BackgroundB‐cell‑specific Moloney MLV insertion site‐1(Bmi‐1)is a crucial osteopenic target molecule. The aim of this study is to explore the effects of Bmi‐1 on alveolar bone resorption and the underlying mechanisms in vitro and vivo.MethodsA <jats:italic>Bmi‐1</jats:italic>‐knockout (<jats:italic>Bmi‐1<jats:sup>−/−</jats:sup></jats:italic>) mouse model was used to investigate the effect of Bmi‐1 on alveolar bone metabolism, with micro‐computed tomography imaging, histology, and immunohistochemistry staining. Furthermore, we utilized a ligature‐induced experimental periodontitis model to examine the impact of <jats:italic>Bmi‐1</jats:italic>‐knockdown (<jats:italic>Bmi‐1</jats:italic><jats:sup>±</jats:sup>) on inflammatory alveolar bone resorption. Finally, we stimulated human periodontal ligament stem cells (hPDLSCs) with lipopolysaccharide (LPS) to explore the potential mechanism of Bmi‐1 overexpression in the process of osteogenesis.ResultsCompared with wild‐type mice, <jats:italic>Bmi‐1</jats:italic><jats:sup>−/−</jats:sup> mice demonstrated more alveolar bone resorption by inhibiting osteogenesis, which was characterized by decreases in Runt‐related transcription factor 2 and type 1 collagen formation. In addition, <jats:italic>Bmi‐1<jats:sup>−/−</jats:sup></jats:italic> mice had lower levels of autophagy markers such as Parkin and LC3, but higher levels of inflammation‐related factors such as interleukin (IL)‐6 and IL‐1β in periodontal tissues. In addition, <jats:italic>Bmi‐1</jats:italic>‐knockdown aggravated ligature‐induced alveolar bone loss. Under in vitro inflammatory conditions, Bmi‐1 overexpression stimulated osteoblast differentiation and inhibited the production of inflammatory factors, as well as the autophagy and apoptosis in hPDLSCs stimulated with LPS. When 3‐methyladenine (3‐MA), an autophagy inhibitor, was added, the osteogenic effect of Bmi‐1 was further enhanced.ConclusionsBmi‐1 alleviates alveolar bone resorption by regulating autophagy, indicating that it could be a potential target for periodontitis prevention and treatment.Plain Language SummaryPeriodontitis is a chronic inflammatory disease, which leads to progressive destruction of periodontal tissues, manifested as periodontal pocket formation, loss of periodontal attachment and alveolar bone resorption. Currently, there is a lack of effective treatments to regenerate damaged periodontal tissues. Therefore, it is of great clinical significance to explore new mechanisms of periodontitis and effective intervention targets. B‐cell‑specific Moloney MLV insertion site‐1 (Bmi‐1) is involved in the regulation of the cell cycle, DNA damage repair, autophagy, bone metabolism, tumor, and other physiopathological processes. Autophagy, as an important mechanism of intracellular self‐regulation, plays an indispensable role in the destruction and repair of periodontal tissues. The aim of this study was to investigate the role of Bmi‐1 on periodontal tissues and its intrinsic mec
{"title":"Bmi‐1 alleviates alveolar bone resorption through the regulation of autophagy","authors":"Yiting Chu, Shuying Liu, Lixueer Yan, Aixiu Gong","doi":"10.1002/jper.23-0796","DOIUrl":"https://doi.org/10.1002/jper.23-0796","url":null,"abstract":"BackgroundB‐cell‑specific Moloney MLV insertion site‐1(Bmi‐1)is a crucial osteopenic target molecule. The aim of this study is to explore the effects of Bmi‐1 on alveolar bone resorption and the underlying mechanisms in vitro and vivo.MethodsA <jats:italic>Bmi‐1</jats:italic>‐knockout (<jats:italic>Bmi‐1<jats:sup>−/−</jats:sup></jats:italic>) mouse model was used to investigate the effect of Bmi‐1 on alveolar bone metabolism, with micro‐computed tomography imaging, histology, and immunohistochemistry staining. Furthermore, we utilized a ligature‐induced experimental periodontitis model to examine the impact of <jats:italic>Bmi‐1</jats:italic>‐knockdown (<jats:italic>Bmi‐1</jats:italic><jats:sup>±</jats:sup>) on inflammatory alveolar bone resorption. Finally, we stimulated human periodontal ligament stem cells (hPDLSCs) with lipopolysaccharide (LPS) to explore the potential mechanism of Bmi‐1 overexpression in the process of osteogenesis.ResultsCompared with wild‐type mice, <jats:italic>Bmi‐1</jats:italic><jats:sup>−/−</jats:sup> mice demonstrated more alveolar bone resorption by inhibiting osteogenesis, which was characterized by decreases in Runt‐related transcription factor 2 and type 1 collagen formation. In addition, <jats:italic>Bmi‐1<jats:sup>−/−</jats:sup></jats:italic> mice had lower levels of autophagy markers such as Parkin and LC3, but higher levels of inflammation‐related factors such as interleukin (IL)‐6 and IL‐1β in periodontal tissues. In addition, <jats:italic>Bmi‐1</jats:italic>‐knockdown aggravated ligature‐induced alveolar bone loss. Under in vitro inflammatory conditions, Bmi‐1 overexpression stimulated osteoblast differentiation and inhibited the production of inflammatory factors, as well as the autophagy and apoptosis in hPDLSCs stimulated with LPS. When 3‐methyladenine (3‐MA), an autophagy inhibitor, was added, the osteogenic effect of Bmi‐1 was further enhanced.ConclusionsBmi‐1 alleviates alveolar bone resorption by regulating autophagy, indicating that it could be a potential target for periodontitis prevention and treatment.Plain Language SummaryPeriodontitis is a chronic inflammatory disease, which leads to progressive destruction of periodontal tissues, manifested as periodontal pocket formation, loss of periodontal attachment and alveolar bone resorption. Currently, there is a lack of effective treatments to regenerate damaged periodontal tissues. Therefore, it is of great clinical significance to explore new mechanisms of periodontitis and effective intervention targets. B‐cell‑specific Moloney MLV insertion site‐1 (Bmi‐1) is involved in the regulation of the cell cycle, DNA damage repair, autophagy, bone metabolism, tumor, and other physiopathological processes. Autophagy, as an important mechanism of intracellular self‐regulation, plays an indispensable role in the destruction and repair of periodontal tissues. The aim of this study was to investigate the role of Bmi‐1 on periodontal tissues and its intrinsic mec","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"1 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142276942","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}
