Titles

Professor, Medicine

Education

Boards

Recognition

Research Interests

My lab studies mechanisms of pathological bone loss.  Most work has focused on the study of osteoclasts, the cells that resorb/remove bone to allow normal bone turnover. These cells are hematopoietic-derived cells of the monocyte lineage that differentiate in the bone microenvironment under the influence of the cytokine RANKL. OCs attach to the bone surface via integrins and form an extracellular compartment, the resorption lacuna, into which they secrete acid and proteases to degrade the organic and mineral components of bone. Activity of these cells is critical for bone homeostasis, but their abnormal activation is responsible for pathological bone loss in many settings, including osteolytic tumor metastases and infection. We use a combination of disease models, genetic mouse models, and in vitro cultures, providing a broad range of potential research projects as well as diverse technical approaches. Our current active projects include investigation of the role of the inflammasome in S. aureus-mediated osteomyelitis, and tumor-bone interactions in HTLV-1/acute T cell leukemia.

My clinical research interests include analyzing bone biopsies for studies of metabolic bone diseases such as osteoporosis and hypophosphatasia, using both qualitative and quantitative histomorphometric approaches. In addition, I work with clinicians to describe new or rare bone diseases and collaborate on basic and translational breast cancer studies.

Editorial Responsibilities

DBBS Affiliations

Selected Publications

• Myofibroblastic CAFs arising from bone-resident osteoblast precursors retain an osteolineage signature and support breast cancer progression via Osterix-mediated signaling

  Publication

• LAIR1 prevents excess inflammatory tissue damage in Staphylococcus aureus skin infection and Cutaneous T-cell Lymphoma

  Publication

• Ablation of CD38 in multiple myeloma cells leads to an aggressive phenotype in a mouse xenograft model

  Publication

• <em>Staphylococcus aureus</em> inhibits the NLRP3 inflammasome in macrophages during the early phases of intracellular infection, but not the late phases

  Publication

Assistant