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Periodontitis and Diabetes Complications: A Danish Population-Based Study. 牙周炎与糖尿病并发症:一项基于丹麦人口的研究
Pub Date : 2024-08-01 Epub Date: 2024-08-05 DOI: 10.1177/00220345241259954
F V Bitencourt, A Andersen, L Bjerg, A Sandbæk, H Li, G G Nascimento, R Spin-Neto, M A Peres, F R M Leite

Conflicting evidence suggests a link between diabetes-related microvascular complications and periodontitis. Reliable estimates have been hindered by small sample sizes and residual confounding. Moreover, the combined effects of microvascular complications and dyslipidemia on periodontitis have not been explored. Therefore, this study aimed to investigate the association between individual and combined diabetic microvascular complications (i.e., neuropathy and retinopathy) and moderate/severe periodontitis in a Danish population-based study. In addition, we assessed whether dyslipidemia modified these associations. This study comprised 15,922 participants with type 2 diabetes from the Health in Central Denmark study. Multinomial logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for individual and joint microvascular diabetes complications. The models adjusted for potential confounders, including sociodemographic factors, lifestyle behaviors, and health conditions. Inverse probability of treatment weighting (IPTW) balanced measured confounders between periodontitis and nonperiodontitis participants. Sensitivity analyses tested the findings' robustness by estimating E-values for unmeasured confounding and varying microvascular complication definitions. After IPTW, adjusted models revealed that diabetic neuropathy (OR 1.36, 95% CI 1.14 to 1.63) and retinopathy (OR 1.21, 95% CI 1.03 to 1.43) were significantly associated with moderate/severe periodontitis. Moreover, the coexistence of microvascular complications increased the odds 1.5-fold for moderate/severe periodontitis (OR 1.51, 95% CI 1.23 to 1.85). An effect modification of dyslipidemia on an additive scale was found, indicated by a positive relative excess risk due to interaction of 0.24 for neuropathy, 0.11 for retinopathy, and 0.44 for both complications. Sensitivity analysis ruled out unmeasured confounders and microvascular complication definitions as explanatory factors. Diabetic neuropathy and retinopathy, individually and combined, were associated with moderate/severe periodontitis. In addition, dyslipidemia had an additive positive effect modification on diabetic microvascular complications, elevating the odds of moderate/severe periodontitis. These findings may aid in identifying at-risk subgroups for diabetes-related microvascular complications and periodontitis, optimizing efforts to mitigate disease burden.

相互矛盾的证据表明,糖尿病相关微血管并发症与牙周炎之间存在联系。由于样本量小和残余混杂因素,可靠的估计结果受到阻碍。此外,尚未探讨微血管并发症和血脂异常对牙周炎的综合影响。因此,本研究旨在通过一项基于丹麦人群的研究,探讨糖尿病微血管并发症(即神经病变和视网膜病变)与中度/重度牙周炎之间的关联。此外,我们还评估了血脂异常是否会改变这些关联。这项研究包括丹麦中部健康研究中的 15,922 名 2 型糖尿病患者。我们采用多叉逻辑回归法估算了单个和联合微血管糖尿病并发症的几率比(OR)和 95% 置信区间(CI)。模型调整了潜在的混杂因素,包括社会人口因素、生活方式行为和健康状况。反向治疗概率加权(IPTW)平衡了牙周炎和非牙周炎参与者之间的测量混杂因素。敏感性分析通过估算未测量混杂因素的 E 值和不同的微血管并发症定义来检验研究结果的稳健性。IPTW调整后的模型显示,糖尿病神经病变(OR 1.36,95% CI 1.14-1.63)和视网膜病变(OR 1.21,95% CI 1.03-1.43)与中度/重度牙周炎显著相关。此外,同时存在微血管并发症会使中度/重度牙周炎的几率增加 1.5 倍(OR 1.51,95% CI 1.23 至 1.85)。研究还发现,血脂异常对并发症的影响具有叠加效应,神经病变、视网膜病变和两种并发症的交互作用导致的正向相对超额风险分别为 0.24、0.11 和 0.44。敏感性分析排除了作为解释因素的未测量混杂因素和微血管并发症定义。糖尿病神经病变和视网膜病变单独或合并与中度/重度牙周炎有关。此外,血脂异常对糖尿病微血管并发症也有叠加的积极影响,提高了中度/重度牙周炎的几率。这些发现有助于确定糖尿病相关微血管并发症和牙周炎的高危亚群,从而优化减轻疾病负担的工作。
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引用次数: 0
Novel Antimitotic Agent SP-1-39 Inhibits Head and Neck Squamous Cell Carcinoma. 新型抗溃疡剂 SP-1-39 抑制头颈部鳞状细胞癌
Pub Date : 2024-08-01 Epub Date: 2024-08-05 DOI: 10.1177/00220345241261982
K L Adeleye, A R Li, Y Xie, S Pochampally, D Hamilton, F Garcia-Godoy, D D Miller, W Li