BackgroundThe aim of this study was to investigate the potential association between vitamin D deficiency and matrix metalloproteinase‐9 (MMP‐9) levels in gingival crevicular fluid (GCF) across various periodontal health and disease statuses.MethodsA total of 200 volunteers were divided into two groups according to serum vitamin D concentration (25(OH)D < 10 ng/mL and 25(OH)D ≥ 10 ng/mL). Periodontal health status was determined based on a full‐mouth periodontal examination and radiographic evaluation. Participants in both groups were categorized according to periodontal diagnoses, encompassing periodontal health, gingivitis, and periodontitis. Following sampling, the MMP‐9 levels in GCF were determined by the enzyme‐linked immunosorbent assay (ELISA) method.ResultsThe GCF MMP‐9 levels were found to be higher in individuals with serum 25(OH)D < 10 ng/mL, in both the healthy and gingivitis and periodontitis groups, compared to those with 25(OH)D ≥ 10 ng/mL. Nevertheless, a statistically significant distinction was observed exclusively within the gingivitis and periodontitis groups. Correlation analysis and robust regression analyses provided additional evidence supporting the predictive role of periodontal disease status and vitamin D concentration in local MMP‐9 levels. These associations remained significant after adjusting for age and sex in robust regression analysis (<jats:italic>p</jats:italic> = 0.002). Furthermore, the inclusion of periodontal clinical parameters in the regression analysis revealed notable associations of clinical attachment loss with local MMP‐9 levels, along with periodontal disease status and serum vitamin D concentration (<jats:italic>p</jats:italic> < 0.001).ConclusionThe findings of our study suggest a potential mechanistic relationship between serum vitamin D levels and periodontitis.PLAIN LANGUAGE SUMMARYVitamin D deficiency is a widespread issue globally due to urban living, less outdoor time, seasonal changes, aging, and sunscreen use, leading to inadequate sun exposure. Low vitamin D levels are linked to several health problems, including hypertension, diabetes, heart diseases, and periodontal diseases, which affect the gums and bones around teeth and can cause tooth loss if untreated. Although the link between vitamin D and periodontal disease is unclear, it may involve the enzyme matrix metalloproteinase‐9 (MMP‐9). Our study examined 200 people, dividing them into two groups based on vitamin D levels. We assessed their gum health and measured MMP‐9 levels in their gingival crevicular fluid, a liquid that seeps out from the tiny space between gums and teeth. We found that people with lower vitamin D levels had higher MMP‐9 levels, especially those with gum disease. Our analysis showed that both vitamin D levels and gum health significantly impact MMP‐9 levels, with gum health being the more influential factor. Maintaining good gum health and adequate vitamin D levels is crucial for managing MMP‐9, an e
背景 本研究旨在探讨维生素D缺乏与不同牙周健康和疾病状态下牙龈缝隙液（GCF）中基质金属蛋白酶-9（MMP-9）水平之间的潜在关联。方法 根据血清维生素D浓度（25(OH)D < 10 ng/mL和25(OH)D ≥ 10 ng/mL）将200名志愿者分为两组。牙周健康状况根据全口牙周检查和放射学评估确定。两组参与者均根据牙周诊断进行分类，包括牙周健康、牙龈炎和牙周炎。采样后，采用酶联免疫吸附试验（ELISA）法测定 GCF 中的 MMP-9 含量。结果发现，在健康组、牙龈炎组和牙周炎组中，与血清 25(OH)D≥10 纳克/毫升的人相比，血清 25(OH)D≥10 纳克/毫升的人的 GCF MMP-9 含量更高。然而，仅在牙龈炎和牙周炎组中观察到了统计学上的显著差异。相关性分析和稳健回归分析提供了更多证据，支持牙周病状态和维生素 D 浓度对当地 MMP-9 水平的预测作用。在稳健回归分析中对年龄和性别进行调整后，这些相关性仍然显著（p = 0.002）。此外，将牙周临床参数纳入回归分析后发现，临床附着丧失与局部 MMP-9 水平以及牙周疾病状态和血清维生素 D 浓度都有显著关联（p < 0.001）。维生素 D 含量低与多种健康问题有关，包括高血压、糖尿病、心脏病和牙周病，牙周病会影响牙齿周围的牙龈和骨骼，如不及时治疗会导致牙齿脱落。虽然维生素 D 与牙周病之间的联系尚不清楚，但可能与基质金属蛋白酶-9（MMP-9）有关。我们的研究调查了 200 人，根据维生素 D 水平将他们分为两组。我们评估了他们的牙龈健康状况，并测量了他们牙龈缝隙液（一种从牙龈和牙齿之间的微小空间渗出的液体）中的MMP-9水平。我们发现，维生素 D 水平较低的人 MMP-9 水平较高，尤其是患有牙龈疾病的人。我们的分析表明，维生素 D 水平和牙龈健康都会对 MMP-9 水平产生重大影响，而牙龈健康是影响更大的因素。保持良好的牙龈健康和充足的维生素 D 水平对管理 MMP-9 至关重要，MMP-9 是一种对愈合和炎症期间组织重塑至关重要的酶。然而，过量的 MMP 可能会迅速破坏牙周组织。
{"title":"Serum vitamin D concentration is inversely associated with matrix metalloproteinase‐9 level in periodontal diseases","authors":"Yeşim Ayhan Yıldırım, Ayla Ozturk, Fatma Doğruel, Hatice Saraçoğlu, Cevat Yazıcı","doi":"10.1002/jper.24-0106","DOIUrl":"https://doi.org/10.1002/jper.24-0106","url":null,"abstract":"BackgroundThe aim of this study was to investigate the potential association between vitamin D deficiency and matrix metalloproteinase‐9 (MMP‐9) levels in gingival crevicular fluid (GCF) across various periodontal health and disease statuses.MethodsA total of 200 volunteers were divided into two groups according to serum vitamin D concentration (25(OH)D < 10 ng/mL and 25(OH)D ≥ 10 ng/mL). Periodontal health status was determined based on a full‐mouth periodontal examination and radiographic evaluation. Participants in both groups were categorized according to periodontal diagnoses, encompassing periodontal health, gingivitis, and periodontitis. Following sampling, the MMP‐9 levels in GCF were determined by the enzyme‐linked immunosorbent assay (ELISA) method.ResultsThe GCF MMP‐9 levels were found to be higher in individuals with serum 25(OH)D < 10 ng/mL, in both the healthy and gingivitis and periodontitis groups, compared to those with 25(OH)D ≥ 10 ng/mL. Nevertheless, a statistically significant distinction was observed exclusively within the gingivitis and periodontitis groups. Correlation analysis and robust regression analyses provided additional evidence supporting the predictive role of periodontal disease status and vitamin D concentration in local MMP‐9 levels. These associations remained significant after adjusting for age and sex in robust regression analysis (<jats:italic>p</jats:italic> = 0.002). Furthermore, the inclusion of periodontal clinical parameters in the regression analysis revealed notable associations of clinical attachment loss with local MMP‐9 levels, along with periodontal disease status and serum vitamin D concentration (<jats:italic>p</jats:italic> < 0.001).ConclusionThe findings of our study suggest a potential mechanistic relationship between serum vitamin D levels and periodontitis.PLAIN LANGUAGE SUMMARYVitamin D deficiency is a widespread issue globally due to urban living, less outdoor time, seasonal changes, aging, and sunscreen use, leading to inadequate sun exposure. Low vitamin D levels are linked to several health problems, including hypertension, diabetes, heart diseases, and periodontal diseases, which affect the gums and bones around teeth and can cause tooth loss if untreated. Although the link between vitamin D and periodontal disease is unclear, it may involve the enzyme matrix metalloproteinase‐9 (MMP‐9). Our study examined 200 people, dividing them into two groups based on vitamin D levels. We assessed their gum health and measured MMP‐9 levels in their gingival crevicular fluid, a liquid that seeps out from the tiny space between gums and teeth. We found that people with lower vitamin D levels had higher MMP‐9 levels, especially those with gum disease. Our analysis showed that both vitamin D levels and gum health significantly impact MMP‐9 levels, with gum health being the more influential factor. Maintaining good gum health and adequate vitamin D levels is crucial for managing MMP‐9, an e","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"132 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277060","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}
