Researchers Identify Immune Culprits Linked to Bone Loss in Gum Disease
Unhealthy microbes in the mouth trigger immune cells that inflame and destroy tissues leading to bone loss associated with gum disease, according to a new study.
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An unhealthy population of microbes in the mouth triggers specialized immune cells that inflame and destroy tissues, leading to the type of bone loss associated with a severe form of gum disease, according to a new study in mice and humans. The research, led by scientists from NIDCR and the University of Pennsylvania School of Dental Medicine, could have implications for new treatment approaches for the condition. The findings appeared online Oct. 17 in Science Translational Medicine.
Periodontal disease is a common disorder that affects nearly half of American adults over age 30, and 70 percent of adults 65 and older. In those affected, bacteria trigger inflammation of the tissues that surround the teeth, which can lead to loss of bone and teeth in an advanced stage of the disease called periodontitis.
“We’ve known for years that microbes stimulate inflammation,” said study senior author Dr. Niki Moutsopoulos, a clinical investigator at NIDCR. “Removing bacteria by tooth-brushing and dental care controls inflammation, but not permanently, suggesting there are other factors at play. Our results suggest that immune cells known as T helper 17 cells are drivers of this process, providing the link between oral bacteria and inflammation.”
Moutsopoulos and colleagues observed that T helper (Th) 17 cells were much more prevalent in the gum tissue of humans with periodontitis than in the gums of their healthy counterparts, and that the amount of Th17 cells correlated with disease severity.
Th17 cells normally live in so-called barrier sites—such as the mouth, skin and digestive tract—where germs make first contact with the body. Th17 cells are known to protect against oral thrush, a fungal infection of the mouth, but they are also linked to inflammatory diseases such as psoriasis and colitis, suggesting that they play dual roles in health and disease.