Angeliki Polymeri, Magda Feres, William V. Giannobile, Bruno G. Loos
Background Glucagon‐like peptide‐1 receptor agonists (GLP‐1 RAs) are analogs of the endogenous incretin hormone GLP‐1 and are increasingly used in the treatment of diabetes and obesity. Beyond glycemic control and weight loss, they have demonstrated anti‐inflammatory, antioxidative, and immunomodulatory properties. Given the inflammatory nature of periodontitis and its bidirectional relationship with diabetes mellitus, interest is growing in exploring the potential therapeutic benefits of GLP‐1 RAs in periodontal diseases. This scoping review aims to search the existing literature on the effects of GLP‐1 RAs on periodontitis, focusing on underlying mechanisms and emerging clinical implications. Methods Following PRISMA guidelines for scoping reviews, a comprehensive search was conducted in Medline/PubMed and Embase to identify preclinical and clinical studies in English evaluating the effects of GLP‐1 RAs on periodontal tissues. Data were synthesized thematically to highlight key findings and gaps. Results Evidence from mechanistic and preclinical studies supports a biologically plausible link between GLP‐1 RAs and pathways central to periodontal inflammation and host response. Human studies remain limited and observational but consistently report associations between periodontitis and altered incretin hormone profiles, including reduced endogenous GLP‐1 levels and increases following periodontal treatment. Conclusion This scoping review identifies growing mechanistic and preclinical evidence suggesting potential interactions between GLP‐1 RAs and periodontal inflammatory pathways. Although current human evidence is indirect and insufficient to establish therapeutic benefit, these early signals highlight an important opportunity for future research. Well‐designed clinical trials with periodontal endpoints are needed to clarify whether GLP‐1 RAs may provide adjunctive value in periodontal care. Plain language summary GLP‐1 receptor agonists are medications commonly used to manage diabetes and obesity. In addition to their metabolic effects, laboratory and animal studies suggest that these drugs may influence biological processes also involved in gum disease, such as inflammation, immune response, and bone metabolism. This scoping review examined all available scientific studies on the relationship between GLP‐1 receptor agonists and periodontal disease. Most of the existing evidence comes from mechanistic and preclinical research showing that these medications can reduce inflammation and support tissue repair in experimental models. Human studies are still very limited and have focused mainly on metabolic markers rather than on direct measures of gum health. So far, no clinical trial has tested whether GLP‐1 medications can improve periodontal outcomes. Although no conclusions can be made for clinical dental practice today, the findings highlight an emerging and promising area of research. Well‐designed clinical studies are needed to determine whe
{"title":"GLP‐1 receptor agonists: Bridging diabetes, obesity, and periodontitis—A scoping review of emerging evidence","authors":"Angeliki Polymeri, Magda Feres, William V. Giannobile, Bruno G. Loos","doi":"10.1002/jper.70092","DOIUrl":"https://doi.org/10.1002/jper.70092","url":null,"abstract":"Background Glucagon‐like peptide‐1 receptor agonists (GLP‐1 RAs) are analogs of the endogenous incretin hormone GLP‐1 and are increasingly used in the treatment of diabetes and obesity. Beyond glycemic control and weight loss, they have demonstrated anti‐inflammatory, antioxidative, and immunomodulatory properties. Given the inflammatory nature of periodontitis and its bidirectional relationship with diabetes mellitus, interest is growing in exploring the potential therapeutic benefits of GLP‐1 RAs in periodontal diseases. This scoping review aims to search the existing literature on the effects of GLP‐1 RAs on periodontitis, focusing on underlying mechanisms and emerging clinical implications. Methods Following PRISMA guidelines for scoping reviews, a comprehensive search was conducted in Medline/PubMed and Embase to identify preclinical and clinical studies in English evaluating the effects of GLP‐1 RAs on periodontal tissues. Data were synthesized thematically to highlight key findings and gaps. Results Evidence from mechanistic and preclinical studies supports a biologically plausible link between GLP‐1 RAs and pathways central to periodontal inflammation and host response. Human studies remain limited and observational but consistently report associations between periodontitis and altered incretin hormone profiles, including reduced endogenous GLP‐1 levels and increases following periodontal treatment. Conclusion This scoping review identifies growing mechanistic and preclinical evidence suggesting potential interactions between GLP‐1 RAs and periodontal inflammatory pathways. Although current human evidence is indirect and insufficient to establish therapeutic benefit, these early signals highlight an important opportunity for future research. Well‐designed clinical trials with periodontal endpoints are needed to clarify whether GLP‐1 RAs may provide adjunctive value in periodontal care. Plain language summary GLP‐1 receptor agonists are medications commonly used to manage diabetes and obesity. In addition to their metabolic effects, laboratory and animal studies suggest that these drugs may influence biological processes also involved in gum disease, such as inflammation, immune response, and bone metabolism. This scoping review examined all available scientific studies on the relationship between GLP‐1 receptor agonists and periodontal disease. Most of the existing evidence comes from mechanistic and preclinical research showing that these medications can reduce inflammation and support tissue repair in experimental models. Human studies are still very limited and have focused mainly on metabolic markers rather than on direct measures of gum health. So far, no clinical trial has tested whether GLP‐1 medications can improve periodontal outcomes. Although no conclusions can be made for clinical dental practice today, the findings highlight an emerging and promising area of research. Well‐designed clinical studies are needed to determine whe","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"11 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pedro H. C. Isaias, Paulo G. B. Silva, Isabelly V. do Nascimento, Raul A. D. A. da Silva, Thayla M. do C. Sousa, Ana J. A. de de Vasconcelos, José V. M. Lemos, Fabrício B. Sousa, Ana P. N. N. Alves, Mário R. L. Mota