BACKGROUNDBehçet's disease (BD) pathogenesis involves severe outcomes such as blindness, central nervous system manifestations, and deep venous thrombosis that impacts systemic and local inflammatory changes. We tested the hypothesis that BD negatively affects gingival health and increases the severity of gingivitis.METHODSThe study included 37 BD patients with gingivitis without any sign of periodontitis. Systemically healthy 19 patients with gingivitis (G) and 20 periodontally and systemically healthy individuals (C) were recruited as controls. BD patients were further grouped as stable and unstable based on their responses to BD treatment. Clinical periodontal parameters were measured to determine the impact of BD on gingival health. Serum and saliva levels of ELA-2 (neutrophil elastase-2), SLPI (secretory leukocyte protease inhibitor), α1-AT (alpha1-anti-trypsin), VEGF (vascular endothelial growth factor), IL-6 (interleukin-6), IL-8 (interleukin-8), and TNF-α (tumor necrosis factor alpha) were analyzed using multiplex immunoassay to measure the systemic and local inflammatory impact of BD.RESULTSPlaque index (PI), probing pocket depth (PPD), and bleeding on probing (BOP) were significantly higher in the BD group than in the controls (p < 0.05). IL-6 was higher in both serum and saliva in the BD group than in the G group (p < 0.05). ELA-2 levels in saliva were higher in the stable BD group than in the controls, while TNF-α and SLPI were statistically significantly higher in BD than in the control (p < 0.05). Salivary α1-AT level was statistically lower in the BD group compared to the control group.CONCLUSIONOur study suggested that the gingival inflammatory profile was impaired in patients with BD.
{"title":"Behçet's disease modifies the gingival inflammatory response.","authors":"Selin Sahinkaya,Melis Yilmaz,Ekin Yay,Hilal Toygar,Nur Balci,Dursun Dorukhan Altinisik,Zekayi Kutlubay,Alpdogan Kantarci","doi":"10.1002/jper.24-0182","DOIUrl":"https://doi.org/10.1002/jper.24-0182","url":null,"abstract":"BACKGROUNDBehçet's disease (BD) pathogenesis involves severe outcomes such as blindness, central nervous system manifestations, and deep venous thrombosis that impacts systemic and local inflammatory changes. We tested the hypothesis that BD negatively affects gingival health and increases the severity of gingivitis.METHODSThe study included 37 BD patients with gingivitis without any sign of periodontitis. Systemically healthy 19 patients with gingivitis (G) and 20 periodontally and systemically healthy individuals (C) were recruited as controls. BD patients were further grouped as stable and unstable based on their responses to BD treatment. Clinical periodontal parameters were measured to determine the impact of BD on gingival health. Serum and saliva levels of ELA-2 (neutrophil elastase-2), SLPI (secretory leukocyte protease inhibitor), α1-AT (alpha1-anti-trypsin), VEGF (vascular endothelial growth factor), IL-6 (interleukin-6), IL-8 (interleukin-8), and TNF-α (tumor necrosis factor alpha) were analyzed using multiplex immunoassay to measure the systemic and local inflammatory impact of BD.RESULTSPlaque index (PI), probing pocket depth (PPD), and bleeding on probing (BOP) were significantly higher in the BD group than in the controls (p < 0.05). IL-6 was higher in both serum and saliva in the BD group than in the G group (p < 0.05). ELA-2 levels in saliva were higher in the stable BD group than in the controls, while TNF-α and SLPI were statistically significantly higher in BD than in the control (p < 0.05). Salivary α1-AT level was statistically lower in the BD group compared to the control group.CONCLUSIONOur study suggested that the gingival inflammatory profile was impaired in patients with BD.","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"49 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142246838","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}
Triana Blanco-Pintos, Alba Regueira-Iglesias, Iryna Kuz, Alba Sánchez-Barco, Noelia Seijas-Otero, María Del Pilar Chantada-Vázquez, Carlos Balsa-Castro, Inmaculada Tomás
<p><strong>Background: </strong>Few investigations evaluated smoking's impact on the periodontal proteome. Therefore, this study aimed to analyse the influence of tobacco on the overall periodontal proteome and the differential expression of gingival crevicular fluid (GCF) proteins using sequential window acquisition of all theoretical mass spectra (SWATH-MS).</p><p><strong>Methods: </strong>GCF samples were collected from 40 periodontitis subjects (stages III-IV). These were separated based on smoking status into smokers (17), ex-smokers (10), and non-smokers (13). Samples were analysed using SWATH-MS, and proteins were identified using the UniProt human-specific database. Data are available via ProteomeXchange with the identifier PXD043474. Principal component analysis (PCA) was employed to examine the spectral mass distribution of the proteome. Protein expression was different for a p-value <0.05 and a log2 fold change ≥0.3 (upregulated) or ≤-0.3 (downregulated).</p><p><strong>Results: </strong>The distribution of overall proteome did not differ between non-smokers, smokers, and ex-smokers. Considering protein expression, 23 were differentially expressed in smokers vs. non-smokers (16 upregulated and 7 downregulated), 17 in ex-smokers vs. non-smokers (2 upregulated and 15 downregulated), and only 8 in smokers vs. ex-smokers (7 upregulated and 1 downregulated). Smoking increased the expression of proteins related to epithelial hyperkeratinization (keratins type II cytoskeletal 4, type I cytoskeletal 13 and type I cytoskeletal 19, cornulin, and fatty acid-binding protein 5). However, multiple immunoglobulins were underexpressed when comparing smokers and ex-smokers to non-smokers.</p><p><strong>Conclusion: </strong>Although smoking does not significantly modify the overall GCF proteome associated with periodontitis, it alters the expression of several proteins compared to never-smokers and ex-smokers.</p><p><strong>Plain language summary: </strong>Smoking is a critical risk factor for the development and progression of periodontitis. However, evidence of the effect of smoking on the subgingival proteome is scarce. Therefore, this study aimed to determine the impact of smoking on the overall proteome and differential expression of gingival crevicular fluid (GCF) proteins using the sequential window acquisition of all theoretical mass spectra (SWATH-MS) proteomic technique. For this purpose, GCF samples were collected from 40 subjects with periodontitis, of which 17 were smokers, 10 were ex-smokers, and 13 were non-smokers. These samples were analysed by SWATH-MS, and proteins were identified using the UniProt human-specific database. Analysis of the overall proteome showed that its distribution was not significantly different between smokers, ex-smokers, and non-smokers. However, several proteins were found to be differentially expressed according to the smoking status. Smoking can increase the expression of several keratins and proteins related
