Signaling Network Dysregulation in Periapical Lesions: Interplay of Oxidative Stress, Autophagy, and Apoptosis

Alexandra Popa^1,2, Alexandra Ripszky^1,2,*, Sebastian Andrei Bancu^1,2, Melis Izet¹, Radu Vasile Radulescu^2,*, Florentina Rus², Ecaterina Andronescu^3,4, Ana Cernega⁵, Silviu Mirel Pituru⁵
1 The Interdisciplinary Center for Dental Research and Development, “Carol Davila” University of Medicine and Pharmacy, 19-21 Jean Louis Calderon, Bucharest, Romania
2 Department of Biochemistry, Faculty of Dental Medicine, University of Medicine and Pharmacy Carol Davila, 37 Dionisie Lupu Street, District 2, Bucharest, Romania
3 National Research Center for Micro and Nanomaterials, National Polytechnic University of Science and Technology of Bucharest, Bucharest, Romania
4 Department of Science and Engineering of Oxide Materials and Nanomaterials, Faculty of Chemical Engineering and Biotechnologies, National Polytechnic University of Science and Technology of Bucharest, Bucharest, Romania
5 Department of Professional Organization and Medical Legislation-Malpractice, “Carol Davila” University of Medicine and Pharmacy, 37 Dionisie Lupu Street, District 2, Bucharest, Romania
* Corresponding Author: Alexandra Ripszky. Email: email ; Radu Vasile Radulescu. Email: email
(This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)

BIOCELL https://doi.org/10.32604/biocell.2026.084761

Received 29 April 2026; Accepted 29 June 2026; Published online 17 July 2026

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Abstract

Periapical lesions (PAL) are chronic inflammatory conditions resulting from microbial invasion of the root canal system. Despite available treatments, failure rates of 20–35% highlight the need for a deeper understanding of their molecular mechanisms. This review provides an in-depth look at three interconnected cellular processes—oxidative stress, autophagy, and apoptosis—and examines their roles in PAL development and progression. Reactive oxygen species (ROS) activate redox-sensitive signaling pathways such as NF-κB, the Keap1–Nrf2/ARE axis, and MAPK cascades, disrupting bone homeostasis by inhibiting osteoblast formation and enhancing osteoclast activity via the RANKL–RANK–OPG pathway. Cell survival or death during inflammation primarily depends on the balance between the pro-survival autophagy process and the pro-death process of apoptosis. Apoptosis, regulated through intrinsic and extrinsic routes, is heavily affected by ROS and autophagic signals. Additional cell death mechanisms, such as necroptosis and pyroptosis, exacerbate tissue damage and prolong inflammation. The interactions among these pathways have direct clinical relevance: endodontic sealers differentially influence redox balance and inflammatory signaling in periapical cells. Understanding the interplay among oxidative stress, autophagy, and apoptosis offers a valuable framework for developing targeted therapies to improve clinical outcomes in endodontic practice.

Keywords

Periapical lesion; oxidative stress; autophagy; apoptosis; osteoclast; osteoblast; endodontic sealers; nuclear erythroid factor 2-related 2; receptor activator of nuclear factor-kappa B

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Signaling Network Dysregulation in Periapical Lesions: Interplay of Oxidative Stress, Autophagy, and Apoptosis

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