Effective management of head and neck cancer (HNC) poses a significant challenge in the field of oncology, due to its intricate pathophysiology and limited treatment options. The most common HNC malignancy is head and neck squamous cell carcinoma (HNSCC). HNSCC treatment includes a combination of surgery, radiation, and chemotherapy. While HNSCC is treatable if diagnosed early, this is often not the case and is considered incurable once in its late stages and metastatic disease has developed. Therapies are also limited once resistant disease has occurred. SP-1-39, a novel colchicine-binding site inhibitor (CBSI), has been recently reported for its potential efficacy in a variety of cancer cell lines including breast, melanoma, pancreatic, and prostate. SP-1-39 also shows abilities to overcome paclitaxel resistance in a paclitaxel-resistant prostate cancer xenograft model. To evaluate the potential of SP-1-39 as a new HNSCC treatment option, herein we systematically performed preclinical studies in HNSCC models using SP-1-39 and demonstrated that, in vitro, SP-1-39 inhibits the proliferation of 2 HNSCC cell lines with low nanomolar IC50 values (1.4 to 2.1 nM), induces HNSCC cell apoptosis in a dose-dependent manner, interferes with migration of HNSCC cells, and leads to HNSCC cell cycle arrest in the G2/M phase. In vivo, SP-1-39 suppresses the primary tumor growth of a Detroit 562 subcutaneous xenograft mouse model in 6- to 8-wk-old, male NSG (NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ) mice, with no detectable cytotoxic effects at a low dose of 2.5 mg/kg. This efficacy of SP-1-39 is better when compared with the treatment using a reference chemotherapy drug, paclitaxel at 10 mg/kg. Collectively, these data demonstrate that SP-1-39 is a promising candidate for further development for more efficacious HNSCC treatment.

头颈癌(HNC)的病理生理学错综复杂,治疗方案有限,因此有效治疗头颈癌是肿瘤学领域的一项重大挑战。最常见的 HNC 恶性肿瘤是头颈部鳞状细胞癌(HNSCC)。HNSCC 的治疗包括手术、放疗和化疗。虽然 HNSCC 在早期诊断的情况下是可以治疗的,但情况往往并非如此,一旦进入晚期并出现转移性疾病,就会被认为是无法治愈的。一旦出现耐药性疾病,治疗方法也会受到限制。SP-1-39 是一种新型秋水仙碱结合位点抑制剂 (CBSI),最近有报道称它对乳腺癌、黑色素瘤、胰腺癌和前列腺癌等多种癌症细胞系具有潜在疗效。SP-1-39 还能在紫杉醇抗性前列腺癌异种移植模型中克服紫杉醇抗性。为了评估 SP-1-39 作为一种新的 HNSCC 治疗方案的潜力,我们在此使用 SP-1-39 对 HNSCC 模型进行了系统的临床前研究,结果表明,在体外,SP-1-39 能以较低的纳摩尔 IC50 值(1.4 至 2.1 nM)抑制 2 种 HNSCC 细胞株的增殖,以剂量依赖性方式诱导 HNSCC 细胞凋亡,干扰 HNSCC 细胞的迁移,并导致 HNSCC 细胞周期停滞在 G2/M 期。在体内,SP-1-39 可抑制 Detroit 562 皮下异种移植小鼠模型中 6 至 8 周大雄性 NSG(NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ)小鼠的原发性肿瘤生长,在 2.5 毫克/千克的低剂量下没有检测到细胞毒性作用。与使用参考化疗药物紫杉醇(10 毫克/千克)进行治疗相比,SP-1-39 的疗效更好。这些数据共同表明,SP-1-39 是一种有望进一步开发的候选药物,可用于更有效的 HNSCC 治疗。
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引用次数: 0
PIEZO1 Promotes Odontoblast-Mediated Reactionary Dentinogenesis via SEMA3A. PIEZO1 通过 SEMA3A 促进牙本质母细胞介导的反应性牙本质生成
Pub Date : 2024-08-01 Epub Date: 2024-06-24 DOI: 10.1177/00220345241257866
P Huang, R X Jiang, F Wang, W W Qiao, Y T Ji, L Y Meng, Z Bian