Background Sodium alendronate (ALN) is widely used to treat postmenopausal osteoporosis, but both estrogen deficiency and antiresorptive therapy may impair alveolar bone repair after tooth extraction. A clinically relevant but insufficiently explored scenario involves estrogen‐deficient individuals receiving hormone replacement therapy (HRT) who subsequently initiate ALN treatment. This study investigated whether estradiol valerate (E) replacement attenuates ALN‐associated disturbances in alveolar bone repair in ovariectomized (OVX) rats. Methods Sixty‐three female Wistar rats were divided into sham‐operated (SHAM) or OVX groups and treated with ALN (5 or 10 mg/kg) or 0.9% sodium chloride saline solution (SAL), with or without E replacement (0.8 mg/kg). The left first molar was extracted, and alveolar repair was evaluated 28 days later through clinical, radiographic, histological, and immunohistochemical (tumor necrosis factor alpha [TNF‐α], receptor activator of nuclear factor kappa‐B ligand [RANKL], osteoprotegerin [OPG], and tartrate‐resistant acid phosphatase [TRAP]) analyses. Results OVX increased body mass and reduced uterine wet mass ( <jats:italic>p</jats:italic> < 0.001). Radiographically, ALN‐treated groups exhibited increased socket radiolucency, particularly at the higher dose ( <jats:italic>p</jats:italic> = 0.040). Microscopic analysis revealed more empty osteocyte lacunae ( <jats:italic>p</jats:italic> = 0.012) and connective tissue ( <jats:italic>p</jats:italic> = 0.010), particularly in ALN‐treated OVX groups. OVX and ALN increased TNF‐α, RANKL, and TRAP expression and reduced OPG levels ( <jats:italic>p</jats:italic> = 0.004; = 0.002; = 0.030; < 0.001). E replacement mitigated these effects and reduced type III collagen deposition ( <jats:italic>p</jats:italic> < 0.001). Conclusions Chronic ALN impaired alveolar bone repair, exacerbated by estrogen deficiency. HRT with E partially attenuated these effects without fully restoring healing. The persistent remodeling disturbances highlight the relevance of hormonal status for dental risk assessment in patients receiving bisphosphonates. Plain Language Summary Osteoporosis is common in postmenopausal women due to reduced estrogen levels and leads to weaker bones. Alendronate is widely prescribed to lower fracture risk, but it may interfere with bone healing after dental procedures such as tooth extraction. Using a rat model that mimics postmenopausal bone loss, this study examined how estrogen deficiency, alendronate treatment, and estrogen replacement together influence healing of the tooth socket, a process highly relevant to periodontal and oral surgical care. The results showed that estrogen deficiency alone already compromised bone repair, and this effect became more pronounced when alendronate was used. Estrogen replacement with estradiol valerate did not fully restore normal healing, but it reduced several harmful changes in bone structure and local inflammatory activ
{"title":"Estradiol replacement attenuates alendronate‐associated adverse effects on alveolar bone repair in ovariectomized rats","authors":"Pedro H. C. Isaias, Paulo G. B. Silva, Isabelly V. do Nascimento, Raul A. D. A. da Silva, Thayla M. do C. Sousa, Ana J. A. de de Vasconcelos, José V. M. Lemos, Fabrício B. Sousa, Ana P. N. N. Alves, Mário R. L. Mota","doi":"10.1002/jper.70088","DOIUrl":"https://doi.org/10.1002/jper.70088","url":null,"abstract":"Background Sodium alendronate (ALN) is widely used to treat postmenopausal osteoporosis, but both estrogen deficiency and antiresorptive therapy may impair alveolar bone repair after tooth extraction. A clinically relevant but insufficiently explored scenario involves estrogen‐deficient individuals receiving hormone replacement therapy (HRT) who subsequently initiate ALN treatment. This study investigated whether estradiol valerate (E) replacement attenuates ALN‐associated disturbances in alveolar bone repair in ovariectomized (OVX) rats. Methods Sixty‐three female Wistar rats were divided into sham‐operated (SHAM) or OVX groups and treated with ALN (5 or 10 mg/kg) or 0.9% sodium chloride saline solution (SAL), with or without E replacement (0.8 mg/kg). The left first molar was extracted, and alveolar repair was evaluated 28 days later through clinical, radiographic, histological, and immunohistochemical (tumor necrosis factor alpha [TNF‐α], receptor activator of nuclear factor kappa‐B ligand [RANKL], osteoprotegerin [OPG], and tartrate‐resistant acid phosphatase [TRAP]) analyses. Results OVX increased body mass and reduced uterine wet mass ( <jats:italic>p</jats:italic> < 0.001). Radiographically, ALN‐treated groups exhibited increased socket radiolucency, particularly at the higher dose ( <jats:italic>p</jats:italic> = 0.040). Microscopic analysis revealed more empty osteocyte lacunae ( <jats:italic>p</jats:italic> = 0.012) and connective tissue ( <jats:italic>p</jats:italic> = 0.010), particularly in ALN‐treated OVX groups. OVX and ALN increased TNF‐α, RANKL, and TRAP expression and reduced OPG levels ( <jats:italic>p</jats:italic> = 0.004; = 0.002; = 0.030; < 0.001). E replacement mitigated these effects and reduced type III collagen deposition ( <jats:italic>p</jats:italic> < 0.001). Conclusions Chronic ALN impaired alveolar bone repair, exacerbated by estrogen deficiency. HRT with E partially attenuated these effects without fully restoring healing. The persistent remodeling disturbances highlight the relevance of hormonal status for dental risk assessment in patients receiving bisphosphonates. Plain Language Summary Osteoporosis is common in postmenopausal women due to reduced estrogen levels and leads to weaker bones. Alendronate is widely prescribed to lower fracture risk, but it may interfere with bone healing after dental procedures such as tooth extraction. Using a rat model that mimics postmenopausal bone loss, this study examined how estrogen deficiency, alendronate treatment, and estrogen replacement together influence healing of the tooth socket, a process highly relevant to periodontal and oral surgical care. The results showed that estrogen deficiency alone already compromised bone repair, and this effect became more pronounced when alendronate was used. Estrogen replacement with estradiol valerate did not fully restore normal healing, but it reduced several harmful changes in bone structure and local inflammatory activ","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"1 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Maayan Atzmon‐Shavit, Marilena Vered, Michael Saminsky, Liat Chaushu
Background Free palatal gingival grafts (FGG) are commonly harvested during mucogingival procedures. The present study investigates age‐related local and systemic early secondary wound healing outcomes, following FGG harvest in a rat model. Methods A 4.2 mm diameter defect was created in the palate of 24 younger (2 m) and 24 older (6 m) Wistar male rats. They were divided according to experimental days 1–4. Values of complete blood count, chemistry analysis, and inflammatory biomarkers were assessed. Specimens were examined histologically. Results Wound healing was similar between groups, with a significant de‐epithelized surface reduction from day 1 to day 2 ( <jats:italic>p</jats:italic> = 0.0007) and day 2 to day 3 ( <jats:italic>p</jats:italic> = 0.002), without a significant difference between day 3 and day 4 ( <jats:italic>p</jats:italic> = 0.4). Histological inflammation scores were consistently higher in younger individuals, suggesting a more pronounced local inflammatory response. Picrosirius red staining revealed more dynamic collagen fiber organization in the younger rats, with significant differences at days 2 ( <jats:italic>p </jats:italic> = 0.01), 3 ( <jats:italic>p </jats:italic> = 0.03), and 4 ( <jats:italic>p </jats:italic> = 0.03). Age‐related differences were noted regarding levels of WBC (white blood cells), RBC (red blood cells), HGB (hemoglobin), HCT (hematocrit), MCV (mean corpuscular volume), MCH (mean corpuscular hemoglobin), platelet counts, creatinine, SGPT (serum glutamic pyruvic transaminase), SGOT (serum glutamic‐oxaloacetic transaminase), and AlkPhos. Younger rats displayed higher MCV, MCH, platelet counts, and a delayed rise in SGPT, creatinine, and AlkPhos over time, whereas older rats presented constantly higher WBC, RBC, HGB, HCT, and creatinine levels. Serum TNF‐α levels were initially higher in the older rats but declined rapidly. In contrast, IL‐6 peaked earlier and was higher in the older rats. IL‐18 peaked earlier in the older (day 2) compared with the younger rats (day 3). Conclusions Local and systemic early events following surgery of the palatal mucosa revealed age‐related differences. The older rats demonstrated in general a decreased local response vs. an increased systemic response. Plain language summary Free palatal gingival grafts are commonly harvested during mucogingival procedures around teeth and implants. The present study investigated age‐related local and systemic early phase outcomes following palatal free gingival harvest with a 4.2 mm diameter punch in a rat model. Younger and older Wistar male rats were included and divided into four experimental groups according to experimental days 1–4. Systemic outcome parameters included complete blood count, chemistry analysis, and immunological parameters. Biopsies were examined for local histological‐inflammatory outcome and collagen immunohistochemistry. Wound healing was similar between the older and younger groups. Local inflammation scores w
{"title":"Age‐related local versus systemic early phase wound healing dynamics following free gingival graft harvest","authors":"Maayan Atzmon‐Shavit, Marilena Vered, Michael Saminsky, Liat Chaushu","doi":"10.1002/jper.70089","DOIUrl":"https://doi.org/10.1002/jper.70089","url":null,"abstract":"Background Free palatal gingival grafts (FGG) are commonly harvested during mucogingival procedures. The present study investigates age‐related local and systemic early secondary wound healing outcomes, following FGG harvest in a rat model. Methods A 4.2 mm diameter defect was created in the palate of 24 younger (2 m) and 24 older (6 m) Wistar male rats. They were divided according to experimental days 1–4. Values of complete blood count, chemistry analysis, and inflammatory biomarkers were assessed. Specimens were examined histologically. Results Wound healing was similar between groups, with a significant de‐epithelized surface reduction from day 1 to day 2 ( <jats:italic>p</jats:italic> = 0.0007) and day 2 to day 3 ( <jats:italic>p</jats:italic> = 0.002), without a significant difference between day 3 and day 4 ( <jats:italic>p</jats:italic> = 0.4). Histological inflammation scores were consistently higher in younger individuals, suggesting a more pronounced local inflammatory response. Picrosirius red staining revealed more dynamic collagen fiber organization in the younger rats, with significant differences at days 2 ( <jats:italic>p </jats:italic> = 0.01), 3 ( <jats:italic>p </jats:italic> = 0.03), and 4 ( <jats:italic>p </jats:italic> = 0.03). Age‐related differences were noted regarding levels of WBC (white blood cells), RBC (red blood cells), HGB (hemoglobin), HCT (hematocrit), MCV (mean corpuscular volume), MCH (mean corpuscular hemoglobin), platelet counts, creatinine, SGPT (serum glutamic pyruvic transaminase), SGOT (serum glutamic‐oxaloacetic transaminase), and AlkPhos. Younger rats displayed higher MCV, MCH, platelet counts, and a delayed rise in SGPT, creatinine, and AlkPhos over time, whereas older rats presented constantly higher WBC, RBC, HGB, HCT, and creatinine levels. Serum TNF‐α levels were initially higher in the older rats but declined rapidly. In contrast, IL‐6 peaked earlier and was higher in the older rats. IL‐18 peaked earlier in the older (day 2) compared with the younger rats (day 3). Conclusions Local and systemic early events following surgery of the palatal mucosa revealed age‐related differences. The older rats demonstrated in general a decreased local response vs. an increased systemic response. Plain language summary Free palatal gingival grafts are commonly harvested during mucogingival procedures around teeth and implants. The present study investigated age‐related local and systemic early phase outcomes following palatal free gingival harvest with a 4.2 mm diameter punch in a rat model. Younger and older Wistar male rats were included and divided into four experimental groups according to experimental days 1–4. Systemic outcome parameters included complete blood count, chemistry analysis, and immunological parameters. Biopsies were examined for local histological‐inflammatory outcome and collagen immunohistochemistry. Wound healing was similar between the older and younger groups. Local inflammation scores w","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"23 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leticia Helena Theodoro, João Victor Soares Rodrigues, Marta A. A. Nuernberg, Pedro Henrique Petrilli, Mabelle de Freitas Monteiro, Valdir Gouveia Garcia, Rafael Scaf de Molon, Renato Correa Viana Casarin
Background Individuals with Down syndrome (DS) are particularly vulnerable to early‐onset and rapidly progressing periodontitis, yet the local immune‐inflammatory alterations that contribute to this susceptibility are not fully understood. This study aimed to characterize cytokine profiles in gingival crevicular fluid (GCF) from individuals with DS and periodontitis and to compare them with those of periodontitis patients without DS and periodontally healthy controls. Methods Forty‐five participants were enrolled and divided equally into three groups ( <jats:italic>n</jats:italic> = 15 each): DS with periodontitis (DSP), periodontitis without DS (P), and systemically and periodontally healthy controls (C). GCF samples were collected from two interproximal sites per participant and analyzed for IL‐1β, IL‐4, IL‐6, IL‐10, TNF‐α, and IFN‐γ using multiplex immunoassays. Standard periodontal parameters, including probing depth, attachment level, bleeding on probing, and plaque index, were also recorded. Non‐parametric comparisons and multivariate approaches, including principal component analysis and hierarchical clustering, were employed to explore cytokine distribution patterns. Results Individuals with DS and periodontitis exhibited a heterogeneous but predominantly pro‐inflammatory cytokine profile, characterized by elevated IL‐1β, IL‐6, TNF‐α, and higher Th1/Th2 and IL‐1β/IL‐10 ratios. In contrast, the P group demonstrated a Th2‐skewed response with higher levels of IL‐4, IL‐10, and IFN‐γ, suggestive of compensatory immune regulation. Healthy controls consistently displayed the lowest cytokine concentrations. Conclusion This preliminary study identifies a distinct pro‐inflammatory cytokine profile in Down syndrome‐associated periodontitis, characterized by heightened IL‐1β responses and a Th1‐skewed immune pattern. While limited by sample size and the absence of a DS‐healthy control group, these findings provide initial mechanistic insights into the accelerated periodontal breakdown observed in DS and lay the groundwork for future, larger‐scale investigations. Plain language summary People with Down syndrome (DS) often develop gum disease, called periodontitis, much earlier and more severely than others. This condition damages the tissues and bone that support the teeth and can lead to tooth loss. Researchers believe that an overactive immune system may play a role, but the exact reasons are not well understood. In this study, we examined the levels of several immune signaling molecules, called cytokines, in the fluid around the gums of people with DS and periodontitis, comparing them with individuals with periodontitis but without DS and with healthy participants. We found that people with DS and periodontitis had higher levels of inflammatory cytokines, showing an exaggerated immune reaction dominated by molecules that promote inflammation. In contrast, people with periodontitis but without DS showed signs of a more balanced immune response, inc
