表观遗传修饰和牙周病的相关性

牙周病是一种多因素的感染性疾病,主要表现为牙周支持组织的炎症反应和破坏,是失牙最主要的原因之一。其发病机制复杂,不只是牙周致病菌及其产物对牙齿周围组织的直接破坏作用,还与机体在免疫应答中产生的细胞因子密切联系。近年来研究表明,人细胞因子基因的表达与表观遗传修饰有关。表观遗传修饰通过调节细胞因子与牙周病相联系。     

白细胞介素-6与牙周病

白细胞介素-6(IL-6)是一种多功能的细胞因子,在牙周病的发生、发展和组织破坏中,尤其是在牙槽骨吸收过程中发挥着重要作用.牙周组织中的大多数细胞类型都可以组成性地和(或)在多种因素的刺激下反应性地生成IL-6,并且产生的IL-6量也受到众多因素的影响和调控.     

白细胞介素—6与牙周病

白细胞介素－6（IL－6）是一种多功能的细胞因子,在牙周病的发生、发展和组织破坏中,尤其是在牙槽骨吸收过程中发挥着重要作用。牙周组织中的大多数细胞类型都可以组成性地和（或）在多种因素的刺激下反应性地生成IL－6,并且产生的IL－6量也受到众多因素的影响和调控。     

牙周膜干细胞表观遗传学研究进展

牙周膜干细胞(periodontal ligament stem cells,PDLSCs)是牙周膜组织中的间充质干细胞,是牙周组织再生和修复的重要细胞群,牙周微环境的变化会影响牙周膜干细胞的生物学特性.表观遗传(epigenetics)是指不基于DNA序列的变化,而出现稳定可遗传的基因表达水平及功能的改变.环境因素是影响表观遗传的重要因素之一,暴露环境的不同可以引起表观修饰改变,进而影响基因表达.表观遗传是干细胞生物学特性的重要内源性调控机制,在干细胞中的变化稳定可遗传,并具有可逆性.近年来牙周膜干细胞的表观遗传调控已成为研究热点,本文通过对表观遗传调控对牙周膜干细胞生物学特性的影响进行综述,以期使牙周膜干细胞更好地应用于牙周再生修复.     

表观遗传学在口腔鳞状细胞癌分子机制中的研究进展

口腔鳞状细胞癌（oral sqaumous cell carcinoma,OSCC）是来源于口腔粘膜不同程度鳞状分化的上皮性恶性肿瘤.找到OSCC发生的根本原因是提高生存率和减少发生率的关键,而分子标志物的筛查成为早发现早诊断的重要依据,表观遗传学是肿瘤标志物的研究方法之一.表观遗传学在口腔鳞癌分子机制研究中的应用历经了DNA甲基化、组蛋白修饰、染色质重塑、组蛋白变体和非编码RNA（microRNA）等调控模式的变迁,近来新出现的lncRNA对肿瘤等各种疾病的调控模式在表观遗传学中越来越重要.本文就表观遗传学在口腔鳞癌发生机制探索中的研究内容做一全面综述,展望表观遗传学在口腔鳞癌领域的应用前景.     

白细胞介素折-6与牙周病

白细胞介素-6(IL-6)是一种多功能的细胞因子,在牙周病的发生、发展和组织破坏中,尤其是在牙槽骨吸收过程中发挥着重要作用。牙周组织中的大多数细胞类型都可以组成性地和(或)在多种因素的刺激下反应性地生成IL-6,并且产生的IL-6量也受到众多因素的影响和调控。     

牙周病致牙槽骨缺损的治疗进展

牙周病最终造成的损害是牙槽骨吸收，牙齿脱落。近年来随着生物材料学，分子生物学和细胞生物学研究的进展，牙槽骨缺损的治疗也有较大发展。本文系统回顾了近年来对牙周病所致牙槽骨缺损的治疗情况，阐述了组织工程化骨在牙槽骨缺损治疗中的应用前景。     

牙周病与细胞凋亡的相关研究进展

细胞凋亡是由特定的信号分子启动，在基因调控下遵循自身的程序而自我消亡的过程。目前对牙周病的发病机制与细胞凋亡的相关研究涉及细菌及其产物，白细胞，巨噬细胞，破骨细胞，成骨细胞，以及IL－1，TNF等细胞因子。本文对近来涉及上述方面的研究作一综述。     

