本研究由中国国家自然科学基金U21A20368（L.Y.）、82101000（H.W.）和82100982（F.L.）以及四川省科技计划2023NSFSC1499（H.W.）资助。所有原始数据和图像均包含在本文中。

本研究的实验程序经四川大学华西口腔医学院伦理委员会（WCHSIRB-D-2021-125）批准。成年C57BL / 6小鼠购自中国成都的Gempharmatech实验动物公司。上颌第一磨牙的整个牙冠在出生后 21 天萌出。手术小鼠的年龄应大于21天，具有正常活力11。在这里，使用 6 至 8 周龄的小鼠进行建模。 图 1 是一个流程图，显示了所使用的协议。
1.术前准备（图2）
<ol><li>获取以下仪器：立体显微镜、固定板、医用胶带、口腔堵嘴、直径0.6mm的微创牙科毛刺、牙科高速牙科手机、8# C+锉、加热垫、1 mL注射器、无菌棉球、眼钳。</li>
	<li>获得以下药物：麻醉混合物，兽药膏。</li>
</ol>2.口塞的准备
<ol><li>通过腹膜内注射麻醉混合溶液（10%盐酸氯胺酮+ 5%甲苯噻嗪+ 85%无菌等渗盐水）以0.007mL / g体重称重并麻醉小鼠，并通过脚趾捏法确认适当的麻醉。将眼科润滑膏涂抹在眼睛上，以防止手术时因干燥而造成眼睛受伤。 注意：医用帽子、口罩、手套和工作服以及其他基本保护措施是必要的。确保手术环境和小鼠室清洁安全。在整个过程中，用于热支撑的加热垫是必要的。</li>
	<li>如下所述准备嘴巴堵嘴（图3）。<ol><li>获得以下材料：直径为 8 μm 的正畸弓丝、年轻的环弯曲钳、重型钢丝钳、记号笔、长度为 3 mm、横截面直径为 1 mm 的橡胶帽。</li>
		<li>首先，用左手拉直弓形线进行固定，右手的拇指、食指稍微弯曲以抵挡线的弧度。重复此动作几次，将有助于弯曲到正确的三维角度。</li>
		<li>使用Yong环弯曲钳将梯形（图3C，a-l-k-b）的顶部边缘（图3G，a-i）弯曲在弓形丝的中点长约8 mm。确保点 a（图 3）位于钳嘴的边缘。</li>
		<li>用左手握住钳子，用右手拇指和食指夹住弓线的自由端，从a点弯曲弓线，形成约120°的角度。在点i处复制上一个操作（图3G）。将弓形线放在水平台上而不撬动，检查弓形线是否在一个平面上。</li>
		<li>每侧留出约 9 毫米的长度（图 3D、a-b、l-k），并使用与步骤 2.2.4 相同的技能将自由端弯曲到 75° 角，同时确保每条边都在一个平面上。用钳嘴的尖端弯曲这个锐角。</li>
		<li>找到距离 b 点约 5 毫米的 c 点。按照相同的技巧在点 c 上弯曲 105° 角。在距离 c 点 5 毫米的 d 点再弯曲 105° 角。距 d 点约 4.5 mm，找到 e 点。在点 e 处弯曲自由端以形成约 100 -105° 的角度（图 3E）。 注意：我们使用的 6-8 周龄的 C57 小鼠约为 20 g。5毫米的间距不仅可以卡住小鼠的上下颚而不动弹，而且不会压迫小鼠的皮肤而引起不适。如果使用其他种类或年龄的小鼠，请根据实际情况调整c-d和i-h部分的长度（图3E，G）。</li>
		<li>为下颌部分弯曲一个额外的压舌板（图3G，j-i-h-g）。</li>
