Pub Date : 2024-07-01Epub Date: 2024-06-14DOI: 10.1177/00220345241255325
K Rattanaprukskul, X-J Xia, M Jiang, E Albuquerque-Souza, D Bandyopadhyay, S E Sahingur
Most of the elderly population is afflicted by periodontal diseases, creating a health burden worldwide. Cellular senescence is one of the hallmarks of aging and associated with several chronic comorbidities. Senescent cells produce a variety of deleterious secretions, collectively termed the senescence-associated secretory phenotype (SASP). This disrupts neighboring cells, leading to further senescence propagation and inciting chronic inflammation, known as "inflammaging." Detrimental repercussions within the tissue microenvironment can trigger senescence at a younger age, accelerate biological aging, and drive the initiation or progression of diseases. Here, we investigated the biological signatures of senescence in healthy and diseased gingival tissues by assessing the levels of key senescence markers (p16, lipofuscin, and β-galactosidase) and inflammatory mediators (interleukin [IL]-1β, IL-6, IL-8, matrix metalloproteinase [MMP]-1, MMP-3, and tumor necrosis factor-α). Our results showed significantly increased senescence features including p16, lipofuscin, and β-galactosidase in both epithelial and connective tissues of periodontitis patients compared with healthy sites in all age groups, indicating that an inflammatory microenvironment can trigger senescence-like alterations in younger diseased gingival tissues as well. Subsequent analyses using double staining with specific cell markers noted the enrichment of β-galactosidase in fibroblasts and macrophages. Concurrently, inflammatory mediators consistent with SASP were increased in the gingival biopsies obtained from periodontitis lesions. Together, our findings provide the first clinical report revealing susceptibility to elevated senescence and inflammatory milieu consistent with senescence secretome in gingival tissues, thus introducing senescence as one of the drivers of pathological events in the oral mucosa and a novel strategy for targeted interventions.
{"title":"Molecular Signatures of Senescence in Periodontitis: Clinical Insights.","authors":"K Rattanaprukskul, X-J Xia, M Jiang, E Albuquerque-Souza, D Bandyopadhyay, S E Sahingur","doi":"10.1177/00220345241255325","DOIUrl":"10.1177/00220345241255325","url":null,"abstract":"<p><p>Most of the elderly population is afflicted by periodontal diseases, creating a health burden worldwide. Cellular senescence is one of the hallmarks of aging and associated with several chronic comorbidities. Senescent cells produce a variety of deleterious secretions, collectively termed the <i>senescence-associated secretory phenotype</i> (SASP). This disrupts neighboring cells, leading to further senescence propagation and inciting chronic inflammation, known as \"inflammaging.\" Detrimental repercussions within the tissue microenvironment can trigger senescence at a younger age, accelerate biological aging, and drive the initiation or progression of diseases. Here, we investigated the biological signatures of senescence in healthy and diseased gingival tissues by assessing the levels of key senescence markers (p16, lipofuscin, and β-galactosidase) and inflammatory mediators (interleukin [IL]-1β, IL-6, IL-8, matrix metalloproteinase [MMP]-1, MMP-3, and tumor necrosis factor-α). Our results showed significantly increased senescence features including p16, lipofuscin, and β-galactosidase in both epithelial and connective tissues of periodontitis patients compared with healthy sites in all age groups, indicating that an inflammatory microenvironment can trigger senescence-like alterations in younger diseased gingival tissues as well. Subsequent analyses using double staining with specific cell markers noted the enrichment of β-galactosidase in fibroblasts and macrophages. Concurrently, inflammatory mediators consistent with SASP were increased in the gingival biopsies obtained from periodontitis lesions. Together, our findings provide the first clinical report revealing susceptibility to elevated senescence and inflammatory milieu consistent with senescence secretome in gingival tissues, thus introducing senescence as one of the drivers of pathological events in the oral mucosa and a novel strategy for targeted interventions.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"800-808"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11308264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141322202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-05-16DOI: 10.1177/00220345241245033
R Xu, R Sheng, W Lin, S Jiang, D Zhang, L Liu, K Lei, X Li, Z Liu, X Zhang, Y Wang, D Seriwatanachai, X Zhou, Q Yuan