牙周病患者牙槽骨状况评价方法研究进展

牙周病的发生发展是一个缓慢的病理过程,患者牙槽骨状况的改变,包括牙槽骨的吸收与改建,对治疗方案的选择及预后的评估极为重要。本文对牙周病患者牙槽骨状况现有的评价方法作一综述,着重比较锥形束CT与牙槽骨状况传统评价方法的优缺点,并就锥形束CT在指导牙周病治疗的前景提出展望。     

Role of epigenetics in alveolar bone resorption and regeneration around periodontal and peri‐implant tissues

Periodontitis and peri‐implantitis are multifactorial diseases characterized by alveolar bone destruction mediated by the host response to a microbial challenge. Alveolar bone resorption mediated by epigenetics could be one of the mechanisms responsible for this destruction of alveolar bone. The relationship between epigenetic modifications and bone metabolism has been thoroughly investigated in bone remodeling, cancer, and rheumatoid arthritis, but evidence is low regarding the relationship between epigenetic modifications and alveolar bone loss related to periodontal and peri‐implant diseases. Therefore, we conducted a review of the pertinent literature based on a priori‐formulated focused questions and a screening strategy, in an attempt to comprehend the role of different epigenetic mechanisms in alveolar bone loss and to determine the current state with respect to their possible therapeutic applications in regenerative medicine. The review showed that the roles of DNA methylation, histone modifications, and non‐coding RNAs in bone loss have been investigated. The results indicate that epigenetic mechanisms can participate in periodontal and peri‐implant alveolar bone breakdown, suggesting their potential as therapeutic targets in alveolar bone regeneration. However, there is still only preliminary information regarding the possible therapeutic utility of these epigenetic mechanisms, suggesting a need for basic and translational research to assess the potential of such mechanisms in promoting alveolar bone regeneration.     

甲状旁腺激素调控牙周组织改建的研究进展

甲状旁腺激素是由甲状旁腺主细胞合成并分泌的多肽类分子,是维持机体钙磷代谢平衡的一种重要的调钙激素,可促进骨形成与骨吸收,加快骨转换.目前临床上甲状旁腺激素主要用于防治妇女绝经期骨质疏松症和降低骨折的发生率.甲状旁腺激素通过刺激成骨细胞、破骨细胞、牙周膜细胞、成牙骨质细胞等的增殖和分化来促进牙周组织改建和愈合,有效地控制牙槽骨的丧失,加速正畸牙的移动,以及促进种植体与牙槽骨的骨结合.本文就近年来甲状旁腺激素对牙周组织再生与改建的相关临床和基础研究作一综述,旨在为甲状旁腺激素在牙周组织的应用与研究提供参考.     

The effect of ketoprofen creams on periodontal disease in rhesus monkeys

Ketoprofen creams were evaluated for the treatment of periodontal disease in a placebo-controlled, double-blind study in the rhesus monkeys, Macaca mulatta. Two formulations containing ketoprofen (1%), with or without vitamin E, were evaluated against appropriate controls (8 monkeys per group). Two weeks prior to treatment, the animals received prophylaxis on only the left side of the mouth (spontaneous model). Selected teeth on the right side of the mouth were ligated (ligature model). The creams were administered to the gingiva once daily at a standard dose of 1.8 ml per monkey for 6 months. Clinical assessments were made 2 wk before initiation, at baseline and 1, 2, 3 and 6 months post-treatment. The clinical parameters included plaque formation, gingival redness, edema, bleeding on probing and Ramfjord Attachment Level measurements (RAL). Radiographs were taken at 2 wk before initiation, baseline and at 3 and 6 months post-treatment. Digital subtraction radiography was used to measure vertical linear bone loss along the interproximal root surfaces of the left and right mandibular first molars. Gingival crevicular fluid (GCF) was collected for biochemical assays on PGE₂, TxB₂, LTB₄, IL-1β and TNFα. There were no significant differences among groups with respect to gingival indices. Radiographic data demonstrated significant positive effects on bone activity in both groups treated with ketoprofen formulations with improvement over time in the ligature model (0.01 ≤p≤ 0.04). The placebo group exhibited bone loss of 1.96±0.48 and 1.40±0.56 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream showed an apparent bone gain of 0.28±0.41 and 0.78±0.47 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream containing vitamin E showed a mean bone loss of 0.41–0.48 mm per site at 3 months with improvement to an apparent bone gain of 0.31±0.44 mm per site at 6 months. The biochemical data demonstrated early and significant suppression of GCF-LTB₄ by both ketoprofen formulations at 1 month, which preceded the significant suppression of GCF-PGE₂ at 2 and 3 months in the ligature model (p≤0.003) and at 2 to 6 months in the spontaneous model (p≤0.02). We conclude that ketoprofen at 1% level in suitable topical vehicles can effectively inhibit GCF-LTB₄ and GCF-PGE₂ and positively alter alveolar bone activity in the ligature-induced model of periodontitis in the monkey.     

