Periodontosis is one of the most widespread dental conditions in the world – according to WHO statistics, it affects about 20% of the adult population. Its main cause factor is Porphyromonas gingivalis bacteria, whose abundance (usually occurs due to poor oral hygiene) leads to systemic inflammation and, in some cases, may lead to cardiovascular disease, cancer, and increase the risk of Alzheimer's disease, entering the bloodstream.
One key factor explaining why this bacteria spreads rapidly is its unique biochemical trick, allowing it to avoid an individual's immune system. Recently, a group of Israeli scientists precisely described this molecular mechanism – let's take a look at their main conclusions.
How does it work?
There are a few key proteins involved in the process. Our organism detects P. gingivalis using Toll-like receptor 2 (TLR2), which, in turn, is associated with another protein called CD47.
The latter causes the suppression of phagocytosis, worsening the bactericidal process in the organism. Thus, in mice models lacking CD47, animals effectively cleared the pathogen.
Additionally, the increased expression of CD47 protein significantly enhances the secretion of another molecule called thrombospondin-1 (TSP-1), which protects P. gingivalis and some other periodontosis-causing bacteria from immune system reactions.
Why it's important?
Summarizing the abovementioned discoveries, we can state that P. gingivalis bacteria uses CD47 protein to avoid the organism's immune response, suppressing its detection and phagocytic functions.
This discovery may significantly contribute to periodontitis treatment – with a specific drug, pharmacists may alter the CDR47 or TSP-1 protein secretion, decreasing the pathogen's "stealth mode."
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