普鲁卡因封闭颈交感神经节治疗急性浆液性淋巴结炎

植物性神经系统在机体生命活动中起着重要作用,机体组织的供血、物质代谢、营养以及适应能力、体内环境的稳定等等均受该系统的制约。植物性神经系统参与颌面部软组织的神经支配,因此任何一种炎性疾病都伴有该系统失调的症状。     

低氧诱导因子-1α与口腔扁平苔藓

低氧诱导因子(HIF)-1是机体低氧反应中的重要转录因子,在免疫炎症反应中参与调控免疫细胞分化、促进黏附、影响细胞代谢、诱导新生血管形成、调控细胞增殖与凋亡等。近年研究表明,HIF-1α在口腔扁平苔藓的发生发展过程中可能发挥着重要作用,本文将从HIF-1的结构、功能及调控,免疫炎症反应中HIF-1α的表达,HIF-1α在口腔扁平苔藓发生、发展中的作用等方面作一综述。     

光动力介导的免疫调控作用及其在口腔医学领域中的作用特点

光动力疗法在临床应用中发展迅速，在口腔肿瘤、口腔黏膜病、牙髓牙周疾病治疗以及组织再生等领域有广阔的应用前景。免疫调控在光动力治疗中发挥着重要作用。光动力疗法可诱导细胞凋亡或直接破坏细胞，暴露抗原物质，进而刺激免疫细胞的增殖与活化并释放炎症细胞因子，从而破坏病变组织，抑制肿瘤增殖；通过改变血管通透性等方式调节局部炎症进程，促进免疫细胞抗炎极化，同时减少炎性细胞浸润；通过改变局部细胞因子的分泌模式间接促进组织再生，或直接靶向免疫细胞引起内皮细胞、软骨细胞和成纤维细胞等的增殖或分化。文章就光动力介导的免疫调控作用特点及其在口腔医学领域中的应用方向做一综述。     

补肾固齿丸对人牙周膜成纤维细胞分泌白细胞介素-6的影响

牙周病是在致病菌和宿主免疫反应失衡情况下发生的感染性疾病。多种炎性介质和细胞因子参与了牙周病的发生发展过程,其中白细胞介素-6（interleukin-6,IL-6）是一种重要的细胞因子,其分泌增多时会产生明显的致炎作用。牙周膜成纤维细胞（periodontal ligament cell,PDLC）是牙周组织中合成分泌IL-6的重要细胞,在受到细菌刺激时,合成分泌IL-6的能力增强。     

维生素D3对老年糖尿病性牙周炎的免疫调节作用

糖尿病性牙周炎是一种易造成牙周组织显著破坏的难治性疾病,在老年人群具有较高的发病率,是目前牙周疾病治疗的难点和热点之一.作为机体固有免疫的组成部分,炎症反应及其相关的炎症因子在糖尿病性牙周炎发生发展过程中扮演了主要角色.近年来研究发现维生素D3除了具有经典的调节钙磷代谢等作用以外,还具有调节免疫系统的功能.维生素D3通过参与炎症反应的相关细胞和炎症介质、抗炎因子进行调节,对老年糖尿病性牙周炎的防治具有重要作用.     

IL-8与牙髓炎的研究探讨

牙髓炎是一种以G^-厌氧菌感染为主的炎性疾病。细菌在损害组织的同时，还释放各类毒性产物，如LPS等激发机体免疫系统，产生多种细胞因子，参与免疫炎性反应。白细胞介素-8（Interleukin-8，IL-8）是人们在牙髓组织中发现的一种重要的细胞因子，它能趋化中性粒白细胞（Polymorphonuclear leukocyte，PMN）、T淋巴细胞、嗜碱性粒细胞和单核细胞；并能诱导PMN上粘附分子的表达，引导它穿越血管内皮并介导炎症反应。因此IL-8在牙髓炎的病理过程中发挥重要作用。     

叉头转录因子-1与骨代谢关系的研究进展

叉头转录因子-1（FoxO1）可调控细胞增殖、葡萄糖异生、能量代谢和氧化应激等生物学过程,近年来研究表明,其在骨重塑过程中也发挥着重要的作用,影响机体骨量。其主要通过调控成骨细胞形成新骨,破骨细胞吸收矿化骨基质和前体细胞的分化增殖,影响骨代谢过程,调控机体骨量。本文通过对FoxO1在骨代谢中的研究进行回顾,对其在骨代谢中的作用途径和机制进行综述。     