N6-methyladenosine (m6A) modification, a eukaryotic messenger RNA modification catalyzed by methyltransferase-like 3 (METTL3), plays a pivotal role in stem cell fate determination. Calvarial bone development and maintenance are orchestrated by the cranial sutures. Cathepsin K (CTSK)-positive calvarial stem cells (CSCs) contribute to mice calvarial ossification. However, the role of m6A modification in regulating Ctsk+ lineage cells during calvarial development remains elusive. Here, we showed that METTL3 was colocalized with cranial nonosteoclastic Ctsk+ lineage cells, which were also associated with GLI1 expression. During neonatal development, depletion of Mettl3 in the Ctsk+ lineage cells delayed suture formation and decreased mineralization. During adulthood maintenance, loss of Mettl3 in the Ctsk+ lineage cells impaired calvarial bone formation, which was featured by the increased bone porosity, enhanced bone marrow cavity, and decreased number of osteocytes with the less-developed cellular outline. The analysis of methylated RNA immunoprecipitation sequencing and RNA sequencing data indicated that loss of METTL3 reduced Hedgehog (Hh) signaling pathway. Restoration of Hh signaling pathway by crossing Sufufl/+ alleles or by local administration of SAG21 partially rescued the abnormity. Our data indicate that METTL3 modulates Ctsk+ lineage cells supporting calvarial bone formation by regulating the Hh signaling pathway, providing new insights for clinical treatment of skull vault osseous diseases.
{"title":"METTL3 Modulates Ctsk<sup>+</sup> Lineage Supporting Cranial Osteogenesis via Hedgehog.","authors":"R Xu, R Sheng, W Lin, S Jiang, D Zhang, L Liu, K Lei, X Li, Z Liu, X Zhang, Y Wang, D Seriwatanachai, X Zhou, Q Yuan","doi":"10.1177/00220345241245033","DOIUrl":"10.1177/00220345241245033","url":null,"abstract":"<p><p>N6-methyladenosine (m<sup>6</sup>A) modification, a eukaryotic messenger RNA modification catalyzed by methyltransferase-like 3 (METTL3), plays a pivotal role in stem cell fate determination. Calvarial bone development and maintenance are orchestrated by the cranial sutures. Cathepsin K (CTSK)-positive calvarial stem cells (CSCs) contribute to mice calvarial ossification. However, the role of m<sup>6</sup>A modification in regulating Ctsk<sup>+</sup> lineage cells during calvarial development remains elusive. Here, we showed that METTL3 was colocalized with cranial nonosteoclastic Ctsk<sup>+</sup> lineage cells, which were also associated with GLI1 expression. During neonatal development, depletion of <i>Mettl3</i> in the Ctsk<sup>+</sup> lineage cells delayed suture formation and decreased mineralization. During adulthood maintenance, loss of <i>Mettl3</i> in the Ctsk<sup>+</sup> lineage cells impaired calvarial bone formation, which was featured by the increased bone porosity, enhanced bone marrow cavity, and decreased number of osteocytes with the less-developed cellular outline. The analysis of methylated RNA immunoprecipitation sequencing and RNA sequencing data indicated that loss of METTL3 reduced Hedgehog (Hh) signaling pathway. Restoration of Hh signaling pathway by crossing <i>Sufu<sup>fl/+</sup></i> alleles or by local administration of SAG21 partially rescued the abnormity. Our data indicate that METTL3 modulates Ctsk<sup>+</sup> lineage cells supporting calvarial bone formation by regulating the Hh signaling pathway, providing new insights for clinical treatment of skull vault osseous diseases.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"734-744"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140946755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-05-29DOI: 10.1177/00220345241253186
J Bao, X Zhang, S Xiang, H Liu, M Cheng, Y Yang, X Huang, W Xiang, W Cui, H C Lai, S Huang, Y Wang, D Qian, H Yu
The increasing application of virtual surgical planning (VSP) in orthognathic surgery implies a critical need for accurate prediction of facial and skeletal shapes. The craniofacial relationship in patients with dentofacial deformities is still not understood, and transformations between facial and skeletal shapes remain a challenging task due to intricate anatomical structures and nonlinear relationships between the facial soft tissue and bones. In this study, a novel bidirectional 3-dimensional (3D) deep learning framework, named P2P-ConvGC, was developed and validated based on a large-scale data set for accurate subject-specific transformations between facial and skeletal shapes. Specifically, the 2-stage point-sampling strategy was used to generate multiple nonoverlapping point subsets to represent high-resolution facial and skeletal shapes. Facial and skeletal point subsets were separately input into the prediction system to predict the corresponding skeletal and facial point subsets via the skeletal prediction subnetwork and facial prediction subnetwork. For quantitative evaluation, the accuracy was calculated with shape errors and landmark errors between the predicted skeleton or face with corresponding ground truths. The shape error was calculated by comparing the predicted point sets with the ground truths, with P2P-ConvGC outperforming existing state-of-the-art algorithms including P2P-Net, P2P-ASNL, and P2P-Conv. The total landmark errors (Euclidean distances of craniomaxillofacial landmarks) of P2P-ConvGC in the upper skull, mandible, and facial soft tissues were 1.964 ± 0.904 mm, 2.398 ± 1.174 mm, and 2.226 ± 0.774 mm, respectively. Furthermore, the clinical feasibility of the bidirectional model was validated using a clinical cohort. The result demonstrated its prediction ability with average surface deviation errors of 0.895 ± 0.175 mm for facial prediction and 0.906 ± 0.082 mm for skeletal prediction. To conclude, our proposed model achieved good performance on the subject-specific prediction of facial and skeletal shapes and showed clinical application potential in postoperative facial prediction and VSP for orthognathic surgery.
