Host response mechanisms in periodontal diseases.
Host response mechanisms in periodontal diseases.
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DOI：
10.1590/1678-775720140259
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发表时间：
2015-05
期刊：
影响因子：
--
通讯作者：
Gamonal J
中科院分区：
文献类型：
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作者：
Silva N;Abusleme L;Bravo D;Dutzan N;Garcia-Sesnich J;Vernal R;Hernández M;Gamonal J
牙周病通常是指称为牙龈炎和牙周炎的常见炎症性疾病，其由龈下生物膜中的致病性微生物群引起，包括牙龈卟啉单胞菌、伴放线菌聚集菌、嗜酸坦那杆菌和齿垢密螺旋体，其触发先天性、炎症性和适应性免疫应答。这些过程导致牙齿周围和支撑牙齿的组织的破坏，最终导致组织、骨骼和牙齿脱落。先天免疫反应构成了一个稳态系统，这是第一道防线，能够识别入侵的微生物为非自身，触发免疫反应以消除它们。除了先天免疫外，适应性免疫细胞和特征性细胞因子已被描述为牙周病发病机制中的重要参与者，特别关注CD 4 + T细胞（T辅助细胞）。有趣的是，T细胞介导的适应性免疫发展高度依赖于先天免疫相关的抗原呈递细胞，其在抗原捕获后经历成熟过程并向淋巴结迁移，在淋巴结中它们产生不同的细胞因子模式，这些细胞因子将有助于特异性T CD 4+淋巴细胞的后续极化和活化。骨稳态依赖于骨形成成骨细胞（OBL）和骨吸收破骨细胞（OCL）活性之间的动态平衡。这种平衡受到各种调节系统（如内分泌系统）的严格控制，并受到免疫系统（一种依赖于淋巴细胞和巨噬细胞来源的细胞因子的骨免疫调节）的影响。所有这些细胞因子和炎症介质能够单独或协同作用，以通过组织来源的基质金属蛋白酶刺激牙周分解和胶原破坏，牙周炎进展的特征是作为对微生物挑战呈现显著宿主免疫和炎症反应的阶段，其决定在多种行为的影响下发展破坏性/进行性牙周炎的易感性，环境和遗传因素。
Periodontal diseases usually refer to common inflammatory disorders known as gingivitis and periodontitis, which are caused by a pathogenic microbiota in the subgingival biofilm, including Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Treponema denticola that trigger innate, inflammatory, and adaptive immune responses. These processes result in the destruction of the tissues surrounding and supporting the teeth, and eventually in tissue, bone and finally, tooth loss. The innate immune response constitutes a homeostatic system, which is the first line of defense, and is able to recognize invading microorganisms as non-self, triggering immune responses to eliminate them. In addition to the innate immunity, adaptive immunity cells and characteristic cytokines have been described as important players in the periodontal disease pathogenesis scenario, with a special attention to CD4+ T-cells (T-helper cells). Interestingly, the T cell-mediated adaptive immunity development is highly dependent on innate immunity-associated antigen presenting cells, which after antigen capture undergo into a maturation process and migrate towards the lymph nodes, where they produce distinct patterns of cytokines that will contribute to the subsequent polarization and activation of specific T CD4+ lymphocytes. Skeletal homeostasis depends on a dynamic balance between the activities of the bone-forming osteoblasts (OBLs) and bone-resorbing osteoclasts (OCLs). This balance is tightly controlled by various regulatory systems, such as the endocrine system, and is influenced by the immune system, an osteoimmunological regulation depending on lymphocyte- and macrophage-derived cytokines. All these cytokines and inflammatory mediators are capable of acting alone or in concert, to stimulate periodontal breakdown and collagen destruction via tissue-derived matrix metalloproteinases, a characterization of the progression of periodontitis as a stage that presents a significantly host immune and inflammatory response to the microbial challenge that determine of susceptibility to develop the destructive/progressive periodontitis under the influence of multiple behavioral, environmental and genetic factors.