American journal of kidney diseases : the official journal of the National Kidney Foundation · 2007
Minimodeling reduces the rate of cortical bone loss in patients with secondary hyperparathyroidism.
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Yajima Aiji, Inaba Masaaki, Tominaga Yoshihiro, Ito Akemi
Аннотация
BACKGROUND: Secondary hyperparathyroidism often causes progressive cortical thinning because of increased bone resorption at the endocortical surface and increases cortical porosity because of increased resorption at the intracortical surface. Because bone formation by minimodeling has not yet been reported in cortical bone, we investigated the effects of cortical minimodeling on the decrease in rate of bone loss.
METHODS: Thirty-five patients with secondary hyperparathyroidism were enrolled. Remodeling and minimodeling parameters at the endocortical and periosteal surfaces, as well as at the intracortical surface, were measured. Relationships between remodeling parameters and minimodeling parameters at each surface were investigated by using linear regression analysis. Cortical bone specimens were classified into 3 groups according to cortical width and cortical porosity values. Relationships of minimodeling parameters at the endocortical surface with cortical width and at the intracortical surface with cortical porosity were investigated.
RESULTS: Some minimodeling parameters showed positive correlations with serum parathyroid hormone levels and remodeling parameters. Minimodeling bone volume at the endocortical surface was greater in the narrow-cortical-width group than wide-cortical-width group, possibly slowing the progression of cortical thinning. Minimodeling volume at the intracortical surface was greater in the high-porosity than low-porosity group, possibly slowing the progression of intracortical resorption space enlargement. Minimodeling of the periosteal surface was found in 1 specimen.
CONCLUSION: Results show enhanced cortical minimodeling in patients with secondary hyperparathyroidism, possibly representing the decrease in rate of cortical bone loss.
METHODS: Thirty-five patients with secondary hyperparathyroidism were enrolled. Remodeling and minimodeling parameters at the endocortical and periosteal surfaces, as well as at the intracortical surface, were measured. Relationships between remodeling parameters and minimodeling parameters at each surface were investigated by using linear regression analysis. Cortical bone specimens were classified into 3 groups according to cortical width and cortical porosity values. Relationships of minimodeling parameters at the endocortical surface with cortical width and at the intracortical surface with cortical porosity were investigated.
RESULTS: Some minimodeling parameters showed positive correlations with serum parathyroid hormone levels and remodeling parameters. Minimodeling bone volume at the endocortical surface was greater in the narrow-cortical-width group than wide-cortical-width group, possibly slowing the progression of cortical thinning. Minimodeling volume at the intracortical surface was greater in the high-porosity than low-porosity group, possibly slowing the progression of intracortical resorption space enlargement. Minimodeling of the periosteal surface was found in 1 specimen.
CONCLUSION: Results show enhanced cortical minimodeling in patients with secondary hyperparathyroidism, possibly representing the decrease in rate of cortical bone loss.