Marie P J, Glorieux F H
Metab Bone Dis Relat Res. 1981;3(3):159-64. doi: 10.1016/0221-8747(81)90002-3.
Besides rachitic and osteomalacic bone lesions specific disturbances of intracortical bone remodeling have been described in children with vitamin D-resistant rickets (VDRR). The effects of phosphate and 1,25-dihydroxyvitamin D3 [Pi + 1,25(OH)2D] on the abnormal cortical bone remodeling were assessed by static and dynamic histomorphometric analysis of dual labeled undecalcified iliac crest bone biopsies obtained from 12 young VDRR children. Bone mineralization was markedly improved as shown by reduction of the osteoid thickness, shortening of the mineralization lag time and of the osteon calcification period. In conjunction with improved bone mineralization the extent of dual labeled bone surface was increased together with the osteoblast population, indicating that normal bone calcification requires the presence of osteoblasts. At the tissue level the birthrate of new Basic Multicellular remodeling Units (BMU) was clearly enhanced; while at the cellular level, the low calcification rate remained unchanged in most cases. The data show that treatment with Pi + 1,25(OH)2D stimulates the bone turnover in young patients with VDRR by inducing creation of new BMU after restoration of bone mineralization. Unlike the increased recruitment of new BMU caused by treatment, the persistence of a low calcification rate may reflect the existence of a primary osteoblast defect in some VDRR patients.
