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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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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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All bones comprise an outer layer of compact bone, and an interior made up of spongy bone tissue, also called cancellous or trabecular bone. In long bones, spongy bone tissue is mainly found in the interior of the epiphyses (broad ends of the bone).
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Most bones contain compact and spongy osseous tissue, but their distribution and concentration vary based on the bone's overall function.
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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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Analysis and Imaging of Osteocytes
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Microstructural changes associated with osteoporosis negatively affect loading-induced fluid flow around osteocytes

Vittorio Gatti1, Evan M Azoulay1, Susannah P Fritton1

  • 1Department of Biomedical Engineering, The City College of New York, New York, NY 10031, USA.

Journal of Biomechanics
|December 9, 2017
PubMed
Summary

Postmenopausal osteoporosis in rats significantly reduces bone interstitial fluid flow, impairing osteocyte communication. This microstructural change, particularly altered vascular porosity, may contribute to age-related bone loss.

Keywords:
Bone fluid flowLacunar-canalicular systemOsteocyteOsteoporosisPoroelasticity

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Area of Science:

  • Biomechanical Engineering
  • Skeletal Biology
  • Computational Biology

Background:

  • Loading-induced interstitial fluid flow is vital for osteocyte mechanotransduction and bone health.
  • Osteoporosis alters bone microarchitecture, including vascular porosity and the lacunar-canalicular system.
  • Previous studies in our group identified these microstructural changes in a rat model of postmenopausal osteoporosis.

Purpose of the Study:

  • To investigate the impact of osteoporosis-induced microstructural changes on interstitial fluid flow around osteocytes.
  • To quantify the reduction in fluid flow within the lacunar-canalicular system of ovariectomized rats compared to controls.
  • To determine the influence of vascular porosity and lacunar-canalicular permeability on fluid velocity.

Main Methods:

  • Poroelastic finite element analysis was employed.
  • Animal-specific models were created using micro-CT reconstructions and poroelastic properties.
  • Loading-induced fluid flow was quantified and compared between ovariectomized and sham-operated rats.

Main Results:

  • Mechanically-induced interstitial fluid velocity was significantly reduced in the lacunar-canalicular system of ovariectomized rats.
  • Vascular porosity demonstrated a major influence on interstitial fluid flow.
  • Lacunar-canalicular permeability had a limited influence on fluid velocity when exceeding 10-20m2.

Conclusions:

  • Microstructural alterations in osteoporosis negatively affect interstitial fluid flow in cortical bone.
  • Reduced fluid flow may impair osteocyte mechanosensation, contributing to bone loss.
  • These findings highlight a potential mechanism in the progression of postmenopausal osteoporosis.