Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis
By Hyun Sook Hwang, H. Kim. International Journal of Molecular Sciences, 2015
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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.
Subfields: Pharmacology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/c69c488bd904b7ce4a485aae576a01d9a5dfe666
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Citations in the corpus
- Hyaluronic Acid: Molecular Mechanisms and Therapeutic Trajectory (2019, background): “The common molecular inducers of chondroptosis may include ROS, RNS, cytokines [IL-1β, TNF-α, TNF-related apoptosisinducing ligand (TRAIL), and Fas ligand], and mechanical stress (131).”
- The role of metabolism in chondrocyte dysfunction and the progression of osteoarthritis. (2020, background): “apoptosis, which is an important characteristic in OA pathogenesis (Hwang and Kim, 2015; Lauber et al., 2003).”
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets (2023, background): “Apoptosis, a highly regulated programmed cell death, is the earliest reported cell death form.(117) While it is known that a low level of apoptosis detected by TUNEL assay exists in normal articular cartilage, the number of apoptotic cells is dramatically increased in the early and late stages of OA”