Dentistry

Recent study reveals potential new treatment for periodontal disease

British scientists have identified the type of cells that regulate the inflammatory process that occurs in periodontal disease.

Recent research revealed a potential new treatment for periodontal disease

Although understanding of the causes and potential treatments for periodontal disease has advanced significantly in recent decades, new research continues to expand these horizons. A study by King's College London has shed light on the role that a particular cell type plays in the progression of this condition and how this may provide a therapeutic intervention.

The research team was able to identify and describe the role of a cell type known as telocytes in regulating the inflammatory process that occurs in periodontal disease. According to the authors, telocytes are involved in direct cell-to-cell communication between macrophages, a type of white blood cell involved in the response to infection or the accumulation of damaged and dead cells. Macrophages that stimulate the inflammatory response are known as M1 macrophages, while M2 macrophages counteract inflammation and stimulate tissue repair. The balance between M1 and M2 macrophages is critical for effective regulation of the body's immune response.

Using single-cell RNA sequencing and cell-based assays, the researchers determined the role of telocytes in regulating the balance of M1-M2 macrophages in periodontal disease and demonstrated their natural ability to shift macrophages from the M1 state to the M2 state. This ability will facilitate these transitions and may provide a possible strategy for the future treatment of periodontal disease as well as other inflammatory conditions such as arthritis.

“My hope is that this research can not only lead to a better understanding of periodontal disease, but also serve as a stimulus for others to explore the potential role of telocytes in other tissues,” said Dr. Paul Sharpe, professor of craniofacial biology and research co-author.