磷酸氯喹在口腔扁平苔藓中的临床应用

综述了氯喹的药物代谢动力学、作用机制、临床应用及药物不良反应。氯喹通过抗炎、免疫抑制、抗感染等作用，应用于口腔扁平苔藓，在改善病情中可发挥重要作用，此药安全有效。     

NLRP3及其在口腔疾病中的研究进展

NLRP3受体是天然免疫系统细胞浆型模式识别受体中核苷酸结合寡聚化结构域样受体(NLR)家族的一个重要成员,在机体固有免疫应答中发挥独特的功能,其特点是可以通过形成复杂的蛋白质复合体——炎性体,介导炎症反应和细胞死亡。NLRP3炎性体在多种疾病和炎症反应中发挥重要作用,下面就NLRP3受体的结构、功能及其在口腔疾病中的作用作一综述。     

牙周炎性牙槽骨吸收与T细胞间的关系

牙周炎性牙槽骨吸收是常见的牙周组织炎症性破坏性疾病,是导致牙丧失的主要原因。T细胞在牙周炎的发生发展过程中发挥了重要的作用。一方面,牙周致病菌抗原活化T细胞是机体抗牙周致病菌感染所必需;另一方面,活化的T细胞是破骨细胞分化成熟和骨吸收活性的重要调节细胞,也是牙周炎性牙槽骨吸收的损伤细胞。本文就牙周炎性牙槽骨吸收,T细胞在牙周炎性牙槽骨吸收中的作用,T细胞和干扰素一1对破骨细胞的作用等研究进展作一综述。     

Cytotoxicity of polymerized commercial cyanoacrylate adhesive on cultured human oral fibroblasts

Cyanoacrylate (CA) has been used as both a commercial and tissue adhesive. Dentists may have had the experience of patients repairing their own acrylic-based dentures using a cyanoacrylate (CA) adhesive known as 'super glue'. This study evaluated the cytotoxicity of commercial CA adhesives when fully polymerized, as well as the toxicity of substances released from polymerized commercial CA adhesives after incubation of these materials for various periods of time. Toxicity was tested on cultured oral fibroblasts. Dead cells found around the various CA-coated filter papers constituted inhibitory zones which varied from 200-1000 microns and which persisted for two weeks. Control oral fibroblasts grew to approach the wax-coated filter paper. Cell viability testing using MTT and crystal violet staining methods supported the conclusion that polymerized CA-coated filter paper released substances that are toxic to cells, while wax-coated filter paper gave the same result as the control. The crystal violet staining method was also used to investigate the cytotoxicity of various CA materials after incubation for one, three, seven and 14 days and showed that CA continued to release cytotoxic substances at about the same level for at least two weeks. It can be concluded that, if CA adhesive is used for repair of broken dentures, it will release substances which are toxic to human oral fibroblast cells. This release of substances may persist for at least two weeks.     

Chemokines in oral inflammatory diseases: apical periodontitis and periodontal disease

The inflammatory oral diseases are characterized by the persistent migration of polymorphonuclear leukocytes, monocytes, lymphocytes, plasma and mast cells, and osteoblasts and osteoclasts. In the last decade, there has been a great interest in the mediators responsible for the selective recruitment and activation of these cell types at inflammatory sites. Of these mediators, the chemokines have received particular attention in recent years. Chemokine messages are decoded by specific receptors that initiate signal transduction events, leading to a multitude of cellular responses, including chemotaxis and activation of inflammatory and bone cells. However, little is known about their role in the pathogenesis of inflammatory oral diseases. The purpose of this review is to summarize the findings regarding the role of chemokines in periapical and periodontal tissue inflammation, and the integration, into experimental models, of the information about the role of chemokines in human diseases.     

外泌体在骨髓间充质干细胞骨向分化及其在牙周再生中的研究进展

外泌体是多种细胞在生理或病理状态下分泌到细胞外的纳米级囊泡,富含蛋白质、核酸、脂质等生物活性物质,是细胞间信息交流传递和物质交换转移的重要介质。研究证实,外泌体可通过蛋白、miRNAs等调控干细胞的增殖、分化,在免疫应答、炎症反应等过程中均发挥重要的调节作用。本文就炎性环境下不同细胞来源的外泌体生物学性能及其在成骨分化中的作用作一综述,以期为牙周炎所致骨缺损的治疗方法提供参考。     

Microbiological, pathological, inflammatory, immunological and molecular biological aspects of periradicular disease

