~ 404 ~ International Journal of Applied Dental Sciences 2021; 7(3): 404-406 ISSN Print: 2394-7489 ISSN Online: 2394-7497 IJADS 2021; 7(3): 404-406 © 2021 IJADS www.oraljournal.com Received: 25-05-2021 Accepted: 27-06-2021 Nasir A Salati Assistant Professor Department of Oral Pathology, Oral Medicine & Radiology, Dr Z.A. Dental College., AMU, Aligarh, Uttar Pradesh, India Md Asadullah Assistant Professor Department of Oral Pathology, Oral Medicine & Radiology, Dr Z.A. Dental College., AMU, Aligarh, Uttar Pradesh, India Masood H Khan Assistant Professor Department of Oral Pathology, Oral Medicine & Radiology, Dr Z.A. Dental College., AMU, Aligarh, Uttar Pradesh, India Pradhuman Verma Chairman, Department of Oral Pathology, Oral Medicine & Radiology, Dr. Z. A Dental College., AMU, Aligarh, Uttar Pradesh, India Corresponding Author: Md Asadullah Assistant Professor Department of Oral Pathology, Oral Medicine & Radiology, Dr Z.A. Dental College., AMU, Aligarh, Uttar Pradesh, India Role of apoptosis in pathogenesis of oral lesions: Molecular approach Nasir A Salati, Md Asadullah, Masood H Khan and Pradhuman Verma DOI: https://doi.org/10.22271/oral.2021.v7.i3f.1330 Abstract Research in histology, genetics, and molecular biology indicate that virtually all animal cells are armed with the genetic machinery to die. Under normal physiological circumstances, damaged cells are removed through a genetically programmed type of cell death. The aberrations in the regulation of genetically programmed cell death have been found to cause disease and deformity. Cell death, the ultimate result of cell injury, is one of the most crucial events in pathology, affecting every cell type and being the major consequence of ischemia (lack of blood flow), infection, toxins and immune reactions. Cell death is critical during normal embryogenosis, lymphoid tissue development and normally induced involution and is the aim of cancer radiotherapy and chemotherapy. This article discusses role of apoptotis in pathologies of potentially malignant, malignant, autoimmune and reactive lesions of oral cavity. Keywords: apoptotic bodies, BCL-2, caspases, MDM2 gene, necrosis, PMDs 1. Introduction The term programmed cell death was introduced in 1964, proposing that cell death during development is not of accidential nature but follows a sequence of controlled steps leading to locally and temporally defined self-destruction [1] . During necrosis, the cellular contents are released uncontrolled into the cell's environment which results in damage of surrounding cells and a strong inflammatory response in the corresponding tissue [2, 3] . Apoptosis, by contrast, is a process in which cells play an active role in their own death. Light microscopic identification of apoptosis usually involves single cells or occasionally small groups of cells. The apoptotic cell shrinks and separates from its neighbors and is surrounded by a halo like clear space. The nuclear chromatin breaks up into irregular crescentic, beaded or nodular masses; small basophilic apoptotic bodies may be identified. The complete absence of normal cellular detail is due to protein denaturation and nuclear dissolution. Ultra structurally necrotic cell initially swells because cell membrane volume control is lost; the cell then lyses, organelles disintegrate, and with nuclear dissolution, there is random DNA degradation [4] . The cytoplasmic contents of lysed necrotic cells excite an inflammatory reaction. Ultra structurally, apoptosis has a characteristic morphology: initially there is loss of cell junctions and specialized membrane structures, such as microvilli, with the fomation of contorted surface protuberances (or) blebs. Condensation beneath the nuclear membrane is irregular, crescentic or bead like, highly osmiophilic chromatin, which corresponds to cleavage of DNA into large fragments. The cell then breaks up into resistant, membrane bound fragments called apoptotic bodies [5] . Genetic basis of Apoptosis Important genes involved in cell cycle regulation are: c-myc,c-fos,c-jun,p53, kinases and phosphatases [6] The major determinants of the ‘‘apoptotic phenotype’’ in lymphocytes are the levels of expression of Bcl-2,Bcl-x L, Fas and Fas ligand(FasL) [7-10] . Both apoptotic signaling pathways converge at the level of the specific proteases-the caspases. There are 14 mammalian caspases which are synthesized as pro-enzymes, which usually undergo proteolysis and activation by other caspases in a cascade [11-13] Peptide caspase inhibitors can inhibit