Cellular apoptosis is programmed cell death. The concept has been studied for a century but the idea of programmed cell death was first identified in 1964, and the greek term apoptosis referring to the falling of leaves in autumn coined to describe the process in 1972. In the average human 50 to 70 billion cells undergo aptoptosis, which makes room for cell renewal. Physiologic growth and development as well as tissue homeostatis rely on this ability. Injury results in a period of rapid cell proliferation which can extend over weeks yet at the end of several weeks, there may be the number of cells as there were a few weeks into the process, due to concommitant apoptosis. Orchestrated cell death and proliferation is going on similtaneously.
Under certain conditions a given cell needs to shut down for good, Blunt trauma to cartilage of sufficient severity is associated by apoptosis of 35% of the cells. In vivo models of osteonecrosis of the femoral head due to glucocorticoids is associated with cellular apoptosis of the osteocyte with resultant loss of their mechanosensing function and with that loss of structural integrity resulting in joint collapse. The apoptosis caused by glucocorticoids in some cell lines in prevented by inhibiting protein synthesis, a point which emphasizes the active nature of the process. Many oncologic treatments work by inducing apoptosis in the neoplastic cell.
If there is a catastrophic failure, say a car crash for instance, if the engine is still going, the concern is for fire or explosion, in other words, wide spread damage due to the continued functioning of the aparatus. It may be that programmed cell death is useful overall in a similar way. If there is sufficient damage to a cell its continued function may it be detrimental to the organism as a whole making programmed cell death the best option.
If you have a breakdown say on a boat far away from land, it may be necessary to pirate the parts from something non essential in order to get the sail or the engine to work. In some cartilage injuries, especially if the full thickness of the cartilage is not violated, there is no migration of pluripotential cells to the sight of injury. The cells that undergo apoptosis, do they provide a local reservoir for recycling of parts, allowing for an in situ healing process?
If a virus infects a cell it takes over the reproductive aparatus for its own purpose. In such a case would not a mechanism for programmed cell death be desirable. Extrinsic triggering of apoptosis in an infected cell or a cell that had undergone malignant transformation is an essential defense mechanism. Not surprisingly then, the search word apoptosis in HighWire Press generates over one hundred thousand references.
Apoptosis is different than necrosis. It is an active process and highly regulated, an orchestrated suicide rather than an accidental demise of the cell. The process requires specific effectors, studies implicate an intrinsic mechanism involving translocation of the cytochome c aparatus from the mitochondria initiated by a cascade of proteases called caspases. When the effectors are lost apoptosis may fail to occur and the cell continues to proliferate, evading the apoptosis inducing defense mechanism. We can't get to the shut down switch.