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Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis.
Int J Mol Sci. 2015 Oct 30; 16(11):26035-54.IJ

Abstract

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.

Authors+Show Affiliations

Division of Rheumatology, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Kyunggi 431-060, Korea. wazzup@hallym.ac.kr. Institute for Skeletal Aging, Hallym University, Chunchon 200-702, Korea. wazzup@hallym.ac.kr.Division of Rheumatology, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Kyunggi 431-060, Korea. kimha@hallym.ac.kr. Institute for Skeletal Aging, Hallym University, Chunchon 200-702, Korea. kimha@hallym.ac.kr.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

26528972

Citation

Hwang, Hyun Sook, and Hyun Ah Kim. "Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis." International Journal of Molecular Sciences, vol. 16, no. 11, 2015, pp. 26035-54.
Hwang HS, Kim HA. Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis. Int J Mol Sci. 2015;16(11):26035-54.
Hwang, H. S., & Kim, H. A. (2015). Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis. International Journal of Molecular Sciences, 16(11), 26035-54. https://doi.org/10.3390/ijms161125943
Hwang HS, Kim HA. Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis. Int J Mol Sci. 2015 Oct 30;16(11):26035-54. PubMed PMID: 26528972.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis. AU - Hwang,Hyun Sook, AU - Kim,Hyun Ah, Y1 - 2015/10/30/ PY - 2015/8/9/received PY - 2015/10/3/revised PY - 2015/10/21/accepted PY - 2015/11/4/entrez PY - 2015/11/4/pubmed PY - 2016/8/20/medline KW - apoptosis KW - autophagy KW - cartilage KW - caspase KW - chondrocyte KW - chondroptosis KW - endoplasmic reticulum stress KW - mitochondria KW - osteoarthritis SP - 26035 EP - 54 JF - International journal of molecular sciences JO - Int J Mol Sci VL - 16 IS - 11 N2 - 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. SN - 1422-0067 UR - https://www.unboundmedicine.com/medline/citation/26528972/Chondrocyte_Apoptosis_in_the_Pathogenesis_of_Osteoarthritis_ DB - PRIME DP - Unbound Medicine ER -