The long term goal of The Sasaki Lab is the development of novel therapeutic approaches for the prevention and treatment of inflammation-associated diseases. Also, our laboratory will contribute to students/residents for their acquisition of scientific knowledge through our research.
The goal of our research is to develop novel therapeutic approaches for the prevention and treatment of inflammation-associated diseases and to provide better environment for wound healing and tissue regeneration. We are interested in 1) understanding how innate immunity regulates the development and healing of dental inflammatory diseases; and 2) how cytokines, damage-associated molecular patterns, and hypoxia-inducible factors are involved in these processes.
The innate immune system senses invading microbial pathogens and also endogenous damage-associated molecules. The innate immune system plays crucial roles in induction and resolution of inflammation. We are interested in the role of Toll-like receptors (TLRs) and their crosstalk, in particular TLR2 and TLR4.
Apical and marginal periodontitis are infection-induced inflammatory diseases. Therefore, to date, most researches focused on the details of host-microbial interaction. However, there is increasing interest in damage-associated molecular patterns (DAMPs), including HMGB1 (high-mobility group box 1), S100A8, S100A9, and SAA (serum amyloid A), which are endogenous molecules released by damaged/necrotic host cells. We test a hypothesis SAA, produced in response to dental infections, exacerbates dentoalveolar bone destruction, and furthermore contributes to systemic inflammation and its sequellae in obesity/type 2 diabetes.
In marginal and apical periodontitis, inflammation and bone destruction are stimulated by various cytokines that are induced by infection rather than by direct interaction of bacteria with bone-eating osteoclasts and other host cells. These mediators help to fight with infection, but failure of bacteria clearance will lead to the unwanted destruction of periodontal tissue by these mediators. We investigate the functional role of cytokines in dental inflammations.
Hypoxia (low oxygen level) is an important feature during infections and affects the host defence mechanisms largely through the activation of hypoxia-inducible factor 1 (HIF-1). At the same time, HIF-1 mediates pro-healing responses including accelerated bone regeneration, improved resolution of inflammation and wound healing. We research into the importance of HIFs in dental inflammations.
Dr. Hajime Sasaki received his DDS in 1989 and Ph.D in 1998 from the Iwate Medical University (Morioka, Japan). He took a postdoctoral trainee position at the Forsyth Dental Center (Boston, MA) and built his academic career in there until February, 2017. His last appointment in Forsyth was an Associate Member of the Staff in the Department of Immunology and Infectious Diseases. He started his carrier at the University of Michigan School of Dentistry from March, 2017.
The most recent publications are reported below.
2018; Journal of dental research; Hirai K | Furusho H | Kawashima N | Xu S | de Beer MC | Battaglino R | Van Dyke T | Stashenko P | Sasaki H.
2018; International journal of oral science; Hirai K | Furusho H | Hirota K | Sasaki H