{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T10:15:13Z","timestamp":1784542513342,"version":"3.55.0"},"reference-count":37,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2018,8,14]],"date-time":"2018-08-14T00:00:00Z","timestamp":1534204800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Graduate School and Faculty of Dentistry, Prince of Songkla University"}],"content-domain":{"domain":["aap.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[2018,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Although vibration combined with orthodontic force may accelerate orthodontic tooth movement, little is known about the mechanisms that regulate the associated cellular responses. The goal of this study was to investigate whether mechanical vibration combined with compressive force regulates cyclooxygenase (<jats:italic>COX<\/jats:italic>)<jats:italic>\u20102<\/jats:italic>\/prostaglandin E2 (PGE<jats:sub>2<\/jats:sub>) and interleukin (IL)\u20106 and IL\u20108 messenger RNA (mRNA) and protein expression in human periodontal ligament (hPDL) cells via the COX pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The primary cultured hPDL cells were exposed to mechanical vibration, compressive force or a combination of both mechanical vibration and compressive force at 24, 48, and 72\u00a0hours. The <jats:italic>COX\u20102<\/jats:italic>, <jats:italic>IL\u20106<\/jats:italic>, <jats:italic>IL\u20108<\/jats:italic>, receptor activator of nuclear factor kappa\u2010\u0392 ligand (<jats:italic>RANKL<\/jats:italic>), and osteoprotegrin (<jats:italic>OPG<\/jats:italic>) mRNA expressions were determined using quantitative real\u2010time polymerase chain reaction (qPCR). The PGE<jats:sub>2<\/jats:sub>, IL\u20106, and IL\u20108 protein expressions were quantified by enzyme\u2010linked immunosorbent assay (ELISA). To demonstrate whether the expression of PGE<jats:sub>2<\/jats:sub>, IL\u20106, and IL\u20108 was in the COX\u2010dependent pathway, the hPDL cells were treated with indomethacin. To determine whether PGE<jats:sub>2<\/jats:sub> stimulated the hPDL cells to express IL\u20106 and IL\u20108, exogenous PGE<jats:sub>2<\/jats:sub> was added to the culture media.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The combination of mechanical vibration and compressive force synergistically upregulated <jats:italic>RANKL\/OPG<\/jats:italic>, <jats:italic>COX\u20102<\/jats:italic>\/PGE<jats:sub>2<\/jats:sub>, IL\u20106 and IL\u20108 mRNA, and protein expression. The indomethacin significantly attenuated the increases of PGE<jats:sub>2<\/jats:sub>, IL\u20106, and IL\u20108 expression in cells stimulated with compressive force or mechanical vibration combined with compressive force. In addition, exogenous PGE<jats:sub>2<\/jats:sub> increased IL\u20106 and IL\u20108 mRNA and protein expressions in hPDL cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Mechanical vibration may enhance alveolar bone resorption at the compression side during orthodontic tooth movement via a mechanism involving the cyclooxygenase pathway.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jper.17-0653","type":"journal-article","created":{"date-parts":[[2018,5,14]],"date-time":"2018-05-14T22:24:37Z","timestamp":1526336677000},"page":"1131-1141","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Vibration enhances PGE<sub>2<\/sub>, IL\u20106, and IL\u20108 expression in compressed hPDL cells via cyclooxygenase pathway"],"prefix":"10.1002","volume":"89","author":[{"given":"Pussadee","family":"Phusuntornsakul","sequence":"first","affiliation":[{"name":"Orthodontic Section Department of Preventive 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