Abstract

Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. The induction of autophagy has been shown to have both protective and pathological effects in periodontitis. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy is an evolutionarily conserved process essential for cellular homeostasis and human health. Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. It also participates in various biological processes, such as cellular differentiation, cell function, and defense against pathogens. In addition, autophagic dysfunction is associated with multiple diseases such as autoimmune disease, cancer, diabetes, and oral disease. Nowadays research has ascertained the role of autophagy in Periodontal disease, especially its role in the host defence against periodontal disease drivers. A bulk of research has recognized several pharmaceuticals and nutraceuticals that can potentially modulate this kind of cell death and serve as useful therapies. However, further research is warranted in order to reach a clinical translation, which could be of help in the discovery of novel host modulation therapies for Periodontal disease.
 Keywords: Autophagy, Apoptosis, Micro autophagy, immune response, Periodontitis, Periodontal pathogens, Periapical lesion

Highlights

  • Review Article|| Print ISSN: 2589-7837 || Online ISSN: 2581-3935 || International Journal of Medical Science and Diagnosis Research (IJMSDR)

  • The term autophagy was first coined by Christian de Duve over 40 years ago, which was largely based on the observation in degradation of mitochondria and other intracellular structures within lysosomes of rat liver perfused with the pancreatic hormone, glucagon

  • Butyrate, produced by anaerobic bacteria and highly concentrated in mature subgingival dental plaques, activates autophagic cell death in gingival epithelial cells. This butyrate-induced cell death can be significantly reversed by the autophagic inhibitor 3-MA, but not by caspase inhibitors, which confirms the existence of caspase-independent cell death mediated by autophagy

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Summary

Review Article

|| Print ISSN: 2589-7837 || Online ISSN: 2581-3935 || International Journal of Medical Science and Diagnosis Research (IJMSDR). DUAL ROLE OF AUTOPHAGY IN PERIODONTAL DISEASE Dr Priyanka Muwal, Dr Navneet Kaur, Dr Gurpreet Kaur3 1MDS Post Graduate Student, Department of Periodontology and Oral Implantology, National Dental College and Hospital, Derabassi, Mohali, Punjab. Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. It participates in various biological processes, such as cellular differentiation, cell function, and defense against pathogens.

Introduction
THE MAJOR DEVELOPMENT IN THE FIELD OF AUTOPHAGY
TYPES OF AUTOPHAGY
Autophagosome formation
IMPLICATION OF AUTOPHAGY IN PERIODONTAL DISEASE RELATED DRIVERS
Successful establishment of persistent colonization in subgingival crevices by
AUTOPHAGY DEPENDENT LINK WITH HUMAN ORAL DISEASES
ROLE OF AUTOPHAGY IN BONE HOMEOSTATSIS
In Osteoclast Cell
In Osteoblast and Osteocytes cells
Autophagy and Oral Cancer
Autophagy and Oral Candidiasis
Autophagy and Periapical Lesions
Future Direction of Autophagy Research in Periodontal Disease
Findings
Conclusion
Full Text
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