{"title":"Deep Learning-Based Facial and Skeletal Transformations for Surgical Planning.","authors":"J Bao, X Zhang, S Xiang, H Liu, M Cheng, Y Yang, X Huang, W Xiang, W Cui, H C Lai, S Huang, Y Wang, D Qian, H Yu","doi":"10.1177/00220345241253186","DOIUrl":"10.1177/00220345241253186","url":null,"abstract":"<p><p>The increasing application of virtual surgical planning (VSP) in orthognathic surgery implies a critical need for accurate prediction of facial and skeletal shapes. The craniofacial relationship in patients with dentofacial deformities is still not understood, and transformations between facial and skeletal shapes remain a challenging task due to intricate anatomical structures and nonlinear relationships between the facial soft tissue and bones. In this study, a novel bidirectional 3-dimensional (3D) deep learning framework, named P2P-ConvGC, was developed and validated based on a large-scale data set for accurate subject-specific transformations between facial and skeletal shapes. Specifically, the 2-stage point-sampling strategy was used to generate multiple nonoverlapping point subsets to represent high-resolution facial and skeletal shapes. Facial and skeletal point subsets were separately input into the prediction system to predict the corresponding skeletal and facial point subsets via the skeletal prediction subnetwork and facial prediction subnetwork. For quantitative evaluation, the accuracy was calculated with shape errors and landmark errors between the predicted skeleton or face with corresponding ground truths. The shape error was calculated by comparing the predicted point sets with the ground truths, with P2P-ConvGC outperforming existing state-of-the-art algorithms including P2P-Net, P2P-ASNL, and P2P-Conv. The total landmark errors (Euclidean distances of craniomaxillofacial landmarks) of P2P-ConvGC in the upper skull, mandible, and facial soft tissues were 1.964 ± 0.904 mm, 2.398 ± 1.174 mm, and 2.226 ± 0.774 mm, respectively. Furthermore, the clinical feasibility of the bidirectional model was validated using a clinical cohort. The result demonstrated its prediction ability with average surface deviation errors of 0.895 ± 0.175 mm for facial prediction and 0.906 ± 0.082 mm for skeletal prediction. To conclude, our proposed model achieved good performance on the subject-specific prediction of facial and skeletal shapes and showed clinical application potential in postoperative facial prediction and VSP for orthognathic surgery.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"809-819"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141163163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-05-31DOI: 10.1177/00220345241253794
J Wang, B Wang, Y Y Liu, Y L Luo, Y Y Wu, L Xiang, X M Yang, Y L Qu, T R Tian, Y Man
Digital technology has emerged as a transformative tool in dental implantation, profoundly enhancing accuracy and effectiveness across multiple facets, such as diagnosis, preoperative treatment planning, surgical procedures, and restoration delivery. The multiple integration of radiographic data and intraoral data, sometimes with facial scan data or electronic facebow through virtual planning software, enables comprehensive 3-dimensional visualization of the hard and soft tissue and the position of future restoration, resulting in heightened diagnostic precision. In virtual surgery design, the incorporation of both prosthetic arrangement and individual anatomical details enables the virtual execution of critical procedures (e.g., implant placement, extended applications, etc.) through analysis of cross-sectional images and the reconstruction of 3-dimensional surface models. After verification, the utilization of digital technology including templates, navigation, combined techniques, and implant robots achieved seamless transfer of the virtual treatment plan to the actual surgical sites, ultimately leading to enhanced surgical outcomes with highly improved accuracy. In restoration delivery, digital techniques for impression, shade matching, and prosthesis fabrication have advanced, enabling seamless digital data conversion and efficient communication among clinicians and technicians. Compared with clinical medicine, artificial intelligence (AI) technology in dental implantology primarily focuses on diagnosis and prediction. AI-supported preoperative planning and surgery remain in developmental phases, impeded by the complexity of clinical cases and ethical considerations, thereby constraining widespread adoption.
