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Related Concept Videos

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...
Degenerative Disc Disease ll: Pathophysiology01:23

Degenerative Disc Disease ll: Pathophysiology

The symptoms of degenerative disc disease arise from a combination of mechanical compression, vascular compromise, and biochemical inflammation, which together disrupt nerve function and produce pain.Mechanical CompressionDisc degeneration reduces height and elasticity, predisposing to herniation of the nucleus pulposus, a major cause of radicular pain. Herniations may be protrusion (bulging with intact annulus), extrusion (nucleus extends beyond disc but remains connected), or sequestration...
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.
Degenerative Disc Disease I: Introduction01:27

Degenerative Disc Disease I: Introduction

Degenerative disc disease is a chronic condition in which intervertebral discs gradually lose structure and function. It is not infectious or autoimmune; rather, it results from age-related biochemical and mechanical changes, influenced by genetic, metabolic, and environmental factors.Structure and Function of DiscsThe spine contains 23 intervertebral discs that absorb load, distribute forces, maintain spacing, and allow flexibility. Each disc consists of a nucleus pulposus, a gel-like core...
Bone Disorders01:29

Bone Disorders

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Related Experiment Video

Updated: Jun 9, 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

Evolving concepts in neurogenic osteoporosis.

Weiping Qin1, William A Bauman, Christopher P Cardozo

  • 1Center of Excellence for the Medical Consequences of Spinal Cord Injury, Bronx, NY 10468, USA. Weiping.qin@mssm.edu

Current Osteoporosis Reports
|September 8, 2010
PubMed
Summary

The central nervous system regulates bone mass through neurotransmitters and neuropeptides. Sympathetic nervous system activity contributes to bone loss, while blocking specific receptors can increase bone density.

Related Experiment Videos

Last Updated: Jun 9, 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

Area of Science:

  • Neuroscience
  • Endocrinology
  • Bone Biology

Background:

  • Growing evidence links the central nervous system (CNS) to bone regulation.
  • Neural pathways involve neurotransmitters and neuropeptides acting both centrally and peripherally.
  • The sympathetic nervous system (SNS) plays a critical role in bone metabolism.

Purpose of the Study:

  • To review the neural regulation of bone mass.
  • To elucidate the mechanisms by which the nervous system influences bone density.
  • To highlight the roles of neurotransmitters, neuropeptides, and the SNS in bone health.

Main Methods:

  • Review of existing literature on neuro-osseous interactions.
  • Analysis of studies investigating neurotransmitter and neuropeptide effects on bone cells.
  • Examination of the impact of sympathetic nervous system activity on bone mass.

Main Results:

  • Pharmacologic blockade of ß2-adrenergic receptors or gene disruption increases bone mass.
  • Increased sympathetic nervous system activity is associated with bone loss.
  • Serotonergic neurons in the brainstem modulate SNS activity and leptin signaling.
  • Nicotinic receptor stimulation promotes bone formation, while higher levels inhibit it.

Conclusions:

  • The CNS exerts significant control over bone mass through complex neural pathways.
  • Autonomic, sensory, and peripheral nervous system interactions are crucial for bone homeostasis.
  • Further research is needed to clarify these interactions in both healthy and pathological conditions.