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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

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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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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.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
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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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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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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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Oogenesis,  the process of developing egg cells (female gametes), occurs within the ovaries and is fundamental to female fertility. This sequence begins during fetal development when diploid oogonia in the developing ovaries undergo mitotic divisions to produce primary oocytes. By birth, these primary oocytes enter prophase I of meiosis but become arrested in this stage, remaining suspended until puberty.
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Osteoclast Derivation from Mouse Bone Marrow
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Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in

Ha-Neui Kim1, Filipa Ponte1, Intawat Nookaew2

  • 1Division of Endocrinology and Metabolism, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, 4301 W. Markham St. #587, Little Rock, 72205-7199, USA.

Scientific Reports
|July 21, 2020
PubMed
Summary
This summary is machine-generated.

Estrogen loss causes osteoporosis by increasing osteoclast numbers. Estrogen (E2) reduces osteoclast progenitors via apoptosis, by decreasing mitochondrial respiration and complex I activity, not through FasL.

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Cellular Biology

Background:

  • Menopause-associated estrogen loss accelerates osteoporosis and fracture risk.
  • Estrogens normally inhibit bone resorption by reducing osteoclast numbers.
  • The precise molecular mechanisms underlying estrogen's anti-osteoclastogenic effects require elucidation.

Purpose of the Study:

  • To investigate the molecular mechanism by which 17β-estradiol (E2) reduces osteoclast number.
  • To determine if FasL mediates the anti-osteoclastogenic effects of E2.
  • To identify the cellular pathways involved in E2-induced osteoclast progenitor apoptosis.

Main Methods:

  • Utilized ovariectomized mouse models and isolated osteoclast progenitors.
  • Assessed apoptosis via Bak/Bax and mitochondrial pathways.
  • Performed microarray analysis to identify gene expression changes.
  • Measured mitochondrial complex I activity and oxygen consumption rates.

Main Results:

  • E2 induced apoptosis in early osteoclast progenitors, not mature osteoclasts, dependent on Bak/Bax.
  • FasL-deficient mice exhibited bone loss similar to controls, indicating FasL is not critical.
  • E2 signaling via ERα downregulated oxidative phosphorylation and mitochondrial complex I gene expression.
  • E2 inhibited complex I activity and oxygen consumption; Rotenone mimicked E2's effects.

Conclusions:

  • Estrogens decrease osteoclast number by promoting apoptosis in osteoclast progenitors.
  • This effect is mediated by E2-induced attenuation of mitochondrial respiration and complex I activity.
  • Estrogen's protective role against bone loss involves regulating progenitor cell bioenergetics via ERα.