In diseases characterized by bone loss — such as periodontitis, rheumatoid arthritis, and osteoporosis — there are many that scientists still do not understand. What is the role of the immune response in the process? What happens to the regulatory mechanisms that protect bone?
In a paper recently published in Scientific Reports, researchers from the Forsyth Institute and the Universidad de Chile describe a device that solved a piece of the puzzle. Looking at periodontal disease in a mouse model, scientists found that a specific type of T cell, called regulatory T cells, is beginning to behave in unexpected ways. These cells lose the ability to regulate bone loss and instead begin to stimulate inflammation.
This is important because, in many treatments studied in in-vivo models, researchers typically examine whether the number of regulatory T cells has increased. But they should make sure that those cells are actually working. “
Dr. Carla Alvarez, Principal Research Author, Postdoctoral Researcher, Forsyth Institute
T regulatory cells control the body’s immune response. In periodontal disease, bone loss occurs because the body’s immune system responds unequally to the microbial threat, causing inflammation and destroying healthy tissue. Normally, regulatory T cells help eliminate that destruction, but they appear to lose their suppressive capacity during periodontal disease.
In terms of science, this process has been studied in the field of osteoimmunology, which examines the complex interactions between the immune system and bone metabolism.
“This is an interesting tool that illustrates how bone loss occurs in periodontal disease,” said Dr. Alpdogan Kantarci, Chief of Staff at Forsyth and co-author of the paper with the Dr. Rolando Vernal, Professor from the School of Dentistry at Universidad de Chile.
In the case of periodontal disease, treatment that may target T cells could restore the normal activity regulation of T cells, not just increase their numbers.
“Unfortunately, this is not a linear process – that’s the complex part,” Kantarci says.
Periodontal disease is initiated by microbes in the mouth, making it more complex.
“The relationship between immune response and bone is not as simple,” says Alvarez. “There are several components. You have to think of a complex network of signals and participating cells.”
It is this cellular and microbial complexity that makes the disease so difficult to diagnose in humans. However, the next step of the research is to study this apparatus in humans, Alvarez says. The research team is designing a collaborative study to look at healthy and diseased patients, with a view to monitoring devices similar to those seen in an animal model.
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Magazine Reference:
Alvarez, C., et al. (2020) regulatory T cell phenotype and anti-osteoclastogenic activity in experimental periodontitis. Scientific Reports. doi.org/10.1038/s41598-020-76038-w.