. Author manuscript; available in PMC: 2016 Mar 1.

Published in final edited form as: J Bone Miner Res. 2015 Mar;30(3):539–549. doi: 10.1002/jbmr.2372

Table 2.

	N, #	MAR, um/day	MS/BS, %	BFR/BS, um³/um²/year
CKD High PTH
CTL	11	2.2 ± 1.1	31 ± 8	280 ± 156
Scl-Ab	12	2.8 ± 1.7	29 ± 8	323 ± 221
Zol	9	2.0 ± 1.0	21 ± 10	166 ± 117
CKD Low PTH
CTL	10	1.2 ± 0.3	11 ± 5	49 ± 18
Scl-Ab	12	1.2 ± 0.6	28 ± 17	154 ± 154
Zol	9	0.4 ± 0.2	5 ± 4	8 ± 7
Normal animals
CTL	8	1.2 ± 0.3	21 ± 7	94 ± 42
Scl-Ab	8	1.4 ± 0.3	24 ± 9	133 ± 66

CTL= control or no treatment; Scl-Ab = treatment with anti-sclerostin Ab; Zol = treatment with zoledronic acid; MAR = mineral apposition rate; MS/BS = mineralizing surface per bone surface; BFR/BS = bone formation rate per bone surface. Data presented as mean and standard deviation. The CKD animals were compared by two-way ANOVA evaluating the effect of PTH and drug treatment. After log transformation, there were significant PTH (all < 0.001) and overall drug treatment (p < 0.02 for all) effects for MAR, MS/BS and BFR/BS, and a significant PTH*drug treatment interaction for MS/BS% (p = 0.006) and BFR/BS (p = 0.009). Between group analyses revealed that Animals with higher PTH had values compared to low PTH (p < 0.002 for all three measurements). The MAR and BFR/BS were both different in ZOL compared to anti-sclerostin Ab and control (both p < 0.02) but the anti-sclerostin Ab was not different from control. All three treatments were different from each other for the MS/BS% (all p < 0.03). The Normal animals with and without treatment with anti-sclerostin Ab were compared by t-test but there was no significant difference for any parameter.