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Analysis of NT3.catK mice demonstrated that, at baseline, the number of OCs was increased, as were serum levels of CTX, a marker of OC activity, indicating that bone resorption was increased.
In addition, the serum level of TRAP, which is responsible for enhanced osteoclastogenesis and activation of mature osteoclasts for bone resorption, was increased in the OVX group, but JSOG-6 treatment significantly reduced TRAP activity in a dose-dependent manner (P < 0.01).
In these experiments, the serum concentration of cross-linking telopeptide of type 1 collagen (a marker of bone resorption) was increased whereas the activity of serum alkaline phosphatase (a marker of bone formation) was decreased, indicating a disturbance of normal bone metabolism due to Cd exposure.
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Histomorphometric analysis revealed that osteoblast maturation and bone formation are disturbed in Col1a1-Krm2 mice, whereas bone resorption is increased.
Histomorphometric analysis of femoral trabecular bone confirmed that the number of OCs per bone surface (N.Oc/BS) and the OC surface per bone surface (Oc.S/BS), two indices of bone resorption, were increased by cPTH in WT but not in TNF −/− mice (Fig. 5d,e).
Histomorphometric analysis of femoral trabecular bone revealed that the number of OCs per bone surface (NOc/BS) and the OC surface per bone surface (Oc.S/BS), two indices of bone resorption, were increased by cPTH to a greater amount in control mice than in PPRT cells −/− mice (Fig. 2f,g).
Bone resorption is increased in RA.
Bone resorption is increased by the TZD in vitro (9).
Bone resorption is increased in RA and AS.
In RA, the former scenarios appear to be relevant since bone resorption is increased and bone formation is decreased.
In patients with RA, markers of bone resorption are increased in comparison with controls [ 51].
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