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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 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 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 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

Updated: May 28, 2026

Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model
07:32

Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model

Published on: May 6, 2020

Osteochondral alterations in osteoarthritis.

Sunita Suri1, David A Walsh

  • 1Arthritis Research UK Pain Centre, Academic Rheumatology, University of Nottingham, Clinical Sciences Building, Nottingham City Hospital, Nottingham, NG5 1PB, UK.

Bone
|October 26, 2011
PubMed
Summary
This summary is machine-generated.

Osteoarthritis (OA) involves early changes at the osteochondral junction, including bone changes, blood vessel, and nerve growth. Understanding these alterations may lead to new OA pain and progression therapies.

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Area of Science:

  • Orthopedics and Musculoskeletal Research
  • Cell Biology
  • Pain Medicine

Background:

  • Osteoarthritis (OA) is a leading cause of pain and disability, particularly in aging populations.
  • The pathogenesis of OA is not fully understood, with early changes at the osteochondral junction gaining attention.
  • Osteochondral alterations may drive pain and structural damage in OA, impacting joint health.

Purpose of the Study:

  • To review pathological changes occurring at the osteochondral junction in OA.
  • To explore the potential therapeutic implications of these osteochondral changes for OA treatment.

Main Methods:

  • Review of existing literature on osteochondral junction pathology in OA.
  • Analysis of cellular signaling, bone turnover, angiogenesis, and nerve growth at the osteochondral junction.

Main Results:

  • Osteochondral junction alterations, including loss of integrity and tissue merging, occur early in OA.
  • These changes involve subchondral bone turnover, angiogenesis, and sensory nerve invasion into articular cartilage.
  • Cross-talk between cells across the osteochondral junction contributes to pathological changes.

Conclusions:

  • The osteochondral junction is a critical site for OA pathogenesis.
  • Understanding these early pathological changes offers potential therapeutic targets for OA management.
  • Similarities with other diseases suggest existing therapeutic strategies may be adaptable for OA.