		<li>a-b-c零件在l-k-j零件上的重复弯曲步骤。同时夹紧 i-k 和 k-j 零件，并在 j 点弯曲自由端，使其垂直于 i-k-j 平面。夹紧点 i 距点 j 5 mm，弯曲自由端以使其平行于 i-k-j 平面和 c-d 部分（图 3H）。</li>
		<li>从 i 点起留 5 mm 长度，在 h 点处，将拱形弯曲垂直于 i-h 部分并平行于 j-i-h 平面。在距点 h 5 毫米处找到点 g。夹紧 j-i-h-g 平面并弯曲对称于 k-j 部分的自由端。然后，点f之后的自由端应与点e的自由端对称（图3H）。</li>
		<li>将橡胶帽放在自由端（图3F）。</li>
	</ol></li>
</ol>3. 固定
<ol><li>将小鼠仰卧固定在固定板上，四肢用皮胶带固定。用拇指和食指压缩嘴巴的自由端。</li>
	<li>将鼠标前门牙固定在两条手臂的梯形凹槽中。确保带有压舌板的手臂用于下颌骨。调整嘴巴堵嘴，确保老鼠的舌头被固定但不会缺血。</li>
</ol>4. 牙齿评估
<ol><li>确保手术时上颌第一磨牙应没有龋齿、外伤和牙龈生成。确保周围的牙龈没有发红、肿胀或瘘管。确保对面的牙齿健康，并可以作为健康的对照组。</li>
</ol>5. 纸浆暴露
<ol><li>使用牙齿毛刺以 20,000 rpm 的速度在上颌第一磨牙的咬合侧钻孔。确保去除牙釉质。仅在牙本质的浅层中保持牙科手机的操作，以防止对牙髓组织进行过度热刺激12.</li>
	<li>同时，在手术过程中每 3 分钟使用注射器将生理盐水滴在牙齿上，以防止过热。</li>
	<li>将 8# 或 10# C+ 锉刀放在钻坑的最低位置，然后刺穿最后一个牙本质，露出牙髓室。当局部牙本质被彻底去除时，会有一种明显的坠落感。不要探得太深，否则牙髓组织可能会从牙髓室中带出。</li>
	<li>清洁牙齿周围的碎片。取下嘴巴堵嘴;手术已经完成。使用对面的上颌第一磨牙作为对照，无需手术。</li>
</ol>6. 术后护理
<ol><li>手术后，皮下给予卡洛芬（5mg / kg），并将小鼠置于化学热加热垫上，以俯卧姿势，直到从麻醉中恢复。喂老鼠并提供饮用水。恢复过程应该受到监督。在小鼠完全恢复之前，其他动物不应在同一腔室中。</li>
</ol>7. 样本采集和储存
<ol><li>在手术后 24 小时或根据实验9 的任何其他时间点，在深度麻醉条件下对颈椎脱位的小鼠实施安乐死。用眼科剪刀剪开附着在上颌骨和颧骨上的骨骼肌。去除骨骼、额骨和软组织，取出带有上颌磨牙的蚋臼片。 注意：根据 He 等人的说法，建议在手术后不到 72 小时收集牙髓炎样本，以避免牙髓组织广泛坏死13。</li>
	<li>矢状地将蚊蚋石分成两半，并将组织储存在PBS（pH 7.4）中的4%多聚甲醛中，在4°C下进行24小时固定。</li>
</ol>8. 组织学分析
<ol><li>用磷酸盐缓冲盐水（PBS）洗涤组织，并在每日更换的5%EDTA和4%蔗糖的PBS（pH 7.4）脱钙溶液中脱钙，在4°C下2-4周10。</li>
	<li>将 1/2 蚊蚋石嵌入石蜡中，并确保没有牙齿的矢状面位于组织盒的底部。</li>
	<li>用石蜡切片机将石蜡块切成5μm厚的切片。根据显微镜下观察到的近端、远端、上部和下部关系调整石蜡块的角度，以确保可以切割完整的冠髓和第一磨牙的穿孔。</li>
</ol>

