细胞焦亡参与牙周炎发生发展的研究进展

牙周炎是一种慢性感染性炎症疾病,探究牙周炎发生发展过程中炎症调节机制是预防和治疗牙周炎的关键,但目前其尚不明确。细胞焦亡是一种新发现的炎症性细胞程序性死亡方式,以细胞裂解并释放大量促炎因子为主要特征。菌斑微生物、局部及全身促进因素等多种牙周炎相关因素可能通过细胞焦亡引起牙周组织损伤。文章就细胞焦亡参与牙周炎发生发展的相关研究进展做一综述。     

铁死亡相关口腔颌面部疾病的研究进展

铁死亡是区别于凋亡、坏死、焦亡等细胞死亡方式的胞内铁依赖程序性细胞死亡方式,研究显示其参与神经系统、心血管系统、消化系统、免疫系统等相关疾病的发生、发展。近年来,谷胱甘肽超氧化物酶-谷胱甘肽-(半)胱氨酸[GPX4-GSH-Cyst(e)ine]途径介导的铁死亡在口腔疾病中也有报道。本文就铁死亡在口腔颌面部疾病中的研究进展及其作用机制作一综述,以期为铁死亡相关口腔疾病的防治提供新思路。     

细胞焦亡在糖尿病牙周炎中的研究进展

细胞焦亡作为细胞程序性死亡之一,自2001年被命名至今,一直在诸多疾病领域中被探索与研究.细胞焦亡的发生主要依赖于caspase?1/4/5/11对消皮素D(GSDMD)的裂解并介导诸如白细胞介素18(IL?18)和IL?1β等非活性细胞因子和其他细胞内容物的释放.目前,越来越多的证据表明,细胞焦亡在引发牙周病的间接和...     

探究焦亡与原发性干燥综合征的关系

目的:探究焦亡与原发性干燥综合征的关系,方法:干扰素-γ(interferon-γ,IFN-γ)处理A253细胞系,通过CCK-8、细胞活死染色检测细胞活力,实时定量荧光PCR(qRT-PCR)检测焦亡相关指标mRNA水平,免疫荧光检测焦亡相关蛋白水平,免疫组织化学染色检测人组织标本中焦亡相关蛋白水平,再用焦亡抑制剂Vx765分别处理受IFN-γ刺激和经二甲基亚砜(Dimethyl sulfoxide, DMSO)处理的A253细胞,检测对应组别的细胞活力和相关因子的mRNA水平。结果:IFN-γ处理组细胞活力明显下降,焦亡相关指标的mRNA和蛋白水平均升高,人唇腺组织标本中的焦亡相关通路蛋白表达也升高,且经Vx765处理后,IFN-γ组细胞活力增加,且焦亡相关炎性因子的mRNA水平降低。结论:原发性干燥综合征在发生的同时可能伴随着焦亡。     

口腔黏膜癌变中程序性细胞死亡相关基因的研究进展

细胞凋亡是基因控制的程序性死亡,与口腔黏膜癌变密切相关。为进一步探讨程序性细胞死亡调控与口腔黏膜癌变的关系,进而了解口腔黏膜癌变的发病机制,探索预防和治疗口腔黏膜癌变的手段,研究程序性细胞死亡相关基因是必要的。下面就与口腔黏膜癌变相关的程序性细胞死亡调控基因的研究进展作一综述。     

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自噬是细胞程序性死亡的一种方式,人类多种肿瘤存在自噬异常。自噬过程受自噬相关基因调控,Beclin1是目前惟一被证实的哺乳动物"自噬基因",是自噬的直接执行者,通过诱导自噬、促进凋亡抑制肿瘤进程。本文就Beclin1与肿瘤发生、发展的关系进行综述,并对口腔癌自噬研究做一简要介绍。     

