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• W1973478304 abstract "The apoptosis is the programmed cell death, a distinct process compared to cellular necrosis, which plays an important role in both human embryonic development and adult tissue homeostasis. Apoptosis represents a physiological form of cell death. The role of apoptosis is to remove harmful, damaged or unwanted cells without inducing inflammatory response by the release of cell contents [1]. Apoptosis is activated through two principal signaling pathways: intrinsic and extrinsic, both of which are potential anticancer therapeutic targets. In contrast to necrosis, which is a form of cell death resulting from an acute cellular stress or trauma, apoptosis is a death orderly and regular, does not induce inflammation, requires energy (ATP) and generally lead to an advantage during the body life. Besides its importance as a biological phenomenon, it has acquired a huge medical value, since imperfect process of apoptosis covers many diseases. Excessive activity can cause trouble by apoptotic cell loss (see, for example neurodegenerative diseases such as Parkinson’s disease), while a weak apoptosis may involve uncontrolled cell growth in malignancy mechanism [2]. Apoptosis is the most common mechanism by which the body eliminates damaged or unneeded cells, without local inflammation from leakage of cell contents. Cells that are undergoing apoptosis exhibit a characteristic pattern of morphologic changes, including cell shrinkage, condensation, fragmentation of the nucleus and bubbling of the plasma membrane, known as “blebbing,” and chromatin condensation and nucleosomal fragmentation [1,3]. Apoptosis functions through two main, alternative pathways: death receptor-mediated (or extrinsic) and mitochondria-dependent (or intrinsic). The former pathway is initiated by ligation of specific death receptors by their ligands. The main death receptors—Fas and tumour necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) receptors R1 and R2—induce cell death following ligation with Fas ligand (FasL) or TRAIL, respectively [4-7]. Ligation of TRAIL R1 by TNFα also induces apoptosis after inhibition of nuclear factor kappa-B (NF-kB). Fas ligation by FasL is followed by recruitment of FADD (Fas-associated via death domain) and subsequently of caspase 8. This process gives rise to caspase 8 activation, which can be inhibited by the anti-apoptotic molecule FLICE inhibitory protein (Flip). Caspase 8 induces apoptosis by directly activating caspase 3 or by cleaving bid (BH3 interacting domain death agonist), resulting in mitochondrial dysfunction and subsequent release of cytochrome c and activation of caspases 9 and 3. Caspase 3 promotes the typical apoptosis features, including DNA fragmentation and cell death in several tissues [8,9]. It is unclear whether repetitive loading and apoptosis are quantitatively related in any type of cartilage. Several studies have demonstrated the crucial function of apoptotic mechanisms in intervertebral disc degeneration, and the involvement of apoptosis in various conditions associated with intervertebral disc degeneration has been thoroughly explored [10]. However, apoptosis has been documented to have a central role not only in intervertebral disc degeneration [10]. Although a number of features of temporomandibular joint (TMJ) disc degeneration have been thoroughly studied, data on the involvement of apoptotic mechanisms and their mediators are few and quite recent; indeed most of the research conducted on disc apoptosis has focused on the intervertebral disc. TMJ disc degeneration is believed to be a consequence of mechanical and biological events affecting the equilibrium between matrix synthesis and degradation. According to this hypothesis loss of cellularity, collagen fibre fragmentation and TMJ disc tears and clefts would all depend on excessive apoptosis, a situation where collagen fibre degradation is not offset by synthesis of new fibres because of apoptosis-induced cell loss. The findings correlating TMJ disc internal derangement and apoptosis largely come from animal models [11]. However, our group has extensively analyzed programmed cell death in human TMJ discs with and without internal derangement [12,13]. We have advanced Corresponding author." @default.
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• W1973478304 date "2013-01-01" @default.
• W1973478304 modified "2023-09-29" @default.
• W1973478304 title "Apoptosis in TMJ Disc Diseases" @default.
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• W1973478304 doi "https://doi.org/10.4236/ojapo.2013.24007" @default.
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