使用新型 Mouth-Gag 创建牙髓炎症小鼠模型 

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作者声明没有利益冲突。

作为牙齿内孤立的软组织，牙髓在维持牙齿的生物活性方面发挥着至关重要的作用，但仍然高度敏感。保留这种重要的牙髓已成为最近牙髓治疗中首选的初始方法，因此需要全面了解牙髓的炎症机制16。炎症微环境的时空波动和牙髓炎中驻留细胞类型之间的相互作用使其通过 体外 研究的研究变得复杂11.相反， 体内 研究通过复制在人类中发现的生?...

牙髓是牙齿的一个组成部分，负责多种基本功能，如营养供应、牙本质形成、感觉功能和防御反应1。然而，被硬组织包围的牙髓容易受到深龋、牙髓炎、创伤或后续治疗的伤害和损伤 2,3。功能性牙髓的缺失会增加牙齿脆弱的风险4.此外，年轻恒牙牙髓活力的丧失会对牙齿成熟产生不利影响，而目前的假牙技术无法恢复健康牙髓提供的神经反馈4.这种情况促使研究人员探索管理发炎牙髓的替代解决方案，而不仅仅是去除。
2007 年，Murray 等人开始将组织工程应用于再生牙髓学，从而引发了人们对牙髓保存和再生的兴趣5。然而，发炎的牙髓组织带来了挑战，因为细胞会释放 IL-6 等炎症因子，IL-6 会招募炎症细胞并导致细胞坏死、牙髓活力丧失和功能恢复并发症 6,7。因此，了解炎症和相关的细胞死亡对于保护重要牙髓的进展至关重要。已经进行了许多实验来探索炎症牙髓在体内或体外的分子生物学 8,9。尽管像 2D 或 3D 细胞培养这样的体外实验已经发展了多年，并且已经变得成熟并广泛用于测试牙髓细胞对炎症因子的反应，但这些实验无法反映牙髓组织与全身免疫系统之间的相互作用10。如果正在研究的现象来源于其他组织来源的细胞，如免疫、血管和神经系统，那么纯牙髓细胞培养将导致死胡同。因此，体内实验是非常必要和具有参考意义的。
小鼠因其成本效益、高生育率和活力而日益成为 体内炎症研究中的常见选择。然而，目前尚无针对小鼠牙髓炎模型的综合方案，可作为参考。小鼠的小尺寸和它们对刺激的敏感性在实验过程中构成了重大挑战。观察隐藏在小鼠口腔深处的微小牙齿通常需要使用悬臂显微镜，尽管桌面显微镜在实验室中更为普遍。没有张口器需要其他人的帮助。为了解决这个问题，该小组使用现成的材料设计了一种口腔堵嘴器，旨在为构建小鼠牙髓炎模型提供标准化和可重复的协议。本文详细介绍了该过程，涵盖 C57 小鼠的术前准备、固定、牙髓暴露手术和样本采集。该协议建议使用口腔堵嘴，提供有关其结构、生产和应用的信息，以方便其他研究人员复制该程序。

<table><tbody><tr><td>&lt;strong&gt;Animal&lt;/strong&gt;</td><td></td><td></td><td></td></tr><tr><td>C57/B6J mice</td><td>Gempharmatech Experimental Animals Company</td><td>C57/B6J</td><td>For the establishment of pulp exposure</td></tr><tr><td>&lt;strong&gt;Equipment&lt;/strong&gt;</td><td></td><td></td><td></td></tr><tr><td>1 mL syringe</td><td>Chengdu Xinjin Shifeng Medical Apparatus &amp;amp; Instruments Co. LTD.</td><td>SB1-074(IV)</td><td>Apply in drug injection.</td></tr><tr><td>8# C+ file</td><td>Readysteel</td><td>0010047</td><td>Apply in exposing the roof of pulp chamber.</td></tr><tr><td>Anesthesia Mix solution</td><td></td><td></td><td>10% ketamine hydrochloride+ 5% xylazine + 85% sterile isotonic saline.&amp;nbsp;</td></tr><tr><td>DAPI Staining Solution</td><td>Beyotime</td><td>C1005</td><td>Apply in immunofluorescence staining for counter-staining of nucleus.</td></tr><tr><td>Dental high-speed dental handpiece</td><td>Jing yuan electronic commerce technology</td><td>WJ-422</td><td>Apply in pulp exposure.</td></tr><tr><td>Heavy wire cutter</td><td>Jirui Medical Instrument Co., Ltd.</td><td>none</td><td>Apply inarc cutting.</td></tr><tr><td>Hematoxylin and Eosin Stain kit</td><td>Biosharp</td><td>BL700B</td><td>For the histological analysis of the slides.</td></tr><tr><td>IL-6 antibody</td><td>Novus</td><td>NBP2-89149</td><td>Apply in immunofluorescence staining to detect the inflammation of the dental pulp.</td></tr><tr><td>Ketamine(Ketamine hydrochloride)</td><td>Vet One, Boise, Idaho, USA</td><td>C3N VT1</td><td>100mg/kg, IP. Apply in nesthetization.</td></tr><tr><td>Medical tap</td><td>3M</td><td>1530</td><td>Apply in mice immobilization.</td></tr><tr><td>Orthodontic arch wire&amp;nbsp;</td><td>Shanghai Wei Rong Medical Apparatus Co. LTD.</td><td>K417</td><td>Diameter of 8&amp;micro;m</td></tr><tr><td>Round dental burr (0.6 mm)</td><td>Shofu global</td><td>072208</td><td>Apply in removing enamel and shallow layer of dentin.</td></tr><tr><td>Young loop bending plier</td><td>Jirui Medical Instrument Co., Ltd.</td><td>none</td><td>Apply in arc bending.</td></tr></tbody></table>

