To understand gum disease, researchers examine the abrupt behavior of T cells

In diseases characterized by bone loss – such as gingivitis, rheumatoid arthritis, and osteoporosis – scientists still don’t understand much. What is the role of the immune response in the process? What happens to the regulatory mechanisms that protect the bones?

In a paper recently published in Scientific Reports, Researchers from the Forsyth Institute and the University of Chile describe a mechanism that unlocks a piece of the puzzle. Looking at gum disease in a mouse model, the scientists found that a specific type of T cell, known as regulatory T cells, begins to behave in unexpected ways. These cells lose their ability to regulate bone loss and instead begin to promote inflammation.

“This is important because, in many treatments that have been analyzed in in vivo models, researchers usually check whether the number of regulatory T cells has increased. But they must have increased,” says Dr. Carla Alvarez, postdoctoral researcher at Forsyth and lead author of the paper. Check to see if these cells are actually working. “

Regulatory T cells control the body’s immune response. In periodontal disease, bone loss occurs because the body’s immune system responds disproportionately to the microbial threat, which causes inflammation and damages healthy tissue. Usually, regulatory T cells help suppress this destruction, but they appear to lose their suppressive capabilities during gum disease.

Scientifically, this process is analyzed in the field of bone immunology, which explores the complex interactions between the immune system and bone metabolism.

“This is an interesting mechanism that sheds light on how bone loss occurs in periodontal disease,” said Dr. Albdugan Cantaresi, Senior Task Team Member at Forsyth and co-author of the paper with Dr. Rolando Vernal, Professor from the School of Dentistry at the University of Chile.

In the case of periodontal disease, a potential treatment targeting regulatory T cells could restore the normal functioning of T cells, not just increase their numbers.

“Unfortunately, this is not a linear process – that’s the complicated part,” says Kantarci.

Gum disease is triggered by microbes in the mouth, which make it more complicated.

“The relationship between the immune response and bone is not entirely clear,” says Alvarez. “There are multiple components. You have to imagine a complex network of signals and cells that are participating.”

It is this cellular and microbial complexity that makes the disease difficult to study in humans. However, studying this mechanism in humans is the next step in the research, says Alvarez. The research team is planning a collaborative study to screen healthy and ill patients, with the goal of observing mechanisms similar to those seen in the animal model.


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