Located at the interface of the dentin-pulp complex, the odontoblasts are specialized cells responsible for dentin synthesis and nociceptive signal detection in response to external stimuli. Recent studies have shown that the mechanosensitive ion channel PIEZO1 is involved in bone formation and remodeling through the influx of calcium ions, and it is abundantly expressed in odontoblasts. However, the specific role of PIEZO1 in reactionary dentinogenesis and the underlying mechanisms remain elusive. In this study, we found intense PIEZO1 expression in the plasma membrane and cytoplasm of odontoblasts in healthy human third molars, mouse mandibular molars, and human odontoblast-like cells (hOBLCs). In hOBLCs, PIEZO1 positively regulated DSPP, DMP1, and COL1A1 expression through the Ca2+/PI3K-Akt/SEMA3A signaling pathway. In addition, exogenous SEMA3A supplementation effectively reversed reduced mineralization capacity in PIEZO1-knockdown hOBLCs. In vivo, Piezo1 expression peaked at day 7 and returned to baseline at day 21 in a wild-type mice dentin injury model, with Sema3a presenting a similar expression pattern. To investigate the specific role of PIEZO1 in odontoblast-mediated reactionary dentinogenesis, mice with a conditional knockout of Piezo1 in odontoblasts were generated, and no significant differences in teeth phenotypes were observed between the control and conditional knockout (cKO) mice. Nevertheless, cKO mice exhibited reduced reactionary dentin formation and decreased Sema3a and Dsp positive staining after dentin injury, indicating impaired dental pulp repair by odontoblasts. In summary, these findings suggest that PIEZO1 enhances the mineralization capacity of hOBLCs in vitro via the Ca2+/PI3K-Akt/SEMA3A signaling pathway and contributes to reactionary dentinogenesis in vivo.

牙本质母细胞位于牙本质-牙髓复合体的界面,是负责牙本质合成和对外界刺激的痛觉信号检测的特化细胞。最近的研究表明,机械敏感性离子通道 PIEZO1 通过钙离子的流入参与骨形成和重塑,它在牙本质母细胞中大量表达。然而,PIEZO1 在反应性牙本质形成中的具体作用及其内在机制仍未确定。在这项研究中,我们发现 PIEZO1 在健康人类第三磨牙、小鼠下颌磨牙和人类牙本质母细胞样细胞(hOBLCs)的牙本质母细胞的质膜和细胞质中都有大量表达。在hOBLCs中,PIEZO1通过Ca2+/PI3K-Akt/SEMA3A信号通路正向调节DSPP、DMP1和COL1A1的表达。此外,补充外源 SEMA3A 能有效逆转 PIEZO1 敲除的 hOBLCs 矿化能力的降低。在体内,野生型小鼠牙本质损伤模型中,Piezo1的表达在第7天达到峰值,在第21天恢复到基线水平,Sema3a也呈现类似的表达模式。为了研究 PIEZO1 在牙本质母细胞介导的反应性牙本质生成中的特殊作用,我们在牙本质母细胞中产生了条件性敲除 Piezo1 的小鼠,在对照组和条件性敲除(cKO)小鼠之间没有观察到牙齿表型的显著差异。然而,cKO 小鼠的反应性牙本质形成减少,牙本质损伤后 Sema3a 和 Dsp 阳性染色减少,表明牙本质母细胞的牙髓修复功能受损。总之,这些研究结果表明,PIEZO1在体外通过Ca2+/PI3K-Akt/SEMA3A信号通路增强了hOBLCs的矿化能力,并有助于体内的反应性牙本质形成。
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引用次数: 0
The Use of Artificial Intelligence in Endodontics. 人工智能在牙髓病学中的应用。
Pub Date : 2024-08-01 Epub Date: 2024-05-31 DOI: 10.1177/00220345241255593
F C Setzer, J Li, A A Khan

Endodontics is the dental specialty foremost concerned with diseases of the pulp and periradicular tissues. Clinicians often face patients with varying symptoms, must critically assess radiographic images in 2 and 3 dimensions, derive complex diagnoses and decision making, and deliver sophisticated treatment. Paired with low intra- and interobserver agreement for radiographic interpretation and variations in treatment outcome resulting from nonstandardized clinical techniques, there exists an unmet need for support in the form of artificial intelligence (AI), providing automated biomedical image analysis, decision support, and assistance during treatment. In the past decade, there has been a steady increase in AI studies in endodontics but limited clinical application. This review focuses on critically assessing the recent advancements in endodontic AI research for clinical applications, including the detection and diagnosis of endodontic pathologies such as periapical lesions, fractures and resorptions, as well as clinical treatment outcome predictions. It discusses the benefits of AI-assisted diagnosis, treatment planning and execution, and future directions including augmented reality and robotics. It critically reviews the limitations and challenges imposed by the nature of endodontic data sets, AI transparency and generalization, and potential ethical dilemmas. In the near future, AI will significantly affect the everyday endodontic workflow, education, and continuous learning.