establishment of a murine pulp exposure model with a novel mouth-gag for pulpitis research

牙髓炎是自然牙齿脱落的常见原因，会导致发炎牙髓中的坏死和生物活性丧失。揭示牙髓炎的机制及其有效治疗是牙髓病学研究的持续重点。因此，了解牙髓内的炎症过程对于改善牙髓保存至关重要。与其他体 外 实验相比，鼠牙髓炎模型为观察牙髓炎的病理进展提供了更真实和遗传多样化的背景。然而，尽管小鼠具有成本效益和可及性，但由于它们的体积小、协调性差和耐受性低，使用小鼠会带来困难，使口腔内和牙科手术复杂化。该协议引入了一种新颖的设计和应用，即口腔堵嘴以暴露小鼠牙髓，从而促进更有效的口内手术。口腔堵嘴由大多数牙医都可以轻松使用的牙弓组成，可以显着加快手术准备，即使是第一次手术也是如此。Micro-CT、苏木精-伊红（hematoxylin-eosin，HE）染色和免疫荧光染色（immunofluescing sing）检测形态和细胞表达的变化。本文的目的是帮助研究人员建立一种更具可重复性且要求更低的程序，以使用这种新型的口腔堵嘴创建牙髓炎症模型。

在3,6-8周龄C57BL / 6小鼠的右上颌第一磨牙上进行上述程序，同时保留左上颌第一磨牙作为对照。空白对照、12 h牙髓炎和24 h牙髓炎样品的组织学和免疫荧光结果用于示范。
根据 Goldman 等人 15 的 CT 分析方案，通过 图 4 A-C 中的显微 CT 和重建建模确认了牙髓暴露。来自对照侧和手术侧的上颌第一磨牙的矢状面切片都进行了 HE ?...

Watch this Scientific Journal Video about Establishment of a Murine Pulp Exposure Model with a Novel Mouth-Gag for Pulpitis Research at JoVE.com

作者聚焦：通过改进的小鼠模型增强牙髓研究

本文提出了一种简化的方案，用于使用创新的口堵在小鼠中建立牙髓炎模型，然后进行随后的组织学分析。

基于新型口堵的鼠牙髓暴露模型的建立及其在牙髓炎研究中的应用

Pulpitis, a common cause of natural tooth loss, leads to necrosis and loss of bioactivity in the inflamed dental pulp. Unraveling the mechanisms ...

2D或3D细胞培养等单个实验已被广泛用于测试牙髓细胞的反应。这些实验不能反映牙髓组织与全身免疫系统之间的相互作用。因此，体内实验在牙髓研究中越来越受欢迎。C57小鼠因其成本效益、高生育率和活力而日益成为牙髓炎症研究中的常见选择。然而，小鼠体积小和缺乏协调性在实验过程中带来了重大挑战。固定过程是提高技术门槛的重要因素。我们使用现成的材料和简单的组装设计了一种新颖的口腔堵嘴器，以帮助研究人员进行牙髓暴露手术。根据我们的研究，这种口腔堵嘴可以大大缩短初学者固定嘴巴和暴露小鼠上颌第一磨牙所需的时间。

establishment-murine-pulp-exposure-model-with-novel-mouth-gag-for

Research

JoVE Journal

Medicine

Establishment of a Murine Pulp Exposure Model with a Novel Mouth-Gag for Pulpitis Research

897 次观看.  Sichuan University. 2D或3D细胞培养等单个实验已被广泛用于测试牙髓细胞的反应。这些实验不能反映牙髓组织与全身免疫系统之间的相互作用。因此，体内实验在牙髓研究中越来越受欢迎。C57小鼠因其成本效益、高生育率和活力而日益成为牙髓炎症研究中的常见选择。然而，小鼠体积小和缺乏协调性在实验过程中带来了重大挑战。固定过程是提高技术门槛的重要因素。我们使用现成?...

