Common medicines reverse devastating gum disease

Scientists have found that drugs approved for treatment of multiple sclerosis and psoriasis have shown great hope in combating periodontitis, one of the main causes of tooth loss worldwide.

Researchers from Wenzhou Medical University found that in experimental models of gum disease, dimethyldimethyl fumarate (DMF) significantly reduces bone loss and inflammation by improving the cellular “cleaning up” mechanism and metastasizing immune responses to healing rather than destruction.

“The ability of fumarate dimethyl to refine macrophage polarization through mitochondria is a game changer for changing periodontal therapy,” said Dr. Shengbin Huang, corresponding author of the study. “By targeting the mitochondrial protein TUFM, we found a molecular switch that controls the inflammatory response in gingival tissue. These insights could redefine how we deal with chronic inflammatory conditions outside the mouth.”

Periodontitis affects millions of millions around the world and occurs when simple chewing gum inflammation progresses to destroy the support structure around the teeth. Traditional treatments are primarily about removing bacterial plaques and administering antibiotics, which usually fail to stop the disease from progressing.

This breakthrough was published in the International Journal of Oral Sciences, which protects the dual capacity of mitochondria (cell power) with the dual capacity of DMF and changes the behavior of macrophages, the behavior of macrophages, and important immune cells can promote inflammation or promote healing.

In healthy gums, there is a balance between proinflammatory (M1) and healing (M2) macrophages. During periodontitis, this balance is pushed in large quantities towards destructive M1 cells. The researchers demonstrate that DMF helps restore this balance by protecting a key protein called TUFM, which keeps cells healthy.

When TUFM is depleted, DMF loses its protective effect, confirming the critical role of this protein in the success of the treatment. The drug appears to play a role in the cells by preventing TUFM degradation, allowing it to coordinate a cell cleaning process called mitochondria, which removes damaged mitochondria.

What makes this discovery particularly promising is that DMF has approved the FDA in other diseases, which may accelerate its clinical pathway for periodontitis. Future applications may include topical formulations directly applied to affected gingival tissue to minimize any systemic side effects.

In addition to saving teeth, these findings may have a wider impact. The cellular mechanisms targeted by DMF are common for many inflammatory diseases, suggesting potential applications in diseases such as rheumatoid arthritis or inflammatory bowel disease.

For patients currently suffering from periodontitis, this study offers hope that treatment options may soon exceed the limitations of the current approach. A drug that addresses potential imbalances rather than just fighting bacteria can alter the outcome of this common but devastating oral disease.

Related