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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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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 Disorders01:29

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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.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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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.
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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Related Experiment Video

Updated: Mar 31, 2026

Author Spotlight: Integrating Traditional Chinese Medicine with Modern Pharmacology and Genomics for Assessing Postmenopausal Osteoporosis in Mice
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[Treatment for hepatic osteodystrophy].

Hiroshi Kaji1

  • 1Department of Physiology and Regenerative Medicine,Kinki University Faculty of Medicine, Japan.

Clinical Calcium
|October 28, 2015
PubMed
Summary
This summary is machine-generated.

Bisphosphonates and Vitamin D show promise for treating bone density loss in chronic liver disease patients. Estrogen use is limited due to risks of liver dysfunction and cancer.

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Area of Science:

  • Hepatology and Endocrinology
  • Bone Metabolism in Liver Disease

Context:

  • Chronic liver diseases (e.g., cirrhosis) have diverse causes like viral hepatitis and steatohepatitis.
  • Hepatic osteodystrophy lacks sufficient clinical evidence for effective treatment strategies.
  • Vitamin D deficiency is common in hepatic osteodystrophy pathogenesis.

Purpose:

  • To review current evidence on treating hepatic osteodystrophy in chronic liver disease.
  • To evaluate the efficacy of bisphosphonates and Vitamin D for bone health in these patients.
  • To discuss the limitations of estrogen therapy in liver disease patients.

Summary:

  • Bisphosphonates, such as alendronate, may increase bone mineral density in chronic liver disease.
  • Vitamin D treatment could address prevalent deficiencies contributing to hepatic osteodystrophy.
  • Estrogen therapy is cautioned against due to potential liver dysfunction and hepatocellular carcinoma risks.

Impact:

  • Informs clinical practice regarding bone health management in chronic liver disease.
  • Highlights potential therapeutic avenues for hepatic osteodystrophy.
  • Provides guidance on medication selection, considering liver-specific risks.