{"title":"Surveying immune and inflammatory alterations in periodontitis among individuals with Down syndrome: A preliminary cross‐sectional study","authors":"Leticia Helena Theodoro, João Victor Soares Rodrigues, Marta A. A. Nuernberg, Pedro Henrique Petrilli, Mabelle de Freitas Monteiro, Valdir Gouveia Garcia, Rafael Scaf de Molon, Renato Correa Viana Casarin","doi":"10.1002/jper.70087","DOIUrl":"https://doi.org/10.1002/jper.70087","url":null,"abstract":"Background Individuals with Down syndrome (DS) are particularly vulnerable to early‐onset and rapidly progressing periodontitis, yet the local immune‐inflammatory alterations that contribute to this susceptibility are not fully understood. This study aimed to characterize cytokine profiles in gingival crevicular fluid (GCF) from individuals with DS and periodontitis and to compare them with those of periodontitis patients without DS and periodontally healthy controls. Methods Forty‐five participants were enrolled and divided equally into three groups ( <jats:italic>n</jats:italic> = 15 each): DS with periodontitis (DSP), periodontitis without DS (P), and systemically and periodontally healthy controls (C). GCF samples were collected from two interproximal sites per participant and analyzed for IL‐1β, IL‐4, IL‐6, IL‐10, TNF‐α, and IFN‐γ using multiplex immunoassays. Standard periodontal parameters, including probing depth, attachment level, bleeding on probing, and plaque index, were also recorded. Non‐parametric comparisons and multivariate approaches, including principal component analysis and hierarchical clustering, were employed to explore cytokine distribution patterns. Results Individuals with DS and periodontitis exhibited a heterogeneous but predominantly pro‐inflammatory cytokine profile, characterized by elevated IL‐1β, IL‐6, TNF‐α, and higher Th1/Th2 and IL‐1β/IL‐10 ratios. In contrast, the P group demonstrated a Th2‐skewed response with higher levels of IL‐4, IL‐10, and IFN‐γ, suggestive of compensatory immune regulation. Healthy controls consistently displayed the lowest cytokine concentrations. Conclusion This preliminary study identifies a distinct pro‐inflammatory cytokine profile in Down syndrome‐associated periodontitis, characterized by heightened IL‐1β responses and a Th1‐skewed immune pattern. While limited by sample size and the absence of a DS‐healthy control group, these findings provide initial mechanistic insights into the accelerated periodontal breakdown observed in DS and lay the groundwork for future, larger‐scale investigations. Plain language summary People with Down syndrome (DS) often develop gum disease, called periodontitis, much earlier and more severely than others. This condition damages the tissues and bone that support the teeth and can lead to tooth loss. Researchers believe that an overactive immune system may play a role, but the exact reasons are not well understood. In this study, we examined the levels of several immune signaling molecules, called cytokines, in the fluid around the gums of people with DS and periodontitis, comparing them with individuals with periodontitis but without DS and with healthy participants. We found that people with DS and periodontitis had higher levels of inflammatory cytokines, showing an exaggerated immune reaction dominated by molecules that promote inflammation. In contrast, people with periodontitis but without DS showed signs of a more balanced immune response, inc","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"5 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background Chronic obstructive pulmonary disease (COPD) is a chronic lung disease with bronchitis and pulmonary emphysema phenotypes, with high morbidity and mortality. COPD is predicted to be the third leading cause of death by 2030. Periodontitis results from oral microbe dysbiosis, such as enrichment of periodontitis pathogens (e.g., Porphyromonas gingivalis ), which could disseminate to the lung via the blood stream or aspiration. Periodontitis pathogens are suggested to contribute to chronic inflammation and mucin secretion in the lung. Accordingly, periodontitis pathogens are associated with the pathogenesis and progression of COPD. However, clinical observation of a correlation between COPD and periodontitis is limited and the involved mechanism is not fully understood. Methods We used a mouse model with ligature‐induced periodontitis and porcine pancreatic elastase (PPE)‐induced pulmonary emphysema to evaluate the roles of P. gingivalis and Scardovia wiggsiae in COPD progression. We analyzed proinflammatory cytokines, immune cells, apoptosis, and the extent of COPD progression using a multiplex assay/enzyme‐linked immunosorbent assay, Hemacolor kit, terminal deoxynucleotidyl transferase nick‐end labeling assay, and the mean linear intercept and lung function, respectively. Results The results suggest that both oral bacterial species contributed to the periodontitis phenotype, promoted PPE‐induced proinflammatory cytokines in serum and bronchoalveolar lavage, and facilitated neutrophil infiltration in the lung. The abundance of neutrophils increased neutrophil elastase (NE) and downstream placenta growth factor (PGF) in the lung and led to alveolar epithelial cell apoptosis, pulmonary emphysema and lung function decline in the PPE‐treated mice. All pathological phenotype were attenuated by Ly6G antibody‐mediated neutrophil depletion in mice. Conclusions We demonstrated a potential mechanism for periodontal‐associated progression to COPD via the neutrophil‐NE‐PGF pathway. Plain Language Summary We demonstrated that the oral bacteria Porphyromonas gingivalis and Scardovia wiggsiae exacerbate ligature‐induced inflammation and increase proinflammatory cytokines in local gingival crevicular fluid, systemic serum, and distal bronchoalveolar lavage, and are associated with more neutrophil infiltration in the lung. The in vivo experiment indicated that gingival infection with P. gingivalis and S. wiggsiae worsens porcine pancreatic elastase‐induced pulmonary apoptosis and emphysema. Here, we show that P. gingivalis and S. wiggsiae are potential pathogenic factors for COPD.