牙髓病学是牙科专业中最主要研究牙髓和根周组织疾病的学科。临床医生经常面对症状各异的患者,必须严格评估二维和三维放射影像,做出复杂的诊断和决策,并进行复杂的治疗。由于放射影像判读的观察者内部和观察者之间的一致性较低,以及非标准化临床技术导致的治疗效果差异,因此对人工智能(AI)形式的支持存在着尚未满足的需求,即在治疗过程中提供自动生物医学图像分析、决策支持和帮助。在过去十年中,人工智能在牙髓病学领域的研究稳步增加,但临床应用有限。这篇综述着重于批判性地评估牙髓病学人工智能研究在临床应用方面的最新进展,包括根尖周病变、骨折和吸收等牙髓病学病理的检测和诊断,以及临床治疗结果预测。报告讨论了人工智能辅助诊断、治疗规划和执行的优势,以及包括增强现实技术和机器人技术在内的未来发展方向。它批判性地回顾了牙髓病学数据集的性质、人工智能的透明度和通用性以及潜在的道德困境所带来的限制和挑战。在不久的将来,人工智能将极大地影响牙髓病学的日常工作流程、教育和持续学习。
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引用次数: 0
Changes in Use of Prenatal Dental Care After Brazil's Incentive Policy. 巴西实施激励政策后产前牙科保健使用情况的变化。
Pub Date : 2024-08-01 Epub Date: 2024-08-05 DOI: 10.1177/00220345241258459
H S Schuch, M Furtado, A D P Chiavegatto Filho, H W Elani

In 2020, the Brazilian federal government launched the "Prevent Brazil" program to incentivize cities to improve their performance across 7 health care indicators, including prenatal dental care. Our study examines the impact of this policy on the use of oral health care among pregnant women in Brazil. We used a series of cross-sectional data from the Brazilian Public Health System from 2018 to 2023. We linked publicly available data from the Brazilian Ministry of Health and the Brazilian Institute of Geography and Statistics. Our outcome was the proportion of pregnant women receiving prenatal care who had at least 1 dental visit during the past year. Covariates included city-level socioeconomic (income and literacy), demographic (gender, race, and urban areas), and workforce variables (number of dentists working in the public health system per city/year). We estimated the impact of the policy on prenatal dental visits nationwide and stratified by geographic region using interrupted time-series analysis. Our analyses included 99.9% of all Brazilian cities (n = 5,562). The use of oral health care among pregnant women increased from 15% in 2018 to 69% in 2023. Adjusted estimates show that, after initiation of the Prevent Brazil, dental care use among pregnant women increased nationally at a rate of 4.6 percentage points per 4-mo period (95% confidence interval [CI] 4.5; 4.7). The policy's largest impact was in the North and Northeast regions, which have the lowest socioeconomic profiles (adjusted time-series rate 5.7 [95% CI 5.3; 6.1] and 5.2 [5.0; 5.4] percent points, respectively). Our findings support the positive impact of the Prevent Brazil policy on prenatal dental care in Brazil. The policy was associated with a countrywide improvement in prenatal dental care use, with a greater impact in socioeconomically disadvantaged regions.

2020 年,巴西联邦政府启动了 "预防巴西 "计划,激励各城市改善其在 7 项医疗保健指标方面的表现,其中包括产前牙科保健。我们的研究探讨了这一政策对巴西孕妇使用口腔保健的影响。我们使用了巴西公共卫生系统从 2018 年到 2023 年的一系列横截面数据。我们链接了巴西卫生部和巴西地理统计研究所的公开数据。我们的研究结果是接受产前检查的孕妇在过去一年中至少接受过一次牙科检查的比例。协变量包括城市一级的社会经济(收入和文化程度)、人口(性别、种族和城市地区)和劳动力变量(每个城市每年在公共卫生系统工作的牙医人数)。我们使用间断时间序列分析法估算了该政策对全国产前牙科就诊的影响,并按地理区域进行了分层。我们的分析包括 99.9% 的巴西城市(n = 5,562)。孕妇使用口腔保健的比例从 2018 年的 15%增至 2023 年的 69%。调整后的估计值显示,在巴西预防计划启动后,全国孕妇牙科保健使用率每 4 个月增加 4.6 个百分点(95% 置信区间 [CI] 4.5; 4.7)。该政策对社会经济地位最低的北部和东北部地区影响最大(调整后的时间序列比率分别为 5.7 [95% CI 5.3; 6.1] 和 5.2 [5.0; 5.4] 个百分点)。我们的研究结果支持 "预防巴西 "政策对巴西产前牙科保健的积极影响。该政策与全国范围内产前牙科保健使用率的提高有关,在社会经济条件较差的地区影响更大。
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引用次数: 0
Type VI Collagen Deficiency Causes Enhanced Periodontal Tissue Destruction. VI 型胶原蛋白缺乏导致牙周组织破坏加剧
Pub Date : 2024-08-01 Epub Date: 2024-06-24 DOI: 10.1177/00220345241256306
T Komori, V Kram, S Perry, H T Pham, P Jani, T M Kilts, K Watanabe, D G Kim, D Martin, M F Young

