Cytokine profile in synovial fluid from patients with internal derangement of the temporomandibular joint: a preliminary study

颞下颌关节 医学 细胞因子 骨保护素 血管内皮生长因子 滑液 生长因子 内科学 碱性成纤维细胞生长因子 内分泌学 成纤维细胞生长因子 病理 骨关节炎 替代医学 受体 血管内皮生长因子受体 激活剂(遗传学)
作者
K Matsumoto,K. Honda,Mitsuhiro Ohshima,Yoshihiro Yamaguchi,Ikuyo Nakajima,Patrick Micke,K. Otsuka
出处
期刊:Dentomaxillofacial Radiology [Oxford University Press]
卷期号:35 (6): 432-441 被引量:60
标识
DOI:10.1259/dmfr/77288976
摘要

Objectives: Temporomandibular joint disorders (TMD) comprise a group of chronic painful conditions of mastication in the temporomandibular joint (TMJ). Although the association between TMD and internal derangement of the TMJ is well documented, the functional relevance is still unclear. Increased concentrations of inflammatory mediators have been identified in the synovial fluid of affected patients with TMD, suggesting an underlying degenerative or inflammatory process. The aim of this study was to generate a comprehensive cytokine expression profile in TMD. Methods: 15 samples from patients with internal derangement of TMJ were analysed using a novel cytokine array that enables the analysis of 79 different cytokines simultaneously. Results: Cytokine levels were correlated with the presence of joint effusion (JE) determined by MRI. In the majority of synovial fluid samples, angiogenin (Ang), fibroblast growth factor (FGF)-9, insulin-like growth factor-binding protein (IGFBP)-3, interleukin (IL)-1α, IL-1β, IL-8, inducible protein (IP)-10, macrophage inflammatory protein (MIP)-1β, osteoprotegerin (OPG), transforming growth factor (TGF)-β2, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, tumour necrosis factor (TNF)-β and vascular endothelial growth factor (VEGF) were detectable. Furthermore, the expression levels of Ang, brain-derived neurotrophic factor (BDNF), FGF-4, FGF-9, IGFBP-2, IL-8, MIP-1β, OPG, pulmonary and activation-regulated protein (PARC), TGF-β2, TIMP-2 and VEGF were significantly associated with the presence of JE; among these, nine cytokines (Ang, BDNF, FGF-4, FGF-9, IGFBP-2, MIP-1β, PARC, TGF-β2 and TIMP-2) were hitherto not described in TMD. Conclusions: This study confirmed previous reports of elevated cytokine levels in TMD. Additionally, we identified previously undescribed cytokines that were upregulated and correlated significantly with the presence of JE. We were able to identify novel cytokines that have hitherto not been described in TMD. Strategies targeting the identified cytokines may represent a novel therapy option in TMD.
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