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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in 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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Bone Remodeling01:40

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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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Bone Formation by Endochondral Ossification01:24

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Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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Bone Disorders01:29

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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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Growth of Cartilage and Bone Tissue01:27

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Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

Updated: Mar 3, 2026

Flow Cytometry Analysis of Immune Cell Subsets within the Murine Spleen, Bone Marrow, Lymph Nodes and Synovial Tissue in an Osteoarthritis Model
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Osteoblast role in osteoarthritis pathogenesis.

Nicola Maruotti1, Addolorata Corrado1, Francesco P Cantatore1

  • 1Rheumatology Clinic, Department of Medical and Surgical Sciences, University of Foggia Medical School, Foggia, Italy.

Journal of Cellular Physiology
|April 21, 2017
PubMed
Summary

Osteoblast dysregulation is a key factor in osteoarthritis development, affecting bone remodeling and mineralization. Understanding these cellular changes is crucial for developing new osteoarthritis treatments.

Keywords:
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Area of Science:

  • Cellular and Molecular Biology
  • Orthopedics
  • Rheumatology

Background:

  • Osteoarthritis (OA) pathogenesis remains incompletely understood.
  • Osteoblast (bone-forming cell) dysregulation is increasingly implicated in OA.
  • Abnormalities in osteoblast function contribute to OA development.

Purpose of the Study:

  • To highlight the critical role of osteoblast dysregulation in osteoarthritis pathogenesis.
  • To explore the molecular mechanisms underlying osteoblast dysfunction in OA.
  • To identify key molecular players involved in OA development.

Main Methods:

  • Review of existing evidence on osteoblast function in OA.
  • Analysis of gene expression patterns in osteoblasts from OA patients.
  • Examination of signaling pathways involving osteoblasts in bone remodeling.

Main Results:

  • Osteoarthritis osteoblasts exhibit abnormal expression of Osteoprotegerin (OPG) and Receptor Activator of Nuclear Factor kappa-B Ligand (RANKL).
  • This dysregulation leads to aberrant bone remodeling and reduced mineralization.
  • Altered gene expression in osteoblasts disrupts their function, contributing to OA.

Conclusions:

  • Osteoblast dysregulation is a significant driver of osteoarthritis.
  • Abnormal OPG/RANKL expression and altered gene expression are key mechanisms.
  • Osteoblast-derived factors play a crucial role in OA pathogenesis.