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Molecular Signatures of Senescence in Periodontitis: Clinical Insights. 牙周炎中衰老的分子特征:临床见解。
Pub Date : 2024-07-01 Epub Date: 2024-06-14 DOI: 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.

大多数老年人都患有牙周病,给全世界的健康造成了负担。细胞衰老是衰老的标志之一,与多种慢性并发症有关。衰老细胞会产生多种有害分泌物,统称为衰老相关分泌表型(SASP)。这会破坏邻近细胞,导致衰老进一步扩散,并引发慢性炎症,即所谓的 "炎症"。组织微环境中的有害反响可在较年轻时触发衰老,加速生物衰老,并推动疾病的发生或发展。在这里,我们通过评估关键衰老标志物(p16、脂质褐素和β-半乳糖苷酶)和炎症介质(白细胞介素[IL]-1β、IL-6、IL-8、基质金属蛋白酶[MMP]-1、MMP-3 和肿瘤坏死因子-α)的水平,研究了健康和患病牙龈组织中衰老的生物学特征。我们的研究结果表明,与所有年龄组的健康部位相比,牙周炎患者上皮组织和结缔组织的衰老特征(包括 p16、脂褐素和 β-半乳糖苷酶)均明显增加,这表明炎症微环境也会引发年轻病变牙龈组织的衰老样改变。随后使用特异性细胞标记物进行双重染色分析发现,β-半乳糖苷酶在成纤维细胞和巨噬细胞中富集。同时,从牙周炎病变中获取的牙龈活检组织中与 SASP 一致的炎症介质也有所增加。总之,我们的研究结果提供了第一份临床报告,揭示了牙龈组织易受衰老和炎症环境升高的影响,这与衰老分泌组一致,因此衰老是口腔黏膜病理事件的驱动因素之一,也是有针对性干预的新策略。
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引用次数: 0
METTL3 Modulates Ctsk+ Lineage Supporting Cranial Osteogenesis via Hedgehog. METTL3通过刺猬调节支持颅骨生成的Ctsk+系谱
Pub Date : 2024-07-01 Epub Date: 2024-05-16 DOI: 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.

N6-甲基腺苷(m6A)修饰是由甲基转移酶样3(METTL3)催化的真核信使RNA修饰,在干细胞命运决定中起着关键作用。颅骨的发育和维持由颅缝协调。Cathepsin K(CTSK)阳性的钙质干细胞(CSCs)有助于小鼠钙质骨化。然而,m6A修饰在调控钙骨发育过程中Ctsk+系细胞的作用仍不明确。在这里,我们发现 METTL3 与颅骨非骨形成的 Ctsk+ 系细胞共定位,这些细胞也与 GLI1 的表达有关。在新生儿发育过程中,Ctsk+系细胞中的Mettl3缺失会延迟缝合线的形成并降低矿化度。在成年期的维持过程中,Ctsk+系细胞中Mettl3的缺失会影响犊骨的形成,其特点是骨孔隙率增加、骨髓腔增大、骨细胞数量减少且细胞轮廓不发达。甲基化 RNA 免疫沉淀测序和 RNA 测序数据的分析表明,METTL3 的缺失减少了 Hedgehog(Hh)信号通路。通过杂交 Sufufl/+ 等位基因或局部注射 SAG21 恢复 Hh 信号通路可部分缓解异常。我们的数据表明,METTL3通过调节Hh信号通路来调节支持钙骨形成的Ctsk+系细胞,为临床治疗颅顶骨疾病提供了新的思路。
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引用次数: 0
Deep Learning-Based Facial and Skeletal Transformations for Surgical Planning. 基于深度学习的面部和骨骼变换手术规划。
Pub Date : 2024-07-01 Epub Date: 2024-05-29 DOI: 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.

