When Quinn T. Easter looks at gum tissue under a microscope, he sees something that could change how doctors treat a painful condition affecting millions of people worldwide. Easter, a research scientist at the VCU School of Dentistry, and his team have discovered a hidden pattern in the blood vessels of patients with fast-moving oral inflammatory diseases. Their findings, published in the journal Nature Communications, point toward a potential new way to treat these conditions—and possibly other inflammatory diseases too.
The research team, working across three major institutions—VCU Massey Comprehensive Cancer Center, the VCU School of Dentistry, and the University of Pennsylvania—set out to understand why some gum diseases destroy tissue much faster than others. They compared three conditions: chronic periodontitis (common gum disease), rapidly advancing periodontitis (a more aggressive form), and peri-implantitis (inflammation around dental implants). All three cause tissue damage, but the fast-moving versions were their main focus.
At first, the researchers expected to find that harmful bacteria were the main culprit. But their analysis revealed something surprising: the amount of bacteria in the tissue did not explain the difference in how quickly disease progressed. Instead, the key lay in changes happening inside the body itself—specifically, in the blood vessels that feed the damaged tissue.
The team found that a protein called CD38 was more abundant in the blood vessel cells of patients with rapidly advancing periodontitis and peri-implantitis. CD38 is linked to inflammation, aging, and how cells produce energy. This shared pattern across two different fast-moving conditions suggests a common biological mechanism that drives rapid tissue destruction.
"This hasn't been described before in peri-implantitis," Easter said. "This is a new mechanism that could potentially change the way this disease is thought about or even treated."
To make this discovery, the researchers used and expanded a powerful tool they created earlier: the Human Periodontal Atlas, the world's leading atlas of gum disease at the cellular level. Kevin Matthew Byrd, an assistant professor at VCU School of Dentistry, compared the process to building with LEGO blocks. "Each dataset gives us another set of pieces," he said. "By putting them together, we can see which disease patterns are unique to one condition and which ones show up across related inflammatory diseases."
The team is now planning to expand their work to study more than 20 human diseases, including various cancers. By mapping how diseases share common patterns at the cellular level, they hope to find new drug targets that could help patients with multiple conditions—not just oral inflammatory diseases, but possibly other illnesses driven by similar biological mechanisms.
The discovery of this shared blood vessel pattern is more than a dental finding. It represents a new way of thinking about how inflammatory diseases work, and it offers hope that treatments developed for one condition might help patients suffering from others too.