慢性阻塞性肺疾病（COPD）是一种慢性肺部疾病，具有支气管炎和肺气肿表型，发病率和死亡率高。预计到2030年，慢性阻塞性肺病将成为第三大死因。牙周炎是由口腔微生物失调引起的，如牙周炎病原体（如牙龈卟啉单胞菌）的富集，可通过血流或吸入传播到肺部。牙周炎病原体被认为与慢性炎症和肺黏液分泌有关。因此，牙周炎病原体与慢性阻塞性肺病的发病和进展有关。然而，慢性阻塞性肺病与牙周炎之间相关性的临床观察有限，涉及的机制尚未完全了解。方法采用结扎性牙周炎和猪胰腺弹性酶（PPE）诱导肺气肿小鼠模型，评估牙龈假单胞菌和wiggsiscardovia在COPD进展中的作用。我们分别使用多重试验/酶联免疫吸附试验、Hemacolor试剂盒、末端脱氧核苷酸转移酶末端标记试验和平均线性截距和肺功能分析促炎细胞因子、免疫细胞、细胞凋亡和COPD进展程度。结果两种口腔细菌均参与了牙周炎表型的形成，促进了PPE诱导的血清和支气管肺泡灌洗液中促炎细胞因子的表达，促进了肺部中性粒细胞的浸润。大量的中性粒细胞增加了肺中中性粒细胞弹性酶（NE）和下游胎盘生长因子（PGF），导致肺泡上皮细胞凋亡、肺气肿和肺功能下降。通过Ly6G抗体介导的小鼠中性粒细胞耗竭，所有病理表型均减弱。结论：我们证明了通过中性粒细胞- NE - PGF途径牙周相关进展为COPD的潜在机制。我们证明了口腔细菌牙龈卟啉单胞菌和威氏斯卡多氏菌会加剧结扎诱导的炎症，增加局部牙龈沟液、全身血清和远端支气管肺泡灌洗液中的促炎细胞因子，并与肺中更多的中性粒细胞浸润有关。体内实验表明，牙龈假单胞菌和wiggsiae感染可使猪胰腺弹性酶诱导的肺细胞凋亡和肺气肿恶化。本研究表明，牙龈假单胞菌和wiggsiae是COPD的潜在致病因子。
{"title":"Porphyromonas gingivalis and Scardovia wiggsiae promote neutrophil‐induced lung epithelial cell apoptosis and emphysema","authors":"Hsin‐Han Hou, Yen‐Fu Chen, Yi‐Wen Chen, Chung‐Wei Wang, Shih‐Jung Cheng, Chun‐Pin Lin, Hao‐Chien Wang, Yen‐Ling Chu, Chong‐Jen Yu","doi":"10.1002/jper.70091","DOIUrl":"https://doi.org/10.1002/jper.70091","url":null,"abstract":"Background Chronic obstructive pulmonary disease (COPD) is a chronic lung disease with bronchitis and pulmonary emphysema phenotypes, with high morbidity and mortality. COPD is predicted to be the third leading cause of death by 2030. Periodontitis results from oral microbe dysbiosis, such as enrichment of periodontitis pathogens (e.g., <jats:italic>Porphyromonas gingivalis</jats:italic> ), which could disseminate to the lung via the blood stream or aspiration. Periodontitis pathogens are suggested to contribute to chronic inflammation and mucin secretion in the lung. Accordingly, periodontitis pathogens are associated with the pathogenesis and progression of COPD. However, clinical observation of a correlation between COPD and periodontitis is limited and the involved mechanism is not fully understood. Methods We used a mouse model with ligature‐induced periodontitis and porcine pancreatic elastase (PPE)‐induced pulmonary emphysema to evaluate the roles of <jats:italic>P. gingivalis</jats:italic> and <jats:italic>Scardovia wiggsiae</jats:italic> in COPD progression. We analyzed proinflammatory cytokines, immune cells, apoptosis, and the extent of COPD progression using a multiplex assay/enzyme‐linked immunosorbent assay, Hemacolor kit, terminal deoxynucleotidyl transferase nick‐end labeling assay, and the mean linear intercept and lung function, respectively. Results The results suggest that both oral bacterial species contributed to the periodontitis phenotype, promoted PPE‐induced proinflammatory cytokines in serum and bronchoalveolar lavage, and facilitated neutrophil infiltration in the lung. The abundance of neutrophils increased neutrophil elastase (NE) and downstream placenta growth factor (PGF) in the lung and led to alveolar epithelial cell apoptosis, pulmonary emphysema and lung function decline in the PPE‐treated mice. All pathological phenotype were attenuated by Ly6G antibody‐mediated neutrophil depletion in mice. Conclusions We demonstrated a potential mechanism for periodontal‐associated progression to COPD via the neutrophil‐NE‐PGF pathway. Plain Language Summary We demonstrated that the oral bacteria <jats:italic>Porphyromonas gingivalis</jats:italic> and <jats:italic>Scardovia wiggsiae</jats:italic> exacerbate ligature‐induced inflammation and increase proinflammatory cytokines in local gingival crevicular fluid, systemic serum, and distal bronchoalveolar lavage, and are associated with more neutrophil infiltration in the lung. The in vivo experiment indicated that gingival infection with <jats:italic>P. gingivalis</jats:italic> and <jats:italic>S. wiggsiae</jats:italic> worsens porcine pancreatic elastase‐induced pulmonary apoptosis and emphysema. Here, we show that <jats:italic>P. gingivalis and S. wiggsiae</jats:italic> are potential pathogenic factors for COPD.","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"20 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Takanari Miyamoto, Michael McGuire, E. Todd Scheyer, Becki Cole, Rick Heard, Shayan Barootchi
Background The purpose of this study is to report on the development of an artificial intelligence (AI) model designed to improve compliance in periodontal maintenance patients. Methods Fifty adult patients (32 females and 18 males; aged 25 to 78 years) with diagnosis and treatment of Generalized or Localized Periodontitis stages I, II, or III; grades A–C who were following a 3‐month periodontal maintenance interval were provided an AI‐based smartphone application (app) that provided personalized educational, motivational, and risk‐awareness information every week between maintenance visits. Recession (REC), probing pocket depth (PPD), clinical attachment level (CAL), plaque index (PI), bleeding on probing (BOP), and gingival index (GI) captured at each maintenance visit out to 6 months were compared with baseline. In‐office interviews were conducted to assess subjective data points, and cognitive interviews were conducted to validate patient‐reported outcomes (PRO). Results REC, PPD, and CAL remained stable through all timepoints. PI, BOP, and GI demonstrated significant improvement compared with baseline ( <jats:italic>p</jats:italic> < 0.01). PRO were validated and revealed that most subjects found the app to be easy to use, desired more interaction, perceived it as educational by raising their awareness of their oral hygiene, and would recommend the use of the app to a friend. Conclusions An AI‐based smartphone application was trained on a private practice maintenance population of three periodontists. The subjects demonstrated improvements in PI, BOP, and GI with no changes in REC, PPD, or CAL. Patients found the app to be educational and beneficial by improving their understanding of their periodontal disease risk. Plain language summary An artificial intelligence model (AI) was developed to improve periodontal maintenance compliance. Compliance with periodontal maintenance in patients decreases dramatically after 1 year. This is a proof‐of‐concept study using an AI‐based smartphone application (app) that communicates individualized periodontal disease risk awareness messages that were educational and motivational to effect a behavioral change in hopes of improving compliance. Measurements of disease stability/instability, such as gum inflammation, bleeding, bone loss, and assessment of brushing effectiveness, were captured at baseline and at subsequent office visits every 3 months for a total of 6 months. Subjective patient information was captured via in‐office interviews to supplement clinical data and provide the AI model with multimodal data points. Patient‐reported outcome surveys were developed via cognitive interviews. Results showed improvements in brushing effectiveness, which translated to less gum bleeding and inflammation. Other clinical measurements of disease activity showed no change, which could translate to a lack of disease progression. Patient‐reported outcome development revealed that most of the subjects found the i