虚拟手术规划(VSP)在正颌外科手术中的应用越来越广泛,这意味着准确预测面部和骨骼形状的需求非常迫切。由于面部软组织和骨骼之间错综复杂的解剖结构和非线性关系,颌面部畸形患者的颅颌面关系仍不为人所知,面部和骨骼形状之间的转换仍是一项具有挑战性的任务。本研究基于大规模数据集,开发并验证了一种名为 P2P-ConvGC 的新型双向三维(3D)深度学习框架,可实现面部和骨骼形状之间的精确转换。具体来说,该框架采用两阶段点采样策略生成多个非重叠点子集,以表示高分辨率的面部和骨骼形状。面部和骨骼点子集分别输入预测系统,通过骨骼预测子网络和面部预测子网络预测相应的骨骼和面部点子集。在定量评估中,准确度是根据预测的骨骼或面部与相应的地面实况之间的形状误差和地标误差来计算的。形状误差是通过比较预测点集和地面实况计算得出的,P2P-ConvGC 优于现有的最先进算法,包括 P2P-Net、P2P-ASNL 和 P2P-Conv。P2P-ConvGC 在上颅骨、下颌骨和面部软组织的总地标误差(颅颌面地标欧氏距离)分别为 1.964 ± 0.904 mm、2.398 ± 1.174 mm 和 2.226 ± 0.774 mm。此外,双向模型的临床可行性还通过临床队列进行了验证。结果表明,该模型的预测能力很强,面部预测的平均表面偏差误差为 0.895 ± 0.175 毫米,骨骼预测的平均表面偏差误差为 0.906 ± 0.082 毫米。总之,我们提出的模型在特定对象的面部和骨骼形状预测方面取得了良好的性能,并在正颌手术的术后面部预测和 VSP 方面显示出了临床应用潜力。
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引用次数: 0
Recent Advances in Digital Technology in Implant Dentistry. 种植牙数字技术的最新进展。
Pub Date : 2024-07-01 Epub Date: 2024-05-31 DOI: 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.

数字技术已成为牙科种植领域的变革性工具,可在诊断、术前治疗规划、手术过程和修复交付等多个方面显著提高准确性和有效性。通过虚拟规划软件将放射影像数据和口内数据(有时还包括面部扫描数据或电子面弓)进行多重整合,可实现软硬组织和未来修复体位置的全面三维可视化,从而提高诊断精度。在虚拟手术设计中,通过分析横截面图像和重建三维表面模型,结合修复体的排列和个体解剖细节,可以虚拟执行关键程序(如植入、扩展应用等)。经过验证后,利用包括模板、导航、组合技术和种植机器人在内的数字技术,实现了虚拟治疗方案与实际手术部位的无缝对接,最终提高了手术效果和准确性。在修复服务方面,印模、色调匹配和修复体制作的数字化技术不断进步,实现了无缝数字数据转换以及临床医生和技术人员之间的高效沟通。与临床医学相比,人工智能(AI)技术在牙科种植中的应用主要集中在诊断和预测方面。人工智能支持的术前规划和手术仍处于发展阶段,受到临床病例的复杂性和伦理因素的阻碍,从而限制了其广泛应用。
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引用次数: 0
The Role of Pericyte Migration and Osteogenesis in Periodontitis. 牙周膜迁移和骨生成在牙周炎中的作用。
Pub Date : 2024-07-01 Epub Date: 2024-05-31 DOI: 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.

为了探索周细胞在牙槽骨形成中的功能,我们在野生型小鼠和CD146CreERT2; RosatdTomato小鼠中建立了结扎诱导的牙周炎模型。我们发现,在牙周炎进展和牙周伤口愈合过程中,CD146+/NG2+周细胞在牙周组织区域富集,它们可以迁移到牙槽骨表面并与ALP+/OCN+成骨细胞共定位。使用AMD3100抑制趋化因子C-X-C受体4(CXCR4)可阻断CD146-Cre+周细胞的迁移和成骨,并进一步加剧牙周炎相关骨质流失。接着,用磁激活细胞分选法分选出原发性周细胞,并证明 C-X-C motif趋化因子配体 12(CXCL12)通过 CXCL12-CXCR4-Rac1 信号传导促进周细胞迁移和成骨。最后,在局部注射腺相关病毒使 Rac1 在 NG2+周细胞中过度表达,可促进周细胞的成骨细胞分化,并增加牙周炎患者的牙槽骨体积。因此,我们的研究结果为牙周炎病理过程中周细胞可能通过CXCL12-CXCR4-Rac1轴迁移和成骨提供了证据。
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引用次数: 0
Increased Fluorohydroxyapatite across Dentin after Fluoride Iontophoresis. 氟化物离子注入后牙本质上的氟羟基磷灰石增加
Pub Date : 2024-07-01 Epub Date: 2024-05-29 DOI: 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。
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引用次数: 0
Brittle-Ductile Threshold in Lithium Disilicate under Sharp Sliding Contact. 尖锐滑动接触下二硅酸锂的脆性-延展阈值
Pub Date : 2024-07-01 Epub Date: 2024-06-14 DOI: 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.

