{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T14:22:51Z","timestamp":1783088571330,"version":"3.54.6"},"reference-count":34,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,1,18]],"date-time":"2013-01-18T00:00:00Z","timestamp":1358467200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Oral Pathology Medicine"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Non\u2010steroidal anti\u2010inflammatory drugs (<jats:styled-content style=\"fixed-case\">NSAIDs<\/jats:styled-content>) have been widely used for the management of pain and inflammation. However, little remains known about the effects of <jats:styled-content style=\"fixed-case\">NSAIDs<\/jats:styled-content> on synovitis of the human temporomandibular joint (<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>). The aims of this study were to investigate the potential anti\u2010inflammatory effects of <jats:styled-content style=\"fixed-case\">NSAIDs<\/jats:styled-content> on synovitis of the <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> and the inflammatory effects of <jats:styled-content style=\"fixed-case\">PGE2<\/jats:styled-content> on fibroblast\u2010like synoviocytes (<jats:styled-content style=\"fixed-case\">FLS<\/jats:styled-content>) derived from the <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Human synovial tissue was obtained from patients with internal derangement who underwent arthroscopy of the <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">FLSs<\/jats:styled-content> were prepared from the tissues using the outgrowth method. A <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content> inhibitor (indomethacin or celecoxib) was added to the <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2\u2010stimulated cells in culture. The cells were also stimulated with <jats:styled-content style=\"fixed-case\">PGE2<\/jats:styled-content> or an <jats:styled-content style=\"fixed-case\">EP<\/jats:styled-content> agonist. The <jats:styled-content style=\"fixed-case\">PGE2<\/jats:styled-content> production and <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content>\u20102 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 expression levels were examined using enzyme\u2010linked immunosorbent assays, real\u2010time <jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>, and a microarray analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content> inhibitors decreased not only <jats:styled-content style=\"fixed-case\">PGE2<\/jats:styled-content> production, but also the expression of <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content>\u20102 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 in <jats:styled-content style=\"fixed-case\">FLS<\/jats:styled-content> stimulated with <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2. <jats:styled-content style=\"fixed-case\">EP2<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">EP4<\/jats:styled-content> were both expressed in the <jats:styled-content style=\"fixed-case\">FLS<\/jats:styled-content>, and the treatment with <jats:styled-content style=\"fixed-case\">EP2<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">EP4<\/jats:styled-content> agonists induced <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 production in these cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content> inhibitors indomethacin and celecoxib reduce the expression of inflammatory factors, such as <jats:styled-content style=\"fixed-case\">COX<\/jats:styled-content>\u20102 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, in <jats:styled-content style=\"fixed-case\">FLS<\/jats:styled-content> from the <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> via suppression of <jats:styled-content style=\"fixed-case\">PGE2<\/jats:styled-content> production. <jats:styled-content style=\"fixed-case\">EP2<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">EP4<\/jats:styled-content> were the main receptors for <jats:styled-content style=\"fixed-case\">PGE2<\/jats:styled-content> present in the <jats:styled-content style=\"fixed-case\">FLS<\/jats:styled-content>. The approach used in this study may be useful for revealing how drugs such as <jats:styled-content style=\"fixed-case\">NSAIDs<\/jats:styled-content> affect the cellular functions of <jats:styled-content style=\"fixed-case\">FLS<\/jats:styled-content> from the <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jop.12045","type":"journal-article","created":{"date-parts":[[2013,1,18]],"date-time":"2013-01-18T10:49:15Z","timestamp":1358506155000},"page":"499-506","source":"Crossref","is-referenced-by-count":31,"title":["The anti\u2010inflammatory effect of cyclooxygenase inhibitors in fibroblast\u2010like synoviocytes from the human temporomandibular joint results from the suppression of <scp>PGE2<\/scp> production"],"prefix":"10.1111","volume":"42","author":[{"given":"Mutsumi","family":"Kawashima","sequence":"first","affiliation":[{"name":"Department of Maxillofacial Surgery Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naomi","family":"Ogura","sequence":"additional","affiliation":[{"name":"Department of Maxillofacial Surgery Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"},{"name":"Research Institute of Oral Science Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miwa","family":"Akutsu","sequence":"additional","affiliation":[{"name":"Department of Maxillofacial Surgery Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"},{"name":"Research Institute of Oral Science Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ko","family":"Ito","sequence":"additional","affiliation":[{"name":"Department of Maxillofacial Surgery Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"},{"name":"Research Institute of Oral Science Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshirou","family":"Kondoh","sequence":"additional","affiliation":[{"name":"Department of Maxillofacial Surgery Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"},{"name":"Research Institute of Oral Science Nihon University School of Dentistry at Matsudo Matsudo Chiba Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,1,18]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1010-5182(05)80452-4"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1079-2104(97)90246-8"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/0278-2391(91)90407-D"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0278-2391(98)90868-0"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1079-2104(98)90415-2"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.173.3.569"},{"key":"e_1_2_5_8_1","doi-asserted-by":"crossref","first-page":"1902","DOI":"10.4049\/jimmunol.139.6.1902","article-title":"Interleukin 1 induces interleukin 1. 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