{"title":"Development of an artificial intelligence platform to improve compliance in periodontal maintenance patients: A proof‐of‐concept study","authors":"Takanari Miyamoto, Michael McGuire, E. Todd Scheyer, Becki Cole, Rick Heard, Shayan Barootchi","doi":"10.1002/jper.25-0037","DOIUrl":"https://doi.org/10.1002/jper.25-0037","url":null,"abstract":"Background The purpose of this study is to report on the development of an artificial intelligence (AI) model designed to improve compliance in periodontal maintenance patients. Methods Fifty adult patients (32 females and 18 males; aged 25 to 78 years) with diagnosis and treatment of Generalized or Localized Periodontitis stages I, II, or III; grades A–C who were following a 3‐month periodontal maintenance interval were provided an AI‐based smartphone application (app) that provided personalized educational, motivational, and risk‐awareness information every week between maintenance visits. Recession (REC), probing pocket depth (PPD), clinical attachment level (CAL), plaque index (PI), bleeding on probing (BOP), and gingival index (GI) captured at each maintenance visit out to 6 months were compared with baseline. In‐office interviews were conducted to assess subjective data points, and cognitive interviews were conducted to validate patient‐reported outcomes (PRO). Results REC, PPD, and CAL remained stable through all timepoints. PI, BOP, and GI demonstrated significant improvement compared with baseline ( <jats:italic>p</jats:italic> < 0.01). PRO were validated and revealed that most subjects found the app to be easy to use, desired more interaction, perceived it as educational by raising their awareness of their oral hygiene, and would recommend the use of the app to a friend. Conclusions An AI‐based smartphone application was trained on a private practice maintenance population of three periodontists. The subjects demonstrated improvements in PI, BOP, and GI with no changes in REC, PPD, or CAL. Patients found the app to be educational and beneficial by improving their understanding of their periodontal disease risk. Plain language summary An artificial intelligence model (AI) was developed to improve periodontal maintenance compliance. Compliance with periodontal maintenance in patients decreases dramatically after 1 year. This is a proof‐of‐concept study using an AI‐based smartphone application (app) that communicates individualized periodontal disease risk awareness messages that were educational and motivational to effect a behavioral change in hopes of improving compliance. Measurements of disease stability/instability, such as gum inflammation, bleeding, bone loss, and assessment of brushing effectiveness, were captured at baseline and at subsequent office visits every 3 months for a total of 6 months. Subjective patient information was captured via in‐office interviews to supplement clinical data and provide the AI model with multimodal data points. Patient‐reported outcome surveys were developed via cognitive interviews. Results showed improvements in brushing effectiveness, which translated to less gum bleeding and inflammation. Other clinical measurements of disease activity showed no change, which could translate to a lack of disease progression. Patient‐reported outcome development revealed that most of the subjects found the i","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"3 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luiz G. Fiorin, Henrique Rinaldi Matheus, Gabriela Carrara Simionato, Ester Oliveira Santos, Ruan Delmonica Barra, Francisley Avila Souza, Edilson Ervolino, Claudia Dellavia, Juliano M de Almeida
Background The proposition of the present study was to evaluate the influence of the secondary effect of tamoxifen (TAM) associated with cisplatin (CIS) in the bone remodeling of osseointegrated titanium implants installed in rat tibiae. Methods One hundred female rats underwent bilateral ovariectomy (OVX) and received titanium implants in both tibiae. Six weeks later, animals were treated with tamoxifen (15 mg/kg) or saline, with further subdivisions receiving cisplatin (5 mg/kg or 2.5 mg/kg) or saline. A non‐ovariectomized group served as a negative control. Animals were euthanized at 30 and 90 days after treatment initiation. Tibiae were harvested for histometric analysis of bone‐to‐implant contact (BIC) and bone ingrowth (BIN), histology, and immunohistochemistry (tartrate‐resistant acid phosphatase [TRAP], osteocalcin [OCN], and runt‐related transcription factor [RUNX2]). Additionally, scanning electron microscopy (SEM) and energy‐dispersive X‐ray spectroscopy (EDS) were used for ultrastructural and elemental analyses. Results The groups that received TAM showed higher BIC and BIN, increased expression of RUNX‐2 and OCN, and a lower number of TRAP‐positive cells. At 30 and 90 days, almost all spaces were filled with vital, well‐vascularized bone tissue without inflammatory foci. TAM groups also exhibited an increased calcium/phosphate (Ca/P) ratio compared to their respective controls, and a progressive thickening of collagen fibril bundles was observed in the bone matrix. Conclusion Tamoxifen positively influenced bone remodeling around osseointegrated titanium implants in rats undergoing cisplatin‐based cancer therapy. Plain Language Summary Dental implant surgery in patients undergoing chemotherapy is frequently approached with caution, as these pharmacological treatments can impair bone metabolism and jeopardize the integration of the implant with the bone. This study investigated whether tamoxifen, a medication widely utilized in breast cancer therapy, could potentially enhance bone healing around titanium implants, specifically when administered alongside the chemotherapeutic agent cisplatin. Utilizing a laboratory model that simulates postmenopausal bone loss, the research demonstrated that tamoxifen significantly improved both the volume and the structural quality of the bone surrounding the implants, partially mitigating the adverse effects associated with cisplatin. These findings are of clinical importance as they suggest that a history of chemotherapy should not be considered a definitive barrier to successful dental rehabilitation. Instead, with appropriate pharmacological support, dental implant procedures may be a more viable and predictable treatment option for cancer survivors than previously recognized. This research provides a foundation for clinicians to better evaluate the feasibility of oral rehabilitation in this patient population, ultimately aiming to improve their long‐term oral health and quality of life.