计算机辅助设计(CAD)/计算机辅助制造(CAM)铣削和手机研磨是制作和调整陶瓷牙科修复体的关键程序。然而,由于微裂纹的形成,这些程序对陶瓷的强度不利。本研究分析了当前脆性机制研磨所造成的损害,并提出了一种潜在的补救措施,即应用一种更安全但仍然有效的研磨机制,即 "韧性机制研磨"。根据制造商的说明,通过切割和结晶偏硅酸锂 CAD/CAM 坯料(即所谓的蓝块),获得了二硅酸锂玻璃陶瓷材料(IPS e.max CAD)的圆盘状试样。然后将圆盘抛光至 1 µm 的金刚石悬浮表面。使用锥形金刚石压头进行单颗粒微划痕测试(n = 10),以再现变形和断裂的基本模式。记录了摩擦系数和穿透深度等关键参数与划痕载荷的函数关系。此外,在施加各种划痕载荷后还进行了双轴挠曲强度测试(n = 6),以分析它们对陶瓷强度的影响。扫描电子显微镜(SEM)和聚焦离子束(FIB)用于表征表面和次表面损伤。统计分析采用单因子方差分析和 Tukey 检验。虽然扫描电子显微镜(SEM)对划痕痕迹的表面分析表明存在韧性和脆性去除模式,但未能准确确定脆性-韧性转变的阈值载荷。根据结合强度退化研究进行的 FIB 表面下损伤分析,脆性-韧性转变的阈值载荷被确定为 70 mN。低于 70 mN 时,试样既不会出现强度下降,也不会形成表面下裂纹。脆性-韧性阈值的确定具有重要意义,因为它为今后研究实施韧性机制研磨/磨削协议以制造无损伤陶瓷牙科修复体的可行性奠定了基础。
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引用次数: 0
Inflammation Triggers Chondrocyte Ferroptosis in TMJOA via HIF-1α/TFRC. 炎症通过 HIF-1α/TFRC 触发颞下颌关节畸形中的软骨细胞铁凋亡
Pub Date : 2024-07-01 Epub Date: 2024-05-20 DOI: 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.

颞下颌关节骨关节炎(TMJOA)是颞下颌关节(TMJ)的一种疼痛性疾病,炎症和关节软骨损失被认为是其主要原因。为了确定这些患者颞下颌关节骨关节炎的病因,我们比较了透明质酸灌洗前后颞下颌关节骨关节炎患者滑膜液的情况,结果发现白细胞介素(IL)1β、反应性氧化应激(ROS)水平大幅升高,灌洗前Fe3+和Fe2+超负荷,这表明软骨细胞死亡的一种模式是铁变态反应。为了探究长期的炎症条件是否会导致体外的类铁变态反应,我们让颞下颌关节软骨细胞接受IL-1β处理,结果发现与铁平衡和氧化应激相关的细胞死亡有关的信使RNA测序基因本体发生了变化。在大鼠单侧前交叉咬合条件下,COL2A1表达减少,软骨细胞减少,谷胱甘肽过氧化物酶4(GPX4)下调,4-羟基壬烯醛(4-HNE)上调。我们的研究表明,铁变态反应会影响线粒体的结构和功能,而抑制剂 Fer-1 可恢复线粒体结构,抑制缺氧诱导因子 1α(HIF-1α)或转铁蛋白受体 1(TFRC)可挽救 IL-1β 诱导的线粒体膜电位损失。抑制 HIF-1α 会下调 IL-1β 诱导的 TFRC 表达,而抑制 TFRC 不会下调 IL-1β 诱导的 HIF-1α 在软骨细胞中的表达。此外,抑制 HIF-1α 或 TFRC 可下调 IL-1β 诱导的 MMP13 在软骨细胞中的表达,而抑制 HIF-1α 或 TFRC 可挽救 IL-1β 抑制的 COL2A1 在软骨细胞中的表达。此外,TFRC 的上调会促进 Fe2+ 进入软骨细胞,诱导 Fenton 反应和脂质过氧化反应,进而引起铁变态反应、软骨细胞功能紊乱和髁状软骨退化加剧。这些发现共同说明了软骨细胞铁变态反应在 TMJOA 中的深远影响,它是一种通过铁超载、氧化应激和关节软骨变性导致软骨细胞死亡的机制,也是 TMJOA 的潜在主要病因。
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引用次数: 0
Expression of Concern: "Porphyromonas gingivalis Evades Immune Clearance by Regulating Lysosome Efflux". 表达关切:"牙龈卟啉单胞菌通过调节溶酶体外流逃避免疫清除"。
Pub Date : 2024-07-01 Epub Date: 2024-05-23 DOI: 10.1177/00220345241251822
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引用次数: 0
Letter to the Editor, "Cannabinoids and Acute Dental Pain". 致编辑的信,"大麻素与急性牙痛"。
Pub Date : 2024-07-01 Epub Date: 2024-06-18 DOI: 10.1177/00220345241238688
M S Mozaffari
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引用次数: 0
期刊
Journal of dental research
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