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Furthermore, mice lacking MMP-13 are reported to have increased bone volume due to decreased osteoclast formation and function, but also demonstrate enhanced osteoblast function [56]; [56].
Our observations may implicate an increase in bone turnover with increasing ALP gene expression and, thus, a decrease in bone volume due to decreasing Tb.N.
An overestimation of bone volume due to μCT was shown in analysis with [ 13] and without [ 18] implants and was explained by the definition of the threshold procedure for μCT analysis.
Leptin-deficient ob/ob mice and leptin receptor-deficient db/db mice are extremely obese, with increased vertebral trabecular bone volume due to increased bone formation, despite hypogonadism and hypercortisolism.
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Taken together, PLCγ2−/− animals have increased trabecular bone volume likely due to an osteoclast defect.
Thus, the observed differences in alveolar bone volume are due to differences in the time after ovariectomy.
Similarly high correlations of bone volume determined due to histomorphometry and μCT were approved by Chappard et al. (r = 0.93) [ 18] and Park (r = 0.85) [ 19].
An in vivo study on the designed scaffolds implanted in rat calvarium defect demonstrated significantly enhanced bone formation, evidenced by new bone volume and bone density, due to the release of BMP2 and Co ions.
The loss of bone volume and quality due to the lack of mechanical stimuli has been recognized and explained since 1870 by Wolff's Law [ 26].
In contrast to Fazzalari and colleagues [ 24], we did not observe age-related changes in bone volume fraction in controls, due to the fact that the aforementioned study analysed a broader age range of subjects.
Implant stability quotient (ISQ), ratio of bone volume to total volume (BV/TV), bone growth rate, and bone-to-implant contact (BIC) were evaluated.
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