Chondroptosis: a variant of apoptotic cell death in chondrocytes?
Evidence has accumulated in recent years that programmed cell death (PCD) is not necessarily synonymous with the classical apoptosis, as defined by Kerr and Wyllie, but that cells use a variety of pathways to undergo cell death, which are reflected by different morphologies. Although chondrocytes with the hallmark features of classical apoptosis have been demonstrated in culture, such cells are extremely rare in vivo. The present review focuses on the morphological differences between dying chondrocytes and classical apoptotic cells. We propose the term 'chondroptosis' to reflect the fact that such cells are undergoing apoptosis in a non-classical manner that appears to be typical of programmed chondrocyte death in vivo. Unlike classical apoptosis, chondroptosis involves an initial increase in the endoplasmic reticulum and Golgi apparatus, reflecting an increase in protein synthesis. The increased ER membranes also segment the cytoplasm and provide compartments within which cytoplasm and organelles are digested. In addition, destruction occurs within autophagic vacuoles and cell remnants are blebbed into the lacunae. Together these processes lead to complete self-destruction of the chondrocyte as evidenced by the presence of empty lacunae. It is speculated that the endoplasmic reticulum pathway of apoptosis plays a greater role in chondroptosis than receptor-mediated or mitochondrial pathways and that lysosomal proteases are at least as important as caspases. Because chondroptosis does not depend on phagocytosis, it may be more advantageous in vivo, where chondrocytes are isolated within their lacunae. At present the initiation factors or the molecular pathways involved in chondroptosis remain unclear.
Roach
H I
HI
University Orthopaedics, Bone & Joint Research Unit, General Hospital and University of Southampton, Southampton, UK. hr@soton.ac.uk
Aigner
T
T
Kouri
J B
JB
D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D002451:Cell Compartmentation; D019902:Chondrocytes / Q000473:pathology* / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D006056:Golgi Apparatus / Q000648:ultrastructure; D006132:Growth Plate / Q000473:pathology / Q000648:ultrastructure; D006801:Humans; D008954:Models, Biological; D010003:Osteoarthritis / Q000473:pathology; D011506:Proteins / Q000378:metabolism; D014617:Vacuoles / Q000648:ultrastructure
D011506:Proteins