视频: 作者聚焦：通过改进的小鼠模型增强牙髓研究

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure

Fetal alcohol syndrome (FAS) is a severe manifestation of embryonic exposure to ethanol. It presents with characteristic defects to the face and organs, including mental retardation due to disordered and damaged brain development. Fetal alcohol spectrum disorder (FASD) is a term used to cover a continuum of birth defects that occur due to maternal alcohol consumption, and occurs in approximately 4% of children born in the United States. With 50% of child-bearing age women reporting consumption of alcohol, and half of all pregnancies being unplanned, unintentional exposure is a continuing issue2. In order to best understand the damage produced by ethanol, plus produce a model with which to test potential interventions, we developed a model of developmental ethanol exposure using the zebrafish embryo. Zebrafish are ideal for this kind of teratogen study3-8. Each pair lays hundreds of eggs, which can then be collected without harming the adult fish. The zebrafish embryo is transparent and can be readily imaged with any number of stains. Analysis of these embryos after exposure to ethanol at different doses and times of duration and application shows that the gross developmental defects produced by ethanol are consistent with the human birth defect. Described here are the basic techniques used to study and manipulate the zebrafish FAS model.

In order to understand the molecular mechanisms of the ethanol-induced developmental damage, we have developed a zebrafish model of ethanol exposure and are exploring the physical, cellular, and genetic alterations that occur after ethanol exposure1. We then seek to find potential interventions and rapidly test them in this animal model.

在斑马鱼模型的胎儿酒精暴露评估致畸的变化

Fetal alcohol syndrome (FAS) is a severe manifestation of embryonic exposure to ethanol. It presents with characteristic defects to the face and organs, ...

科研

医学

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Chronic inflammation is a major driver of pathological tissue damage and a unifying characteristic of many chronic diseases in humans including neoplastic, autoimmune, and chronic inflammatory diseases. Emerging evidence implicates pathogen-induced chronic inflammation in the development and progression of chronic diseases with a wide variety of clinical manifestations. Due to the complex and multifactorial etiology of chronic disease, designing experiments for proof of causality and the establishment of mechanistic links is nearly impossible in humans. An advantage of using animal models is that both genetic and environmental factors that may influence the course of a particular disease can be controlled. Thus, designing relevant animal models of infection represents a key step in identifying host and pathogen specific mechanisms that contribute to chronic inflammation.
Here we describe a mouse model of pathogen-induced chronic inflammation at local and systemic sites following infection with the oral pathogen Porphyromonas gingivalis, a bacterium closely associated with human periodontal disease. Oral infection of specific-pathogen free mice induces a local inflammatory response resulting in destruction of tooth supporting alveolar bone, a hallmark of periodontal disease. In an established mouse model of atherosclerosis, infection with P. gingivalis accelerates inflammatory plaque deposition within the aortic sinus and innominate artery, accompanied by activation of the vascular endothelium, an increased immune cell infiltrate, and elevated expression of inflammatory mediators within lesions. We detail methodologies for the assessment of inflammation at local and systemic sites. The use of transgenic mice and defined bacterial mutants makes this model particularly suitable for identifying both host and microbial factors involved in the initiation, progression, and outcome of disease. Additionally, the model can be used to screen for novel therapeutic strategies, including vaccination and pharmacological intervention.

Animal models have proven to be invaluable tools in defining host and pathogen specific mechanisms that contribute to the development of chronic inflammation. Here we describe a mouse model of oral infection with the human pathogen Porphyromonas gingivalis and detail methodologies to assess the progression of inflammation at local and systemic sites.

鼠标型号病原体引起的慢性炎症局部及全身站点

Chronic inflammation is a major driver of pathological tissue damage and a unifying characteristic of many chronic diseases in humans including ...

