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Zoledronate promotes bone formation by blocking osteocyte-osteoblast communication during bone defect healing

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dc.contributor.authorCui, Pingping
dc.contributor.authorLiu, Hongrui
dc.contributor.authorSun, Jing
dc.contributor.authorAmizuka, Norio
dc.contributor.authorSun, Qinfeng
dc.contributor.authorLi, Minqi
dc.date.accessioned2022-03-24T10:42:56Z
dc.date.available2022-03-24T10:42:56Z
dc.date.issued2018
dc.description.abstractNitrogen-containing bisphosphonates (NBPs) are potent antiresorptive drugs and their actions on osteoclasts have been studied extensively. Recent studies have suggested that N-BPs also target bone-forming cells. However, the precise mechanism of N-BPs in osteoblasts is paradoxical, and the specific role of osteocytes is worthy of in-depth study. Here, we investigated the cellular mechanisms of N-BPs regulating bone defect healing by zoledronate (ZA). Bone histomorphometry confirmed an increase in new bone formation by systemic ZA administration. ZA induced more alkaline phosphatase-positive osteoblasts and tartrate-resistant acid phosphatase-positive osteoclasts residing on the bone surface. Inexplicably, ZA increased SOST expression in osteocytes embedded in the bone matrix, which was not compatible with the intense osteoblast activity on the bone surface. ZA induced heterogeneous osteocytes and disturbed the distribution of the osteocytic-canalicular system (OLCS). Furthermore, according to the degree of OLCS regularity, dentin matrix protein 1 reactivity had accumulated around osteocytes in the ZA group, but it was distributed evenly in the OLCS of the control group. The control group showed a dense array of the gap junction protein connexin 43. However, connexin 43 was extremely sparse after ZA administration. In summary, ZA treatment reduces gap junction connections and blocks cellular communication between osteocytes and osteoblasts. Retaining SOST expression in osteocytes leads to activation of the Wnt signaling pathway and subsequent bone formation.es
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dc.format.extent11es
dc.identifier.citationHistology and Histopathology, Vol.33, nÂş1, (2018)
dc.identifier.doiDOI: 10.14670/HH-11-893
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/118308
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de BiologĂ­a Celular e HistologĂ­aes
dc.relationSin financiaciĂłn externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectZoledronatees
dc.subjectOsteoblastses
dc.subjectOsteocyteses
dc.subjectConnexin 43es
dc.subjectBone defectes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - PatologĂ­a. Medicina clĂ­nica. OncologĂ­aes
dc.titleZoledronate promotes bone formation by blocking osteocyte-osteoblast communication during bone defect healinges
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.33, nÂş1 (2018)