Multiple bacteria types found to contribute to bone loss in gum disease

In a previous study, the researchers injected lipopolysaccharide (LPS) from Gram-negative bacteria into mice engineered without the gene that produces molecules that gather at sites of damaged tissue. Without these molecules, called prostaglandin E2 (PGE2), the LPS failed to induce bone loss. This suggested, Inada said, that PGE2 is required for periodontitis to progress.

"LPS is considered to be a dominant pathogen causing inflammatory bone resorption in periodontitis," Inada said. "On the other hand, Gram-positive bacteria have been known to contribute to the inflammation of the periodontal gums in the initial phases of periodontitis; however, there was little evidence to show that these pathogens contribute to the induction of inflammatory bone resorption in the late phase of periodontitis."

It comes down to bone remodeling, according to Inada. At what point does cell death from the infection outpace the body's effort to create new bone cells?

"Several reasons could be counting and explaining on these phenomena, " Inada said.

In the case of LPS in the PGE2-deficient mice, the balance stayed in favor of bone formation. But when the researchers introduced lipoteichoic acid (LTA), a major component of the cell wall in Gram-positive bacteria, the balance tipped to bone resorption. The researchers injected mice with periodontitis with LTA and found that it increased the amount of PGE2, resulting in bone resorption. They also saw that Gram-positive bacteria proliferated at a higher rate than Gram-negative bacteria and they preferred to occupy the depths of the teeth pockets — suggesting a more potent dose of LTA closer to the site of bone lose, according to Inada.

"Our goal is to clarify the crosstalk of Gram-positive and -negative bacteria for the pathogenesis and progression of periodontal bone loss," Inada said. "The understanding of the mechanisms will contribute to developing novel drugs for the treatment of periodontal bone loss."

https://www.nature.com/articles/s41598-021-92744-5