The periodontal ligament (PDL) is a fibrillar connective tissue that lies between the alveolar bone and the tooth and is composed of highly specialized extracellular matrix (ECM) molecules and a heterogeneous population of cells that are responsible for collagen formation, immune response, bone formation, and chewing force sensation. Type VI collagen (COL6), a widely distributed ECM molecule, plays a critical role in the structural integrity and mechanical properties of various tissues including muscle, tendon, bone, cartilage, and skin. However, its role in the PDL remains largely unknown. Our study shows that deficiency of COL6 impairs PDL fibrillogenesis and exacerbates tissue destruction in ligature-induced periodontitis (LIP). We found that COL6-deficient mice exhibited increased bone loss and degraded PDL in LIP and that fibroblasts expressing high levels of Col6α2 are pivotal in ECM organization and cell-ECM interactions. Moreover, COL6 deficiency in the PDL led to an increased number of fibroblasts geared toward the inflammatory response. We also observed that cultured COL6-deficient fibroblasts from the PDL exhibited decreased expression of genes related to collagen fiber turnover and ECM organization as well as migration and proliferation. Our findings suggest that COL6 plays a crucial role in the PDL, influencing fibroblast function in fibrillogenesis and affecting the immune response in periodontitis. These insights advance our understanding of the molecular mechanisms underlying PDL maturation and periodontal disease.

牙周韧带(PDL)是位于牙槽骨和牙齿之间的纤维结缔组织,由高度特化的细胞外基质(ECM)分子和负责胶原形成、免疫反应、骨形成和咀嚼力感觉的异质细胞群组成。六型胶原蛋白(COL6)是一种广泛分布的细胞外基质分子,在肌肉、肌腱、骨骼、软骨和皮肤等各种组织的结构完整性和机械性能方面发挥着至关重要的作用。然而,它在 PDL 中的作用在很大程度上仍不为人所知。我们的研究表明,在结扎诱导的牙周炎(LIP)中,缺乏 COL6 会影响 PDL 纤维的生成并加剧组织破坏。我们发现,缺乏 COL6 的小鼠在 LIP 中表现出骨质流失增加和 PDL 降解,而表达高水平 Col6α2 的成纤维细胞在 ECM 组织和细胞-ECM 相互作用中起着关键作用。此外,PDL 中 COL6 的缺乏导致了炎症反应成纤维细胞数量的增加。我们还观察到,从 PDL 中培养出的 COL6 缺乏成纤维细胞表现出与胶原纤维周转和 ECM 组织以及迁移和增殖相关的基因表达减少。我们的研究结果表明,COL6 在 PDL 中起着至关重要的作用,它影响成纤维细胞在纤维生成过程中的功能,并影响牙周炎的免疫反应。这些见解加深了我们对 PDL 成熟和牙周疾病的分子机制的理解。
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引用次数: 0
Melatonin and Metformin Mitigate Doxorubicin-Induced Alveolar Bone Toxicity. 褪黑素和二甲双胍可减轻多柔比星诱发的肺泡骨毒性
Pub Date : 2024-08-01 Epub Date: 2024-08-05 DOI: 10.1177/00220345241261980
B Srivichit, C Thonusin, R Aeimlapa, A Arinno, T Chunchai, N Charoenphandhu, N Chattipakorn, S C Chattipakorn

Evidence concerning the osteotoxic effects of chemotherapy (doxorubicin) has been previously described. Periodontitis also progressively increases in patients receiving chemotherapy; however, the beneficial effects of melatonin and metformin on the alleviation of doxorubicin-induced osteotoxicity have never been investigated. Therefore, we investigated the negative impact of doxorubicin on alveolar bone homeostasis and the benefits of melatonin and metformin on the attenuation of doxorubicin-induced alveolar bone toxicity. Male Wistar rats were divided into 4 groups to receive either 1 mL of normal saline solution as a control group, 3 mg/kg of doxorubicin, 3 mg/kg of doxorubicin plus 10 mg/kg of melatonin, or 3 mg/kg of doxorubicin plus 250 mg/kg of metformin. Doxorubicin treatment was given on days 0, 4, 8, 15, 22, and 29, while interventions were given daily on days 0 to 29. Following euthanasia, blood and alveolar bones were collected for evaluation of oxidative stress, bone remodeling, inflammation, microarchitecture, and periodontal condition. We found that doxorubicin increased systemic oxidative stress, decreased antioxidative capacity, increased inflammation, decreased bone formation, increased bone reabsorption, impaired microarchitecture, and impaired periodontal condition of the alveolar bone. Although cotreatment with melatonin or metformin resulted in some improvement in these parameters, cotreatment with melatonin was more effective than cotreatment with metformin in terms of decreasing oxidative stress, reducing bone resorption, and improving microarchitecture and periodontal condition. All of these findings highlight the potential for antioxidants, especially melatonin, to ameliorate doxorubicin-induced alveolar bone toxicity.

