Study identifies gingival cells that can protect against periodontitis.
PHILADELPHIA, U.S./CHENGDU, China: Periodontitis remains the sixth most prevalent infectious disease worldwide, and the most common cause of tooth loss despite significant advancements in oral health care. A new cell type discovered in the gingival epithelium that helps protect against harmful bacteria has renewed the interest in the immunological regulation of periodontal diseases.
Periodontitis is a chronic inflammation of the tooth-supporting tissues induced by a bacterial infection. Recent studies have shown that periodontitis results from a condition known as polymicrobial dysbiosis, which disturbs the ecologically balanced oral microbiota needed for maintaining normal periodontal homeostasis. The host innate immune system remains highly active in order to maintain the homeostasis in healthy periodontal tissue; however, an imbalance or disruption in innate immunity also contributes to the destruction of periodontal tissue. The host-microbiota interactions that determine periodontal homeostasis are complex and remain poorly defined. We have very limited knowledge of the specific host receptors that detect pathogenic oral bacteria.
However, this study appears to have taken us closer to the point of understanding the receptors and molecules that can influence the onset of periodontitis and its management.
Researchers from Monell Chemical Senses Center, a nonprofit independent scientific institute, collaborated with the scientists from Sichuan University in Chengdu in China and examined the gingivae of mice, where they found a cell type called solitary chemosensory cells (SCCs) that expressed different types of taste receptors as well as the protein gustducin. SCCs, which have previously been found in the urinary tract, the gut and the nasal cavities, function by sensing irritants and bacteria.
The study showed that when the researchers genetically removed gustducin and/or SCCs from the mice’s gingivae, often pathogenic oral bacteria quickly grew in numbers, resulting in periodontitis. In contrast, when they stimulated the bitter taste receptors in SCCs, it promoted the production of antimicrobial molecules.
Overall, mice without gustducin in their SCCs harboured more potentially harmful oral microbiome than those with gustducin present in their SCCs. Most importantly, the researchers identified these differences in oral flora compositions much before any periodontal bone loss occurred, which implies that the presence or absence of gustducin in SCCs could be regarded as a forerunner to periodontitis and help us in the early identification of the disease.
“Our study adds to a growing list of tissues we now know contain SCCs and indicates that the common molecular pathways in gum SCCs are involved in the regulation of oral microbiota,” said Dr Marco Tizzano, a researcher & the co-author of this study at Monell Chemical Senses Center. “In the absence of taste signalling in the gums, the oral microbiome changed in mice without gustducin.”
Topical treatment with bitter-tasting denatonium could increase the expression of antimicrobial
peptides against ligature-induced periodontitis in gustducin positive mice, and not in others.
The research team, based on this study and other unpublished work relating to humans, has suggested that periodontal SCCs in humans may play a similar regulatory role in regard to our own oral microbiomes.
The study, titled “Gingival solitary chemosensory cells are immune sentinels for periodontitis,” was published online on Oct. 3, 2019, in Nature Communications.