Analysis of inflammatory mediators in temporomandibular joint synovial fluid lavage samples of symptomatic patients and asymptomatic controls
Analysis of inflammatory mediators in temporomandibular joint synovial fluid lavage samples of symptomatic patients and asymptomatic controls
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DOI：
10.1016/j.joms.2005.02.009
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发表时间：
2005-06-01
影响因子：
1.9
通讯作者：
Israel, H
中科院分区：
文献类型：
--
作者：
Chang, H;Israel, H
目的：这是我们的目的是研究伊加，IgG和β-葡萄糖醛酸酶水平的颞下颌关节液灌洗样本，以找到一个生化标志物和关节pathology.Materials和方法之间的相关性：我们的患者人群包括20例（18名女性和2名男性），严重的疼痛和下颌运动的限制，未能改善至少3个月的一个完整的非手术治疗过程。在机构审查委员会批准后，获得了13名对照受试者（6名女性和7名男性），无颞下颌关节疼痛/功能障碍病史。患者和对照组的关节镜检查涉及使用视觉分级系统对骨关节炎和滑膜炎的关节进行分类。结果：与对照组（4.13 +/- 8.30 vs 0.9 +/- 0.83 [mean +/- SD]）相比，患者组β-葡萄糖醛酸酶显著升高（P <0.05，t检验）。IgG水平的差异也具有统计学意义（31，638 +/-70，714对4，407 +/-1，324）（P <0.05，t检验）。伊加水平在患者组和对照组之间显示出相似的趋势（6，315 +/-19，037对425 +/- 192）（P = 0.10，t检验）。结论：β-葡萄糖醛酸酶、伊加和IgG的定量滑液分析表明，与无症状的非患病关节相比，患病关节中炎症介质水平升高。我们推测TMJ滑液中高水平的伊加、IgG和β-葡萄糖醛酸酶是由于血清和滑膜中慢性炎症细胞的浸润所致。在封闭的关节间隙中，高水平的免疫球蛋白可引起强烈的炎症反应，并通过补体激活和免疫复合物沉积对关节组织造成破坏。补体激活增加血管渗透性，使嗜中性白细胞能够募集，然后释放各种溶酶体酶并损伤关节软骨。(c)2005年美国口腔颌面外科医师协会。
Purpose: It was our purpose to study IgA, IgG, and beta-glucuronidase levels in temporomandibular joint fluid lavage samples in order to find a correlation between biochemical markers and joint pathology.Materials and Methods: Our patient population included 20 patients (18 female and 2 male) with severe pain and limitation of mandibular movement that failed to improve with at least 3 months of a full course of nonsurgical therapy. After institutional review board approval, 13 control subjects (6 female and 7 male), with no history of temporomandibular joint pain/dysfunction, were obtained. Arthroscopic examination of the patient and control groups involved classification of joints for osteoarthritis and synovitis using a visual grading system. All synovial fluid samples were analyzed for beta-glucuronidase, IgA, and IgG using fluorometric assay and enzyme-linked immunosorbent assay.Results: beta-Glucuronidase was significantly elevated (P < .05, t test) in the patient group compared with the control group (4.13 +/- 8.30 versus 0.9 +/- 0.83 [mean +/- SD]). The difference in the IgG level was also statistically significant (31,638 +/- 70,714 versus 4,407 +/- 1,324) (P < .05, t test). IgA level showed a similar trend between the patient and control groups (6,315 +/- 19,037 versus 425 +/- 192) (P = .10, t test).Conclusions: Quantitative synovial fluid analysis of beta-glucuronidase, IgA, and IgG demonstrates elevated levels of inflammatory mediators in diseased joints compared with asymptomatic nondiseased joints. We hypothesize that high levels of IgA, IgG, and beta-glucuronidase in the TMJ synovial fluids are due to infiltration from the sera and chronic inflammatory cells residing in the synovium. High levels of immunoglobulins in a closed joint space can elicit strong inflammatory reaction and cause destruction to the joint tissues via complement activation and immune complex deposition. Complement activation increases blood vessel permeability to enable recruitment of neutrophilic leukocytes, which then liberate various lysosomal enzymes and damage the articular cartilage. (c) 2005 American Association of Oral and Maxillofacial Surgeons.