{"title":"Recent Advances in Digital Technology in Implant Dentistry.","authors":"J Wang, B Wang, Y Y Liu, Y L Luo, Y Y Wu, L Xiang, X M Yang, Y L Qu, T R Tian, Y Man","doi":"10.1177/00220345241253794","DOIUrl":"10.1177/00220345241253794","url":null,"abstract":"<p><p>Digital technology has emerged as a transformative tool in dental implantation, profoundly enhancing accuracy and effectiveness across multiple facets, such as diagnosis, preoperative treatment planning, surgical procedures, and restoration delivery. The multiple integration of radiographic data and intraoral data, sometimes with facial scan data or electronic facebow through virtual planning software, enables comprehensive 3-dimensional visualization of the hard and soft tissue and the position of future restoration, resulting in heightened diagnostic precision. In virtual surgery design, the incorporation of both prosthetic arrangement and individual anatomical details enables the virtual execution of critical procedures (e.g., implant placement, extended applications, etc.) through analysis of cross-sectional images and the reconstruction of 3-dimensional surface models. After verification, the utilization of digital technology including templates, navigation, combined techniques, and implant robots achieved seamless transfer of the virtual treatment plan to the actual surgical sites, ultimately leading to enhanced surgical outcomes with highly improved accuracy. In restoration delivery, digital techniques for impression, shade matching, and prosthesis fabrication have advanced, enabling seamless digital data conversion and efficient communication among clinicians and technicians. Compared with clinical medicine, artificial intelligence (AI) technology in dental implantology primarily focuses on diagnosis and prediction. AI-supported preoperative planning and surgery remain in developmental phases, impeded by the complexity of clinical cases and ethical considerations, thereby constraining widespread adoption.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"787-799"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-05-31DOI: 10.1177/00220345241244687
Y Cao, Q Ni, C Bao, C Cai, T Wang, X Ruan, Y Li, H Wang, R Wang, W Sun
A ligature-induced periodontitis model was established in wild-type and CD146CreERT2; RosatdTomato mice to explore the function of pericytes in alveolar bone formation. We found that during periodontitis progression and periodontal wound healing, CD146+/NG2+ pericytes were enriched in the periodontal tissue areas, which could migrate to the alveolar bone surface and colocalize with ALP+/OCN+ osteoblasts. Chemokine C-X-C motif receptor 4 (CXCR4) inhibition using AMD3100 blocked CD146-Cre+ pericyte migration and osteogenesis, as well as further exacerbated periodontitis-associated bone loss. Next, primary pericytes were sorted out by magnetic-activated cell sorting and demonstrated that C-X-C motif chemokine ligand 12 (CXCL12) promotes pericyte migration and osteogenesis via CXCL12-CXCR4-Rac1 signaling. Finally, the local administration of an adeno-associated virus for Rac1 overexpression in NG2+ pericytes promotes osteoblast differentiation of pericytes and increases alveolar bone volume in periodontitis. Thus, our results provided the evidence that pericytes may migrate and osteogenesis via the CXCL12-CXCR4-Rac1 axis during the pathological process of periodontitis.
