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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.

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Array comparative genomic hybridization (array CGH) analysis was conducted in chorionic villous samples from 20 first-trimester spontaneous abortions with G-banding normal chromosomes. A microarray, containing 2,173 BAC clones and covering the whole genome with a 1.5-Mb resolution, was constructed and used in the analysis. Two deletions were identified: a 1.4-Mb deletion at 3p26.2-p26.3 and a 13.7-Mb deletion at 13q32.3-qter. Reexamination of chromosome preparations from the sample with the 13.7-Mb deletion documented a mixture of cells with the 13q- chromosome and those with 46,XX chromosomes, the latter of which are likely to have been derived from contaminating decidual cells. This left the 1.4-Mb 3p deletion as the only instance with submicroscopic imbalance detected, giving a frequency of 1 in 19 (5%) G-banding normal abortions.