Internal derangement (ID) and osteoarthritis (OA) are often encountered in temporomandibular joint (TMJ) disorders. It is known that high concentrations of interleukin (IL)-1
β and tumor necrosis factor (TNF)-
α are detected in the synovial fluids of patients with ID and OA. IL-1
β and TNF-
α play key roles in intracapsular pathological conditions of the TMJ. Gene expressions induced by IL-1
β and/or TNF-
α in synoviocytes obtained from human TMJ were analyzed using microarrays. Microarray analysis showed that levels of IL-6 and leukemia inhibitory factor (LIF), which are in the IL-6 cytokine family, were up-regulated in synoviocytes stimulated with IL-1
β and/or TNF-
α. The IL-6 cytokine family, which contains IL-6, LIF, oncostatin M (OSM), IL-11, and IL-12, is associated with inflammation and tissue destruction. We examined the gene expressions of IL-6 cytokine family members and their receptors in synoviocytes stimulated with IL-1
β and/or TNF-
α using RT-PCR, and real-time PCR. The up-regulated levels of IL-6 and LIF were greatest following stimulation with both IL-1
β and TNF-
α and least following stimulation with only TNF-
α. Protein production of IL-6 and LIF also increased in synoviocytes stimulated with IL-1
β and/or TNF-
α. The up-regulated levels of IL-6 and LIF protein productions reflected the gene expression levels. The gene expressions of OSM, IL-11, and IL-12 were not detected in synoviocytes. Glycoprotein 130 (gp130), which is a receptor subunit for signal transduction of the IL-6 cytokine family, LIF receptor, OSM receptor, and IL-11 receptor were expressed in synoviocytes constitutively. In conclusion, IL-1
β and TNF-
α may cause abnormalities associated with intracapsular pathological conditions of the TMJ through the enhanced expression of IL-6 and LIF in synoviocytes.
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