{"title":"The Role of Pericyte Migration and Osteogenesis in Periodontitis.","authors":"Y Cao, Q Ni, C Bao, C Cai, T Wang, X Ruan, Y Li, H Wang, R Wang, W Sun","doi":"10.1177/00220345241244687","DOIUrl":"10.1177/00220345241244687","url":null,"abstract":"<p><p>A ligature-induced periodontitis model was established in wild-type and CD146<sup>CreERT2</sup>; Rosa<sup>tdTomato</sup> mice to explore the function of pericytes in alveolar bone formation. We found that during periodontitis progression and periodontal wound healing, CD146<sup>+</sup>/NG2<sup>+</sup> pericytes were enriched in the periodontal tissue areas, which could migrate to the alveolar bone surface and colocalize with ALP<sup>+</sup>/OCN<sup>+</sup> osteoblasts. Chemokine C-X-C motif receptor 4 (CXCR4) inhibition using AMD3100 blocked CD146-Cre<sup>+</sup> pericyte migration and osteogenesis, as well as further exacerbated periodontitis-associated bone loss. Next, primary pericytes were sorted out by magnetic-activated cell sorting and demonstrated that C-X-C motif chemokine ligand 12 (CXCL12) promotes pericyte migration and osteogenesis via CXCL12-CXCR4-Rac1 signaling. Finally, the local administration of an adeno-associated virus for Rac1 overexpression in NG2<sup>+</sup> pericytes promotes osteoblast differentiation of pericytes and increases alveolar bone volume in periodontitis. Thus, our results provided the evidence that pericytes may migrate and osteogenesis via the CXCL12-CXCR4-Rac1 axis during the pathological process of periodontitis.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"723-733"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-05-29DOI: 10.1177/00220345241254017
O Ajcharanukul, P Kosakarn, M Sujjapong, S Berkbandee, P Bussabong
Due to the multiple factors contributing to dentin demineralization and hypersensitivity among individuals, the effectiveness of the available treatments in the long term remains unclear. A recent study reported a simple strategy to potentially mimic natural remineralization with increased crystallization on the enamel caries using fluoride iontophoresis. Such an effect is also ideal for accomplishing dentin biomineralization and structural strength. This study aimed to investigate structural and compositional characteristics and permeability changes after fluoride iontophoresis with different polarities, cathodal iontophoresis (CIP), anodal iontophoresis (AIP), and the control without iontophoresis for the treatment of etched dentin under simulated pulpal pressure. The 24 premolars were divided into 3 groups: CIP, AIP, and topical application of 5% sodium fluoride (NaF) for 40 s. Relative to before treatment, iontophoresis with both polarities significantly decreased the permeability with a visible increase in occluding tubules containing crystal formation and growth throughout the dentin structure and depth. The CIP not only restored the etched dentin surface into a sound condition but also reinforced the dentin across the structure and depth by the synergistic effects of remineralization, increasing crystal formation and transformation toward the more crystalline structure of fluorohydroxyapatite. Following topical treatment, X-ray diffraction analysis and Raman spectra revealed a significant reduction in the crystal size and crystallinity associated with the raised B-type carbonate substitution into the hydroxyapatite compared with that in the sound dentin. The result was the first to reveal the ideal strategy to rapidly restore the etched dentin surface into a sound condition, including reinforcing the dentin across the structure and depth by the synergistic effects of decreasing permeability, increasing crystal formation, and transformation toward the more crystalline structure of fluorohydroxyapatite using the 5% NaF applied with the DC cathode iontophoresis. The technique is noninvasive and simple and deserves further development for clinical application.