Radiographic and clinical assessments of destructive periodontal disease

191 subjects, aged 35-80 years, were examined for periodontal disease using radiographic and clinical means. At all approximal tooth surfaces, assessments were made of (i) the distance on radiographs between the cementoenamel junction and the most coronal level of the alveolar bone, and (ii) probing attachment loss. The results revealed that (i) a strong correlation existed between the radiographic and the clinical assessments (r = 0.80, p = 0.0001), (ii) the difference between the 2 types of assessments was within 2 mm in 92% of the tooth sites examined, (iii) the degree of agreement between the 2 methods was similar, irrespective of tooth type and tooth surface, but (iv) the agreement was poor at sites with severe periodontal tissue breakdown.     

Autophagy and its significance in periodontal disease

Autophagy is an evolutionarily conserved process essential for cellular homeostasis and human health. As a lysosome‐dependent degradation pathway, autophagy acts as a modulator of the pathogenesis of diverse diseases. The relationship between autophagy and oral diseases has been explored in recent years, and there is increasing interest in the role of autophagy in periodontal disease. Periodontal disease is a prevalent chronic inflammatory disorder characterized by the destruction of periodontal tissues. It is initiated through pathogenic bacterial infection and interacts with the host immune defense, leading to inflammation and alveolar bone resorption. In this review, we outline the machinery of autophagy and present an overview of work on the significance of autophagy in regulating pathogen invasion, the immune response, inflammation, and alveolar bone homeostasis of periodontal disease. Existing data provide support for the importance of autophagy as a multi‐dimensional regulator in the pathogenesis of periodontal disease and demonstrate the importance of future research on the potential roles of autophagy in periodontal disease.     

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牙周炎造成的骨缺损以及骨形态的改变在很大程度上影响牙周治疗效果.牙周基础治疗对骨组织再生的影响有限,而牙周骨外科手术因其备受肯定的疗效已被广泛应用于临床,通过牙周骨外科手术达到牙周组织缺损的修复重建成为牙周临床治疗领域的关注热点.     

自体骨髓基质细胞用于牙周骨缺损移植的动物实验研究

目的：应用分离的骨髓干细胞（ＭＳＣ）进行牙周骨缺损的自体移植动物实验,观察ＭＳＣ用于牙周再生治疗的可行性。方法：体外分离狗髂骨的ＭＳＣ,体外培养,移植前进行ＭＳＣ的体外钙化实验,以胶原膜为移植载体,将ＭＳＣ移植到狗下颌后牙的根分叉骨缺损中,覆盖国产聚四氟乙烯膜,３０ｄ后进行组织学观察。结果：分离的ＭＳＣ在体外均出现了不同程度的钙化;动物实验结果发现,ＭＳＣ移植组达到了骨缺损的完全修复,无根面吸收;     

Mineral status of skeleton and advanced periodontal disease

Abstract Studies of the effect of general bone loss on periodontal condition and on development of periodontal pockets suggest that there is no clear correlation between periodontal health or number of teeth and the general mineral status of the skeleton. In some reports, however, deep periodontal pockets have been correlated with good mineral status in the jawbones and skeleton. The purpose of this study of 227 healthy postmenopausal women aged 48 to 56 years was to determine whether advanced alveolar bone loss, diagnosed by panoramic radiographs, and periodontal probing depths or number of remaining teeth were correlated with the bone mineral status of the skeleton and cortical bone in the mandible. The results suggest that individuals with high mineral values in the skeleton seem to retain their teeth with deep periodontal pockets more easily than those with osteoporosis. This finding may especially motivate treatment of persons suffering from advanced periodontal disease but having good mineral status.     

氯化锂促进大鼠牙周组织缺损修复效果研究

目的 观察分析氯化锂促进大鼠牙周组织缺损修复的实验效果.方法 将25只SD大鼠随机分为5组(每组5只),构建大鼠急性牙周缺损模型.采取腹腔注射氯化锂及缺损处放置氯化锂明胶海绵两种给药方式,并在牙周缺损表面覆盖Guidor?可吸收基质膜.术后4周取材制作组织学切片,光镜下观察牙周组织缺损修复情况,测量各组缺损区域新生牙槽...