Xiaozhe Han, DDS, MSc, PhD

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Xiaozhe Han is interested in the host immune response in periodontal disease tissue destruction, particularly in the area of osteoimmunology, the interaction between the immune system and bone metabolism and its role in inflammatory bone destruction. He focuses on a specific immune cell subset, B-cells, and their novel and significant role in ameliorating gum diseases.

“As a practicing dentist, I know how important, and at times difficult, it is for patients to keep their teeth,” said Han. “As a scientist, I am fortunate to be working behind the scenes to help my patients. My ultimate goal is for my science to provide the answers that will allow me to improve patient care.”

Periodontitis is an inflammatory disease triggered by host immune response to pathogenic microorganisms in the periodontal biofilm, leading to the loosening and subsequent loss of teeth, and increased risk for the development of various systemic conditions. Current treatments do not offer complete amelioration of periodontal tissue destruction because they do not directly address the biological causes of periodontal pathogenesis—unbalanced, overly aggressive immune responses.

There is compelling interest in developing targeted immunological interventions to treat periodontitis before it progresses to an expensive and refractory disease. B cells with a regulatory function (BREG) play a key role in immune system balance, restraining the excessive inflammatory responses by inhibiting pro-inflammatory cytokines and promoting regulatory T cell differentiation. The goal of Han’s current work is to characterize in vitro activated and expanded BREG in response to Toll-like receptor (TLR) agonists and co-stimulatory molecules, and to test these BREG to ameliorate periodontal bone resorption in vivo in a mouse model of experimental periodontal disease. His central hypothesis is that enhancing BREG function can reduce immune-mediated periodontal disease bone loss. Successful completion of this project would be expected to pave the way for systematic translational research to delineate BREG-directed amelioration of periodontitis pathogenesis.