Bone is a dynamic tissue continuously remodeled by osteoblasts, osteoclasts, immune cells, vascular signals, and systemic metabolic factors. Our lab studies how bone remodeling and mineral metabolism are regulated under physiological and pathological conditions, with a particular focus on jawbone pathology and medication-related osteonecrosis of the jaw (MRONJ).

Key Questions

• Why does MRONJ preferentially occur in the jawbone?

• How do antiresorptive and antiangiogenic medications alter bone remodeling and wound healing?

• How do vascular dysfunction, immune dysregulation, infection, and hypoxia contribute to jawbone necrosis?

• Can we identify biomarkers or therapeutic targets to predict, prevent, or treat MRONJ?

• How do systemic metabolic and neuro-immune factors regulate bone disease?

Approaches

• Osteoblast and osteoclast differentiation assays

• Molecular and cellular studies of bone remodeling

• Animal models of jawbone disease and bone pathology

• Histology, bone imaging, and tissue-based analysis

• Serum biomarker and human data analysis

• Human genetics-guided mechanistic studies

Research Topics

• Mechanisms underlying MRONJ development

• Bone remodeling and mineral metabolism

• Osteoblast and osteoclast biology

• Vascular and immune regulation of jawbone disease

• Hypoxia, infection, and impaired wound healing in bone pathology

• Biomarker and therapeutic target discovery for MRONJ

• Systemic regulation of bone metabolism

• Cholesterol sulfate and bone biology

Keywords

MRONJ, jawbone necrosis, bone remodeling, mineral metabolism, osteoblast, osteoclast, angiogenesis, immune regulation, hypoxia, wound healing, biomarker, therapeutic target