由于导致牙本质脱矿和个人过敏症的因素多种多样,现有治疗方法的长期有效性仍不明确。最近的一项研究报告了一种简单的策略,即使用氟离子透入疗法,通过增加釉质龋齿的结晶来模拟自然再矿化。这种效果也是实现牙本质生物矿化和结构强度的理想方法。本研究旨在调查不同极性的氟离子透入(阴极离子透入(CIP)、阳极离子透入(AIP)和不使用离子透入的对照组)治疗模拟牙髓压力下蚀刻牙本质后的结构和成分特征以及渗透性变化。24 颗前臼齿分为 3 组:与治疗前相比,两种极性的离子透入疗法都能显著降低渗透性,在整个牙本质结构和深度中,含有晶体形成和生长的闭塞小管明显增加。CIP 不仅能将蚀刻的牙本质表面恢复到良好状态,还能通过再矿化、增加晶体形成和向氟羟基磷灰石晶体结构转化的协同作用,在整个牙本质结构和深度上强化牙本质。局部治疗后,X 射线衍射分析和拉曼光谱显示,与健全牙本质相比,晶体尺寸和结晶度显著减小,这与羟基磷灰石中的 B 型碳酸盐取代度提高有关。该结果首次揭示了将蚀刻牙本质表面快速恢复到健全状态的理想策略,包括通过使用直流阴极离子透入法施加 5%NaF,在降低渗透性、增加晶体形成以及向氟羟磷灰石更多晶体结构转化的协同作用下,在整个牙本质结构和深度上对其进行加固。该技术无创、简单,值得进一步开发用于临床。
{"title":"Increased Fluorohydroxyapatite across Dentin after Fluoride Iontophoresis.","authors":"O Ajcharanukul, P Kosakarn, M Sujjapong, S Berkbandee, P Bussabong","doi":"10.1177/00220345241254017","DOIUrl":"10.1177/00220345241254017","url":null,"abstract":"<p><p>Due to the multiple factors contributing to dentin demineralization and hypersensitivity among individuals, the effectiveness of the available treatments in the long term remains unclear. A recent study reported a simple strategy to potentially mimic natural remineralization with increased crystallization on the enamel caries using fluoride iontophoresis. Such an effect is also ideal for accomplishing dentin biomineralization and structural strength. This study aimed to investigate structural and compositional characteristics and permeability changes after fluoride iontophoresis with different polarities, cathodal iontophoresis (CIP), anodal iontophoresis (AIP), and the control without iontophoresis for the treatment of etched dentin under simulated pulpal pressure. The 24 premolars were divided into 3 groups: CIP, AIP, and topical application of 5% sodium fluoride (NaF) for 40 s. Relative to before treatment, iontophoresis with both polarities significantly decreased the permeability with a visible increase in occluding tubules containing crystal formation and growth throughout the dentin structure and depth. The CIP not only restored the etched dentin surface into a sound condition but also reinforced the dentin across the structure and depth by the synergistic effects of remineralization, increasing crystal formation and transformation toward the more crystalline structure of fluorohydroxyapatite. Following topical treatment, X-ray diffraction analysis and Raman spectra revealed a significant reduction in the crystal size and crystallinity associated with the raised B-type carbonate substitution into the hydroxyapatite compared with that in the sound dentin. The result was the first to reveal the ideal strategy to rapidly restore the etched dentin surface into a sound condition, including reinforcing the dentin across the structure and depth by the synergistic effects of decreasing permeability, increasing crystal formation, and transformation toward the more crystalline structure of fluorohydroxyapatite using the 5% NaF applied with the DC cathode iontophoresis. The technique is noninvasive and simple and deserves further development for clinical application.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"830-838"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141163164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-06-14DOI: 10.1177/00220345241256279
M Bawazir, C H Lim, P Arnés-Urgellés, M Lu, H Huang, Y Zhang
Computer-aided design (CAD)/computer-aided manufacturing (CAM) milling and handpiece grinding are critical procedures in the fabrication and adjustment of ceramic dental restorations. However, due to the formation of microfractures, these procedures are detrimental to the strength of ceramics. This study analyzes the damage associated with current brittle-regime grinding and presents a potential remedy in the application of a safer yet still efficient grinding regime known as "ductile-regime grinding." Disc-shaped specimens of a lithium disilicate glass-ceramic material (IPS e.max CAD) were obtained by cutting and crystallizing the lithium metasilicate CAD/CAM blanks (the so-called blue blocks) following the manufacturer's instructions. The discs were then polished to a 1 µm diamond suspension finish. Single-particle micro-scratch tests (n = 10) with a conical diamond indenter were conducted to reproduce basic modes of deformation and fracture. Key parameters such as coefficient of friction and penetration depth were recorded as a function of scratch load. Further, biaxial flexure strength tests (n = 6) were performed after applying various scratch loads to analyze their effects on ceramic strength. Scanning electron microscopy (SEM) and focused ion beam (FIB) were used to characterize surface and subsurface damage. Statistical analysis was performed using one-way analysis of variance and Tukey tests. While the SEM surface analysis of scratch tracks revealed the occurrence of both ductile and brittle removal modes, it failed to accurately determine the threshold load for the brittle-ductile transition. The threshold load for brittle-ductile transition was determined to be 70 mN based on FIB subsurface damage analyses in conjunction with strength degradation studies. Below 70 mN, the specimens exhibited neither strength degradation nor the formation of subsurface cracks. Determination of the brittle-ductile thresholds is significant because it sets a foundation for future research on the feasibility of implementing ductile-regime milling/grinding protocols for fabricating damage-free ceramic dental restorations.