化疗(多柔比星)对骨毒性的影响已有相关证据。然而,褪黑素和二甲双胍对缓解多柔比星引起的骨毒性的有益作用却从未被研究过。因此,我们研究了多柔比星对牙槽骨稳态的负面影响,以及褪黑素和二甲双胍对减轻多柔比星诱导的牙槽骨毒性的益处。雄性 Wistar 大鼠被分为 4 组,分别接受 1 mL 生理盐水作为对照组、3 mg/kg 多柔比星、3 mg/kg 多柔比星加 10 mg/kg 褪黑激素或 3 mg/kg 多柔比星加 250 mg/kg 二甲双胍。多柔比星治疗在第0、4、8、15、22和29天进行,而干预则在第0至29天每天进行。安乐死后,收集血液和牙槽骨以评估氧化应激、骨重塑、炎症、微结构和牙周状况。我们发现,多柔比星增加了全身氧化应激,降低了抗氧化能力,增加了炎症,减少了骨形成,增加了骨再吸收,损害了微结构,损害了牙槽骨的牙周状况。虽然褪黑素或二甲双胍联合治疗可在一定程度上改善这些参数,但在降低氧化应激、减少骨吸收、改善微结构和牙周状况方面,褪黑素联合治疗比二甲双胍联合治疗更有效。所有这些发现都凸显了抗氧化剂,尤其是褪黑素在改善多柔比星诱导的牙槽骨毒性方面的潜力。
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引用次数: 0
Topical Vitamin D Prevents Bone Loss and Inflammation in a Mouse Model. 外用维生素 D 可防止小鼠模型中的骨质流失和炎症。
Pub Date : 2024-08-01 Epub Date: 2024-08-05 DOI: 10.1177/00220345241259417
K L Kirkwood, T E Van Dyke, C L Kirkwood, L Zhang, J Panezai, A E Duran-Pinedo, E L Figgins, L K Ryan, J J Frias-Lopez, G Diamond

There is a strong association between vitamin D levels and periodontal disease based on numerous epidemiological studies. We have previously shown that experimental deficiency of serum vitamin D in mice leads to gingival inflammation and alveolar bone loss. Treatment of cultured oral epithelial cells with the active form of vitamin D, 1,25(OH)2 vitamin D3 (1,25(OH)2D3), inhibits the extracellular growth and intracellular invasion of bacteria associated with periodontal disease. Maintenance of periodontal health may be due in part to the anti-inflammatory activities of vitamin D. Furthermore, this hormone can induce the expression of an antimicrobial peptide in cultured oral epithelial cells. We have shown that oral epithelial cells are capable of converting inactive vitamin D to the active form, suggesting that topical treatment of the oral epithelium with inactive vitamin D could prevent the development of periodontitis. We subjected mice to ligature-induced periodontitis (LIP), followed by daily treatment with inactive vitamin D or 1,25(OH)2D3. Treatment with both forms led to a reduction in ligature-induced bone loss and inflammation. Gingival tissues obtained from vitamin D-treated LIP showed production of specialized proresolving mediators (SPM) of inflammation. To examine the mechanism, we demonstrated that apical treatment of 3-dimensional cultures of primary gingival epithelial cells with vitamin D prevented lipopolysaccharide-induced secretion of proinflammatory cytokines and led to a similar production of SPM. Analysis of the oral microbiome of the mice treated with vitamin D showed significant changes in resident bacteria, which reflects a shift toward health-associated species. Together, our results show that topical treatment of oral tissues with inactive vitamin D can lead to the maintenance of periodontal health through the regulation of a healthy microbiome and the stimulation of resolution of inflammation. This strongly supports the development of a safe and effective vitamin D-based topical treatment or preventive agent for periodontal inflammation and disease.

