炎症过程在正畸牙齿移动中的作用

Lucia Avornic-Ciumeico, Valentina Trifan, Igor Uzun, Sabina Calfa, Irina Zumbreanu, Igor Ciumeico
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引用次数: 0

摘要

简介众所周知,牙齿矫正过程中总会在牙周产生压力和张力区。压力区的特点是局部血流部分或完全中断,这将不可避免地导致一些细胞死亡。作为任何生命机体的典型生理反应,炎症过程很快就会出现。尽管从业人员现在已经意识到正畸牙齿移动(OTM)过程中的炎症,但其目的是什么,对正畸治疗是有益还是有害,仍不总是很清楚。研究目的研究正畸牙齿移动过程中炎症过程的作用和特征。材料和方法:研究设计包括对电子资源中的英文文章、教科书和手册中的信息进行系统回顾。只使用原始内容,没有翻译。使用网络平台作为数据库:PubMed、ScrienceDirect、Reserch4Life、Oxford Academic。包含 "正畸装置"、"正畸技术"、"生物力学 "等术语的文章被排除在外,因为本研究不是为了评估正畸治疗的原理。研究结果OTM 总是与无菌性炎症过程相关联。牙周的压力和张力区域会影响局部血管和神经网络。细胞死亡区域以及血管内皮的改变及其通透性的增加导致血液中出现白细胞、单核细胞、巨噬细胞和血小板。这些细胞与局部牙周细胞一起释放出细胞因子(IL1β、IL-6、IL-10、TNF-α、TGF-b、M-CSF)、趋化因子(MCP-1、CCL5)、花生四烯酸衍生物(前列腺素、白三烯、一氧化氮)等炎症因子,导致局部组织重塑。IL-1β 和 TNF-α 在牙周压力区释放,作用于破骨细胞及其前体,刺激其分化,增强其活性和抵抗力。它们还有助于维持和促进炎症过程,提高基质金属蛋白酶(MMPs)的水平。TNF-α 或其受体、PGE2 或白三烯的缺失会导致 OTM 的速率显著下降。将正畸力转化为牙周组织结构变化的最重要因素是 RANKL/RANK/OPG 通路。它通过调节破骨细胞的功能来控制骨重塑/建模过程。大多数促炎细胞因子通过以下三种途径之一发挥其破骨细胞生成作用:刺激 RANK 合成、改变 RANK 诱导的细胞间相互作用或刺激 RANKL 合成。一些原始研究认为,正畸力会导致编码 RANKL 的基因表达增加。RANKL 的缺失会导致 OTM 完全停止。在牙周韧带的张力侧和压力侧都发现了 OPG 和 RANKL 的存在。无论 RANKL/OPG 的确切含量如何,它们都会影响特定牙周区域破骨细胞的活性。在某些情况下,对患有炎症性牙周病的患者进行正畸治疗会导致新生的无菌性炎症与原有的化脓性炎症相结合。这会导致牙周病加速恶化。结论1) OTM 期间的炎症过程本质上是无菌性的,是牙周组织的生理和有利(预期)反应。释放的炎症因子在正畸移动的牙齿的不同部位导致了相反的结果:在压力侧导致组织吸收,在张力侧导致组织形成。2)RANK-RANKL-OPG 机制是外力通过炎症过程转化为骨吸收和附着的关键途径。破骨细胞活动和牙齿移位的速度在很大程度上取决于 RANKL/OPG 的比例,而这些物质的数量则是一个不太重要的因素。在压迫的一侧,炎症因素会改变这一比例,使 RANKL 配体(RANKL)更有利,而在另一侧则观察到相反的现象。3) 患有牙周炎症的患者在接受正畸治疗时,有可能导致原有病情恶化。建议在开始正畸治疗前进行彻底的牙周治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of the inflammatory process in orthodontic tooth movement
Introduction: It is now well-known that an orthodontic tooth movement will always create areas of pressure and tension within periodontium. The pressure area is characterized by partial and complete interruption of the local blood flow which will inevitably result in death of some cells. As a typical physiological reaction of any vital organism an inflammation process soon emerges. Although practitioners are now aware of inflammation during orthodontic tooth movement (OTM) it is still not always clear what is its purpose and whether it’s beneficial or harmful for orthodontic treatment. Objective of the study: To study the role and features of the inflammatory process during orthodontic dental displacement. Material and methods: The design of the study involves a systematic review of information from articles, textbooks and manuals in English found in electronic sources. Only the original content without translation was used. Web platforms were used as a database: PubMed, ScrienceDirect, Reserch4Life, Oxford Academic. Articles that contained the terms ‚Orthodontic appliances’, ‚Orthodontic techniques’, ‚Biomechanics’ were excluded because this study was not conducted to assess the principles of orthodontic treatment. Results: The OTM is always associated with an aseptic inflammatory process. The areas of pressure and tension in the periodontium affect the local vascular and nerve network. Areas of cell death as well as the alteration of the vessel endothelium with increase of its permeability lead to the emergence of leukocytes, monocytes, macrophages, and platelets from the bloodstream. These cells together with the local periodontal cells release inflammatory factors such as cytokines (IL1β, IL-6, IL-10, TNF-α, TGF-b, M-CSF), chemokines (MCP-1, CCL5), arachidonic acid derivatives (prostaglandins, leukotrienes, nitric oxide), which lead to remodeling of local tissues. IL-1β and TNF-α are released at periodontal pressure areas and act on osteoclasts and their precursors, stimulating their differentiation, increasing their activity and resistance. They also contribute to the maintenance and promotion of the inflammatory process and increase the level of matrix metalloproteinases (MMPs). The absence of TNF-α or its receptor, of PGE2 or leukotrienes result in a significant decrease in the rate of OTM. The most important element responsible for the transfer of orthodontic force into structural changing in periodontal tissues is RANKL/RANK/OPG pathway. It controls bone remodeling/modeling processes by regulating the osteoclastic function. Most pro-inflammatory cytokines exert their osteoclastogenetic effects via one of three pathways: stimulation of RANK synthesis, modification of RANK-induced intercellular interactions, or stimulation of RANKL synthesis. Several original studies have concluded that orthodontic forces lead to an increased expression of the gene encoding RANKL. The absence of RANKL leads to a complete cessation of OTM. The presence of OPG and RANKL has been revealed on both the tension side of the periodontal ligament and the compression side. RANKL/OPG ratio, regardless of the exact amount of each substance, affects the activity of osteoclasts in a particular periodontal area. Orthodontic treatment of patients with inflammatory periodontal diseases in some cases results in a combination of a de novo aseptic inflammation with a preexisting septic inflammation. This leads to accelerated progression of periodontal disease. Conclusions: 1) The inflammatory process during OTM is aseptic in nature and represents a physiological and favorable (expected) response of periodontal tissues. The released inflammatory factors lead to opposite results in different parts of the orthodontically moved teeth: to tissue resorption on the pressure side and to its formation on the tension side. 2) The RANK-RANKL-OPG mechanism represents the key pathway for the transformation of exogenous forces into bone resorption and apposition through the inflammatory process. The rate of osteoclast activity and tooth displacement depends largely on the RANKL/OPG ratio, with the amount of these substances being a less relevant factor. On the side of compression, inflammatory factors change this ratio in favour of RANKL-ligand (RANKL), while on the other side the opposite phenomenon is observed. 3) Patients with an inflammatory disease of periodontium are at risk of worsening the preexisting condition when being treated orthodontically. A thorough periodontological therapy is recommended before starting an orthodontic therapy.
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