Necroptosis in apical periodontitis: A programmed cell death with multiple roles

Area of Science:

• Cellular Biology
• Immunology
• Pathology

Background:

• Programmed cell death (PCD) encompasses various mechanisms, including necroptosis, pyroptosis, ferroptosis, and cuproptosis.
• Necroptosis, a caspase-independent inflammatory cell death pathway mediated by MLKL, is increasingly recognized for its role in disease.
• Unlike apoptosis, necroptosis involves cell enlargement and plasma membrane rupture, and can be triggered by bacterial infections.

Purpose of the Study:

• To provide a comprehensive review of necroptosis in the context of apical periodontitis (AP).
• To summarize necroptosis activation pathways in AP.
• To discuss the interplay of different cell death types and potential therapeutic strategies targeting necroptosis in AP.

Main Methods:

• Literature review of recent advances in necroptosis research.
• Analysis of bacterial pathogen interactions with necroptosis pathways.
• Discussion of the role of necroptosis in AP pathogenesis and treatment.

Main Results:

• Bacterial infections can trigger necroptosis, serving as a host defense but also potentially exacerbating inflammation and aiding bacterial survival.
• Necroptosis is implicated in the progression and development of apical periodontitis.
• Understanding necroptosis mechanisms offers insights into AP pathogenesis.

Conclusions:

• Necroptosis is a critical inflammatory cell death pathway in apical periodontitis.
• Targeting necroptosis presents a potential therapeutic avenue for treating apical periodontitis.
• Further research is needed to fully elucidate the complex roles of necroptosis and other cell death modalities in AP.