{"title":"Effects of cisplatin and tamoxifen chemotherapy on peri‐implant bone remodeling around titanium implants in ovariectomized rats: An in vivo study","authors":"Luiz G. Fiorin, Henrique Rinaldi Matheus, Gabriela Carrara Simionato, Ester Oliveira Santos, Ruan Delmonica Barra, Francisley Avila Souza, Edilson Ervolino, Claudia Dellavia, Juliano M de Almeida","doi":"10.1002/jper.70096","DOIUrl":"https://doi.org/10.1002/jper.70096","url":null,"abstract":"Background The proposition of the present study was to evaluate the influence of the secondary effect of tamoxifen (TAM) associated with cisplatin (CIS) in the bone remodeling of osseointegrated titanium implants installed in rat tibiae. Methods One hundred female rats underwent bilateral ovariectomy (OVX) and received titanium implants in both tibiae. Six weeks later, animals were treated with tamoxifen (15 mg/kg) or saline, with further subdivisions receiving cisplatin (5 mg/kg or 2.5 mg/kg) or saline. A non‐ovariectomized group served as a negative control. Animals were euthanized at 30 and 90 days after treatment initiation. Tibiae were harvested for histometric analysis of bone‐to‐implant contact (BIC) and bone ingrowth (BIN), histology, and immunohistochemistry (tartrate‐resistant acid phosphatase [TRAP], osteocalcin [OCN], and runt‐related transcription factor [RUNX2]). Additionally, scanning electron microscopy (SEM) and energy‐dispersive X‐ray spectroscopy (EDS) were used for ultrastructural and elemental analyses. Results The groups that received TAM showed higher BIC and BIN, increased expression of RUNX‐2 and OCN, and a lower number of TRAP‐positive cells. At 30 and 90 days, almost all spaces were filled with vital, well‐vascularized bone tissue without inflammatory foci. TAM groups also exhibited an increased calcium/phosphate (Ca/P) ratio compared to their respective controls, and a progressive thickening of collagen fibril bundles was observed in the bone matrix. Conclusion Tamoxifen positively influenced bone remodeling around osseointegrated titanium implants in rats undergoing cisplatin‐based cancer therapy. Plain Language Summary Dental implant surgery in patients undergoing chemotherapy is frequently approached with caution, as these pharmacological treatments can impair bone metabolism and jeopardize the integration of the implant with the bone. This study investigated whether tamoxifen, a medication widely utilized in breast cancer therapy, could potentially enhance bone healing around titanium implants, specifically when administered alongside the chemotherapeutic agent cisplatin. Utilizing a laboratory model that simulates postmenopausal bone loss, the research demonstrated that tamoxifen significantly improved both the volume and the structural quality of the bone surrounding the implants, partially mitigating the adverse effects associated with cisplatin. These findings are of clinical importance as they suggest that a history of chemotherapy should not be considered a definitive barrier to successful dental rehabilitation. Instead, with appropriate pharmacological support, dental implant procedures may be a more viable and predictable treatment option for cancer survivors than previously recognized. This research provides a foundation for clinicians to better evaluate the feasibility of oral rehabilitation in this patient population, ultimately aiming to improve their long‐term oral health and quality of life.","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"35 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Periodontology is entering a transformative era driven by advances in diagnostics, therapeutics, and digital integration. Emerging technologies and conceptual shifts are currently reshaping the specialty, with a focus on predictive, preventive, and personalized care. Salivary diagnostics, artificial intelligence, and sensor‐based monitoring are expanding the potential for early detection and individualized treatment. Innovations such as host modulation, regenerative therapies, gene and exosome delivery, and microbiome‐preserving strategies offer promising new avenues for managing periodontal disease. The increased use of digital workflows and robotics can be leveraged to enhance precision and efficiency in clinical settings. The future of periodontology will see clinicians working in interprofessional teams that share integrated health data and collaborate for systemic health management where the periodontist assumes the role of a “sentinel of inflammation” to help maintain oral and overall health. To meet these demands, educational programs must evolve to prepare practitioners for a data‐driven, patient‐centered landscape. Balancing technological innovation with equitable access and ethical frameworks will allow the clinicians of the future to deliver the best possible care to patients.
{"title":"The future of periodontology: Emerging technologies and conceptual shifts","authors":"Michael S. Reddy","doi":"10.1002/jper.70079","DOIUrl":"https://doi.org/10.1002/jper.70079","url":null,"abstract":"<jats:label/> Periodontology is entering a transformative era driven by advances in diagnostics, therapeutics, and digital integration. Emerging technologies and conceptual shifts are currently reshaping the specialty, with a focus on predictive, preventive, and personalized care. Salivary diagnostics, artificial intelligence, and sensor‐based monitoring are expanding the potential for early detection and individualized treatment. Innovations such as host modulation, regenerative therapies, gene and exosome delivery, and microbiome‐preserving strategies offer promising new avenues for managing periodontal disease. The increased use of digital workflows and robotics can be leveraged to enhance precision and efficiency in clinical settings. The future of periodontology will see clinicians working in interprofessional teams that share integrated health data and collaborate for systemic health management where the periodontist assumes the role of a “sentinel of inflammation” to help maintain oral and overall health. To meet these demands, educational programs must evolve to prepare practitioners for a data‐driven, patient‐centered landscape. Balancing technological innovation with equitable access and ethical frameworks will allow the clinicians of the future to deliver the best possible care to patients.","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"59 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background While discrepancies in periodontal diagnosis and classification among dental providers with various educational backgrounds have been reported when the 2017 Classification of Periodontal Conditions was applied, the cognitive reasoning processes underlying these discrepancies remain underexplored. This observational study investigated the underlying reasoning for errors in periodontal assessment and diagnosis by analyzing dental students’ responses to open‐ended questions (OEQs) using a mixed‐methods approach. Methods A total of 138 dental students responded to three OEQs addressing periodontal diagnosis, risk factor identification, and periodontitis staging. Quantitative analysis using descriptive statistics assessed overall performance. Qualitative content analysis—independently conducted by two investigators—identified key periodontal diagnostic terms and reasoning trends. Alluvial plots visualized cognitive reasoning pathways. Results Only 39 respondents (28%) correctly diagnosed a gingivitis case by integrating clinical and radiographic assessments. Fifty‐three respondents (38%) answered smoking as the appropriate risk factor for periodontal disease; the remaining included systemic diseases, etiologic and local contributing factors, and/or clinical signs along with smoking. One hundred respondents (72%) correctly assigned Stage III for a periodontitis case, which demonstrated the highest accuracy among the three tasks; the remaining showed an overestimation tendency, often skipping consideration of tooth loss and overemphasizing case complexity. Conclusion The study findings revealed that diagnosing gingivitis was more challenging than determining periodontitis stage, with an overestimation tendency by relying on a single parameter, such as pocket depth. Difficulty in integrating clinical and radiographic data and interpreting case complexity contributed to misdiagnosis and incorrect periodontitis staging. Plain language summary This study explored how dental students think through periodontal cases by analyzing their written responses to three OEQs on real‐world case scenarios involving periodontal diagnosis, risk factor identification, and periodontitis staging. Among 138 respondents, 28% correctly diagnosed the gingivitis case; 38% identified smoking as the risk factor; 72% correctly assigned Stage III. Common errors included overreliance on probing depth, limited use or misinterpretation of bone loss on radiographs. For staging, respondents frequently overlooked the number of teeth lost due to periodontitis and overweighted isolated periodontal complexity features, leading to overrating. These findings indicate a need for structured, case‐based training emphasizing integration of clinical and radiographic data to improve diagnostic accuracy.
