Target Health Blog

The Microbiome Linked to Inflammation and Bone Loss in Gum Disease

October 22, 2018


Periodontal disease is a common disorder that affects nearly half of American adults over age 30, and 70% 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.

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.

According to a new study in mice and humans, published in Science Translational Medicine (17 October 2018), an unhealthy population of microbes in the mouth can trigger specialized immune cells that can inflame and destroy tissues, leading to bone loss associated with a severe form of gum disease. These microbiome-triggered Th17 cells switch from protective to destructive, thus may be potential treatment targets for treatment. The results suggest that these T helper 17 cells are drivers of this process, providing the link between oral bacteria and inflammation. The authors 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.

The authors also found that similar to humans, more Th17 cells accumulated in the gums of mice with periodontitis compared to healthy mice, which served as a control group. To determine if the oral microbiome might be the trigger for Th17 cell accumulation, the authors placed mice on a broad-spectrum antibiotic cocktail. Results showed that by eliminating oral microbes, prevented expansion of Th17 cells in the gums of mice with periodontitis while leaving other immune cells unaffected. According to the authors, this suggested that an unhealthy bacterial population triggers Th17 cell accumulation. Next, the authors wanted to know if blocking Th17 cells could lessen periodontal disease. When the authors genetically engineered mice to lack Th17 cells, or gave the animals a small-molecule drug that prevents Th17 cell development, similar outcomes of reduced bone loss from periodontitis were observed. RNA analysis showed the Th17-blocking drug led to reduced expression of genes involved in inflammation, tissue destruction, and bone loss, suggesting that Th17 cells may mediate these processes in periodontitis.

Finally, the authors studied a group of 35 patients at the NIH Clinical Center with a gene defect causing them to lack Th17 cells. The authors reasoned that if Th17 cells are as important to periodontitis as the animal studies suggested, not having Th17 cells should protect against gum disease. Results showed that these patients were indeed less susceptible to periodontitis, and had less inflammation and bone loss compared to age- and gender-matched volunteers.

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