Periodontosis is a gum inflammatory disease caused by a group of oral bacteria that accumulates around the teeth. One of the main pathogens, A. actinomycetemcomitans, has been a subject of scientific research for the last decades as a bacteria that provokes the occurrence and worsening of rheumatoid arthritis.
Rheumatoid arthritis (RA) – is an autoimmune disease that affects joints, and the nature of its connection with periodontosis was mysterious and unclear until our time.
Recently, a Japanese scientific group from Tokyo Medical and Dental University released research that revealed the molecular mechanism responsible for this phenomenon.
About the Experiment
Scientists do research on the mouse model, which mimics RA in human organisms. As it known, A. actinomycetemcomitans infection increases several arthritis symptoms, including worsened limb swelling and producing a higher level of a specific protein called IL-1β.
This molecule activates the inflammasome – multiprotein complex involved in inflammatory processes in the body as a response to infections, aggravating RA.
Cell Mechanism
Then, scientists dug deeper to find a connection between two links of this process. In further research, they used mice with a deficit of caspase-11 – another protein molecule involved in the immune system reaction.
These mice show less intensive aggravation of arthritis symptoms during inflammasome activation. Such a result means that caspase-11 plays a vital role in that phenomenon, and this information may be used as the basis for future pharmaceutical research.
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