The etiology of the necrosis of the lunate bone is still unclear. In today's theories, the necrosis is explained by impairment of the arterial bone circulation or fracture following mechanical overloading. In this study, six specimen in different stages of the disease were investigated histologically. In all the specimens, focal necrosis was detected, but also signs of regeneration, i.e. immature bone formation. No signs of fracture were seen in all stages of the disease. These findings are not compatible with sudden interruption of arterial blood supply or fracture of the lunate bone as a primary lesion. Comparable histological patterns are known in the necrosis of the femoral head. The etiological model of necrosis of the femoral head is well investigated and postulates primary marrow hypertension, induced by impairment of the venous drainage. Our results are contradictory to the etiological theories of fracture or breakdown of the arterial blood supply as a primary lesion in Kienböck's disease, and support the assumption that the model of intraosseous hypertension is transferable to the necrosis of the lunate bone.
Skin flaps: A novel approach to medical student instruction on integumentary arterial blood supply