{"title":"Reasoning behind discrepancies in periodontal diagnosis and classification: A mixed‐methods analysis","authors":"Seok‐Mo Heo, Thomas W. Oates, Se‐Lim Oh","doi":"10.1002/jper.70083","DOIUrl":"https://doi.org/10.1002/jper.70083","url":null,"abstract":"Background While discrepancies in periodontal diagnosis and classification among dental providers with various educational backgrounds have been reported when the 2017 Classification of Periodontal Conditions was applied, the cognitive reasoning processes underlying these discrepancies remain underexplored. This observational study investigated the underlying reasoning for errors in periodontal assessment and diagnosis by analyzing dental students’ responses to open‐ended questions (OEQs) using a mixed‐methods approach. Methods A total of 138 dental students responded to three OEQs addressing periodontal diagnosis, risk factor identification, and periodontitis staging. Quantitative analysis using descriptive statistics assessed overall performance. Qualitative content analysis—independently conducted by two investigators—identified key periodontal diagnostic terms and reasoning trends. Alluvial plots visualized cognitive reasoning pathways. Results Only 39 respondents (28%) correctly diagnosed a gingivitis case by integrating clinical and radiographic assessments. Fifty‐three respondents (38%) answered smoking as the appropriate risk factor for periodontal disease; the remaining included systemic diseases, etiologic and local contributing factors, and/or clinical signs along with smoking. One hundred respondents (72%) correctly assigned Stage III for a periodontitis case, which demonstrated the highest accuracy among the three tasks; the remaining showed an overestimation tendency, often skipping consideration of tooth loss and overemphasizing case complexity. Conclusion The study findings revealed that diagnosing gingivitis was more challenging than determining periodontitis stage, with an overestimation tendency by relying on a single parameter, such as pocket depth. Difficulty in integrating clinical and radiographic data and interpreting case complexity contributed to misdiagnosis and incorrect periodontitis staging. Plain language summary This study explored how dental students think through periodontal cases by analyzing their written responses to three OEQs on real‐world case scenarios involving periodontal diagnosis, risk factor identification, and periodontitis staging. Among 138 respondents, 28% correctly diagnosed the gingivitis case; 38% identified smoking as the risk factor; 72% correctly assigned Stage III. Common errors included overreliance on probing depth, limited use or misinterpretation of bone loss on radiographs. For staging, respondents frequently overlooked the number of teeth lost due to periodontitis and overweighted isolated periodontal complexity features, leading to overrating. These findings indicate a need for structured, case‐based training emphasizing integration of clinical and radiographic data to improve diagnostic accuracy.","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"41 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Raquel de S. F Nassar, Marcella C. Ribeiro, Ana Carolina P. Hernandes, Laura Z. Gianduzzo, Vanessa de P. S. Pereira, Sérgio L. S. Salvador, Edilson Ervolino, Débora S. F. Sávio, Michel R. Messora, Flávia A. C. Furlaneto
Background Prebiotic therapy is a promising approach for managing periodontitis due to its potential benefits in modulating the microbiome and the immune response. This study aimed to evaluate the effects of the prebiotic (PREB) polydextrose (PDX) on the development of experimental periodontitis (EP) in rats. Methods A total of 44 male adult rats ( Rattus norvegicus, albinus , Wistar) were randomly allocated into groups ( n = 11) C (control), PREB, EP, and EP/PREB. The PREB and EP/PREB groups received 2 g of PDX/day in the drinking water for 44 days. The EP and EP/PREB groups received cotton ligatures around mandibular first molars (M1) for 14 days. Microtomographic, histopathological, and immunohistochemical analyses of periodontal and intestinal tissues were performed. Data were analyzed statistically ( p < 0.05). Results The EP/PREB group showed less alveolar bone destruction than the EP group. The EP/PREB group exhibited higher expressions of IL‐10 and a lower number of TRAP (tartrate‐resistant acid phosphatase)‐positive cells than the EP group in periodontal tissues. The EP/PREB group had increased villus heights in the duodenum and ileum, increased crypt depths in the duodenum, and higher expressions of occludin in all intestinal portions, claudin‐1 in the jejunum, IL‐10 in the duodenum, and lower expressions of IL‐1β in the jejunum compared with the EP group. Conclusion Polydextrose exerted a protective effect against alveolar bone resorption and favorably modulated both local and systemic immune‐inflammatory response in rats with experimental periodontitis. Plain language summary Prebiotic therapy has emerged as a promising approach for treating periodontitis, an immunoinflammatory disease associated with a dysbiotic biofilm that leads to the loss of the supporting structures of the teeth. This is because prebiotics can positively influence the balance of bacteria in the body and the immune system's response. However, current understanding of its potential effects and mechanisms of action remains limited in periodontal therapy. The effects of the prebiotic polydextrose (PDX) on periodontal tissues remain unknown. The results of the present study show that the prebiotic PDX can minimize alveolar bone loss and improve bone microarchitecture through modulation of the immune‐inflammatory response in both intestinal and periodontal tissues of rats with experimental periodontitis. Our findings suggest that the prebiotic PDX may represent a beneficial adjunctive strategy for managing periodontitis.
{"title":"Immunological and periodontal benefits of prebiotic polydextrose in rats with induced periodontitis","authors":"Raquel de S. F Nassar, Marcella C. Ribeiro, Ana Carolina P. Hernandes, Laura Z. Gianduzzo, Vanessa de P. S. Pereira, Sérgio L. S. Salvador, Edilson Ervolino, Débora S. F. Sávio, Michel R. Messora, Flávia A. C. Furlaneto","doi":"10.1002/jper.70095","DOIUrl":"https://doi.org/10.1002/jper.70095","url":null,"abstract":"Background Prebiotic therapy is a promising approach for managing periodontitis due to its potential benefits in modulating the microbiome and the immune response. This study aimed to evaluate the effects of the prebiotic (PREB) polydextrose (PDX) on the development of experimental periodontitis (EP) in rats. Methods A total of 44 male adult rats ( <jats:italic>Rattus norvegicus, albinus</jats:italic> , Wistar) were randomly allocated into groups ( <jats:italic>n</jats:italic> = 11) C (control), PREB, EP, and EP/PREB. The PREB and EP/PREB groups received 2 g of PDX/day in the drinking water for 44 days. The EP and EP/PREB groups received cotton ligatures around mandibular first molars (M1) for 14 days. Microtomographic, histopathological, and immunohistochemical analyses of periodontal and intestinal tissues were performed. Data were analyzed statistically ( <jats:italic>p</jats:italic> < 0.05). Results The EP/PREB group showed less alveolar bone destruction than the EP group. The EP/PREB group exhibited higher expressions of IL‐10 and a lower number of TRAP (tartrate‐resistant acid phosphatase)‐positive cells than the EP group in periodontal tissues. The EP/PREB group had increased villus heights in the duodenum and ileum, increased crypt depths in the duodenum, and higher expressions of occludin in all intestinal portions, claudin‐1 in the jejunum, IL‐10 in the duodenum, and lower expressions of IL‐1β in the jejunum compared with the EP group. Conclusion Polydextrose exerted a protective effect against alveolar bone resorption and favorably modulated both local and systemic immune‐inflammatory response in rats with experimental periodontitis. Plain language summary Prebiotic therapy has emerged as a promising approach for treating periodontitis, an immunoinflammatory disease associated with a dysbiotic biofilm that leads to the loss of the supporting structures of the teeth. This is because prebiotics can positively influence the balance of bacteria in the body and the immune system's response. However, current understanding of its potential effects and mechanisms of action remains limited in periodontal therapy. The effects of the prebiotic polydextrose (PDX) on periodontal tissues remain unknown. The results of the present study show that the prebiotic PDX can minimize alveolar bone loss and improve bone microarchitecture through modulation of the immune‐inflammatory response in both intestinal and periodontal tissues of rats with experimental periodontitis. Our findings suggest that the prebiotic PDX may represent a beneficial adjunctive strategy for managing periodontitis.","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"50 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146215869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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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