Apoptosis in Oral Health and Disease: a Brief Review (original) (raw)
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Apoptosis and Its Significance in Oral Diseases: An Update
Journal of Oral Diseases, 2013
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.
Functional role of apoptosis in oral diseases: An update
Journal of Oral and Maxillofacial Pathology, 2016
Cell death appears to be a basic biological phenomenon which is maintained by the human body. The term apoptosis, also known as programmed cell death, is characterized by several unique morphological and biochemical features. Apoptosis and its different forms are essential for tissue homeostasis. Alteration in molecular mechanisms involved in apoptotic signaling contributes to a vast range of oral diseases. An understanding of the regulation of apoptosis has led to the development of many therapeutic approaches and better management of oral diseases. The review updates us the correlation between apoptosis in normal oral tissues and oral diseases.
Role of apoptosis in pathogenesis of oral lesions: Molecular approach
International Journal of Applied Dental Sciences, 2021
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.
Apoptosis in Oral Diagnostics: An Overview
JDUHS, 2009
Apoptosis describes the molecular and morphological processes leading to controlled cellular self destruction. In recent years, it has been investigated for its biological significance in numerous physiological processes including embryogenesis, differentiation, ...
Apoptosis and genes involved in oral cancer - a comprehensive review
Oncology Reviews, 2020
Oral cancers needs relentless research due to high mortality and morbidity associated with it. Despite of the comparable ease in accessibility to these sites, more than 2/3rd cases are diagnosed in advanced stages. Molecular/genetic studies augment clinical assessment, classification and prediction of malignant potential of oral lesions, thereby reducing its incidence and increasing the scope for early diagnosis and treatment of oral cancers. Herein we aim to review the role of apoptosis and genes associated with it in oral cancer development in order to aid in early diagnosis, prediction of malignant potential and evaluation of possible treatment targets in oral cancer. An internet-based search was done with key words apoptosis, genes, mutations, targets and analysis to extract 72 articles after considering inclusion and exclusion criteria. The knowledge of genetics and genomics of oral cancer is of utmost need in order to stop the rising prevalence of oral cancer. Translational ap...
Oral Oncology, 2004
Oral cancer is one of the most disfiguring types of cancer, since the surgical removal of the tumor may result in facial distortion. Oral cancer is also known to exhibit "field cancerization", resulting in the development of a second primary tumor. Furthermore, the five-year survival rate of this disease has remained approximately 50% during the past 30 years. Prevention and early detection/ treatment of oral cancer could significantly improve the quality of life for individuals at risk. Recently, the targeted elimination of oral squamous cell carcinoma cells by inducing apoptosis has emerged as a valued strategy to combat oral cancer. Studies utilizing a variety of chemical or biological interventions demonstrated promising results for induction of apoptosis in oral malignant cells. This review summarizes the results of a number of investigations focused specifically on induction of apoptosis in oral cancer cells by synthetic compounds and naturally occurring chemopreventive agents with apoptotic potential.
Apoptosis and Predisposition To Oral Cancer
Critical Reviews in Oral Biology & Medicine, 1999
The term apoptosis, also known as programmed cell death (PCD), was coined by developmental biologists a number of years ago to describe a form of cell death characterized by several unique morphological and biochemical features. Genetic studies of the round worm Caeneorhabditis elegans, a simple multicellular organism, first revealed apoptosis to be an integral part of the developmental program. Subsequently, the importance of apoptosis in higher organisms was demonstrated in several eukaryotic systems. In mammals, apoptosis is widespread during embryogenesis and in adult tissues. It is required for normal tissue homeostasis and for clonal selection in the immune system. In both developing and adult organisms, apoptosis plays a central role in reinforcing appropriate cellular patterns and in regulating cell number by eliminating cells that are harmful or no longer needed. It is becoming increasingly clear that disruption in the apoptosis pathway can contribute to the development of a number of developmental, inflammatory, degenerative, and neoplastic diseases. The effector arm of the apoptotic program includes members of the Bcl-2 gene family that function as either death agonists or death antagonists. These proteins participate in an elaborate genetically controlled biochemical pathway that functions to maintain tissue and organ homeostasis and serve as a critical defense mechanism to guard against malignant transformation. Cancer is the result of a series of genetic lesions that include activation of oncogenes and inactivation or loss of tumor suppressor genes. Several groups of investigators have observed that deregulated expression of oncogenes can subvert apoptotic pathways, resulting in prolonged cell survival. In pathological settings such as cancer, members of the Bcl-2 gene family are able to synergize with oncogenes and tumor suppressor genes to transform cells. In this review, we describe the process of apoptosis in mammalian cells and define the role and biochemical pathways through which the Bcl-2 gene family induce and/or protect cells from apoptosis. Last, we will discuss the evidence which suggests that alterations in this pathway may play a central role in tumorigenesis by allowing genetically damaged cells normally destined for elimination to persist, predisposing them to additional mutations and driving them to malignancy.