牙周成纤维细胞铁死亡和牙周炎相关作用的研究进展

牙周成纤维细胞(periodontal fibroblasts, PDLFs)是牙周组织中含量最多的细胞,牙周病原体或炎性细胞因子刺激牙周组织加剧牙周炎进展并诱发细胞程序性死亡。铁死亡(ferroptosis)是一种胞内铁使脂质过氧化物蓄积导致质膜损伤的新型程序性死亡。作为近年来的热点研究方向,它被证明与谷胱甘肽过氧化物酶4(glutathione-dependent peroxidase 4,GPX4)活力休戚相关,主要会出现铁积聚、脂质过氧化和GPX4耗竭等改变,对炎症等疾病的形成和发展起重要的调节作用。研究表明,PDLFs受到刺激诱发牙周炎及发生细胞铁死亡,而通过激活或抑制PDLFs铁死亡可以干预牙周炎的发展,但相关机制研究还很有限。本文就PDLFs铁死亡与牙周炎关联的机制研究进展做一综述。     

鳞状细胞癌抗原的研究进展

鳞状细胞癌抗原(SCCA)是从子宫颈鳞状上皮中分离出来的鳞状上皮细胞相关抗原TA-4的亚单位,由SCCA-1和SCCA-2抗原组成.SCCA与鳞状细胞癌的发生发展关系十分密切,是反映鳞状细胞癌生物学特性的重要标志物,被广泛应用于全身各系统肿瘤的研究中.笔者下面就SCCA的结构和功能、在组织和体液中的表达、与肿瘤细胞程序性死亡以及多种鳞状细胞癌的关系等研究进展作一综述.     

雨虎属Ras同系物-Ⅰ基因及其与口腔肿瘤间的关系

雨虎属Ras同系物(arh)-Ⅰ基因参与细胞周期调控和信号通路的传导,从而负向调节细胞生长和诱发程序性细胞死亡。arh-Ⅰ基因在卵巢、乳腺和胰腺等癌细胞中均有表达缺失,即arh-Ⅰ基因与肿瘤的形成和发展密切相关。本文就arh-Ⅰ基因的定位与结构、作用途径和与肿瘤间的关系等研究进展作一综述。     

雨虎属Ras同系物-I基因及其与口腔肿瘤间的关系

雨虎属Ras同系物（arh）-I基因参与细胞周期调控和信号通路的传导，从而负向调节细胞生长和诱发程序性细胞死亡。arh—I基因在卵巢、乳腺和胰腺等癌细胞中均有表达缺失，即arh—I基因与肿瘤的形成和发展密切相关。本文就arh—I基因的定位与结构、作用途径和与肿瘤间的关系等研究进展作一综述。     

Programmed cell death and its possible relationship with periodontal disease

Cell death occurs in physiological conditions and as a result of injury or disease. Programmed cell death has an important role in the development and homeostasis of human tissue. Aberrant regulation of this process is thought to cause numerous diseases, including developmental disorders, neurodegenerative disease, and cancer. Apoptosis is the main type of programmed cell death and is well understood. However, recent intensive studies have revealed other types of programmed cell death. Here, we include an overview of three types of programmed cell death: apoptosis, necroptosis, and autophagic cell death. We also provide information on damage-associated molecular patterns (DAMPs), which have pro-inflammatory effects and are reportedly associated with cell death. Finally, we discuss the link between programmed cell death and periodontal disease and propose a hypothetical role for programmed cell death and DAMPs-which are released from cytoplasm of necrotic cells-in periodontal disease initiation.     

Programmed cell death in periodontitis: recent advances and future perspectives

Periodontitis is a highly prevalent infectious disease, characterized by destruction of the periodontium, and is the main cause of tooth loss. Periodontitis is initiated by periodontal pathogens, while other risk factors including smoking, stress, and systemic diseases aggravate its progression. Periodontitis affects many people worldwide, but the molecular mechanisms by which pathogens and risk factors destroy the periodontium are unclear. Programmed cell death (PCD), different from necrosis, is an active cell death mediated by a cascade of gene expression events and can be mainly classified into apoptosis, autophagy, necroptosis, and pyroptosis. Although PCD is involved in many inflammatory diseases, its correlation with periodontitis is unclear. After reviewing the relevant published articles, we found that apoptosis has indeed been reported to play a role in periodontitis. However, the role of autophagy in periodontitis needs further verification. Additionally, implication of necroptosis or pyroptosis in periodontitis remains unknown. Therefore, we recommend future studies, which will unravel the pivotal role of PCD in periodontitis, allowing us to prevent, diagnose, and treat the disease, as well as predict its outcomes.     

