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The role of inflammatory mediators such as prostaglandin E2 (PGE2) and osteoclast promoting factors including RANKL in the pathogenesis of osteolysis has been well characterized. However, the PGE2 receptor (EP1, EP2, or EP4), and cell type in which it is expressed, which is responsible for PGE2 induction of RANKL during wear debris\u2013induced osteolysis, has yet to be elucidated. To address this, we used mice genetically deficient in these EP receptors to assess PGE2 and wear debris responses in vitro and in vivo. Wear debris\u2013induced osteolysis and RANKL expression were observed at similar levels in WT, EP1\u2212\/\u2212, and EP2\u2212\/\u2212 mice, indicating that these receptors do not mediate PGE2 signals in this process. A conditional knockout approach was used to eliminate EP4 expression in FSP1+ fibroblasts that are the predominant source of RANKL. In the absence of EP4, fibroblasts do not express RANKL after stimulation with particles or PGE2, nor do they exhibit high levels of osteoclasts and osteolysis. These results show that periprosthetic fibroblasts are important mediators of osteolysis through the expression of RANKL, which is induced after PGE2 signaling through the EP4 receptor.<\/jats:p>","DOI":"10.1359\/jbmr.090412","type":"journal-article","created":{"date-parts":[[2009,5,6]],"date-time":"2009-05-06T18:08:26Z","timestamp":1241633306000},"page":"1753-1762","source":"Crossref","is-referenced-by-count":78,"title":["PGE2 Signaling Through the EP4 Receptor on Fibroblasts Upregulates RANKL and Stimulates Osteolysis"],"prefix":"10.1093","volume":"24","author":[{"given":"Ryosuke","family":"Tsutsumi","sequence":"first","affiliation":[{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Xie","sequence":"additional","affiliation":[{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaochao","family":"Wei","sequence":"additional","affiliation":[{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minjie","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinping","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa M","family":"Flick","sequence":"additional","affiliation":[{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward M","family":"Schwarz","sequence":"additional","affiliation":[{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Regis J","family":"O'Keefe","sequence":"additional","affiliation":[{"name":"Department of Orthopaedics, University of Rochester, Rochester, New York, USA"},{"name":"Center for Musculoskeletal Research, University of Rochester, Rochester, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,12,4]]},"reference":[{"key":"2024020319555831300_bib1","doi-asserted-by":"crossref","first-page":"165","DOI":"10.1186\/ar81","article-title":"Anti-TNF-alpha therapy as a clinical intervention for periprosthetic osteolysis","volume":"2","author":"Schwarz","year":"2000","journal-title":"Arthritis Res"},{"key":"2024020319555831300_bib2","doi-asserted-by":"crossref","first-page":"836","DOI":"10.1002\/art.1780290704","article-title":"Formation of a synovial-like membrane at the bone-cement interface. 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