{"title":"Impact of smoking habit on the subgingival proteome in patients with periodontitis.","authors":"Triana Blanco-Pintos, Alba Regueira-Iglesias, Iryna Kuz, Alba Sánchez-Barco, Noelia Seijas-Otero, María Del Pilar Chantada-Vázquez, Carlos Balsa-Castro, Inmaculada Tomás","doi":"10.1002/JPER.24-0062","DOIUrl":"https://doi.org/10.1002/JPER.24-0062","url":null,"abstract":"<p><strong>Background: </strong>Few investigations evaluated smoking's impact on the periodontal proteome. Therefore, this study aimed to analyse the influence of tobacco on the overall periodontal proteome and the differential expression of gingival crevicular fluid (GCF) proteins using sequential window acquisition of all theoretical mass spectra (SWATH-MS).</p><p><strong>Methods: </strong>GCF samples were collected from 40 periodontitis subjects (stages III-IV). These were separated based on smoking status into smokers (17), ex-smokers (10), and non-smokers (13). Samples were analysed using SWATH-MS, and proteins were identified using the UniProt human-specific database. Data are available via ProteomeXchange with the identifier PXD043474. Principal component analysis (PCA) was employed to examine the spectral mass distribution of the proteome. Protein expression was different for a p-value <0.05 and a log2 fold change ≥0.3 (upregulated) or ≤-0.3 (downregulated).</p><p><strong>Results: </strong>The distribution of overall proteome did not differ between non-smokers, smokers, and ex-smokers. Considering protein expression, 23 were differentially expressed in smokers vs. non-smokers (16 upregulated and 7 downregulated), 17 in ex-smokers vs. non-smokers (2 upregulated and 15 downregulated), and only 8 in smokers vs. ex-smokers (7 upregulated and 1 downregulated). Smoking increased the expression of proteins related to epithelial hyperkeratinization (keratins type II cytoskeletal 4, type I cytoskeletal 13 and type I cytoskeletal 19, cornulin, and fatty acid-binding protein 5). However, multiple immunoglobulins were underexpressed when comparing smokers and ex-smokers to non-smokers.</p><p><strong>Conclusion: </strong>Although smoking does not significantly modify the overall GCF proteome associated with periodontitis, it alters the expression of several proteins compared to never-smokers and ex-smokers.</p><p><strong>Plain language summary: </strong>Smoking is a critical risk factor for the development and progression of periodontitis. However, evidence of the effect of smoking on the subgingival proteome is scarce. Therefore, this study aimed to determine the impact of smoking on the overall proteome and differential expression of gingival crevicular fluid (GCF) proteins using the sequential window acquisition of all theoretical mass spectra (SWATH-MS) proteomic technique. For this purpose, GCF samples were collected from 40 subjects with periodontitis, of which 17 were smokers, 10 were ex-smokers, and 13 were non-smokers. These samples were analysed by SWATH-MS, and proteins were identified using the UniProt human-specific database. Analysis of the overall proteome showed that its distribution was not significantly different between smokers, ex-smokers, and non-smokers. However, several proteins were found to be differentially expressed according to the smoking status. Smoking can increase the expression of several keratins and proteins related ","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289685","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}
{"title":"AAP President's Address*","authors":"David K. Okano","doi":"10.1002/JPER.24-0190","DOIUrl":"10.1002/JPER.24-0190","url":null,"abstract":"","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"95 10","pages":"1011-1013"},"PeriodicalIF":4.2,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231412","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}
BackgroundThe polarization of macrophages into an anti‐inflammatory phenotype is crucial for resolving periodontal inflammation. It has been reported that B10 cells can regulate the immune response of macrophages during inflammation and are also able to regulate inflammation in periodontitis. However, whether B10 cells’ regulation function in periodontitis is related to macrophage polarization remains unclear. This study aims to investigate whether B10 cells can regulate macrophage polarization in periodontitis.MethodsMacrophages were cocultured with B10 cells in vitro for 5 days. After coculture, macrophages were obtained for analysis directly or followed by stimulation with Pg‐LPS/IFN‐γ or IL‐4/IL‐13. Flow cytometry and/or reverse transcriptase‐polymerase chain reaction (RT‐PCR) were employed to detect the expression of IL‐1β, iNOS, TNF‐α, CD206, and ARG‐1 in macrophages. B10 cells were transferred on the 5th day after ligation in wild or macrophage‐depletion mice. Toluidine blue and TRAP staining were used to evaluate alveolar bone resorption and osteoclast activation. Immunohistochemistry was employed to detect the expression of CD68, IL‐1β, TNF‐α, iNOS, ARG‐1, and IL‐10. Immunofluorescence was used to detect the expression of CD68+CD86+M1 macrophages and CD68+CD206+M2 macrophages.ResultsIn vitro, B10 cells inhibit the expression of IL‐1β, iNOS, and TNF‐α in macrophages while increasing the expression of CD206 and ARG‐1. In experimental periodontitis, B10 cells inhibit the polarization of CD68+CD86+M1 macrophages and iNOS expression but enhance the polarization of CD68+CD206+M2 macrophages and ARG‐1 expression. Importantly, the depletion of macrophages partially weakened the regulation function of B10 cells in periodontitis.ConclusionsB10 cells promote M2 macrophage polarization, inhibit M1 macrophage polarization in periodontitis, and alleviate periodontitis partially by regulating macrophage polarization.
