{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T13:26:36Z","timestamp":1790429196638,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2020,12,15]],"date-time":"2020-12-15T00:00:00Z","timestamp":1607990400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2021,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Overexpression of the nucleotide\u2010binding leucine\u2010rich repeat protein 3\u00a0(NLRP3) inflammasome in chronic auto\u2010immune diseases leads to skeletal anomalies, with severe osteopenia due to the activation of osteoclasts. Reproducing this phenotype in<jats:italic>Nlrp3<\/jats:italic>knock\u2010in mice has provided insights into the role of NLRP3 in bone metabolism. We studied the role of NLRP3 in physiological bone development using a complete<jats:italic>Nlrp3<\/jats:italic>knock\u2010out mouse model. We found impaired skeletal development in<jats:italic>Nlrp3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice, resulting in a shorter stature than that of<jats:italic>Nlrp3<\/jats:italic><jats:sup>+\/+\u00a0<\/jats:sup>mice. These growth defects were associated with altered femur bone growth, characterized by a deficient growth plate and an osteopenic profile of the trabeculae. No differences in osteoclast recruitment or activity were observed. Instead,\u00a0<jats:italic>Nlrp3<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>femurs showed a less mineralized matrix in the trabeculae than those of<jats:italic>Nlrp3<\/jats:italic><jats:sup>+\/+<\/jats:sup>\u00a0mice, as well as less bone sialoprotein (BSP) expressing hypertrophic chondrocytes. In vitro, primary osteoblasts lacking NLRP3 expression showed defective mineralization, together with the downregulation of BSP expression. Finally, follow\u2010up by micro\u2010CT highlighted the role of NLPR3 in bone growth, occurring early in living mice, as the osteopenic phenotype diminishes over time. Overall, our data suggest that NLRP3 is involved in bone edification via the regulation of hypertrophic chondrocyte maturation and osteoblast activity. Furthermore, the defect appeared to be transitory, as the skeleton recovered with aging.<\/jats:p>","DOI":"10.1002\/jcp.30162","type":"journal-article","created":{"date-parts":[[2020,12,15]],"date-time":"2020-12-15T22:32:21Z","timestamp":1608071541000},"page":"4455-4469","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["NLRP3 is involved in long bone edification and the maturation of osteogenic cells"],"prefix":"10.1002","volume":"236","author":[{"given":"L.","family":"Detzen","sequence":"first","affiliation":[{"name":"UR 2496, Laboratory Orofacial Pathologies, Imaging and Biotherapies Universit\u00e9 de Paris Montrouge France"},{"name":"D\u00e9partement de Parodontologie, Service d'Odontologie, AP\u2010HP H\u00f4pital Rothschild Paris France"},{"name":"Laboratoire d'Excellence INFLAMEX 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