Autophagy, One of the Main Steps in Periodontitis Pathogenesis and Evolution
Maria Greabu,
Francesca Giampieri,
Marina Melescanu Imre,
Maria Mohora,
Alexandra Totan,
Silviu Mirel Pituru,
Ecaterina Ionescu
Affiliations
Maria Greabu
Department of Biochemistry, Faculty of Dental Medicine, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
Francesca Giampieri
Department of Agricultural, Food and Environmental Sciences, Università Politecnica delle Marche, Via Ranieri 65, 60131 Ancona, Italy
Marina Melescanu Imre
Department of Complete Denture, Faculty of Dental Medicine, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
Maria Mohora
Department of Biochemistry, Faculty of General Medicine, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
Alexandra Totan
Department of Biochemistry, Faculty of Dental Medicine, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
Silviu Mirel Pituru
Department of Professional Organization and Medical Legislation-Malpractice, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
Ecaterina Ionescu
Department of Orthodontics and Dento-Facial Orthopedics’, Faculty of Dental Medicine, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
Periodontitis represents a complex inflammatory disease that compromises the integrity of the tooth-supporting tissue through the interaction of specific periodontal pathogens and the host’s immune system. Experimental data help to outline the idea that the molecular way towards periodontitis initiation and progression presents four key steps: bacterial infection, inflammation, oxidative stress, and autophagy. The aim of this review is to outline the autophagy involvement in the pathogenesis and evolution of periodontitis from at least three points of view: periodontal pathogen invasion control, innate immune signaling pathways regulation and apoptosis inhibition in periodontal cells. The exact roles played by reactive oxygen species (ROS) inside the molecular mechanisms for autophagy initiation in periodontitis still require further investigation. However, clarifying the role and the mechanism of redox regulation of autophagy in the periodontitis context may be particularly beneficial for the elaboration of new therapeutic strategies.