A crucial role for thiol antioxidants in estrogen-deficiency bone loss
J. Clin. Invest. Jenny M. Lean, et al. 112:915 doi:10.1172/JCI18859 [Go to this article.]

Figure 3
BSO induces bone loss in mice. (a and b) Representative sections of femora from a control mouse and a mouse injected with BSO (2 mmol/kg) twice a day for 3 weeks, showing loss of trabecular bone in BSO-treated mouse. (c) BSO caused substantial and significant loss of bone. (d–f) Bone loss was accompanied by an increase in the number of osteoclasts per millimeter of bone surface, the percentage of bone surface covered by osteoclasts, and the percentage of bone surface that showed an eroded surface. (g and h) BSO also significantly increased the number of osteoblasts covering bone surfaces and the percentage of bone surface covered by osteoblasts. (i–k) Dynamic parameters of bone formation: BSO caused a significant increase in the percentage of bone surface that was actively forming bone matrix, as judged by the percentage of surface that incorporated double calcein labels (i). MAR (mineral apposition rate, measured as the distance of separation of the double labels) was not significantly increased (j). There was an overall increase in the quantity of bone formed per unit of time (bone formation rate per unit of bone surface) (k). *P < 0.05 versus vehicle-injected control; n = 6 mice per group. Data expressed as mean ± SEM. Total glutathione fell significantly (P < 0.01) in the bone marrow of BSO-treated mice from 14.5 ± 1.1 to 6.8 ± 0.1 nmol/mg protein. There was no significant change in body weight in either group of mice during the experimental period. Uterine weights of BSO-treated mice did not differ significantly from those of control mice. Oc, osteoclast; ES/BS (%), percentage of bone surface that shows an eroded surface appearance; Ob, osteoblast; dLS/BS, proportion of bone surface that shows fluorochrome double-labeling; BFR/BS, bone formation rate expressed as the volume of bone formed per unit of bone surface.