MCP-1 Production in Temporomandibular Joint Inflammation

Author:

Ogura N.12,Satoh K.1,Akutsu M.12,Tobe M.12,Kuyama K.32,Kuboyama N.42,Sakamaki H.15,Kujiraoka H.6,Kondoh T.12

Affiliation:

1. Department of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo, 2–870–1 Sakaecho-Nishi, Matsudo, Chiba 271–8587, Japan

2. Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo

3. Department of Oral Pathology, Nihon University School of Dentistry at Matsudo

4. Department of Oral Molecular Pharmacology, Nihon University School of Dentistry at Matsudo

5. Department of Dental Hygiene, Faculty of Health Care Sciences, Chiba Prefectural University of Health Sciences, Chiba 261–0014, Japan

6. Department of Dentistry and Oral Surgery, Asahi General Hospital, Asahi, Chiba 289–2511, Japan

Abstract

Synovitis, which is characterized by the infiltration of inflammatory cells, often accompanies progression of temporomandibular joint disorder (TMD) symptoms. Because IL-1β is elevated in synovial fluids obtained from TMDs, we hypothesized that IL-1β-responsive genes in synoviocytes may help identify the putative genes associated with synovitis. Using microarray analysis, we found that monocyte chemoattractant protein-1 (MCP-1) mRNA levels were elevated in IL-1β-stimulated synoviocytes. MCP-1 is a member of the chemokine superfamily. The production of MCP-1 was increased in synoviocytes treated with IL-1β. When IL-1β was injected into the cavities of rat TMJs, inflammatory cells and MCP-1-positive cells were detected in the synovial tissues. Furthermore, MCP-1 levels were higher in synovial fluids from individuals with pain compared with those without pain. Inhibitors of MAP-kinases and NF-κB reduced IL-1β-induced MCP-1 production. These results suggest that MCP-1 stimulated by IL-1β is one of the factors associated with the inflammatory progression of TMDs.

Publisher

SAGE Publications

Subject

General Dentistry

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