免疫与感染

Development of a Direct Pulp-capping Model for the Evaluation of Pulpal Wound Healing and Reparative Dentin Formation in Mice

Dental pulp is a vital organ of a tooth fully protected by enamel and dentin. When the pulp is exposed due to cariogenic or iatrogenic injuries, it is often capped with biocompatible materials in order to expedite pulpal wound healing. The ultimate goal is to regenerate reparative dentin, a physical barrier that functions as a "biological seal" and protects the underlying pulp tissue. Although this direct pulp-capping procedure has long been used in dentistry, the underlying molecular mechanism of pulpal wound healing and reparative dentin formation is still poorly understood. To induce reparative dentin, pulp capping has been performed experimentally in large animals, but less so in mice, presumably due to their small sizes and the ensuing technical difficulties. Here, we present a detailed, step-by-step method of performing a pulp-capping procedure in mice, including the preparation of a Class-I-like cavity, the placement of pulp-capping materials, and the restoration procedure using dental composite. Our pulp-capping mouse model will be instrumental in investigating the fundamental molecular mechanisms of pulpal wound healing in the context of reparative dentin in vivo by enabling the use of transgenic or knockout mice that are widely available in the research community.

We describe a step-by-step method of performing direct pulp capping on mice teeth for the evaluation of pulpal wound healing and reparative dentin formation in vivo.

伤口的牙髓评价一个直接盖髓模型的开发和治疗小鼠中修复性牙本质形成

Dental pulp is a vital organ of a tooth fully protected by enamel and dentin. When the pulp is exposed due to cariogenic or iatrogenic injuries, it is ...

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

The main advantages of studying the pathophysiology of periodontal disease utilizing murine models are the reduced cost of animals, array of genetically modified strains, the vast number of analyses that can be performed on harvested soft and hard tissues. However, many of these systems are subject to procedural criticisms. As an alternative, the ligature-induced model of periodontal disease, driven by the localized development and retention of a dysbiotic oral microbiome, can be employed, which is rapidly induced and relatively reliable. Unfortunately, the variants of ligature-induced murine periodontitis protocol are isolated to focal regions of the periodontium and subject to premature avulsion of the installed ligature. This minimizes the amount of tissue available for subsequent analyses and increases the number of animals required for study. This protocol describes the precise manipulations required to place extended molar ligatures with improved retention and usage of a novel rinse technique to recover oral neutrophils in mice with an alternative approach that mitigates the aforementioned technical challenges.

This article presents a protocol for establishing a ligature-induced model of murine periodontitis involving multiple maxillary molars, resulting in larger areas of the involved gingival tissue and bone for subsequent analysis as well as reduced animal usage. A technique to assess oral neutrophils in a manner analogous to human subjects is also described.

用于口腔中性粒细胞病评价的鼠期牙周炎的强结合诱导模型

The main advantages of studying the pathophysiology of periodontal disease utilizing murine models are the reduced cost of animals, array of genetically ...

Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model

Periodontitis (PD) is a highly prevalent, chronic immune-inflammatory disease of the periodontium, that results in a loss of gingival soft tissue, periodontal ligament, cementum, and alveolar bone. In this study, a simple method of PD induction in rats is described. We provide detailed instructions for placement of the ligature model around the first maxillary molars (M1) and a combination of injections of lipopolysaccharide (LPS), derived from Porphyromonas gingivalis at the mesio-palatal side of the M1. The induction of periodontitis was maintained for 14 days, promoting the accumulation of bacteria biofilm and inflammation. To validate the animal model, IL-1&#946;, a key inflammatory mediator, was determined by an immunoassay in the gingival crevicular fluid (GCF), and alveolar bone loss was calculated using cone beam computed tomography (CBCT). This technique was effective in promoting gingiva recession, alveolar bone loss, and an increase in IL-1&#946; levels in the GCF at the end of the experimental procedure after 14 days. This method was effective in inducing PD, thus being able to be used in studies on disease progression mechanisms and future possible treatments.

Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model

In this study, a rat model of induction of periodontitis is presented via a combination of retentive ligature and repetitive injections of lipopolysaccharide derived from Porphyromonas gingivalis, over 14 days around the first maxillary molars. The ligation and LPS injection techniques were effective in inducing peridontitis, resulting in alveolar bone loss and inflammation.