{"title":"B10 cells regulate macrophage polarization to alleviate inflammation and bone loss in periodontitis","authors":"Guoqin Cao, Qiuping Xu, Shengyuan Huang, Dong Dai, Jilei Wang, Wei Li, Yue Zhao, Jiang Lin, Xiaozhe Han","doi":"10.1002/jper.24-0114","DOIUrl":"https://doi.org/10.1002/jper.24-0114","url":null,"abstract":"BackgroundThe polarization of macrophages into an anti‐inflammatory phenotype is crucial for resolving periodontal inflammation. It has been reported that B10 cells can regulate the immune response of macrophages during inflammation and are also able to regulate inflammation in periodontitis. However, whether B10 cells’ regulation function in periodontitis is related to macrophage polarization remains unclear. This study aims to investigate whether B10 cells can regulate macrophage polarization in periodontitis.MethodsMacrophages were cocultured with B10 cells in vitro for 5 days. After coculture, macrophages were obtained for analysis directly or followed by stimulation with Pg‐LPS/IFN‐γ or IL‐4/IL‐13. Flow cytometry and/or reverse transcriptase‐polymerase chain reaction (RT‐PCR) were employed to detect the expression of IL‐1β, iNOS, TNF‐α, CD206, and ARG‐1 in macrophages. B10 cells were transferred on the 5th day after ligation in wild or macrophage‐depletion mice. Toluidine blue and TRAP staining were used to evaluate alveolar bone resorption and osteoclast activation. Immunohistochemistry was employed to detect the expression of CD68, IL‐1β, TNF‐α, iNOS, ARG‐1, and IL‐10. Immunofluorescence was used to detect the expression of CD68<jats:sup>+</jats:sup>CD86<jats:sup>+</jats:sup>M1 macrophages and CD68<jats:sup>+</jats:sup>CD206<jats:sup>+</jats:sup>M2 macrophages.ResultsIn vitro, B10 cells inhibit the expression of IL‐1β, iNOS, and TNF‐α in macrophages while increasing the expression of CD206 and ARG‐1. In experimental periodontitis, B10 cells inhibit the polarization of CD68<jats:sup>+</jats:sup>CD86<jats:sup>+</jats:sup>M1 macrophages and iNOS expression but enhance the polarization of CD68<jats:sup>+</jats:sup>CD206<jats:sup>+</jats:sup>M2 macrophages and ARG‐1 expression. Importantly, the depletion of macrophages partially weakened the regulation function of B10 cells in periodontitis.ConclusionsB10 cells promote M2 macrophage polarization, inhibit M1 macrophage polarization in periodontitis, and alleviate periodontitis partially by regulating macrophage polarization.","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":"23 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100673","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}
<p><strong>Background: </strong>Lipocalin-2 (LCN-2) is an osteokine that suppresses appetite, stimulates insulin secretion, regulates bone remodeling, and is induced by proinflammatory cytokines. The aim of this work was to investigate the participation of LCN-2 in periodontitis associated with type 2 diabetes (T2D) by evaluating alveolar bone loss, glycemic control, inflammation, and femur fragility.</p><p><strong>Methods: </strong>A murine model of periodontitis with T2D and elevated LCN-2 concentration was used. Functional LCN-2 inhibition was achieved using an anti-LCN-2 polyclonal antibody, and isotype immunoglobulin G was used as a control. The alveolar bone and femur were evaluated by micro-CT. Glucose metabolism was determined. Tumor necrosis factor (TNF-α) and receptor activator of nuclear factor kappa-B ligand (RANKL) levels in alveolar bone lysates were quantified using ELISA, and serum cytokines were quantified using flow cytometry. A three-point bending test was performed in the femur, and RANKL levels were measured in femur lysates using ELISA.</p><p><strong>Results: </strong>Functional inhibition of LCN-2 in T2D-periodontitis mice decreased alveolar bone loss in buccal and palatal surfaces and preserved the microarchitecture of the remaining bone, decreased TNF-α and RANKL in alveolar bone, reduced hyperglycemia, glucose intolerance, and insulin resistance, and increased insulin production through improving the functionality of pancreatic β cells. Furthermore, this inhibition increased serum free-glycerol levels, decreased serum interleukin (IL)-6, increased serum IL-4, and reduced femur fragility and RANKL expression in the femur.</p><p><strong>Conclusions: </strong>LCN-2 participates in periodontitis associated with T2D. Inhibiting its function in mice with T2D and periodontitis improves pancreatic β-cell function, and glucose metabolism and decreases inflammatory cytokines and bone-RANKL levels, which results in the preservation of femoral and alveolar bone microarchitecture.</p><p><strong>Plain language summary: </strong>In this study, we explored the role of a bone protein known as lipocalin-2 (LCN-2) in the connection between periodontitis and type 2 diabetes (T2D). Periodontitis is a destructive gum and alveolar bone disease. LCN-2 levels are increased in both T2D and periodontitis. Using a mouse model of T2D with periodontitis, we examined how blocking LCN-2 function affected various aspects of these two diseases. We found that this inhibition led to significant improvements. First, it reduced alveolar bone loss and preserved bone structure by decreasing local inflammation and bone resorption. Second, it improved glucose and lipid metabolism, leading to better blood-sugar control and decreased insulin resistance. Blocking the functions of LCN-2 also decreased systemic inflammation throughout the body and strengthened bone integrity. Overall, our results suggest that LCN-2 plays a crucial role in the periodontitis associated
{"title":"Lipocalin-2 as a fundamental protein in type 2 diabetes and periodontitis in mice.","authors":"Diana Laura Sólis-Suarez, Saúl Ernesto Cifuentes-Mendiola, Patricia González-Alva, Adriana Patricia Rodríguez-Hernández, Arnulfo Martínez-Dávalos, Fulgencio Eduardo Llamosas-Hernandez, Marycarmen Godínez-Victoria, Ana Lilia García-Hernández","doi":"10.1002/JPER.24-0215","DOIUrl":"https://doi.org/10.1002/JPER.24-0215","url":null,"abstract":"<p><strong>Background: </strong>Lipocalin-2 (LCN-2) is an osteokine that suppresses appetite, stimulates insulin secretion, regulates bone remodeling, and is induced by proinflammatory cytokines. The aim of this work was to investigate the participation of LCN-2 in periodontitis associated with type 2 diabetes (T2D) by evaluating alveolar bone loss, glycemic control, inflammation, and femur fragility.</p><p><strong>Methods: </strong>A murine model of periodontitis with T2D and elevated LCN-2 concentration was used. Functional LCN-2 inhibition was achieved using an anti-LCN-2 polyclonal antibody, and isotype immunoglobulin G was used as a control. The alveolar bone and femur were evaluated by micro-CT. Glucose metabolism was determined. Tumor necrosis factor (TNF-α) and receptor activator of nuclear factor kappa-B ligand (RANKL) levels in alveolar bone lysates were quantified using ELISA, and serum cytokines were quantified using flow cytometry. A three-point bending test was performed in the femur, and RANKL levels were measured in femur lysates using ELISA.