2024-09-21 00:12:52
The inflammatory effects of bacteria associated with periodontitis can extend well beyond the mouth and cause systemic episodes, activating the inflasome and thus contributing to the progression of rheumatoid arthritis which affects the entire joints of the human body.
Periodontitis is a chronic inflammatory disease caused by a bacterial infection in the periodontium leading to the secretion of numerous proinflammatory cytokines. It is one of the most common dental diseases in the world which, if left untreated, can end up causing tooth loss.
Furthermore, the inflammatory effects of periodontal bacteria can extend well beyond the mouth and cause systemic events. This has been demonstrated by several clinical studies, establishing that the periodontal pathogen Aggregatibacter-actinomycetemcomitans-(A.actinomycetemcomitans) It is closely related to the onset and worsening of rheumatoid arthritis (RA), which affects the joints.
In this context, a research group from Tokyo Medical and Dental University (TMDU) (Japan) decided to demonstrate the close link between intraperitoneal infection with this bacterium associated with periodontitis and rheumatoid arthritis.
Swelling of the extremities
To this end, the researchers carried out preliminary experiments to confirm whether infection had occurred A. actinomycetemcomitans influenced arthritis in mice. To do this, they used the mouse model of collagen antibody-induced arthritis, which is a well-established experimental model that mimics several aspects of rheumatoid arthritis in humans. They found that infection with this specific bacterium caused increased swelling of the limbs, cellular infiltration into the joint lining, and higher levels of the inflammatory cytokine interleukin-1β (IL-1β) within the limbs.
In particular, these worsening symptoms of rheumatoid arthritis could be suppressed by administering a chemical agent called clodronate that depletes macrophages, a type of immune cell. This demonstrated that macrophages were somehow involved in the aggravation of rheumatoid arthritis caused by the infection.
Further investigations with mouse bone marrow-derived macrophages revealed that infection by A. actinomycetemcomitans increased production of IL-1β. This in turn triggered the activation of a multiprotein complex known as the inflammasome, which plays a key role in initiating and modulating the body’s inflammatory response to infections.
The researchers added an additional piece to this puzzle by using mice deficient in caspase-11. In these animals, inflammasome activation is due to A. actinomycetemcomitans has been cancelled. More importantly, caspase-11-deficient mice showed less deterioration of arthritis symptoms, indicating the important role caspase-11 plays in this context.
“Our research findings provide new insights into the link between periodontal pathogenic bacteria and arthritis exacerbation through inflammasome activation, offering important insights into the long-debated relationship between periodontal disease and systemic periodontal disease.” said Professor Toshihiko Suzuki, one of the study’s lead authors.
The findings of this research could pave the way for advances in clinical treatments for rheumatoid arthritis induced by rheumatoid infection A. actinomycetemcomitans. “Our suggestion of inhibiting inflammasome activation could attenuate the spread of inflammation to joints, resulting in recovery from arthritis symptoms,” said lead author Dr. Tokuju Okano.
The result of this work, published in the ‘Journal of Oral Science’, it could contribute, according to the authors, to the development of treatment strategies not only for arthritis, but also for other systemic diseases, such as Alzheimer’s disease, apparently also linked to pathogenic periodontal bacteria. Rv: Ana Mera, pharmacist. Barcelona
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