Apoptosis-associated proteins and the development of oral squamous cell carcinoma
Oral Oncology, 1999
Expression of apoptosis-associated proteins was evaluated in premalignant and malignant oral epithelial lesions, to test the hypothesis that protein regulation of apoptosis may be altered in the development of oral squamous cell carcinoma. Ninety archived paran-embedded specimens from 25 patients (two or more sequential biopsies each) and eight control specimens were evaluated in immunohistochemically stained sections for tumor suppressor protein p53, p53 binding protein mdm-2, and apoptosis regulatory proteins Bcl-2, Bcl-X, Bax, and Bak. The initial histologic diagnosis for 17/25 patients was either focal keratosis, mild dysplasia, or moderate dysplasia; the initial diagnosis for the remaining eight patients ranged from severe dysplasia to moderately dierentiated squamous cell carcinoma. Thirty of 90 specimens showed positive p53 expression, nine of which were dysplasias. In patients with one or more lesions displaying p53 expression, there was increased intensity of staining with disease progression. Bak was expressed in 57/90 specimens, including 27 dysplasias of various grades. There was also a signi®cantly increased intensity of Bak staining with disease progression, which did not appear to be dependent upon p53 status. Bcl-X was expressed in 73/90 specimens, with staining displayed earlier in premalignant lesions than either p53 or Bak. Ten of 90 specimens were positive for Bcl-2 (all were dysplasias or carcinomas), and only 2/90 specimens were positive for Bax. Eleven of 90 specimens were positive for mdm-2; six of which were also positive for p53. These data show that apoptosis-associated proteins are altered in variable patterns in both premalignant and malignant oral epithelial lesions. p53 and especially Bak and Bcl-X are expressed early; Bax is largely absent; and Bcl-2 and mdm-2 show sporadic expression in the development of oral premalignant and malignant disease. #
Journal of Oral Pathology and Medicine, 2003
In the last three decades, more work has been done on apoptosis and its role in the pathogenesis of many diseases including cancer. In almost all instances of cancer, dysregulation of cell death (apoptosis) and cell proliferation have been found to play a major role in tumourigenesis. A lot of progress has been made on understanding the molecular basis of apoptosis and its regulatory mechanisms. This review focuses on current knowledge on the regulation of apoptosis in oral squamous cell carcinoma, current methodologies and methodological consideration in estimation of cell death in tissue sections and the clinical significance of apoptosis related molecules in progression of oral squamous cell carcinoma.
Effects of aging on apoptosis gene expression in oral mucosal tissues
Apoptosis, 2013
Apoptotic processes are important for physiologic renewal of an intact epithelial barrier and contribute some antimicrobial resistance for bacteria and viruses, as well as anti-inflammatory effects that benefits the mucosa. The oral cavity presents a model of host-bacterial interactions at mucosal surfaces, in which a panoply of microorganisms colonizes various niches in the oral cavity and creates complex multispecies biofilms that challenge the gingival tissues. This report details gene expression in apoptotic pathways that occur in oral mucosal tissues across the lifespan, using a nonhuman primate model. Macaca mulatta primates from 2 to 23 years of age (n = 23) were used in a cross-sectional study to obtain clinical healthy gingival tissues specimens. Further, mRNA was prepared and evaluated using the Affymetrix Rhesus GeneChip and 88 apoptotic pathway genes were evaluated. The results identified significant positive correlations with age in 12 genes and negative correlations with an additional five genes. The gene effects were predicted to alter apoptosis receptor levels, extrinsic apoptotic pathways through caspases, cytokine effects on apoptotic events, Ca ?2-induced death signaling, cell cycle checkpoints, and potential effects of survival factors. Both the positively and negatively correlated genes within the apoptotic pathways provided evidence that healthy tissues in aging animals exhibit decreased apoptotic potential compared to younger animals. The results suggested that decreased physiologic apoptotic process in the dynamic septic environment of the oral mucosal tissues could increase the risk of aging tissues to undergo destructive disease processes through dysregulated inflammatory responses to the oral microbial burden.