</p><p><strong>Results: </strong>Functional inhibition of LCN-2 in T2D-periodontitis mice decreased alveolar bone loss in buccal and palatal surfaces and preserved the microarchitecture of the remaining bone, decreased TNF-α and RANKL in alveolar bone, reduced hyperglycemia, glucose intolerance, and insulin resistance, and increased insulin production through improving the functionality of pancreatic β cells. Furthermore, this inhibition increased serum free-glycerol levels, decreased serum interleukin (IL)-6, increased serum IL-4, and reduced femur fragility and RANKL expression in the femur.</p><p><strong>Conclusions: </strong>LCN-2 participates in periodontitis associated with T2D. Inhibiting its function in mice with T2D and periodontitis improves pancreatic β-cell function, and glucose metabolism and decreases inflammatory cytokines and bone-RANKL levels, which results in the preservation of femoral and alveolar bone microarchitecture.</p><p><strong>Plain language summary: </strong>In this study, we explored the role of a bone protein known as lipocalin-2 (LCN-2) in the connection between periodontitis and type 2 diabetes (T2D). Periodontitis is a destructive gum and alveolar bone disease. LCN-2 levels are increased in both T2D and periodontitis. Using a mouse model of T2D with periodontitis, we examined how blocking LCN-2 function affected various aspects of these two diseases. We found that this inhibition led to significant improvements. First, it reduced alveolar bone loss and preserved bone structure by decreasing local inflammation and bone resorption. Second, it improved glucose and lipid metabolism, leading to better blood-sugar control and decreased insulin resistance. Blocking the functions of LCN-2 also decreased systemic inflammation throughout the body and strengthened bone integrity. Overall, our results suggest that LCN-2 plays a crucial role in the periodontitis associated","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142073067","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}
Fabio Camacho-Alonso, Juan Carlos Bernabeu-Mira, Joaquín Sánchez, Antonio Julián Buendía, Ana María Mercado-Díaz, Mario Pérez-Sayáns, Alba Pérez-Jardón, José Manuel Somoza Martín, Javier Montero, Cristina Gomez-Polo, Norberto Quispe-López, David Peñarrocha-Oltra
<p><strong>Background: </strong>This study aimed to analyze the influence of concave and cylindrical abutments on peri-implant soft tissue. Dimensions, collagen fiber orientation, and immunohistochemical data were assessed.</p><p><strong>Methods: </strong>A multicenter, split-mouth, double-blind randomized clinical trial was conducted. Two groups were analyzed: cylindrical abutments and concave abutments. After a 12-week healing period, peri-implant soft tissue samples were collected, processed, and evaluated for dimensions, collagen fiber orientation, and immunohistochemical data. Inflammatory infiltration and vascularization were assessed, and the abutment surfaces were analyzed using scanning electron microscopy. The statistical analysis was performed using the SPSS version 20.0 statistical package.</p><p><strong>Results: </strong>A total of 74 samples in 37 patients were evaluated. Histological evaluation of peri-implant soft tissue dimensions revealed significant differences between concave and cylindrical abutments. Concave abutments exhibited greater total height (concave: 3.57 ± 0.28 - cylindrical: 2.95 ± 0.27) and barrier epithelium extension (concave: 2.46 ± 0.17 - cylindrical: 1.89 ± 0.21) (p < 0.05), while the supracrestal connective tissue extension (concave: 1.11 ± 0.17 - cylindrical: 1.03 ± 0.16) was slightly greater (p > 0.05). Collagen fiber orientation favored concave abutments (23.76 ± 5.86), with significantly more transverse/perpendicular fibers than for cylindrical abutments (15.68 ± 4.57). The immunohistochemical analysis evidenced greater inflammatory and vascular intensity in the lower portion for both abutments, though concave abutments showed lower overall intensity (concave: 1.05 ± 0.78 - cylindrical: 1.97 ± 0.68) (p < 0.05). The abutment surface analysis demonstrated a higher percentage of tissue remnants on concave abutments (42.47 ± 1.32; 45.12 ± 3.03) (p < 0.05).</p><p><strong>Conclusions: </strong>Within the limitations of this study, concave abutments presented significantly greater peri-implant tissue height, linked to an extended barrier epithelium, versus cylindrical abutments in thick tissue phenotype. This enhanced soft tissue sealing, favoring a greater percentage of transversely oriented collagen fibers. The concave design reduced chronic inflammatory exudation with T and B cells, thus minimizing the risk of chronic inflammation.</p><p><strong>Plain language summary: </strong>This study looked at how 2 different shapes of dental implant abutments (the parts that connect the implant to the crown), specifically concave and cylindrical, affect the soft tissue around the implants. We wanted to see how these shapes influenced the tissue's size, structure, and health. We conducted a clinical trial with 37 patients, comparing the 2 types of abutments in the same mouth over 12 weeks. Our findings showed that the concave abutments led to a taller and more extensive layer of protective tissue around the implant comp
{"title":"Histological and immunohistochemical soft-tissue response to cylindrical and concave abutments: Multicenter randomized clinical trial.","authors":"Fabio Camacho-Alonso, Juan Carlos Bernabeu-Mira, Joaquín Sánchez, Antonio Julián Buendía, Ana María Mercado-Díaz, Mario Pérez-Sayáns, Alba Pérez-Jardón, José Manuel Somoza Martín, Javier Montero, Cristina Gomez-Polo, Norberto Quispe-López, David Peñarrocha-Oltra","doi":"10.1002/JPER.24-0250","DOIUrl":"https://doi.org/10.1002/JPER.24-0250","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to analyze the influence of concave and cylindrical abutments on peri-implant soft tissue. Dimensions, collagen fiber orientation, and immunohistochemical data were assessed.</p><p><strong>Methods: </strong>A multicenter, split-mouth, double-blind randomized clinical trial was conducted. Two groups were analyzed: cylindrical abutments and concave abutments. After a 12-week healing period, peri-implant soft tissue samples were collected, processed, and evaluated for dimensions, collagen fiber orientation, and immunohistochemical data. Inflammatory infiltration and vascularization were assessed, and the abutment surfaces were analyzed using scanning electron microscopy. The statistical analysis was performed using the SPSS version 20.0 statistical package.</p><p><strong>Results: </strong>A total of 74 samples in 37 patients were evaluated. Histological evaluation of peri-implant soft tissue dimensions revealed significant differences between concave and cylindrical abutments. Concave abutments exhibited greater total height (concave: 3.57 ± 0.28 - cylindrical: 2.95 ± 0.27) and barrier epithelium extension (concave: 2.46 ± 0.17 - cylindrical: 1.89 ± 0.21) (p < 0.05), while the supracrestal connective tissue extension (concave: 1.11 ± 0.17 - cylindrical: 1.03 ± 0.16) was slightly greater (p > 0.05). Collagen fiber orientation favored concave abutments (23.76 ± 5.86), with significantly more transverse/perpendicular fibers than for cylindrical abutments (15.68 ± 4.57). The immunohistochemical analysis evidenced greater inflammatory and vascular intensity in the lower portion for both abutments, though concave abutments showed lower overall intensity (concave: 1.05 ± 0.78 - cylindrical: 1.97 ± 0.68) (p < 0.05). The abutment surface analysis demonstrated a higher percentage of tissue remnants on concave abutments (42.47 ± 1.32; 45.12 ± 3.03) (p < 0.05).