The group is studying the pathophysiology of osteoporosis and in particular the regulation of bone formation with focus on male idopathic osteoporosis (MIO).
In one of the largest bone- histomorphometry studies published, we showed that MIO patients had thin bone structural units indicating a formative dysfunction. In primary osteoblast cultures from patients with MIO we demonstrated inhibited responses to anabolic stimuli as PTHrP and calcitriol.
We have studied the association between bone mineral density, bone histomorphometry and circulating amino acids and anabolic hormone such as GH/IGF-1. Tryptophan in reed blood cells was positively correlated with bone mineral density and bone-histomorphometic parameters of bone formation. Reed blood cells may serve as a model-system for intracellular amino-acid levels. MIO patients had low levels of tryptophan in reed blood cells but normal plasma levels. In the current project we evaluate tryptophan transport in MIO and healthy controls. Tryptophan, a precursor for serotonin, has emerged as an important regulator in bone. Differences in tryptophane metabolism may influence bone mass.
Clinical studies on on bone metabolic disorders, specially vitamin D deficiency.