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Azerbaycan Saytlari

 »  Home  »  Endodontic Articles 16  »  Apoptosis: an introduction for the endodontist
Apoptosis: an introduction for the endodontist
How does necrosis compare to apoptosis?



How does necrosis compare to apoptosis?
Cells usually die either by necrosis or apoptosis. The characteristics of apoptotic death are more clearly understood when compared to the characteristics of necrotic death (Table 1). Necrosis is a pathological death of cells resulting from irreversible damage that occurs in the dental pulp and is a term commonly used in pulpal diagnosis. The earliest irreversible changes are mitochondrial, consisting of swelling and granular calcium deposits. After such changes, the outlines of individual cells are indistinct and affected cells may become merged, sometimes forming a focus of coarsely granular, amorphous or hyaline material (Stedman 1995). These features include cell swelling, membrane lysis and an inflammatory response (Wyllie et al. 1980), and are distinctly different from the features of apoptosis described above.

Table 1. Comparison of classic features of apoptosis (programmed cell death) and necrosis (pathologic cell death) (Polverini & Nor1999).

Comparison of classic features of apoptosis


What role does apoptosis play in development?
Apoptosis plays an important role in all stages of life. Developing human branchial arches, embryonic tails and  finger webbing cannot resorb before birth without organised programmed cell death. In mature organisms, homeostasis is maintained by balancing the continuous mitosis and differentiation of cells with the apoptotic process (Kerr et al.1972).
Apoptosis has multiple roles in tooth development from the beginning of tooth formation to the completion of root development. There is evidence of apoptosis in the reduction of cells of the stellate reticulum, at the initiation of enamel formation (Vaahtokari et al. 1996, Baratella et al. 1999) and in the stratum intermedium (Bronckers et al.1996,Vaahtokari et al.1996).This process also occurs during the transition stage between secretion and maturation of ameloblasts during enamel formation (Nishikawa & Sasaki 1995). After enamel formation, approximately 25% of the ameloblasts die and following enamel matrix maturation, another 25% under goapoptosis (Joseph et al.1994).Apoptosis has been shownto occuraround the crowns of teeth during tooth eruption (Bronckers et al.1996, Kaneko et al.1997), playing a major role in the elimination of reduced ameloblasts located at cusps (Shibata et al. 1995). It is thought that the inhibition of apoptosis in reduced ameloblasts may occur after the elimination of the tooth organ, allowing for the establishment of the junctional epithelium (Shibata et al.1995).Whilst the precise mechanisms for these events remain largely undiscovered, some work has shown that bcl-2, an apoptotic inhibitor, is involved in maintaining the viability of the enamel organ during tooth development (Slootweg & deWeger1994).
Fibroblast-like cells of the periodontal ligament (PDL) exhibit apoptosis during tooth development (Cerri et al. 2000), and apoptotic cells, probably osteoclasts, are also found on the surfaces of developing alveolar bone (Vaahtokari et al. 1996). Apoptosis is also responsible for at least partial elimination of the cells of Hertwig’s epithelial root sheath (HERS) after root formation is complete (Kaneko et al.1999, Cerri et al. 2000). Furthermore, cell rests of Malassez, which can proliferate to produce periradicular cysts, may be partially as a result of incomplete apoptosis of HERS.

What role does apoptosis play in the dental pulp?
Apoptosis is a part of normal pulp homeostasis (Nishikawa & Sasaki1999), occurring more in the occlusal (incisal) than in the apical portions of the pulp (Vermelin et al. 1996, Nishikawa & Sasaki 1999). Most apoptotic cells in normal pulp can be foundat the periphery and are usually associated with the subodontoblastic region rather than with the odontoblastic layer (Vermelin et al. 1996, Piattelli et al. 2001). Odontoblasts seem to compensate for the reduction in pulp chamber volume as a result of physiological (secondary) dentine formation by odontoblastic layering rather than by cell death. Apoptosis is more evident in odontoblasts after injury to odontoblastic processes as seen with cavity preparation (Goldberg et al.1994, Bronckers et al.1996,Kitamura et al. 2001). There is evidence that reparative (tertiary) dentine formation, in response to injury, is associated with a large decrease in the number of odontoblasts. Up to half of the pulp odontoblasts can be eliminated in only 4 years by this process (Franquin et al. 1998). Fibroblasts and vascular endothelial cells of the pulp proper also show evidence of apoptosis (Franquin et al.1998).Although certain characteristics of apoptotic death a re favourable to necrosis (i.e. an inflammatory response is not triggered), apoptosis does not lead to pulp recovery. This may be due in part to the elimination of regenerative cells by apoptosis (Goldberg et al.1994).Ultimately, when apoptosis occurs, apoptotic bodies and debris are phagocytosed by major histocompatibility Class II (MHC II) positive and negative macrophages (Nishikawa & Sasaki1999).