</p><p><strong>Conclusions: </strong>Within the limitations of this study, concave abutments presented significantly greater peri-implant tissue height, linked to an extended barrier epithelium, versus cylindrical abutments in thick tissue phenotype. This enhanced soft tissue sealing, favoring a greater percentage of transversely oriented collagen fibers. The concave design reduced chronic inflammatory exudation with T and B cells, thus minimizing the risk of chronic inflammation.</p><p><strong>Plain language summary: </strong>This study looked at how 2 different shapes of dental implant abutments (the parts that connect the implant to the crown), specifically concave and cylindrical, affect the soft tissue around the implants. We wanted to see how these shapes influenced the tissue's size, structure, and health. We conducted a clinical trial with 37 patients, comparing the 2 types of abutments in the same mouth over 12 weeks. Our findings showed that the concave abutments led to a taller and more extensive layer of protective tissue around the implant comp","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055884","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}
Zhexian Cheng, Wei Li, Jitian Wang, Xuan Huang, Xingyuan Jia, Xuan Zhou
<p><strong>Background: </strong>To compare the efficacy of combined treatment of Er:YAG laser (ERL) and low-level laser therapy (LLLT) with single laser applications, and scaling and root planing (SRP) for non-surgical periodontal treatment.</p><p><strong>Methods: </strong>In a randomized controlled trial, 25 non-smoking Stage II or Stage III periodontitis patients were recruited. The four intraoral quadrants were randomly assigned to four different treatments: (1) combined application with ERL plus SRP plus LLLT; (2) ERL plus SRP; (3) SRP plus LLLT; and (4) SRP. We assessed periodontal indexes, including probing depth (PD), clinical attachment level (CAL), bleeding index (BI), and plaque index (PLI), along with three cytokines (IL-1β, TNF-α, IL-10) from gingival crevicular fluid and red complex pathogens from subgingival dental plaque at baseline, 3 months, and 6 months.</p><p><strong>Results: </strong>For initial moderate pockets (4 mm ≤ PD ≤ 6 mm), quadrants treated with ERL+SRP+LLLT, ERL+SRP, and SRP+LLLT exhibited greater PD improvement compared to the control (SRP) quadrants at the 3-month follow-up (1.25 ± 1.06, 1.23 ± 1.12, 1.00 ± 1.21 vs. 0.98 ± 1.21 mm) and the 6-month follow-up (1.35 ± 1.06, 1.23 ± 1.17, 1.35 ± 0.98 vs. 0.98 ± 1.23 mm) (p = 0.002). Quadrants treated with ERL+SRP+LLLT and SRP+LLLT showed more CAL gain means than the control quadrants at the 3-month follow-up (0.96 ± 1.42, 0.61 ± 1.39 vs. 0.55 ± 1.57 mm) and the 6-month follow-up (0.84 ± 1.54, 0.89 ± 1.49 vs. 0.48 ± 1.68 mm) (p = 0.008). For initial deep pockets (PD ≥ 7 mm), the ERL+SRP+LLLT quadrants had more PD improvement and CAL gain compared to the control quadrants at follow-up. There were no significant differences in BI, PLI, inflammatory cytokines, and periodontal pathogens among the four groups.</p><p><strong>Conclusion: </strong>The combined application of ERL and LLLT demonstrated potential efficacy in reducing PD, particularly for deep pockets.</p><p><strong>Plain language summary: </strong>To compare the therapy effect of combined use of Er:YAG laser (ERL) and low level laser therapy (LLLT) with single laser applications, and traditional periodontal treatment (SRP). A total of 25 non smoking patients with periodontitis were involved, and their mouths were divided into four sections, each receiving a different treatment: ERL+SRP+LLLT, ERL+SRP, SRP+LLLT, and SRP. Clinical indexes and laboratory indicators were assessed at baseline, 3 months, and 6 months. After six months, for initial moderate pockets, combined laser group and single laser group showed better improvements than traditional group in reducing the depth of periodontal pockets and increasing attachment levels. But for initial deep pockets, only combined laser group showed better improvement than traditional group. There were no significant differences in bleeding, plaque, inflammation, or harmful bacterial levels among the groups. These findings suggest that the integration of Er:YAG laser and low
{"title":"Combined application of Er:YAG laser and low-level laser in non-surgical treatment of periodontitis.","authors":"Zhexian Cheng, Wei Li, Jitian Wang, Xuan Huang, Xingyuan Jia, Xuan Zhou","doi":"10.1002/JPER.24-0128","DOIUrl":"https://doi.org/10.1002/JPER.24-0128","url":null,"abstract":"<p><strong>Background: </strong>To compare the efficacy of combined treatment of Er:YAG laser (ERL) and low-level laser therapy (LLLT) with single laser applications, and scaling and root planing (SRP) for non-surgical periodontal treatment.</p><p><strong>Methods: </strong>In a randomized controlled trial, 25 non-smoking Stage II or Stage III periodontitis patients were recruited. The four intraoral quadrants were randomly assigned to four different treatments: (1) combined application with ERL plus SRP plus LLLT; (2) ERL plus SRP; (3) SRP plus LLLT; and (4) SRP. We assessed periodontal indexes, including probing depth (PD), clinical attachment level (CAL), bleeding index (BI), and plaque index (PLI), along with three cytokines (IL-1β, TNF-α, IL-10) from gingival crevicular fluid and red complex pathogens from subgingival dental plaque at baseline, 3 months, and 6 months.</p><p><strong>Results: </strong>For initial moderate pockets (4 mm ≤ PD ≤ 6 mm), quadrants treated with ERL+SRP+LLLT, ERL+SRP, and SRP+LLLT exhibited greater PD improvement compared to the control (SRP) quadrants at the 3-month follow-up (1.25 ± 1.06, 1.23 ± 1.12, 1.00 ± 1.21 vs. 0.98 ± 1.21 mm) and the 6-month follow-up (1.35 ± 1.06, 1.23 ± 1.17, 1.35 ± 0.98 vs. 0.98 ± 1.23 mm) (p = 0.002). Quadrants treated with ERL+SRP+LLLT and SRP+LLLT showed more CAL gain means than the control quadrants at the 3-month follow-up (0.96 ± 1.42, 0.61 ± 1.39 vs. 0.55 ± 1.57 mm) and the 6-month follow-up (0.84 ± 1.54, 0.89 ± 1.49 vs. 0.48 ± 1.68 mm) (p = 0.008). For initial deep pockets (PD ≥ 7 mm), the ERL+SRP+LLLT quadrants had more PD improvement and CAL gain compared to the control quadrants at follow-up. There were no significant differences in BI, PLI, inflammatory cytokines, and periodontal pathogens among the four groups.</p><p><strong>Conclusion: </strong>The combined application of ERL and LLLT demonstrated potential efficacy in reducing PD, particularly for deep pockets.</p><p><strong>Plain language summary: </strong>To compare the therapy effect of combined use of Er:YAG laser (ERL) and low level laser therapy (LLLT) with single laser applications, and traditional periodontal treatment (SRP). A total of 25 non smoking patients with periodontitis were involved, and their mouths were divided into four sections, each receiving a different treatment: ERL+SRP+LLLT, ERL+SRP, SRP+LLLT, and SRP. Clinical indexes and laboratory indicators were assessed at baseline, 3 months, and 6 months. After six months, for initial moderate pockets, combined laser group and single laser group showed better improvements than traditional group in reducing the depth of periodontal pockets and increasing attachment levels. But for initial deep pockets, only combined laser group showed better improvement than traditional group. There were no significant differences in bleeding, plaque, inflammation, or harmful bacterial levels among the groups. These findings suggest that the integration of Er:YAG laser and low","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055881","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}
