Baku, February 24, AZERTAC

In a study that could reshape conventional approaches to both periodontal and systemic health, scientists said on Monday they have uncovered how a bacterium responsible for periodontitis evades the immune system, persists inflamed tissue, and contributes to other diseases, according to The Press Service of Israel (TPS-IL).

Periodontitis is a severe gum infection caused by poor oral hygiene, leading to plaque and tartar buildup that inflames the gums. If untreated, it can cause gum recession and tooth loss. In its early stage, it’s called gingivitis, but if it progresses to periodontitis, it can become linked to other health conditions like heart disease, diabetes, Alzheimer’s and certain types of cancer.

According to the National Institute of Dental and Craniofacial Research, approximately 42.2% of adults aged 30 and older in the United States have some form of periodontitis, with 7.8% experiencing severe periodontitis. Globally, the prevalence of periodontal diseases varies, affecting about 20-50% of the population, as reported by the National Center for Biotechnology Information.

In a groundbreaking Hebrew University study led by Prof. Gabriel Nussbaum, researchers showed how Porphyromonas gingivalis (P. gingivalis) uses a protein CD47 to suppress immune responses, allowing it to persist in inflamed tissues and potentially contribute to other diseases. CD47, known as a “don’t eat me” signal in cancer cells, prevents the immune system from attacking the bacterium.

Additionally, P. gingivalis induces the production of thrombospondin-1 (TSP-1), a protein that further suppresses immune responses, particularly by inhibiting neutrophil activity. This dual immune evasion strategy enables the bacterium to persist in inflamed gum tissue, contributing to chronic periodontal disease and increasing the risk of systemic diseases.

“Our findings suggest that P. gingivalis uses CD47 to hijack immune signaling pathways, effectively disabling the host’s ability to clear the infection,” said Nussbaum. “This mechanism helps explain why this bacterium thrives in inflammatory environments, leading to chronic periodontitis and potentially contributing to other systemic diseases.”

The discovery suggests that targeting CD47 or thrombospondin-1 could enhance immune function and offer new strategies for treating periodontal disease and mitigating its related conditions.

Experiments using both in vitro and in vivo models showed that blocking CD47 or TSP-1 significantly enhanced bacterial clearance by the immune system. Mice lacking CD47 were able to eliminate P. gingivalis more effectively, suggesting that targeting this immune evasion pathway could be a promising strategy for treating periodontitis.

The study was recently published in the peer-reviewed PNAS journal.

“Current periodontal treatments focus on reducing bacterial load mechanically, but understanding how these bacteria evade immune responses opens new therapeutic possibilities,” Nussbaum added.

The potential applications of this research are far-reaching. For periodontal health, targeting CD47 or TSP-1 could lead to new treatments that improve immune function and bacterial clearance, offering alternatives to current methods.

Given the links between periodontitis and systemic conditions such as cardiovascular disease and Alzheimer’s, this approach could also help reduce the risk of these diseases.

Furthermore, the identification of CD47 and TSP-1 as key players in immune evasion could pave the way for the development of immune modulation therapies, not just for periodontitis, but for other chronic infections that involve immune suppression.