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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...
Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
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.
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...
Connective Tissue Cell Types01:22

Connective Tissue Cell Types

Connective tissue develops from the mesoderm of a developing embryo and consists of cells, fibers, and ground substance: a gel-like material containing large complexes of carbohydrates and proteins. Connective tissue was first identified as a separate tissue family in the 18th century, and Johannes Peter Muller coined the term connective tissue.
Fat cells (adipocytes), smooth muscle cells (myoblasts), and bone cells (osteoblasts) are some connective tissue cell types. Some immune system cells...
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...

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Related Experiment Video

Updated: Jun 23, 2026

Murine Hind Limb Long Bone Dissection and Bone Marrow Isolation
07:17

Murine Hind Limb Long Bone Dissection and Bone Marrow Isolation

Published on: April 14, 2016

Adynamic bone disease: clinical and therapeutic implications.

João M Frazão1, Patrícia Martins

  • 1Nephrology Department, Hospital de S. João, Medical School and Nephrology Research and Development Unit, University of Porto, Porto, Portugal. jmmdfrazao@netcabo.pt

Current Opinion in Nephrology and Hypertension
|May 9, 2009
PubMed
Summary

Adynamic bone disease in dialysis patients is linked to vascular calcification. Reducing calcium and vitamin D intake may help manage this condition and restore parathyroid activity.

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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
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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

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Last Updated: Jun 23, 2026

Murine Hind Limb Long Bone Dissection and Bone Marrow Isolation
07:17

Murine Hind Limb Long Bone Dissection and Bone Marrow Isolation

Published on: April 14, 2016

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

Area of Science:

  • Nephrology
  • Endocrinology
  • Vascular Biology

Background:

  • Adynamic bone disease (ABD) is increasingly recognized for its association with vascular calcification.
  • Vascular calcification is a significant predictor of mortality in patients with chronic kidney disease (CKD).
  • There's a need for better diagnostic markers for parathyroid status and bone turnover in CKD patients.

Purpose of the Study:

  • To review emerging data on adynamic bone disease.
  • To explore the clinical consequences of ABD, particularly its link to vascular calcification.
  • To discuss therapeutic implications for managing ABD and associated vascular complications.

Main Methods:

  • Literature review of recent studies on adynamic bone disease.
  • Analysis of data linking bone turnover markers to vascular calcification.
  • Evaluation of therapeutic strategies for ABD in CKD patients.

Main Results:

  • A potential link exists between low bone turnover in ABD and increased vascular calcification.
  • Patients with ABD have a reduced capacity to manage calcium loads, potentially exacerbating calcification.
  • Calcium-based phosphate binders, active vitamin D, and high calcium dialysate may contribute to vascular calcification in ABD.

Conclusions:

  • Elevated calcium and vitamin D loads negatively impact vascular calcification progression in dialysis patients with ABD.
  • Therapeutic strategies should prioritize reducing calcium and vitamin D exposure.
  • Restoring parathyroid activity is a key goal in managing ABD and preventing vascular complications.