Multimicrobial infection of the dental pulp triggers inflammatory responses and ultimately causes bone destruction in the periradicular tissues. Besides bacteria, noxious substances such as degraded protein components and cholesterol could also act as antigens and elicit a host response, which can be harmful to periradicular tissues. Histologically, a dense infiltration of immunocompetent cells is seen in periradicular lesions and their host reactions may induce bone resorption. Polymorphonuclear leucocytes (PMN) and macrophages migrate to the periapical lesions and phagocytose pathogens as a first line of defence. Dead PMN are quickly phagocytosed by macrophages and this disposal system plays a role in maintaining chronicity of the lesions. The pathological roles of periradicular T cells have been assessed through analysing phenotypic markers of cell types, especially CD antigens, but the results are still controversial. Recently, technical developments in immunology and molecular biology have made it possible to investigate the pathogenesis of many diseases at molecular level. The investigation of functional analysis of the immune cells and their regulatory molecules such as apoptosis-associated molecules and adhesion molecules, will lead to a better understanding of the pathogenesis of periradicular lesions. The role of inflammatory mediators including antibodies, cytokines, matrix metalloproteinases, growth factors and arachidonic metabolism is becoming known for these lesions. Knowledge from these investigations improve the understanding of the pathological mechanisms of periradicular infections.     

Salivary IgA and IgG subclasses in oral mucosal diseases

OBJECTIVE: It was hypothesized that serum levels of immunoglobulins may play a role in the pathogenesis of oral mucosal diseases, or reflect clinical changes in these conditions, but little is known about the role of salivary immunoglobulins in the pathogenesis of these diseases. The aim of this study was to investigate possible alterations in salivary immunoglobulin A (IgA) and IgG subclasses in patients with oral mucosal inflammatory diseases. SUBJECTS and METHODS: Levels of IgG1, IgG2, IgG3 and IgG4 were determined by enzyme-linked immunosorbent assay (ELISA), and IgA1 and IgA2 by radial immunodiffusion in the resting whole saliva of 31 patients with acute recurrent aphthous ulceration (RAU) (and followed in remission), 11 patients with chronic hyperplastic candidal infection (CHC), 12 patients with Sjogren's syndrome (SS), six patients with oral lichen planus (OLP), and 18 healthy volunteers using the normal saliva as a comparison point for all. RESULTS: IgG and IgA subclasses were increased in OLP. In CHC all IgG subclasses were increased while IgA1 was decreased, IgG1, IgG3 and IgG4 levels were increased in SS, while all IgG subclasses as well as IgA2 were increased in acute RAU in comparison with healthy controls. No differences in any immunoglobulin subclasses between major and minor acute RAU were found. In remission, IgG1 and IgG4 returned to normal values while IgG2, IgG3, and IgA2 remained increased in patients with RAU. CONCLUSION: Salivary immunoglobulin subclasses vary in different oral mucosal conditions and may play a role in oral mucosal inflammatory diseases and/or reflect clinical changes in these conditions.     

Biologically active substances of the mast cell

The mast cells have been shown to contain a number of biologically active substances, some of which may contribute to the various phases of the inflammatory reaction. The present article deals with an evaluation of the potential role of the products of the mast cell metabolism in inflammation in general and in gingivitis in particular. In order for the various substances contained within the mast cells to act, they must be liberated into the connective tissue by degranulation of the cells. Among the released substances, histamine, proteolytic-esterolytic enzymes, "slow reacting substance", lysolecithins and heparin have been related to the development and course of inflammation in humans. Other factors, including, serotonin, unsaturated fatty acids and β-glucaronidase, seem to be of minor importance. The functions of the mast cell ascorbic acid, and phosphatases are not known.     

Natural resolution of inflammation

Inflammation is a protective response essential for maintaining human health and for fighting disease. As an active innate immune reaction to challenge, inflammation gives rise to clinical cardinal signs: rubor, calor, dolor, tumor and functio laesa. Termination of acute inflammation was previously recognized as a passive process; a natural decay of pro‐inflammatory signals. We now understand that the natural resolution of inflammation involves well‐integrated, active, biochemical programs that return tissues to homeostasis. This review focuses on recent advances in the understanding of the role of endogenous lipid mediators that modulate cellular fate and inflammation. Biosynthesis of eicosanoids and other lipids in exudates coincides with changes in the types of inflammatory cells. Resolution of inflammation is initiated by an active class switch in lipid mediators, such as classic prostaglandins and leukotrienes, to the production of proresolution mediators. Endogenous pro‐resolving lipid mediators, including arachidonic acid‐derived lipoxins, aspirin‐triggered lipoxins, ω3‐eicosapentaenoic acid‐derived resolvins of the E‐series, docosahexaenoic acid‐derived resolvins of the D‐series, protectins and maresins, are biosynthesized during the resolution phase of acute inflammation. Depending on the type of injury and the type of tissue, the initial cells that respond are polymorphonuclear leukocytes, monocytes/macrophages, epithelial cells or endothelial cells. The selective interaction of specific lipid mediators with G protein‐coupled receptors expressed on innate immune cells (e.g. G protein‐coupled receptor 32, lipoxin A4 receptor/formyl peptide receptor2, chemokine‐like receptor 1, leukotriene B4 receptor type 1 and cabannoid receptor 2) induces cessation of leukocyte infiltration; vascular permeability/edema returns to normal with polymorphonuclear neutrophil death (mostly via apoptosis), the nonphlogistic infiltration of monocyte/macrophages and the removal (by macrophages) of apoptotic polymorphonuclear neutrophils, foreign agents (bacteria) and necrotic debris from the site. While an acute inflammatory response that is resolved in a timely manner prevents tissue injury, inadequate resolution and failure to return tissue to homeostasis results in neutrophil‐mediated destruction and chronic inflammation. A better understanding of the complex mechanisms of lipid agonist mediators, cell targets and actions allows us to exploit and develop novel therapeutic strategies to treat human inflammatory diseases, including periodontal diseases.     

