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

Departments of ¹Radiology; ² Biochemistry and; ³ Pediatric Dentistry, Nihon University School of Dentistry, Tokyo, Japan; Divisions of ⁴Advanced Dental Treatment; ⁵ Functional Morphology and; ⁶ Oral and Craniomaxillofacial Research, Dental Research Center, Nihon University School of Dentistry, Tokyo, Japan; ⁷ Cancer Center Karolinska, Department of Pathology-Oncology, Karolinska Institute, Stockholm, Sweden

*Correspondence to: Mitsuhiro Ohshima, Department of Biochemistry, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan; Email: oshima-m{at}dent.nihon-u.ac.jp

Received 9 August 2005; revised 21 December 2005; accepted 28 December 2005

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)-1, IL-1ß, IL-8, inducible protein (IP)-10, macrophage inflammatory protein (MIP)-1ß, osteoprotegerin (OPG), transforming growth factor (TGF)-ß2, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, tumour necrosis factor (TNF)-ß 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-1ß, OPG, pulmonary and activation-regulated protein (PARC), TGF-ß2, 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-1ß, PARC, TGF-ß2 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.

Keywords: temporomandibular joint; cytokine; synovial fluid; joint effusion