@Article{biocell.2026.084761,
AUTHOR = {Alexandra Popa, Alexandra Ripszky, Sebastian Andrei Bancu, Melis Izet, Radu Vasile Radulescu, Florentina Rus, Ecaterina Andronescu, Ana Cernega, Silviu Mirel Pituru},
TITLE = {Signaling Network Dysregulation in Periapical Lesions: Interplay of Oxidative Stress, Autophagy, and Apoptosis},
JOURNAL = {BIOCELL},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/biocell/online/detail/27576},
ISSN = {1667-5746},
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.},
DOI = {10.32604/biocell.2026.084761}
}