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Effect of Vitamin K 2 on Cortical and Cancellous Bones in Orchidectomized and/or Sciatic Neurectomized Rats
Author(s) -
Iwamoto Jun,
Yeh James K,
Takeda Tsuyoshi
Publication year - 2003
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.2003.18.4.776
Subject(s) - medicine , endocrinology , vitamin d and neurology , anatomy
We examined the effect of vitamin K 2 on cortical and cancellous bones in orchidectomized and/or sciatic neurectomized rats. Ninety male Sprague‐Dawley rats, 3 months of age, were randomized by stratified weight method into nine groups with 10 rats in each group: baseline control (BLC), age‐matched intact control (IN), IN+vitamin K 2 administration (K), orchidectomy (ORX), ORX+K, unilateral sciatic neurectomy (NX), NX+K, ORX+NX (ONX), and ONX+K. Vitamin K 2 (menatetrenone) was administered orally twice a week at a dose of 30 mg/kg each. After 10 weeks of feeding, the tibial shaft and proximal tibia were processed for cortical and cancellous bone histomorphometric analyses, respectively. An ORX‐induced reduction in maturation‐related cortical bone gain and ORX‐induced cancellous bone loss were attributable to increased endocortical and trabecular bone turnover, respectively. NX‐ and ONX‐induced reductions in maturation‐related cortical bone gain were attributable to decreased periosteal bone formation and increased endocortical bone turnover, while NX‐ and ONX‐induced cancellous bone loss was attributable to increased bone resorption and decreased bone formation. ORX‐induced cancellous bone loss was more pronounced when combined with immobilization. Vitamin K 2 administration did not significantly alter any parameters in IN rats. Vitamin K 2 administration in ORX rats suppressed endocortical bone resorption and trabecular bone turnover, retarding a reduction in maturation‐related cortical bone gain and cancellous bone loss. This effect on cancellous bone loss was primarily because of prevention of a reduction of trabecular thickness. Vitamin K 2 administration in NX and ONX rats suppressed bone resorption and stimulated bone formation (mineralization), with retardation of a reduction of trabecular thickness without any significant effect on cancellous bone mass, and suppressed endocortical bone resorption, retarding a reduction in maturation‐related cortical bone gain. The present study provides evidence indicating that vitamin K 2 has the potential to suppress bone resorption or bone turnover and/or stimulate bone formation in vivo in ORX and/or NX rats.