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Despite this, the cellular and molecular mechanisms underpinning the sexually dimorphic control of bone quality remain unclear, limiting our ability to effectively prevent fractures, especially in postmenopausal osteoporosis. Recently, using male mice, we found that systemic or osteocyte-intrinsic inhibition of TGF\u03b2 signaling, achieved using the 9.6-kb DMP1 promoter-driven Cre recombinase (T\u03b2RIIocy\u2212\/\u2212 mice), suppresses osteocyte perilacunar\/canalicular remodeling (PLR) and compromises bone quality. Because systemic TGF\u03b2 inhibition more robustly increases bone mass in female than male mice, we postulated that sex-specific differences in bone quality could likewise result, in part, from dimorphic regulation of PLR by TGF\u03b2. Moreover, because lactation induces PLR, we examined the effect of TGF\u03b2 inhibition on the female skeleton during lactation. In contrast to males, female mice that possess an osteocyte-intrinsic defect in TGF\u03b2 signaling were protected from TGF\u03b2-dependent defects in PLR and bone quality. The expression of requisite PLR enzymes, the lacunocanalicular network (LCN), and the flexural strength of female T\u03b2RIIocy\u2212\/\u2212 bone was intact. With lactation, however, bone loss and induction in PLR and osteocytic parathyroid hormone type I receptor (PTHR1) expression, were suppressed in T\u03b2RIIocy\u2212\/\u2212 bone, relative to the control littermates. Indeed, differential control of PTHR1 expression, by TGF\u03b2 and other factors, may contribute to dimorphism in PLR regulation in male and female T\u03b2RIIocy\u2212\/\u2212 mice. These findings provide key insights into the sex-based differences in osteocyte PLR that underlie bone quality and highlight TGF\u03b2 signaling as a crucial regulator of lactation-induced PLR. \u00a9 2020 American Society for Bone and Mineral Research.<\/jats:p>","DOI":"10.1002\/jbmr.4023","type":"journal-article","created":{"date-parts":[[2020,4,13]],"date-time":"2020-04-13T12:49:55Z","timestamp":1586782195000},"page":"1549-1561","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["TGF\u03b2 Regulation of Perilacunar\/Canalicular Remodeling Is Sexually Dimorphic"],"prefix":"10.1093","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4675-2649","authenticated-orcid":false,"given":"Neha S","family":"Dole","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery University of California, San Francisco (UCSF) San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristal S","family":"Yee","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic Surgery University of California, San Francisco (UCSF) San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Courtney M","family":"Mazur","sequence":"additional","affiliation":[{"name":"University of California (UC) Berkeley-UCSF Graduate Program in Bioengineering San Francisco CA USA"},{"name":"Department of Orthopaedic Surgery University of California, San Francisco (UCSF) San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claire","family":"Acevedo","sequence":"additional","affiliation":[{"name":"Department of Mechanical Engineering University of Utah Salt Lake City UT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9992-2897","authenticated-orcid":false,"given":"Tamara","family":"Alliston","sequence":"additional","affiliation":[{"name":"Department of Orthopaedic Surgery University of California, San Francisco (UCSF) San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2020,4,13]]},"reference":[{"issue":"5","key":"2024031503440600400_jbmr4023-bib-0001","doi-asserted-by":"crossref","first-page":"1014","DOI":"10.1002\/jbmr.3084","article-title":"Adaptations in the microarchitecture and load distribution of maternal cortical and trabecular bone in response to multiple reproductive cycles in rats","volume":"32","author":"de Bakker","year":"2017","journal-title":"J Bone Miner 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