Caspase-3 and gasdermin E detection in peri-implantitis

Area of Science:

• Oral biology
• Cellular pathology
• Immunology

Background:

• Peri-implantitis is a major cause of dental implant failure, but its underlying mechanisms are not fully understood.
• Pyroptosis, a pro-inflammatory programmed cell death, is increasingly recognized in oral infectious diseases.

Purpose of the Study:

• To investigate the role of cleaved caspase-3 and gasdermin E (GSDME) in peri-implantitis.
• To establish an in vitro model of pyroptosis in human gingival epithelium cells.

Main Methods:

• Analysis of pyroptosis markers (caspase-3, GSDME, IL-1β) in inflamed peri-implantitis biopsies.
• Induction of pyroptosis in human gingival epithelium cells (HGECs) using tumor necrosis factor-α (TNF-α).
• Inhibition of pyroptosis using a caspase-3 inhibitor (Ac-DEVD-CHO) or GSDME small interference RNA (siRNA).

Main Results:

• Elevated levels of pyroptosis markers (caspase-3, GSDME, IL-1β) were observed in peri-implantitis tissues compared to controls.
• TNF-α induced pyroptosis morphological changes and marker upregulation in HGECs.
• Inhibiting caspase-3 or GSDME attenuated TNF-α-induced pyroptosis in HGECs.

Conclusions:

• The caspase-3/GSDME pathway is a key mediator of TNF-α-induced pyroptosis in human gingival epithelium cells.
• High expression of caspase-3 and GSDME is evident in peri-implantitis.
• Targeting the caspase-3/GSDME pathway presents a novel therapeutic strategy for peri-implantitis.