Heat shock proteins in the pathogenesis of inflammatory skin diseases

Heat shock proteins (HSPs) are highly conserved molecules and distributed widely in nature. They are also distributed in the skin, however, only limited information is available on the role of HSPs in the skin diseases. Immunohistochemical study of HSPs in the skin revealed that HSPs are differently expressed in the epidermal cells of patients with systemic lupus erythematosus (SLE), atopic dermatitis, graft versus host disease (GVHD) and so on. In normal healthy skin HSPs are constantly expressed in the epidermal cells. HSPs are expressed in the skin according to the influence of both external and internal milieu of the diseased conditions. Cytokines released in the skin strongly affect to express HSPs in epidermal cells. HSPs expressed in the skin can be targets for infiltrated T cells to modulate immune response of skin diseases. Roles of HSPs in the pathogenesis of SLE, GVHD, atopic dermatitis and psoriasis are discussed in this review. HSPs play an important role in the pathogenesis of many inflammatory skin diseases. They can be the molecules to evaluate both diseased conditions and inflammatory process of the skin diseases.     

Alterations of neutrophil f-actin kinetics by tobacco smoke: implications for periodontal diseases

Tobacco smoking is a major risk factor in the incidence and severity of periodontal diseases. Alterations of neutrophil function by short-term high levels of smoke during the act of smoking (acute smoke exposure) as well as long-term exposure to lower levels of tobacco substances in the bloodstream (chronic smoke exposure) may play a role in the pathogenesis of periodontal diseases in smokers. The polymerization and depolymerization of f-actin in response to infectious agents or inflammatory mediators is a critical process in a variety of neutrophil functions. In this study, we examined the effects of in vitro smoke exposure on neutrophils from smokers and non-smokers (which may be comparable to in vivo acute smoke exposure) and neutrophils from smokers not exposed to further in vitro smoke (which may be comparable to chronic smoke exposure) on f-actin kinetics. Peripheral neutrophils were isolated from seven healthy smoking subjects and seven healthy age-matched non-smoking subjects and exposed to 1-5 min of acute smoke in a smoke box system or not exposed to further smoke (baseline controls). Selected aliquots of neutrophils from control and 5-min exposures of acute smoke were then stimulated with the chemotactic peptide F-met-leu-phe at 10(-7) M for an additional 30-360 s. Cells were fixed and permeabilized, stained for f-actin with NBD phallacidin, and analyzed by flow cytometry. From baseline to 5 min of in vitro smoke exposure, there was a 38% decline in f-actin stain in non-smokers and a 30% decline in f-actin stain in smokers (p > 0.05) with f-actin values slightly higher in smokers than-non-smokers (p > 0.05). With F-met-leu-phe stimulation, both smokers and-non-smokers demonstrated a characteristic rise in f-actin stain from 0 to 120 s with a subsequent decline to baseline at 360 s and no significant differences in f-actin levels at any time of stimulation between groups. After preincubation with 5 min of in vitro smoke, the magnitude of rise in f-actin was less in both smokers and non-smokers when compared to cells not incubated with 5 min of smoke (p < 0.05 at 120 s for both smokers and non-smokers). F-actin values in smokers were higher than-non-smokers from 30 to 360 s of F-met-leu-phe exposure (p > 0.05). These results demonstrate that in vitro smoke exposure may impair normal f-actin kinetics. These alterations in f-actin kinetics may in turn affect other neutrophil functions which may impact on the pathogenesis of periodontal diseases in smokers.