{"title":"Brittle-Ductile Threshold in Lithium Disilicate under Sharp Sliding Contact.","authors":"M Bawazir, C H Lim, P Arnés-Urgellés, M Lu, H Huang, Y Zhang","doi":"10.1177/00220345241256279","DOIUrl":"10.1177/00220345241256279","url":null,"abstract":"<p><p>Computer-aided design (CAD)/computer-aided manufacturing (CAM) milling and handpiece grinding are critical procedures in the fabrication and adjustment of ceramic dental restorations. However, due to the formation of microfractures, these procedures are detrimental to the strength of ceramics. This study analyzes the damage associated with current brittle-regime grinding and presents a potential remedy in the application of a safer yet still efficient grinding regime known as \"ductile-regime grinding.\" Disc-shaped specimens of a lithium disilicate glass-ceramic material (IPS e.max CAD) were obtained by cutting and crystallizing the lithium metasilicate CAD/CAM blanks (the so-called blue blocks) following the manufacturer's instructions. The discs were then polished to a 1 µm diamond suspension finish. Single-particle micro-scratch tests (<i>n</i> = 10) with a conical diamond indenter were conducted to reproduce basic modes of deformation and fracture. Key parameters such as coefficient of friction and penetration depth were recorded as a function of scratch load. Further, biaxial flexure strength tests (<i>n</i> = 6) were performed after applying various scratch loads to analyze their effects on ceramic strength. Scanning electron microscopy (SEM) and focused ion beam (FIB) were used to characterize surface and subsurface damage. Statistical analysis was performed using one-way analysis of variance and Tukey tests. While the SEM surface analysis of scratch tracks revealed the occurrence of both ductile and brittle removal modes, it failed to accurately determine the threshold load for the brittle-ductile transition. The threshold load for brittle-ductile transition was determined to be 70 mN based on FIB subsurface damage analyses in conjunction with strength degradation studies. Below 70 mN, the specimens exhibited neither strength degradation nor the formation of subsurface cracks. Determination of the brittle-ductile thresholds is significant because it sets a foundation for future research on the feasibility of implementing ductile-regime milling/grinding protocols for fabricating damage-free ceramic dental restorations.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"839-847"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11307199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141322201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-05-20DOI: 10.1177/00220345241242389
B Y Chen, J L Pathak, H Y Lin, W Q Guo, W J Chen, G Luo, L J Wang, X F Sun, Y Ding, J Li, T G H Diekwisch, C Liu
Inflammation and loss of articular cartilage are considered the major cause of temporomandibular joint osteoarthritis (TMJOA), a painful condition of the temporomandibular joint (TMJ). To determine the cause of TMJ osteoarthritis in these patients, synovial fluid of TMJOA patients was compared prior to and after hyaluronic lavage, revealing substantially elevated levels of interleukin (IL) 1β, reactive oxidative stress (ROS), and an overload of Fe3+ and Fe2+ prior to lavage, indicative of ferroptosis as a mode of chondrocyte cell death. To ask whether prolonged inflammatory conditions resulted in ferroptosis-like transformation in vitro, we subjected TMJ chondrocytes to IL-1β treatment, resulting in a shift in messenger RNA sequencing gene ontologies related to iron homeostasis and oxidative stress-related cell death. Exposure to rat unilateral anterior crossbite conditions resulted in reduced COL2A1 expression, fewer chondrocytes, glutathione peroxidase 4 (GPX4) downregulation, and 4-hydroxynonenal (4-HNE) upregulation, an effect that was reversed after intra-articular injections of the ferroptosis inhibitor ferrostatin 1 (Fer-1). Our study demonstrated that ferroptosis conditions affected mitochondrial structure and function, while the inhibitor Fer-1 restored mitochondrial structure and the inhibition of hypoxia-inducible factor 1α (HIF-1α) or the transferrin receptor 1 (TFRC) rescued IL-1β-induced loss of mitochondrial membrane potential. Inhibition of HIF-1α downregulated IL-1β-induced TFRC expression, while inhibition of TFRC did not downregulate IL-1β-induced HIF-1α expression in chondrocytes. Moreover, inhibition of HIF-1α or TFRC downregulated the IL-1β-induced MMP13 expression in chondrocytes, while inhibition of HIF-1α or TFRC rescued IL-1β-inhibited COL2A1 expression in chondrocytes. Furthermore, upregulation of TFRC promoted Fe2+ entry into chondrocytes, inducing the Fenton reaction and lipid peroxidation, which in turn caused ferroptosis, a disruption in chondrocyte functions, and an exacerbation of condylar cartilage degeneration. Together, these findings illustrate the far-reaching effects of chondrocyte ferroptosis in TMJOA as a mechanism causing chondrocyte death through iron overload, oxidative stress, and articular cartilage degeneration and a potential major cause of TMJOA.
