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Growth of Cartilage and Bone Tissue

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...

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Updated: Apr 24, 2026

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

Epigenetic differences in human cartilage between mild and severe OA.

Florentine C Moazedi-Fuerst¹, Manuela Hofner, Gerald Gruber

¹Department of Rheumatology and Immunology, Medical University Graz, Austria.

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society

|September 13, 2014

Summary

Epigenetic regulation influences osteoarthritis (OA) development. Genome-wide methylation screening identified 1,214 differentially methylated genes in mild versus severe OA cartilage, suggesting new therapeutic targets.

Keywords:

methylation osteoarthritis whole-genome array

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Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model

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Published on: May 6, 2020

Area of Science:

Genetics
Epigenetics
Osteoarthritis Research

Background:

Osteoarthritis (OA) development is influenced by genetic and environmental factors affecting chondrocyte biology through epigenetic regulation.
Epigenomic alterations may reveal novel pathogenetic pathways in OA.
Understanding these pathways is crucial for identifying new therapeutic targets.

Purpose of the Study:

To perform genome-wide methylation screening to identify differences between mild and severe human osteoarthritic cartilage.
To discover potential new pathogenetic pathways and therapeutic targets in OA.

Main Methods:

Genome-wide methylation screening using human promoter microarrays on paired mild and severe OA cartilage specimens from 16 female patients.
Histological grading of cartilage damage.
Validation of selected genes using methylation-specific quantitative PCR (qPCR).

Main Results:

Identified 1,214 differentially methylated genetic targets between mild and severe OA cartilage.
1,070 targets were hypermethylated and 144 were hypomethylated.
Gene Ontology, KEGG pathway, and protein domain analyses indicated involvement in development and differentiation pathways.

Conclusions:

Distinct methylation patterns exist between mild and severe OA cartilage.
Differentially methylated genes involved in growth and development pathways may represent novel therapeutic targets for OA.
Further understanding of OA pathogenetic mechanisms can be achieved through epigenomic analysis.