在大鼠模型中通过结扎和脂多糖注射的组合 诱导 牙周炎

Periodontitis (PD) is a highly prevalent, chronic immune-inflammatory disease of the periodontium, that results in a loss of gingival soft tissue, ...

Experimental Model of Ligature-Induced Peri-Implantitis in Mice

Dental implants have a high success and survival rate. However, complications such as peri-implantitis (PI) are highly challenging to treat. PI is characterized by inflammation in the tissues around dental implants with progressive loss of supporting bone. To optimize dental implants' longevity in terms of health and functionality, it is crucial to understand the peri-implantitis pathophysiology. In this regard, using mouse models in research has proven clear benefits in recreating clinical circumstances. This study aimed to describe an experimental model of ligature-induced peri-implantitis in mice and determine whether there is effectiveness in inducing this disease, given the observed bone and tissue changes. The experimental peri-implantitis induction comprehends the following steps: teeth extraction, implant placement, and ligature-inducted PI. A sample of eighteen 3-week-old C57BL/6J male mice was divided into two groups, ligature (N=9) and control non-ligature (N=9). The evaluation of clinical, radiographical, and histological factors was performed. The ligature group showed significantly higher bone loss, increased soft tissue edema, and apical epithelial migration than the non-ligature group. It was concluded that this pre-clinical model can successfully induce peri-implantitis in mice.

This is a report on an experimental model of ligature-induced peri-implantitis in mice. We describe all surgical steps, from pre- and post-operative management of the animals, extractions, implant placement, and ligature-induced peri-implantitis.

小鼠结扎诱导种植体周围炎的实验模型

Dental implants have a high success and survival rate. However, complications such as peri-implantitis (PI) are highly challenging to treat. PI is ...

Inducing Apical Periodontitis in Mice

The mechanisms involved in local induced inflammation can be studied using several available animal models. One of these is the induction of apical periodontitis (AP). Apical periodontitis is a common pathology of an inflammatory nature in the periodontal tissues surrounding the tooth root. In order to better understand the nature and mechanism of this pathology it is advantageous to perform the procedure in mice. The induction of this odontogenic inflammation is achieved by drilling into the mouse tooth until the dental pulp is exposed. Next, the tooth pulp remains exposed to be contaminated by the natural oral flora over time, causing apical periodontitis. After this time period, the animal is sacrificed, and the tooth and the jaw bone can be analyzed in various ways. Typical analyses include micro-CT imaging (to evaluate bone resorption), histological staining, immunohistochemistry, and RNA expression. This protocol is useful for research in the field of oral biology to better understand this inflammatory process in an in vivo experimental setting with uniform conditions. The procedure requires a careful handling of the mice and the isolated jaw, and a visual demonstration of the technique is useful. All technical aspects of the procedures leading to induced apical periodontitis and its characterization in a mouse model are demonstrated.

Here, we present a protocol to locally induce apical periodontitis in mice. We show how to drill a hole in the mouse&#39;s tooth and expose its pulp, in order to cause local inflammation. Analysis methods to investigate the nature of this inflammation, such as micro-CT and histology, are also demonstrated.

诱导小鼠的牙周炎

The mechanisms involved in local induced inflammation can be studied using several available animal models. One of these is the induction of apical ...

生物学

The Establishment of a Murine Mandibular Molar Extraction Socket Healing Model

This study introduces the development of a molar extraction model in the murine mandible to provide a practicable model for studying alveolar bone regeneration and intramembranous ossification. C57/J6 mice were used to extract the mandibular first molar to establish this model. They were euthanized, and the bilateral mandibles harvested, at 1 week and 4 weeks post-surgery, respectively. Subsequent serial stereoscopic harvest, histological assessment, and immunofluorescence staining were performed to demonstrate successful surgery. Immediately after surgery, the stereoscopic images displayed an empty extraction socket. The hematoxylin and eosin (H&#38;E) at 1 week and Masson staining at 4 weeks post-surgery showed that the area of the original root was partially and fully filled with bone trabeculae, respectively. The immunofluorescence staining showed that, compared with the homeostasis side, the Sp7 expression increased at 1 week post-surgery, suggesting vigorous osteogenesis in the alveolar fossa. All these results demonstrated a practicable murine tooth extraction socket healing model. Upcoming studies revealing the mechanisms of jawbone defect healing or socket healing could adopt this method.

