Next Article in Journal
Evaluation of New Fluorescent Lipophosphoramidates for Gene Transfer and Biodistribution Studies after Systemic Administration
Next Article in Special Issue
Transducer of ERBB2.1 (TOB1) as a Tumor Suppressor: A Mechanistic Perspective
Previous Article in Journal
Changes in Ultrastructure and Cytoskeletal Aspects of Human Normal and Osteoarthritic Chondrocytes Exposed to Interleukin-1β and Cyclical Hydrostatic Pressure
Previous Article in Special Issue
Targeting Glutamine Induces Apoptosis: A Cancer Therapy Approach
Article Menu
Issue 11 (November) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2015, 16(11), 26035-26054;

Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis

Division of Rheumatology, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Kyunggi 431-060, Korea
Institute for Skeletal Aging, Hallym University, Chunchon 200-702, Korea
Author to whom correspondence should be addressed.
Academic Editor: Anthony Lemarié
Received: 9 August 2015 / Revised: 3 October 2015 / Accepted: 21 October 2015 / Published: 30 October 2015
(This article belongs to the Collection Programmed Cell Death and Apoptosis)
Full-Text   |   PDF [698 KB, uploaded 30 October 2015]   |  


Apoptosis is a highly-regulated, active process of cell death involved in development, homeostasis and aging. Dysregulation of apoptosis leads to pathological states, such as cancer, developmental anomalies and degenerative diseases. Osteoarthritis (OA), the most common chronic joint disease in the elderly population, is characterized by progressive destruction of articular cartilage, resulting in significant disability. Because articular cartilage depends solely on its resident cells, the chondrocytes, for the maintenance of extracellular matrix, the compromising of chondrocyte function and survival would lead to the failure of the articular cartilage. The role of subchondral bone in the maintenance of proper cartilage matrix has been suggested as well, and it has been proposed that both articular cartilage and subchondral bone interact with each other in the maintenance of articular integrity and physiology. Some investigators include both articular cartilage and subchondral bone as targets for repairing joint degeneration. In late-stage OA, the cartilage becomes hypocellular, often accompanied by lacunar emptying, which has been considered as evidence that chondrocyte death is a central feature in OA progression. Apoptosis clearly occurs in osteoarthritic cartilage; however, the relative contribution of chondrocyte apoptosis in the pathogenesis of OA is difficult to evaluate, and contradictory reports exist on the rate of apoptotic chondrocytes in osteoarthritic cartilage. It is not clear whether chondrocyte apoptosis is the inducer of cartilage degeneration or a byproduct of cartilage destruction. Chondrocyte death and matrix loss may form a vicious cycle, with the progression of one aggravating the other, and the literature reveals that there is a definite correlation between the degree of cartilage damage and chondrocyte apoptosis. Because current treatments for OA act only on symptoms and do not prevent or cure OA, chondrocyte apoptosis would be a valid target to modulate cartilage degeneration. View Full-Text
Keywords: osteoarthritis; chondrocyte; apoptosis; caspase; mitochondria; chondroptosis; autophagy; endoplasmic reticulum stress; cartilage osteoarthritis; chondrocyte; apoptosis; caspase; mitochondria; chondroptosis; autophagy; endoplasmic reticulum stress; cartilage

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Hwang, H.S.; Kim, H.A. Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis. Int. J. Mol. Sci. 2015, 16, 26035-26054.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top