Dentistry

Periodontal disease aggravates chronic obstructive pulmonary disease

A recent study found that bacteria associated with periodontal disease contribute to the development of chronic obstructive pulmonary disease.

Periodontal diseases aggravate chronic obstructive disease lungs

Studies have shown a connection between severe periodontal disease and the progression of chronic obstructive pulmonary disease (COPD). However, the specifics of how this relationship affects the immune system are not yet fully understood. A new study sheds light on this topic, showing that immune system cells play a critical role in the microbial link between COPD and periodontal disease.

Researchers from Sichuan University in China reported that bacteria associated with periodontal disease contribute to the development of COPD by activating two types of immune system cells: gamma delta (γδ) T cells, white blood cells that can quickly respond to infected or cancerous cells , and M2 macrophages, white blood cells that help heal wounds and reduce inflammation. They believe that focusing on this specific mechanism could offer innovative approaches to COPD prevention and management.

“By enhancing periodontal therapy and targeting it to inhibit γδ T cells and M2 macrophages, [we] may be able to help control the progression of COPD,” co-author Dr. Boyu Tang, a microbiologist at West China Stomatological Hospital of Sichuan University, said in a press release. .

COPD is an incurable disease. It is the sixth leading cause of death worldwide, according to the World Health Organization. In higher-income countries, tobacco smoking is the leading cause of COPD, while in low- and middle-income countries, both tobacco smoking and household air pollution play important roles as risk factors.

Previous studies have shown that Porphyromonas gingivalis plays an important role in periodontal disease. In the present study, the researchers demonstrated how this bacterium can worsen the progression of COPD. In one of their experiments, they infected mice in which they induced COPD with P. gingivalis and found that this led to faster progression of COPD compared to mice with COPD alone. Another experiment showed that when mice were orally exposed to P. gingivalis, the bacteria moved into and infected the lung tissue. This led to noticeable changes in the lung microbiota. Further observations showed that periodontitis promotes the proliferation of immune cells in the lung tissue.

In another experiment, researchers were able to show that P. gingivalis can activate immune cells, thereby increasing their ability to produce cytokines associated with exacerbation of COPD.

Future human studies will be conducted to confirm these results. The researchers plan to recruit patients with both COPD and periodontal disease and offer them treatment for periodontitis. Participants' lung function and immune cell counts will then be compared before and after treatment.

“Our discovery could lead to a potential new treatment strategy for COPD,” concluded Boyu Tan.