ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2018
Hormonal Regulation of Osteocyte Perilacunar and Canalicular Remodeling in the Hyp Mouse Model of X-Linked Hypophosphatemia.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Impaired bone matrix maturation and mineralization are prevalent in adolescent end-stage kidney disease.JBMR plus · 2026Article
- Effects of nutritional low phosphorus status caused by extremely low phosphorus diet during lactation and early childhood on endochondral ossification in offspring rats.Frontiers in nutrition · 2026Article
- Articular cartilage degeneration and aberrant osteocyte perilacunar/canalicular remodeling in subchondral bone of patients with developmental dysplasia of the hip.BMC musculoskeletal disorders · 2025Article
- Review
- Evidence for peri-lacunar remodeling and altered osteocyte lacuno-canalicular network in mouse models of myeloma-induced bone disease.JBMR plus · 2024Article
- The role of GDF5 in regulating enthesopathy development in the Hyp mouse model of XLH.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- NFATc1 Is Required for Vitamin D- and Phosphate-Mediated Regulation of Osteocyte Lacuno-Canalicular Remodeling.Endocrinology · 2024Article
- Article
- Impaired 1,25-dihydroxyvitamin D3 action underlies enthesopathy development in the Hyp mouse model of X-linked hypophosphatemia.JCI insight · 2023Article
- Influence of Osteocyte Lacunar-Canalicular Morphology and Network Architecture on Osteocyte Mechanosensitivity.Current osteoporosis reports · 2023Review
- Characterization of hearing-impairment in Generalized Arterial Calcification of Infancy (GACI).Orphanet journal of rare diseases · 2022Article
- Function of PHEX mutations p.Glu145* and p.Trp749Arg in families with X-linked hypophosphatemic rickets by the negative regulation mechanism on FGF23 promoter transcription.Cell death & disease · 2022Article
- Cellular and Molecular Alterations Underlying Abnormal Bone Growth in X-Linked Hypophosphatemia.International journal of molecular sciences · 2022Review
- Prevention of Hypomineralization In Auditory Ossicles of Vitamin D Receptor (Vdr) Deficient Mice.Frontiers in endocrinology · 2022Article
- Conductive Hearing Loss in the Hyp Mouse Model of X-Linked Hypophosphatemia Is Accompanied by Hypomineralization of the Auditory Ossicles.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Effects of Active Vitamin D or FGF23 Antibody onJournal of dental research · 2021Article
- Cementocyte alterations associated with experimentally induced cellular cementum apposition in Hyp mice.Journal of periodontology · 2021Article
- Potential Role of Perilacunar Remodeling in the Progression of Osteoporosis and Implications on Age-Related Decline in Fracture Resistance of Bone.Current osteoporosis reports · 2021Review
- Sclerostin Directly Stimulates Osteocyte Synthesis of Fibroblast Growth Factor-23.Calcified tissue international · 2021Article
- Review
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6 authors at 2 institutions in 1 country.
Funding
Abstract
Osteocytes remodel their surrounding perilacunar matrix and canalicular network to maintain skeletal homeostasis. Perilacunar/canalicular remodeling is also thought to play a role in determining bone quality. X-linked hypophosphatemia (XLH) is characterized by elevated serum fibroblast growth factor 23 (FGF23) levels, resulting in hypophosphatemia and decreased production of 1,25 dihydroxyvitamin D (1,25D). In addition to rickets and osteomalacia, long bones from mice with XLH (Hyp) have impaired whole-bone biomechanical integrity accompanied by increased osteocyte apoptosis. To address whether perilacunar/canalicular remodeling is altered in Hyp mice, histomorphometric analyses of tibia and 3D intravital microscopic analyses of calvaria were performed. These studies demonstrate that Hyp mice have larger osteocyte lacunae in both the tibia and calvaria, accompanied by enhanced osteocyte mRNA and protein expression of matrix metalloproteinase 13 (MMP13) and genes classically used by osteoclasts to resorb bone, such as cathepsin K (CTSK). Hyp mice also exhibit impaired canalicular organization, with a decrease in number and branching of canaliculi extending from tibial and calvarial lacunae. To determine whether improving mineral ion and hormone homeostasis attenuates the lacunocanalicular phenotype, Hyp mice were treated with 1,25D or FGF23 blocking antibody (FGF23Ab). Both therapies were shown to decrease osteocyte lacunar size and to improve canalicular organization in tibia and calvaria. 1,25D treatment of Hyp mice normalizes osteocyte expression of MMP13 and classic osteoclast markers, while FGF23Ab decreases expression of MMP13 and selected osteoclast markers. Taken together, these studies point to regulation of perilacunar/canalicular remodeling by physiologic stimuli including hypophosphatemia and 1,25D. © 2017 American Society for Bone and Mineral Research.
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