The Role of Caspase-11 and Pyroptosis in the Regulation of Inflammation in Peri-Implantitis
Peri-implantitis is an important cause of oral implant failure. In the past, TLR4 and TLR2 in the Toll-like family were generally considered as the key immune recognition receptors regulating peri-implantitis. However, under the guidance of this theory, there are still some unexplainable peri-implan...
Saved in:
Published in | Journal of inflammation research Vol. 16; pp. 4471 - 4479 |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Dove Medical Press Limited
31.10.2023
Dove Dove Medical Press |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Peri-implantitis is an important cause of oral implant failure. In the past, TLR4 and TLR2 in the Toll-like family were generally considered as the key immune recognition receptors regulating peri-implantitis. However, under the guidance of this theory, there are still some unexplainable peri-implantitis symptoms. With the discovery of novel intracellular LPS receptor Caspase-11, a new understanding of inflammatory signaling and immune regulation in the development of peri-implantitis has been gained. However, the regulatory role of Caspase-11 in peri-implantitis and its crosstalk with the TLR4 pathway remain unclear. The therapeutic effect of drugs targeting Caspase-11 on peri-implantitis is still in its early stages. In view of this situation, this paper reviews the possible role of Caspase-11 in peri-implant inflammation, elaborated the entry process of LPS and the activation mechanism of Caspase-11, and analyzes the differences in Caspase-11 between commonly studied animals, mice and humans. The current research hotspots and challenges are also analyzed to provide new insights and ideas for researchers. Keywords: caspase-11, pyroptosis, inflammation, peri-implantitis |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 These authors contributed equally to this work |
ISSN: | 1178-7031 1178-7031 |
DOI: | 10.2147/JIR.S427523 |