A significant other: Non-canonical caspase-4/5/11 inflammasome in periodontitis

Periodontitis is an oral inflammatory disease characterised by the destruction of periodontal soft tissue and alveolar bone resorption, mainly triggered by plaque microbial infection. Pyroptosis is an inflammatory form of programmed cell death mediated by the pore-forming gasdermin proteins, which resist the invasion of pathogens into the body's immune system. Many studies have found that pyroptosis is closely related to the occurrence and development of periodontitis. At present, most of these studies focused on the canonical pathway mediated by caspase-1. Moreover, Gram-negative bacteria's lipopolysaccharide has been shown to activate a new form of the non-canonical inflammasome by directly binding to human caspase-4/5 and mouse caspase-11 in the cytosol. However, most of the functions of non-canonical inflammasome are still gradually being studied. Therefore, in this review, we have summarised and analysed the existence and regulation mechanism of the non-canonical inflammasome in periodontitis.     

Regulated Cell Death in Pulpitis

Regulated cell death (RCD) is a preferred term inclusive of all modes of cell death regulated by multiple intracellular signal transduction pathways under physiological and pathologic conditions. Although cell death programs ensure correct growth and developmental processes as well as protect the host against microbial pathogens, some necrotic cell death pathways, such as pyroptosis, NETosis, and necroptosis, release intracellular damage-associated molecular patterns and inflammatory cytokines, thereby skewing the milieu toward a proinflammatory state. Pulpitis is 1 of the most prevalent oral inflammatory diseases. In response to different types of pulpal injury, RCD may occur either in a “single” or an “overlapped mixed” form, including apoptosis, pyroptosis, and NETosis, which can indicate the severity of pulpal inflammation. RCD has received increasing attention because of the cross talk among cell death pathways. Hence, understanding the molecular switch nodes mediating cross talk between diverse RCD pathways may provide new insights into mechanisms underlying cell-fate decision in pulpitis. In this review, we outlined the potential roles of RCD in the progression of pulpitis and some switch nodes connecting different RCD pathways. Ultimately, an in-depth understanding of molecular mechanisms underlying RCD could be translated into effective approaches to preserve pulpal vitality and integrity under pathologic conditions.     

The role of apoptosis in oral disease: mechanisms; aberrations in neoplastic, autoimmune, infectious, hematologic, and developmental diseases; and therapeutic opportunities

Apoptosis is a genetically programmed form of cell death, which primarily functions to eliminate senescent or altered cells that are useless or harmful for the multicellular organism. Contrary to necrosis, apoptosis represents a physiologic cellular mechanism, normal function and control of which are critical for the development and homeostasis of multicellular organisms. In contrast, aberrations of the apoptotic mechanisms that cause excessive or deficient programmed cell death have been linked to a wide array of pathologic conditions. This review briefly summarizes the major apoptotic pathways and molecules and presents the most important oral diseases that are related to dysregulation of apoptosis. Knowledge of the association between aberrations in apoptotic mechanisms and human pathology hopefully will be implemented for the design of improved diagnostic and prognostic assays and the development of novel, more efficient, therapeutic strategies.     

体外培养观察人牙囊细胞中细胞程序性死亡及其在不同流体静压力下的变化

目的 研究体外培养的人牙囊细胞的特征,以及在不同流体静压力作用下细胞程序性死亡（PCD）的改变,探讨PCD在牙齿萌出过程中的作用。方法 取12岁男孩埋伏阻生牙齿的牙囊进行人牙囊细胞培养,将传代的培养细胞应用TUNEL的方法标记PCD细胞,分别在50 kPa和100 kPa流体静压力作用1 h后观察PCD变化,以不加压的人牙囊细胞作为对照。结果 体外培养的人牙囊细胞呈梭形、纺锤形或多角形,具有成纤维细胞特征。在50 kPa流体静压力下人牙囊细胞PCD阳性细胞率与对照组无统计学差异（P>0.05）,而100 kPa流体静压力下PCD阳性细胞率较对照组增加了31.65％,有统计学差异（P<0.01）。结论 流体静压力可以影响体外培养的人牙囊细胞的程序性死亡。