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Ujjal Bhawal – 講題摘要

Prof. Ujjal Bhawal  (Bangladesh)

EDUCATIONAL BACKGROUND

1987-1993             Dhaka Dental College, Bangladesh(DDS)
1997-2001             Hiroshima University Graduate School of Dentistry, Japan(Ph.D. from Hiroshima University)

RESEARCH AND PROFESSIONAL EXPERIENCE
2004-2006             Research Fellow, Department of Biochemistry, Hiroshima University  School of Dentistry, Japan
2006-present         Researcher, Department of Molecular Pathology, Nara Medical University,Japan
2006-2011             Research Fellow, Kanagawa Dental University, Japan
2011-present         Visiting Lecturer, Kanagawa Dental University, Japan
2011-present         Assistant Professor, Department of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo, Japan

 

Topic :

Low Level Laser Therapy (LLLT): Drug free pain relief and better healing

 

Abstract :

OBJECTIVE: Clinical applications for low-level laser therapy (LLLT) include xerostomia, wound healing, and treatment for various forms of inflammation. However, the mechanisms of cell proliferation and anti-inflammatory effects induced by LLLT are still poorly understood. Diabetes can lead to a marked dysfunction of the secretory capacity in salivary glands.

RESEARCH DESIGN: Experimental diabetic rat model was induced by administration of streptozotocin. Twenty-nine days after the induction, the submandibular glands (SMG) of experimental groups (DL) were irradiated with diode laser with energy density of 20J/cm² (660nm/70mW). The animals were euthanized, and the SMG was dissected 24 hours after irradiation.

RESULTS: LLLT reduced the inflammation markers, HMGB1 and AGE, and increased proliferation of salivary glands cells through cAMP/CREB signaling pathway, mediated by p42/44 MAPK signaling. LLLT also decreased TNF-α-induced apoptosis in diabetic salivary glands via caspase-3 pathway.

CONCLUSIONS: These findings elucidate a mechanism for LLLT that function in cell proliferation and survival of diabetic rat SMG via cAMP/CREB signaling pathway, mediated by p42/44 MAPK signaling. Taken together, LLLT may have a great therapeutic potential in the treatment of degenerative changes in diabetic salivary glands, by attenuating inflammation and cell death. Furthermore, increasing proliferation, that can contribute to improve the salivary gland function in diabetes.