Systemic rheumatic and autoimmune diseases such as inflammatory arthritides are characterized by tissue damage at the site of inflammation that is often responsible for the signs and symptoms of the disease. In arthritis, the target organ primarily is the joint, and inflammatory damage to the joint is irreversible, contributing to reduced quality of life even in the absence of active disease.
In our group, we analyze the mechanisms leading to joint inflammation and subsequently joint destruction, with an emphasis on the contribution of myeloid cells in that process. One of our major areas of interest is osteoclast development and function.
In addition, we are interested in bone homeostasis and regeneration, both in the context of arthritis as well as systemically.
We mostly employ experimental model systems, but also analyze patient derived material to gain insight into mechanisms leading to the pathogenesis of rheumatic diseases.