Riccardo Di Gianfilippo, GiovanPaolo Pini Prato, Debora Franceschi, Walter Castelluzzo, Luigi Barbato, Alessandra Bandel, Maria Di Martino, Claudio M Pannuti, Leandro Chambrone, Francesco Cairo
<p><strong>Background: </strong>To assess how the diagnostic reproducibility of the 2018 Classification of Gingival Recession Defects (GRD) could be applied when comparing in-person chairside measurements with photographic measurements.</p><p><strong>Methods: </strong>Thirty-four GRD were photographed and evaluated by 4 masked operators. For each case, the operators measured twice recession type (RT), recession depth (RD), keratinized tissue width (KTW), gingival thickness (GT), detectability of the cemento-enamel junction (CEJ), and presence of root steps (RSs), chairside, and on photographs. Intraclass correlation coefficient (ICC) with 95% confidence intervals (CI) was calculated for RD and KTW; Kappa with 95% CI was used for GT, CEJ, and RS; quadratic weighted Kappa with 95% CI was used for RT.</p><p><strong>Results: </strong>RD, KTW, and RT showed excellent overall intra-operator agreement (> 0.93), and from good to excellent overall inter-operator agreement (> 0.80), for both clinical and photographic measurements. Agreements were lower for GT, CEJ, and RS. Overall clinical and photographic agreements were within 0.1 difference for every variable, except for inter-operator agreement for RS which was 0.72 for clinical measurements and 0.45 for photographic measurements. The lowest overall agreement between clinical versus photographic measurements existed for CEJ (0.28) and RS (0.35).</p><p><strong>Conclusions: </strong>Variables composing the 2018 Classification of GRD are reproducible, both clinically and on photographs, with comparable agreements. The overall agreement was higher for KTW, RD, and RT, and lower for GT, CEJ, and RS, for both clinical and photographic measurements. The comparison between chairside and photographic evaluations indicated fair to excellent agreement for most variables, with CEJ and RS showing fair agreement.</p><p><strong>Plain language summary: </strong>As digital diagnostics evolve to facilitate clinical diagnostic measurement, we aimed to assess the effectiveness of intraoral photography for diagnosing gingival recession defects (GRD) according to the 2018 Classification of GRD, compared to traditional clinical examination. Standardized photographs of thirty-four GRD cases were captured. Four masked operators evaluated the same gingival recessions twice in a clinical setting and twice using photographs. Measurement repeatability within and between operators was calculated for both clinical and photographic settings, and the two settings were compared. Continuous measurements such as recession depth and keratinized tissue width, as well as the evaluation of interproximal attachment height (recession type), showed excellent agreement both clinically and photographically. Agreement was lower for gingival thickness and the detectability of tooth anatomical landmarks, such as the cemento-enamel junction and the presence of root steps. Overall, the agreement between chairside and photographic evaluations was gener
{"title":"Diagnostic reproducibility of the 2018 Classification of Gingival Recessions: Comparing photographic and in-person diagnoses.","authors":"Riccardo Di Gianfilippo, GiovanPaolo Pini Prato, Debora Franceschi, Walter Castelluzzo, Luigi Barbato, Alessandra Bandel, Maria Di Martino, Claudio M Pannuti, Leandro Chambrone, Francesco Cairo","doi":"10.1002/JPER.24-0173","DOIUrl":"https://doi.org/10.1002/JPER.24-0173","url":null,"abstract":"<p><strong>Background: </strong>To assess how the diagnostic reproducibility of the 2018 Classification of Gingival Recession Defects (GRD) could be applied when comparing in-person chairside measurements with photographic measurements.</p><p><strong>Methods: </strong>Thirty-four GRD were photographed and evaluated by 4 masked operators. For each case, the operators measured twice recession type (RT), recession depth (RD), keratinized tissue width (KTW), gingival thickness (GT), detectability of the cemento-enamel junction (CEJ), and presence of root steps (RSs), chairside, and on photographs. Intraclass correlation coefficient (ICC) with 95% confidence intervals (CI) was calculated for RD and KTW; Kappa with 95% CI was used for GT, CEJ, and RS; quadratic weighted Kappa with 95% CI was used for RT.</p><p><strong>Results: </strong>RD, KTW, and RT showed excellent overall intra-operator agreement (> 0.93), and from good to excellent overall inter-operator agreement (> 0.80), for both clinical and photographic measurements. Agreements were lower for GT, CEJ, and RS. Overall clinical and photographic agreements were within 0.1 difference for every variable, except for inter-operator agreement for RS which was 0.72 for clinical measurements and 0.45 for photographic measurements. The lowest overall agreement between clinical versus photographic measurements existed for CEJ (0.28) and RS (0.35).</p><p><strong>Conclusions: </strong>Variables composing the 2018 Classification of GRD are reproducible, both clinically and on photographs, with comparable agreements. The overall agreement was higher for KTW, RD, and RT, and lower for GT, CEJ, and RS, for both clinical and photographic measurements. The comparison between chairside and photographic evaluations indicated fair to excellent agreement for most variables, with CEJ and RS showing fair agreement.</p><p><strong>Plain language summary: </strong>As digital diagnostics evolve to facilitate clinical diagnostic measurement, we aimed to assess the effectiveness of intraoral photography for diagnosing gingival recession defects (GRD) according to the 2018 Classification of GRD, compared to traditional clinical examination. Standardized photographs of thirty-four GRD cases were captured. Four masked operators evaluated the same gingival recessions twice in a clinical setting and twice using photographs. Measurement repeatability within and between operators was calculated for both clinical and photographic settings, and the two settings were compared. Continuous measurements such as recession depth and keratinized tissue width, as well as the evaluation of interproximal attachment height (recession type), showed excellent agreement both clinically and photographically. Agreement was lower for gingival thickness and the detectability of tooth anatomical landmarks, such as the cemento-enamel junction and the presence of root steps. Overall, the agreement between chairside and photographic evaluations was gener","PeriodicalId":16716,"journal":{"name":"Journal of periodontology","volume":" ","pages":""},"PeriodicalIF":4.2,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055882","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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