93%（校正p = 0.803）。前庭深度正预测颊部KMW增益。组织学上，FGG部位表现为正角化上皮特征，而XCM部位表现为角化不全上皮特征。结论两种方法的skmw均升高。虽然FGG方法的颊部KMW增益往往更大，但非随机设计和潜在的残留混淆限制了明确的比较。REGISTRATIONChiCTR2000041104审判。
{"title":"Free Gingival Grafts With or Without Xenogeneic Collagen Matrix Increase Peri-Implant Keratinised Mucosa in Reconstructed Maxillae: A 1-Year Prospective Cohort Study.","authors":"Xiancheng Zeng,Yanjun Ge,Jiayun Dong,Jianfeng Liufu,Xiaofeng Shan,Ruifang Lu","doi":"10.1111/jcpe.70113","DOIUrl":"https://doi.org/10.1111/jcpe.70113","url":null,"abstract":"AIMTo evaluate peri-implant keratinised mucosa augmentation using free gingival grafts (FGG) versus a combined FGG/xenogeneic collagen matrix (XCM) approach in reconstructed maxillae.MATERIALS AND METHODSThis prospective, non-randomised cohort study included patients with vascularised bone flap reconstructed maxillae. Keratinised mucosa width (KMW) was measured pre-operatively (baseline), immediately after operation and at 1 year. The primary outcome was buccal KMW gain, which was analysed using adjusted mixed-effects models with random intercepts. Exploratory histological evaluation was performed.RESULTSTwenty-five patients (76 implants) were included. Baseline buccal KMW was 0.00 ± 0.00 mm (FGG) and 0.02 ± 0.15 mm (FGG/XCM). At 1 year, it increased to 4.00 ± 1.60 mm (FGG) and 2.51 ± 1.22 mm (FGG/XCM). The adjusted mean difference in buccal KMW gain was 0.84 mm (95% CI: -0.09 to 1.77 mm; p = 0.074); 97% and 93% of implants achieved palatal KMW ≥ 2 mm, respectively (adjusted p = 0.803). Vestibular depth positively predicted buccal KMW gain. Histologically, FGG sites exhibited features of orthokeratinised epithelium, whereas XCM sites resembled parakeratinised epithelium.CONCLUSIONSKMW increased in both approaches. Although buccal KMW gain tended to be greater with the FGG approach, the non-randomised design and potential residual confounding limit definitive comparisons.TRIAL REGISTRATIONChiCTR2000041104.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"33 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147461775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AIMTo investigate the potential role and underlying mechanisms of gut microbiota in type 2 diabetes mellitus (T2DM)-exacerbated periodontitis.MATERIALS AND METHODSA T2DM-associated periodontitis model was established in C57BL/6 mice and analysed using multi-omics sequencing (16S rRNA, metagenomics and metabolomics). Faecal microbiota transplantation (FMT) from T2DM donors was carried out in recipient mice to investigate the impact of gut dysbiosis on periodontitis. FMT from healthy donors, supplementation of intestinal barrier protectant or the metabolite oleic acid (OA) was administered to mice with T2DM-associated gut dysbiosis to examine their ameliorative effects on periodontal damage.RESULTST2DM-associated gut dysbiosis, independent of hyperglycaemia, triggered intestinal barrier disruption, which disturbed systemic redox-related metabolisms and elevated oral oxidative stress, thereby aggravating periodontitis. Restoring gut microbiota via FMT from a healthy donor or protecting the intestinal barrier ameliorated periodontitis. Exogenous supplementary metabolite OA rescued periodontal damage by activating the SIRT1/FoxO1 pathway and enhancing antioxidant enzymes in mice with T2DM-associated gut dysbiosis.CONCLUSIONST2DM-induced gut dysbiosis exacerbates periodontitis through intestinal barrier disruption and redox imbalance. These findings provide new adjunctive therapeutic perspectives including microbiota restoration, intestinal barrier protection and antioxidant supplementation for managing patients with T2DM-induced periodontitis.
{"title":"T2DM-Induced Gut Dysbiosis Exacerbates Periodontitis Through Intestinal Barrier Disruption and Redox Imbalance.","authors":"Xulei Yuan,Haotian Gong,Linyue Zhang,Yangbo Liu,Mengjiao Zhou,Yuanyuan Liu,Jiawei Tang,Shengyuan Pan,Xiaohui Xu,Yunji Wang,Ximu Zhang,Tingwei Zhang,Jinlin Song","doi":"10.1111/jcpe.70116","DOIUrl":"https://doi.org/10.1111/jcpe.70116","url":null,"abstract":"AIMTo investigate the potential role and underlying mechanisms of gut microbiota in type 2 diabetes mellitus (T2DM)-exacerbated periodontitis.MATERIALS AND METHODSA T2DM-associated periodontitis model was established in C57BL/6 mice and analysed using multi-omics sequencing (16S rRNA, metagenomics and metabolomics). Faecal microbiota transplantation (FMT) from T2DM donors was carried out in recipient mice to investigate the impact of gut dysbiosis on periodontitis. FMT from healthy donors, supplementation of intestinal barrier protectant or the metabolite oleic acid (OA) was administered to mice with T2DM-associated gut dysbiosis to examine their ameliorative effects on periodontal damage.RESULTST2DM-associated gut dysbiosis, independent of hyperglycaemia, triggered intestinal barrier disruption, which disturbed systemic redox-related metabolisms and elevated oral oxidative stress, thereby aggravating periodontitis. Restoring gut microbiota via FMT from a healthy donor or protecting the intestinal barrier ameliorated periodontitis. Exogenous supplementary metabolite OA rescued periodontal damage by activating the SIRT1/FoxO1 pathway and enhancing antioxidant enzymes in mice with T2DM-associated gut dysbiosis.CONCLUSIONST2DM-induced gut dysbiosis exacerbates periodontitis through intestinal barrier disruption and redox imbalance. These findings provide new adjunctive therapeutic perspectives including microbiota restoration, intestinal barrier protection and antioxidant supplementation for managing patients with T2DM-induced periodontitis.","PeriodicalId":15380,"journal":{"name":"Journal of Clinical Periodontology","volume":"106 1","pages":""},"PeriodicalIF":6.7,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147461774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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