This protocol demonstrates step-by-step details of how to extract the mandibular first molar in the mouse. It provides an alternative method for researchers focusing on jawbone healing and regeneration.

小鼠下颌磨牙拔牙窝愈合模型的建立

This study introduces the development of a molar extraction model in the murine mandible to provide a practicable model for studying alveolar bone ...

<meta charset="utf8"></head><body>柠檬酸诱导的咳嗽超敏反应小鼠模型

Establishment of a Mouse Model with Cough Hypersensitivity via Inhalation of Citric Acid

Cough is one of the most common symptoms of many respiratory diseases. Chronic cough significantly impacts quality of life and imposes a considerable economic burden. Increased cough sensitivity is a pathophysiological hallmark of chronic cough. It has been observed that cough hypersensitivity is related to airway inflammation, remodeling of airway sensory nerves, and alterations in the central nervous system. However, the precise molecular mechanisms remain unclear and require further elucidation using suitable animal models. Previous studies have utilized guinea pigs as models for studying cough, but these models present several experimental limitations, including high costs, a lack of transgenic tools, and a scarcity of commercial reagents. In addition, guinea pigs typically exhibit poor environmental tolerance and high mortality when exposed to stimuli. In contrast, mice are smaller, easier to maintain, more cost-effective, and amenable to genetic manipulation, making them more suitable for mechanistic investigations. In this study, we established a mouse model with cough hypersensitivity&#160;via&#160;continuous inhalation of citric acid (CA). This model is straightforward to operate and yields reproducible results, making it a valuable tool for further studies on the mechanisms and potential novel treatments for chronic cough.

<meta charset="utf8"></head><body>作者聚焦：研究慢性咳嗽和咳嗽超敏反应的机制：一种用于推进治疗研究的具有成本效益且可遗传修饰的工具

This protocol describes the development of a mouse model with cough hypersensitivity, which can serve as an ideal model for studying the mechanisms of chronic cough.

通过吸入柠檬酸建立咳嗽超敏反应小鼠模型

Cough is one of the most common symptoms of many respiratory diseases. Chronic cough significantly impacts quality of life and imposes a considerable ...

基于新型口堵的鼠牙髓暴露模型的建立及其在牙髓炎研究中的应用

副本

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此视频中的章节

在斑马鱼模型的胎儿酒精暴露评估致畸的变化

鼠标型号病原体引起的慢性炎症局部及全身站点

伤口的牙髓评价一个直接盖髓模型的开发和治疗小鼠中修复性牙本质形成

用于口腔中性粒细胞病评价的鼠期牙周炎的强结合诱导模型

在大鼠模型中通过结扎和脂多糖注射的组合诱导牙周炎

小鼠结扎诱导种植体周围炎的实验模型

诱导小鼠的牙周炎

小鼠下颌磨牙拔牙窝愈合模型的建立

通过吸入柠檬酸建立咳嗽超敏反应小鼠模型

通过吸入柠檬酸建立咳嗽超敏反应小鼠模型

基于新型口堵的鼠牙髓暴露模型的建立及其在牙髓炎研究中的应用

副本

摘要

探索更多视频

此视频中的章节

在斑马鱼模型的胎儿酒精暴露评估致畸的变化

鼠标型号病原体引起的慢性炎症局部及全身站点

伤口的牙髓评价一个直接盖髓模型的开发和治疗小鼠中修复性牙本质形成

用于口腔中性粒细胞病评价的鼠期牙周炎的强结合诱导模型

在大鼠模型中通过结扎和脂多糖注射的组合 诱导 牙周炎

小鼠结扎诱导种植体周围炎的实验模型

诱导小鼠的牙周炎

小鼠下颌磨牙拔牙窝愈合模型的建立

通过吸入柠檬酸建立咳嗽超敏反应小鼠模型

通过吸入柠檬酸建立咳嗽超敏反应小鼠模型

在大鼠模型中通过结扎和脂多糖注射的组合诱导牙周炎