Chondrocyte apoptosis: a cause or consequence of osteoarthritis?

Abstract

Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation and changes in the subchondral bone. Over the last two decades, there has been increasing evidence showing association between cartilage degradation and chondrocyte death, and different types of cell death in cartilage have been reported, including apoptosis and chondroptosis as well as necrosis, but which of these types of cell death predominate in OA is debatable. There are also some methodological difficulties in detecting the specific form of cell death in articular cartilage. Current 'gold standard' for detecting chondrocyte death is electron microscopy which suggests that the morphological changes of chondrocytes in OA cartilage are attributed to apoptosis and/or chondroptosis. However, the current literature appears to suggest that classic apoptosis plays an important role in OA; but whether chondrocyte apoptosis is a cause or a result of cartilage degeneration in OA is hotly contested. Studies of suitable animal models, especially longitudinal studies, are needed to address the cause-and-effect relationship.

Histomorphologic and Histomorphometric Characteristics of Zygapophyseal Joint Remodeling in Ankylosing Spondylitis

“…Reduction in cartilage thickness, indicating cartilage damage, can result from matrix degradation or from chondrocyte apoptosis, mechanisms that accompany cartilage degeneration in OA (18)(19)(20). To investigate the potential contribution of these mechanisms to joint remodeling in AS, we measured the proteoglycan content of the cartilage by analyzing the optical density of Safranin O staining, and we determined the frequency of apoptotic cells among chondrocytes according to caspase 3 expression.…”

Chondroptosis in Alkaptonuric Cartilage

“…Although chondroptosis has some features in common with classical apoptosis and other types of cell death such as cell shrinkage, chromatin condensation and the probable involvement of caspases, other features are different such as a cytoplasmic vacuolization without nuclear fragmentation and prominent Golgi and rough endoplasmic reticulum (RER). Chondroptosis has been reported to play an important role in osteoarthritis (OA) (Roach et al, 2004; Pérez et al, 2005; Almonte‐Becerril et al, 2010; Zamli and Sharif, 2011). …”

Effect of self-assembled peptide–mesenchymal stem cell complex on the progression of osteoarthritis in a rat model

“…1 Although the exact pathophysiology of the condition has not been uncovered yet, it is generally considered to be caused by a combination of cumulative mechanical stresses from aging, destructive biochemical changes taking place in the synovial membrane, and apoptosis of chondrocytes. [2][3][4][5] Clinically, there are several classes of treatments for OA, including nonpharmacological, pharmacological, and surgical treatment modalities. However, these treatments provide largely symptom relief, and do not halt the progression of the disease.…”