根据大量流行病学研究,维生素 D 水平与牙周病之间存在密切联系。我们以前的研究表明,小鼠实验性血清维生素 D 缺乏会导致牙龈炎症和牙槽骨流失。用维生素 D 的活性形式--1,25(OH)2 维生素 D3(1,25(OH)2D3)处理培养的口腔上皮细胞,可抑制与牙周病相关的细菌的胞外生长和胞内侵袭。此外,这种激素还能诱导培养的口腔上皮细胞表达一种抗菌肽。我们已经证明,口腔上皮细胞能够将非活性维生素 D 转化为活性形式,这表明用非活性维生素 D 局部治疗口腔上皮细胞可以预防牙周炎的发生。我们对小鼠进行了结扎诱导的牙周炎(LIP)治疗,然后每天用非活性维生素 D 或 1,25(OH)2D3进行治疗。这两种维生素都能减少结扎诱发的骨质流失和炎症。从经维生素 D 处理的 LIP 中获得的牙龈组织显示,产生了专门的炎症促溶解介质(SPM)。为了研究其机理,我们证明了用维生素 D 对原代牙龈上皮细胞的三维培养物进行根尖处理可防止脂多糖诱导的促炎细胞因子的分泌,并导致产生类似的 SPM。对接受维生素 D 治疗的小鼠口腔微生物组的分析表明,常驻细菌发生了显著变化,这反映出小鼠口腔微生物组向与健康相关的菌种转变。总之,我们的研究结果表明,用非活性维生素 D 局部治疗口腔组织可通过调节健康的微生物群和刺激炎症消退来维持牙周健康。这有力地支持了以安全有效的维生素 D 为基础的牙周炎症和疾病局部治疗或预防剂的开发。
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引用次数: 0
Macrophage Polarization during MRONJ Development in Mice. 小鼠 MRONJ 发育过程中的巨噬细胞分化
Pub Date : 2024-08-01 Epub Date: 2024-08-05 DOI: 10.1177/00220345241258990
A Soundia, N Elzakra, D Hadaya, I Gkouveris, O Bezouglaia, S Dry, T Aghaloo, S Tetradis

Macrophages are important regulators of bone remodeling, and M1 polarization is observed in the setting of medication-related osteonecrosis of the jaws (MRONJ). Here, we characterize the phenotype of macrophages during early stages of MRONJ development in zoledronate (ZA)-treated mice with periodontal disease and explore the role of rosiglitazone, a drug that has been reported to lower the M1/M2 macrophage ratio, in MRONJ burden. Mice received ZA, and experimental periodontal disease (EPD) was induced around their second left maxillary molar. The mice were euthanized 1, 2, or 4 wk later. Micro-computed tomography and histologic and immunohistochemical analyses were carried out. In a separate experiment, mice were treated with ZA in the absence or presence of rosiglitazone, EPD was induced for 5 wk, and the MRONJ burden was assessed. An M1 predilection was noted in ZA versus vehicle (Veh) mice at 1, 2, or 4 wk after ligature placement. M1 cells were found to be positive for MMP-13, and their presence coincided with disruption of the surrounding collagen network in ZA mice. Rosiglitazone caused a reversal in the M1/M2 polarization in Veh and ZA mice. Rosiglitazone did not cause significant radiographic changes 5 wk after EPD in Veh or ZA animals. Importantly, percentage osteonecrosis and bone exposure were decreased in the rosiglitazone-treated versus nontreated ZA sites 5 wk after EPD. Our data point to an important role of M1 macrophage polarization with an overexpression of MMP-13 in the early phases of MRONJ development and provide insight into the use of interventional approaches promoting an M2 phenotype as a preventative means to alleviate MRONJ burden.

巨噬细胞是骨重塑的重要调节因子,在药物相关性颌骨坏死(MRONJ)的情况下可观察到巨噬细胞的M1极化。在这里,我们描述了唑来膦酸钠(ZA)治疗的牙周病小鼠在MRONJ发展早期阶段巨噬细胞的表型,并探讨了罗格列酮(一种据报道能降低M1/M2巨噬细胞比例的药物)在MRONJ负担中的作用。小鼠接受ZA治疗,并在左侧第二颗上颌臼齿周围诱发实验性牙周病(EPD)。小鼠在1、2或4周后被安乐死。对小鼠进行显微计算机断层扫描、组织学和免疫组化分析。在另一项实验中,小鼠在无罗格列酮或有罗格列酮的情况下接受ZA治疗,诱导EPD 5周,并评估MRONJ负担。在结扎后1、2或4周时,ZA与载体(Veh)小鼠相比,发现M1偏好。发现 M1 细胞对 MMP-13 呈阳性反应,它们的存在与ZA 小鼠周围胶原网络的破坏相吻合。罗格列酮导致Veh和ZA小鼠的M1/M2极化发生逆转。罗格列酮不会导致Veh和ZA小鼠在EPD 5周后出现明显的放射学变化。重要的是,在EPD 5周后,罗格列酮处理的ZA部位与未处理的ZA部位相比,骨坏死和骨暴露的百分比均有所下降。我们的数据表明,M1巨噬细胞极化与MMP-13的过度表达在MRONJ发展的早期阶段起着重要作用,并为使用促进M2表型的干预方法作为减轻MRONJ负担的预防手段提供了启示。
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引用次数: 0
New Monomer Capable of Dual Chemical Binding with Dentin to Improve Bonding Durability. 能与牙本质进行双重化学结合的新型单体,可提高粘接耐久性。
Pub Date : 2024-07-01 Epub Date: 2024-06-13 DOI: 10.1177/00220345241253526
H M Wang, K X Li, Z L Tian, Y L Zhu, X Y Liu, S H Yang, S W Qiao, S Zhu, Z S Shi

