Obesity Found to Fuel Periodontal Disease

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Chronic inflammation resulting from obesity may trigger osteoclast production and bone tissue breakdown, including the alveolar bone that holds teeth in place, according to a new animal model study.

The study, reported in the Journal of Dental Research, found that excessive inflammation caused by obesity raises the number of myeloid-derived suppressor cells (MDSC), a group of immune cells that increase during illness to regulate immune function. MDSCs, which originate in the bone marrow, develop into a range of different cell types, including osteoclasts.

Bone loss is a major symptom of periodontal disease which may ultimately lead to tooth loss. Periodontal disease affects more than 47% of adults 30 years and older, according to the Centers for Disease Control and Prevention.

“Although there is a clear relationship between the degree of obesity and periodontal disease, the mechanisms that underpin the links between these conditions were not completely understood,” said Keith Kirkwood, DDS, PhD, professor of oral biology in the UB School of Dental Medicine.

“This research promotes the concept that MDSC expansion during obesity to become osteoclasts during periodontitis is tied to increased alveolar bone destruction. Taken together, this data supports the view that obesity raises the risk of periodontal bone loss,” said Kyuhwan Kwack, PhD, postdoctoral associate in the UB Department of Oral Biology.

In the study, two groups of mice were fed different diets over the course of 16 weeks: one group a low-fat diet that derived 10% of energy from fat, the other group a high-fat diet getting 45% of energy from fat.

The high-fat diet group developed obesity, had more inflammation and a greater increase of MDSCs in the bone marrow and spleen compared to the low-fat diet group. The high-fat diet group also developed a significantly larger number of osteoclasts and lost more alveolar bone, which holds teeth in place.

Additionally, in the group fed a high-fat diet, the expression was significantly elevated for 27 genes tied to osteoclast formation.
The findings may help reveal the mechanisms behind other chronic inflammatory, bone-related diseases that develop concurrently with obesity, such as arthritis and osteoporosis, Prof Kirkwood said.

Source: University at Buffalo