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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Bone Remodeling01:40

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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Hormones and Bone Tissue01:17

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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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Oogenesis02:07

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In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...
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Menopause, a natural biological process marking the end of a woman's fertility, typically occurs between the fifth and sixth decade of life. This phase is characterized by the exhaustion of the ovarian follicle pool, leading to less responsive ovaries despite the high levels of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). The consequential decrease in estrogen production results in symptoms like hot flashes, heavy sweating, headaches, hair loss, muscle pains, vaginal...
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Estrogen-Like Effect of Bazi Bushen Capsule in Ovariectomized Rats
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Osteocytes and Estrogen Deficiency.

Laoise M McNamara1,2

  • 1Mechanobiology and Medical Device Research Group, Biomedical Engineering, College of Science and Engineering, National University of Ireland, Galway, Ireland. Laoise.McNamara@nuigalway.ie.

Current Osteoporosis Reports
|November 26, 2021
PubMed
Summary
This summary is machine-generated.

Estrogen deficiency in postmenopausal osteoporosis alters osteocyte function, impacting bone health. New research highlights osteocyte changes, suggesting novel therapeutic targets beyond bone loss.

Keywords:
ApoptosisEstrogen deficiencyMechanotransductionMineralizationOsteoclastOsteocyteOsteoporosisParacrine

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Area of Science:

  • Bone Biology
  • Endocrinology
  • Mechanobiology

Background:

  • Postmenopausal osteoporosis is characterized by reduced estrogen levels, leading to increased osteoclast activity, bone resorption, and fracture risk.
  • Traditionally viewed as a disease of bone loss, emerging evidence suggests a more complex etiology involving cellular and mechanical factors.

Purpose of the Study:

  • To review emerging evidence on the role of mechanosensitive osteocytes in postmenopausal osteoporosis.
  • To explore how estrogen deficiency impacts osteocyte function and bone remodeling.

Main Methods:

  • This review synthesizes recent research findings on osteocyte biology in the context of estrogen deficiency.
  • Analysis of studies investigating changes in osteocyte mechanosensing, apoptosis, and microenvironment.

Main Results:

  • Estrogen deficiency alters the osteocyte mechanical environment and tissue composition.
  • Osteocyte apoptosis increases, and hypermineralization occurs, impairing mechanobiological responses.
  • Impaired osteocyte function exacerbates osteoclast regulation, contributing to bone loss.

Conclusions:

  • Osteoporosis involves critical changes in osteocytes, not just bone resorption.
  • Understanding these osteocyte alterations is crucial for developing targeted therapies.
  • Future osteoporosis treatments may focus on osteocyte-targeted approaches to inhibit resorption and secondary mineralization.