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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 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...
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.
Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

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...
Development of the Limb Synovial Joints01:07

Development of the Limb Synovial Joints

Joints form during embryonic development in conjunction with the formation and growth of the associated bones. The embryonic tissue that gives rise to all bones, cartilage, and connective tissues of the body is called mesenchyme.
The mesenchymal stem cells differentiate into chondrocytes that form the hyaline cartilage, and later the cartilaginous model of the bone. This model further transforms into a bone. This process is known as endochondral ossification.
During development, the limbs...

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Related Experiment Video

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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

Osteoclastogenesis and arthritis.

Nicola Maruotti1, Maria Grano, Silvia Colucci

  • 1Department of Rheumatology, University of Foggia Medical School, Italy.

Clinical and Experimental Medicine
|November 12, 2010
PubMed
Summary

Osteoclasts drive joint destruction in chronic arthritis by enhancing bone resorption. Targeting osteoclast formation, particularly RANKL and TNF-α, offers a strategy to reduce bone damage.

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A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
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Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes
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Published on: January 27, 2023

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:

  • Immunology
  • Rheumatology
  • Bone Biology

Background:

  • Osteoclasts are implicated in joint destruction in chronic inflammatory arthritis.
  • Psoriatic arthritis and rheumatoid arthritis exhibit juxta-articular bone destruction due to heightened osteoclast activity.
  • Bone erosion results from an imbalance favoring bone resorption over formation, influenced by proinflammatory cytokines.

Purpose of the Study:

  • To highlight the role of osteoclasts in inflammatory bone erosion.
  • To identify key molecular pathways and cellular players involved in osteoclastogenesis in arthritis.
  • To propose therapeutic strategies targeting osteoclast activity for reducing bone damage.

Main Methods:

  • Review of existing literature on osteoclast biology and inflammatory arthritis.
  • Analysis of the roles of cytokines (TNF-α, IL-1β, IL-17) and signaling molecules (RANKL) in osteoclast formation.
  • Examination of cellular contributions (T-cells, stromal cells, synoviocytes) to osteoclastogenesis.

Main Results:

  • Osteoclast activity is enhanced by proinflammatory cytokines like TNF-α, IL-1β, and IL-17.
  • RANKL, expressed by T-cells, stromal cells, and synoviocytes, is crucial for osteoclast formation.
  • An imbalance favoring osteoclast-driven bone resorption over osteoblast-mediated bone formation characterizes inflammatory bone erosion.

Conclusions:

  • Osteoclasts are critical mediators of bone destruction in chronic arthritis.
  • Targeting RANKL production and inhibiting TNF-α are promising therapeutic strategies to mitigate bone damage.
  • Osteoclasts represent a viable therapeutic target for managing joint destruction in inflammatory arthropathies.