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Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

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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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Fractures: Bone Repair01:27

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Treatment for a fracture is based on the type of break, the bone affected, and the patient's age.
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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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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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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.
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The Bone Matrix01:18

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Bone contains a relatively small number of cells entrenched in a matrix of collagen fibers that provide an adherent surface for inorganic salt crystals. Both components of the matrix, organic and inorganic, contribute to the unusual properties of bone. Without collagen, bones would be brittle and shatter easily. Without mineral crystals, bones would flex and provide little support. This can be observed by an experiment: when the minerals of a bone are dissolved by soaking the bone in...
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Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model
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Enhanced Bone Remodeling After Fracture Priming.

Jose L Ramirez-GarciaLuna1,2, Karla Rangel-Berridi1,3,2, Ore-Oluwa Olasubulumi1

  • 1Bone Engineering Labs, Injury, Repair & Recovery Program, Research Institute, McGill University Health Centre, 1650 Cedar Ave., Montreal, QC, H3G 1A4, Canada.

Calcified Tissue International
|October 20, 2021
PubMed
Summary

A prior fracture enhances bone healing. Subsequent fractures in mice led to improved bone structure and increased blood vessel formation, suggesting inflammation aids bone repair.

Keywords:
AngiogenesisBone remodelingFractureMast cellsOsteoimmunology

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Area of Science:

  • Immunology
  • Orthopedics
  • Regenerative Medicine

Background:

  • The immune system plays a crucial role in bone repair processes.
  • Mast cells are known to influence the recruitment of macrophages, osteoclasts, and blood vessels to fracture sites.

Purpose of the Study:

  • To investigate if prior fracture exposure sensitizes immune cells, leading to an enhanced response and improved healing in subsequent fractures.
  • To determine the impact of a sensitized immune response on bone morphometrics, vascularization, and cellular activity during fracture healing.

Main Methods:

  • A two-stage fracture model was established in mice, comparing healing in a subsequent fracture to controls with simultaneous bilateral defects.
  • Micro-computed tomography (micro-CT) and histology were used to assess mineralized tissue quantity and bone morphometric parameters.
  • Histochemistry evaluated the activity of osteoblasts, osteoclasts, vascular endothelial cells, mast cells, and macrophages.

Main Results:

  • No significant difference in the total amount of bone produced was observed between groups at 14 or 56 days.
  • Mice with subsequent fractures exhibited significantly improved bone morphometric parameters at 56 days post-operation.
  • Increased content of blood vessels, osteoclasts, and macrophages was noted in the subsequent fracture group.

Conclusions:

  • A transient increase in the inflammatory state following an initial injury promotes accelerated bone remodeling and enhanced angiogenesis.
  • This enhanced healing is associated with altered mast cell and macrophage populations, facilitating mesenchymal stromal cell recruitment.