{"title":"Inflammation Triggers Chondrocyte Ferroptosis in TMJOA via HIF-1α/TFRC.","authors":"B Y Chen, J L Pathak, H Y Lin, W Q Guo, W J Chen, G Luo, L J Wang, X F Sun, Y Ding, J Li, T G H Diekwisch, C Liu","doi":"10.1177/00220345241242389","DOIUrl":"10.1177/00220345241242389","url":null,"abstract":"<p><p>Inflammation and loss of articular cartilage are considered the major cause of temporomandibular joint osteoarthritis (TMJOA), a painful condition of the temporomandibular joint (TMJ). To determine the cause of TMJ osteoarthritis in these patients, synovial fluid of TMJOA patients was compared prior to and after hyaluronic lavage, revealing substantially elevated levels of interleukin (IL) 1β, reactive oxidative stress (ROS), and an overload of Fe<sup>3+</sup> and Fe<sup>2+</sup> prior to lavage, indicative of ferroptosis as a mode of chondrocyte cell death. To ask whether prolonged inflammatory conditions resulted in ferroptosis-like transformation in vitro, we subjected TMJ chondrocytes to IL-1β treatment, resulting in a shift in messenger RNA sequencing gene ontologies related to iron homeostasis and oxidative stress-related cell death. Exposure to rat unilateral anterior crossbite conditions resulted in reduced COL2A1 expression, fewer chondrocytes, glutathione peroxidase 4 (GPX4) downregulation, and 4-hydroxynonenal (4-HNE) upregulation, an effect that was reversed after intra-articular injections of the ferroptosis inhibitor ferrostatin 1 (Fer-1). Our study demonstrated that ferroptosis conditions affected mitochondrial structure and function, while the inhibitor Fer-1 restored mitochondrial structure and the inhibition of hypoxia-inducible factor 1α (HIF-1α) or the transferrin receptor 1 (TFRC) rescued IL-1β-induced loss of mitochondrial membrane potential. Inhibition of HIF-1α downregulated IL-1β-induced TFRC expression, while inhibition of TFRC did not downregulate IL-1β-induced HIF-1α expression in chondrocytes. Moreover, inhibition of HIF-1α or TFRC downregulated the IL-1β-induced MMP13 expression in chondrocytes, while inhibition of HIF-1α or TFRC rescued IL-1β-inhibited COL2A1 expression in chondrocytes. Furthermore, upregulation of TFRC promoted Fe<sup>2+</sup> entry into chondrocytes, inducing the Fenton reaction and lipid peroxidation, which in turn caused ferroptosis, a disruption in chondrocyte functions, and an exacerbation of condylar cartilage degeneration. Together, these findings illustrate the far-reaching effects of chondrocyte ferroptosis in TMJOA as a mechanism causing chondrocyte death through iron overload, oxidative stress, and articular cartilage degeneration and a potential major cause of TMJOA.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"712-722"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141066649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-01Epub Date: 2024-06-18DOI: 10.1177/00220345241238688
M S Mozaffari
{"title":"Letter to the Editor, \"Cannabinoids and Acute Dental Pain\".","authors":"M S Mozaffari","doi":"10.1177/00220345241238688","DOIUrl":"10.1177/00220345241238688","url":null,"abstract":"","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":"103 7","pages":"765"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141428576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}