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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...
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

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...
Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
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...
Pigmentation01:19

Pigmentation

The color of the skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred to the keratinocytes via melanosomes.
Melanin occurs in two primary forms: eumelanin that provides black and brown pigment and pheomelanin that provides red color. Dark-skinned individuals produce more melanin than those with pale...
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...

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Related Experiment Video

Updated: May 31, 2026

Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes
11:52

Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes

Published on: January 27, 2023

Osteoclast formation and function in pigmented villonodular synovitis.

Richard Taylor1, Takesh G Kashima, Helen Knowles

  • 1Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Nuffield Orthopaedic Centre, Oxford, UK.

The Journal of Pathology
|June 28, 2011
PubMed
Summary
This summary is machine-generated.

Pigmented villonodular synovitis (PVNS) involves osteoclast-like giant cells forming from CD14+ macrophages. Osteoclast formation requires RANKL, suggesting anti-resorptive treatments may help control PVNS osteolysis.

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Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue
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Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes
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Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes

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Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue
09:18

Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue

Published on: February 24, 2023

Area of Science:

  • Cell Biology
  • Pathology
  • Rheumatology

Background:

  • Pigmented villonodular synovitis (PVNS) is a tumor-like lesion of the synovium.
  • PVNS is characterized by macrophages and osteoclast-like giant cells, leading to bone erosion (osteolysis).
  • Understanding the mechanisms of giant cell formation and resorption in PVNS is crucial for treatment.

Purpose of the Study:

  • To analyze the characteristics of mononuclear and multinucleated cells in PVNS.
  • To determine the cellular and humoral mechanisms behind giant cell formation and resorption in PVNS.
  • To investigate the role of RANKL and M-CSF in osteoclastogenesis within PVNS.

Main Methods:

  • Isolation and culture of giant cells and CD14+ / CD14- mononuclear cells from PVNS tissue.
  • Assessment of osteoclast formation and activity via TRAP expression and lacunar resorption.
  • Evaluation of osteoclastogenic factors RANKL and M-CSF, and bisphosphonate zoledronate effects.

Main Results:

  • PVNS giant cells exhibited an osteoclast phenotype (CD51+, TRAP+, CD14-, HLA-DR-).
  • Osteoclast formation occurred from CD14+ mononuclear phagocytes, requiring RANKL.
  • Osteoclast formation was independent of exogenous M-CSF, suggesting its over-expression in PVNS pathogenesis.

Conclusions:

  • Osteoclasts in PVNS originate from CD14+ mononuclear phagocytes via a RANKL-dependent pathway.
  • The findings support a pathogenic role for M-CSF over-expression in PVNS.
  • Anti-osteoclast resorptive therapies may be beneficial for managing osteolysis in PVNS.