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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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...
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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 bone...
Bone Remodeling01:40

Bone Remodeling

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.
What is the Skeletal System?01:02

What is the Skeletal System?

Overview
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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...
Bone Remodeling and Repair01:31

Bone Remodeling and Repair

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 bone...

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Updated: Jun 27, 2026

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

Renal osteodystrophy.

T Bardin

    Journal of Clinical Rheumatology : Practical Reports on Rheumatic & Musculoskeletal Diseases
    |December 17, 2008
    PubMed
    Summary
    This summary is machine-generated.

    Renal osteodystrophy presents as secondary hyperparathyroidism or adynamic bone disease. Managing serum phosphorus and vitamin D is key for secondary hyperparathyroidism, while avoiding over-treatment prevents adynamic bone disease in dialysis patients.

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    Osteoclast Derivation from Mouse Bone Marrow
    06:17

    Osteoclast Derivation from Mouse Bone Marrow

    Published on: November 6, 2014

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    A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
    11:47

    A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

    Published on: June 8, 2014

    Osteoclast Derivation from Mouse Bone Marrow
    06:17

    Osteoclast Derivation from Mouse Bone Marrow

    Published on: November 6, 2014

    Area of Science:

    • Nephrology
    • Endocrinology
    • Bone Metabolism

    Background:

    • Renal osteodystrophy encompasses secondary hyperparathyroidism, aluminum-induced bone disease, and adynamic bone disease.
    • Aluminum intoxication is now rare due to improved dialysis solutions and phosphate binder choices.
    • Secondary hyperparathyroidism is common in renal failure and hemodialysis patients, linked to hyperphosphatemia and low vitamin D.

    Purpose of the Study:

    • To review the pathogenesis, clinical presentation, and management of renal osteodystrophy.
    • To highlight the shift in prevalence from aluminum-induced bone disease to adynamic bone disease.
    • To emphasize optimal management strategies for secondary hyperparathyroidism and adynamic bone disease.

    Main Methods:

    • Review of existing literature on renal osteodystrophy.
    • Analysis of the prevalence and characteristics of different forms of renal osteodystrophy.
    • Discussion of diagnostic criteria and therapeutic interventions.

    Main Results:

    • Secondary hyperparathyroidism remains frequent in hemodialysis patients, influenced by hyperphosphatemia and vitamin D deficiency.
    • Adynamic bone disease is increasingly recognized in peritoneal dialysis patients, associated with fractures.
    • Excessive treatment of hyperparathyroidism can lead to adynamic bone disease.

    Conclusions:

    • Effective management of secondary hyperparathyroidism involves controlling serum phosphorus and considering vitamin D analogs or parathyroidectomy.
    • Maintaining serum parathormone levels between 1.5-3x the upper limit of normal is crucial for dialysis patients.
    • Preventing adynamic bone disease requires careful management to avoid excessive suppression of parathyroid hormone.