The water-rich nature of the dentin bonding microenvironment, coupled with the stresses on the bonding interface, contributes to the hydrolytic degradation of the hybrid layer, resulting in a decline in bonding durability and, ultimately, restoration failure. Currently, the 3-step etch-and-rinse technique remains the gold standard for dentin bonding, and the bonding mechanism mainly involves a physical interaction with little chemical bonding. In this study, we have developed a siloxane-modified polyurethane monomer (SPU) with acrylate and siloxane modifications that chemically binds to both collagen and hydroxyapatite in dentin. Formulated as a bisphenol A-glycidyl methacrylate alternative, the SPU monomer-based adhesive was designed to improve dentin bonding quality and durability. Attenuated total reflection Fourier transform infrared spectroscopy, thermogravimetric analysis, X-ray photoelectron spectroscopy, scanning electron microscopy, transmission electron microscope, and hydroxyproline release assays were performed on SPU-treated collagen, hydroxyapatite, and acid-etched dentin slices to dentin. The physicochemical properties of the configured SPU adhesives were profiled for polymerization behavior, water contact angle, and tensile strain and strength. The bonding effectiveness was assessed through micro-tensile strength, nano-leakage tests conducted on the bonded samples before and after thermal cycle aging. Finally, we further conducted in vivo and in vitro experiments to assess the biocompatibility of adhesives. The results showed that the siloxane groups of SPU monomer could covalently bind to dentin collagen and hydroxyapatite. The incorporation of SPU in the adhesive led to a significant increase in adhesive polymerization (P < 0.05) and tensile strain at break up to 134.11%. Furthermore, the SPU adhesive significantly improved dentin bond strength (P < 0.05), reduced interfacial nano-leakage (P < 0.05), and displayed good biocompatibility. In conclusion, the application of SPU, which achieves dual chemical bonding with dentin, can improve the quality of the hybrid layer, buffer the interfacial stresses, enhance the interfacial resistance to hydrolysis, and provide a feasible strategy to extend the service life of adhesive restorations.

牙本质粘接微环境富含水分,再加上粘接界面上的应力,会导致混合层水解降解,导致粘接耐久性下降,最终导致修复失败。目前,三步蚀刻-冲洗技术仍是牙本质粘接的黄金标准,其粘接机制主要涉及物理相互作用,很少涉及化学粘接。在这项研究中,我们开发了一种硅氧烷改性聚氨酯单体(SPU),它具有丙烯酸酯和硅氧烷改性,能与牙本质中的胶原蛋白和羟基磷灰石发生化学结合。作为双酚 A-甲基丙烯酸缩水甘油酯的替代品,这种基于 SPU 单体的粘合剂旨在提高牙本质粘合质量和耐久性。在 SPU 处理过的胶原、羟基磷灰石和酸蚀牙本质切片上进行了衰减全反射傅立叶变换红外光谱、热重分析、X 射线光电子能谱、扫描电子显微镜、透射电子显微镜和羟脯氨酸释放测定。对配置好的 SPU 粘合剂的物理化学特性进行了分析,包括聚合行为、水接触角、拉伸应变和强度。通过对热循环老化前后的粘合样本进行显微拉伸强度和纳米渗漏测试,评估了粘合效果。最后,我们进一步进行了体内和体外实验,以评估粘合剂的生物相容性。结果表明,SPU 单体的硅氧烷基团可与牙本质胶原和羟基磷灰石共价结合。在粘合剂中加入 SPU 后,粘合剂的聚合度显著提高(P < 0.05),断裂拉伸应变高达 134.11%。此外,SPU 粘合剂明显提高了牙本质粘接强度(P < 0.05),减少了界面纳米渗漏(P < 0.05),并显示出良好的生物相容性。总之,SPU 能与牙本质实现双重化学结合,可以提高混合层的质量,缓冲界面应力,增强界面抗水解性,为延长粘接修复体的使用寿命提供了一种可行的策略。
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引用次数: 0
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Journal of dental research
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