ArticleBone reports2022
Temporal changes in cortical microporosity during estrogen deficiency associated with perilacunar resorption and osteocyte apoptosis: A pilot study.
Article in Bone reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Bone organic matrix quality indices associate with fragility fracture occurrence independently of bone mineral density values.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Article
- Estrogen deficiency as a common driver and integrative mechanism in osteoporosis‑osteoarthritis comorbidity (Review).Molecular medicine reports · 2026Review
- Article
- Calvarial Bone Defects Heal Better in Short-Term Ovariectomized Rats Compared to Healthy Rats.Journal of musculoskeletal & neuronal interactions · 2025Article
- Effects of Ovariectomy and Low-Calcium Diet on Six Different Sites of the Rat Skeleton.Biomimetics (Basel, Switzerland) · 2025Article
- Palm Tocotrienol Preserves Trabecular Osteocyte Indices and Modulates the Expression of Osteocyte Markers in Ovariectomized Rats.Biomedicines · 2025Article
- Altered extracellular matrix and mechanotransduction gene expression in rat bone tissue following long-term estrogen deficiency.JBMR plus · 2024Article
- Influence of Osteocyte Lacunar-Canalicular Morphology and Network Architecture on Osteocyte Mechanosensitivity.Current osteoporosis reports · 2023Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteocytes can actively regulate bone microporosity, through either perilacunar resorption or micropetrosis following apoptosis. Osteocyte apoptosis is more prevalent in estrogen deficiency and changes in the lacunar-canalicular network of osteocytes have been reported. Temporal changes in bone mineralisation and osteocytes cellular strains occur, which might be associated with osteocyte-driven microporosity changes, although time dependant changes in bone microporosity are not yet fully understood. In this pilot study we conducted micro-CT analysis, backscatter electron imaging and histological analysis of femoral cortical bone form an ovariectomized rat model of osteoporosis to investigate whether estrogen deficiency causes temporal changes in lacunar and vascular porosity. We also assessed MMP14 expression, lacunar occupancy and mineral infilling, as indicators of perilacunar resorption and micropetrosis. We report temporal changes in cortical microporosity in estrogen deficiency. Specifically, canalicular and vascular porosity initially increased (4 weeks post-OVX), coinciding with the period of rapid bone loss, whereas in the longer term (14 weeks post-OVX) lacunar and canalicular diameter decreased. Interestingly, these changes coincided with an increased prevalence of empty lacunae and osteocyte lacunae were observed to be more circular with a mineralised border around the lacunar space. In addition we report an increase in MMP14+ osteocytes, which also suggests active matrix degradation by these cells. Together these results provide an insight into the temporal changes in cortical microporosity during estrogen deficiency and suggest the likelihood of occurrence of both perilacunar resorption and osteocyte apoptosis leading to micropetrosis. We propose that microporosity changes arise due to processes driven by distinct populations of osteocytes, which are either actively resorbing their matrix or have undergone apoptosis and are infilling lacunae by micropetrosis.
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