Research Profile

Bone is a dynamic organ system exhibiting continual formation and reformation of resorbed tissue (remodeling). These processes are dependent on the metabolic activity of the constituent cells of bone: osteoblasts form bone, osteocytes maintain bone, and osteoclasts resorb bone.

Nearly all bone diseases, or pathologies in fracture healing, manifest aberrations in bone matrix production and/or mineralization. Cytokines and hormones tightly regulate these cellular activities in bone, in both normal and pathologic states. Parathyroid hormone (PTH) is a major regulator of bone formation, remodeling and fracture healing. Its endocrine function in vivo is to maintain Ca2+ levels in the blood by reabsorbing renal Ca2+ and releasing Ca2+ from bones.

As a therapeutic agent, PTH also manifests somatotrophic effects on bone formation and is one of the most promising prospects as an agent for reversing bone loss (osteopenia) and treating severe osteoporosis.

Our laboratory focuses on the regulation of osteoblast function by PTH. Using cell culture and animal models, we have discovered that PTH can dramatically affect an osteoblast’s ability to produce select matrix macromolecules, alter its ability to assemble these macromolecules into an extracellular matrix, and regulate its mineralization of this matrix.

Our aim is to define the molecular mechanisms operating in these biological responses. This research will advance our knowledge of bone growth and repair and may offer new strategies for using PTH to treat bone disorders.