Apoptosis is a well defined mode of cell death which plays an imperative role in the development, regulation, and maintenance of the cell populations in multicellular organisms. Apoptosis is implicated in both health and diseases. Errors in apoptotic mechanisms have been allied to a wide range of pathologies including oral diseases. This review presents an update focused on the role and significance of apoptosis in various oral diseases ranging from reactive to benign and malignant pathologies. 1. Introduction The word “apoptosis” is of Greek origin, meaning “dropping off” or “falling off” of petals from flowers or leaves from trees. The term “apoptosis” was first introduced by Kerr et al. It is an active, inherently programmed phenomenon which can be initiated or inhibited by a variety of environmental stimuli, both physiological and pathological. Carl Vogt, however, first described the phenomenon more than 100 years earlier in 1842 [1, 2]. There are four major players which are involved in triggering and influencing the apoptotic process. These are the caspases, Bcl-2 family of proteins, tumor necrosis factor receptor (TNF-R) superfamily, and adaptor proteins [3]. Caspases are a family of proteases and are classified into initiator caspases 2, 8, 9, and 10, effector caspases 3, 6, and 7, and inflammatory caspases 1, 4, 5, 11, 12, 13, and 14 [3–5]. The members of Bcl-2 family are a group of crucial regulatory factors in apoptosis which are characterized by presence of conserved sequence motifs known as Bcl-2 homology (BH) domains. They are categorised into proapoptotic proteins (Bad, Bak, Bax, Bcl-rambo, Bcl-xS, Bid, Bik, Bim, Blk, BNIP3, Bok/Mtd, Hrk, and Nip3 in mammals and Egl-1 in C. elegans) and antiapoptotic proteins (A1/Bfl1, Bcl-2, Bcl-w, Bcl-xL, Boo/Diva, Mcl-1, NR-13, and Nrf3 in mammals, BHRF-1, E1B19？K, Ks-Bcl-2, LMW5-HL, and ORF16 in bacteria, and Ced-9 in C. elegans) [3, 5]. Broadly based intrinsic and extrinsic classification is used as platform to describe apoptotic signal cascade. Extrinsic/death receptor activated pathway involves the initiation of apoptosis through ligation of plasma membrane death receptors whereas intrinsic/mitochondrial cell death pathway involves initiation of apoptosis as a result of disturbance of intracellular homeostasis and mitochondria being critical executioner of cell death. While the initiation mechanisms of these pathway are different, both pathways converge (common pathway) resulting ultimately in cellular morphologic and biochemical alterations characteristic of apoptosis [5, 6]. Thus, apoptosis is a
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