Remove all references to SMI and interpretations about plates and rods that flow from it. Salmon et al. are rather stronger in their assessment of SMI's veracity than the mild criticism that your text implies: they advise not to use it at all and especially not when there is a pronounced change in BV/TV as in your specimens. Increasing BV/TV induces a strong artefact due to increased amounts of concave curvature, which SMI assumes is not there but by which it is strongly biased. Salmon et al. provide some suggestions about how to determine whether your SMI measurement is biased (by calculating the CF, SMI+ and SMI- with BoneJ), and unbiased ways to measure rods and plates.
Remove references to Tb.N - it is redundant when you have Conn.D measurements, which are a topological count of trabeculae.
"a tendency (P = 0.06) for trabecular thickness to be lower with treatment." Remove this. If you are using a significance cutoff (already dubious at p = 0.05), then stick to it. This is a non-significant result and should be reported as such. What was your power? From p and power you can work out the likelihood of a false positive or false negative, which can be alarmingly high (I do note in your methods that you have set a false discovery rate of 5%). https://doi.org/10.1098/rsos.140216
"The reduced bone accrual observed in the present study and in longer duration spaceflights is superficially similar to changes observed in rats following hypophysectomy"
And the reduced accrual is explained mostly by reduced mechanical loading, so the GH emphasis here seems like a red herring or false equivalence. GH and mechanical loading effects are then conflated. The Halloran paper you cite suggests that both GH and mechanical loading are necessary for normal bone mass, which they deduce from creating a severe GH deficiency by hypophysectomy which is rescued by GH only in the presence of mechanical loading. Were your untreated rats GH-deficient? I find the logic around GH administration to this group of animals confused and unconvincing. The observation itself is fine and should be published, but the discussion and rationale of why administering additional GH to GH-sufficient animals would rescue space-flight-induced osteopenia is unclear. In particular the assertion that "It is plausible that GH resistance rather than GH deficiency contributes to the observed effect" lacks sufficient justification; could it simply be that no effect of rhGH would be expected in GH-sufficient animals?
Underlying all this is the concept that trabecular morphology and in particular trabecular bone accrual during growth is strongly influenced by growth hormone, in a dose-dependent (or plasma concentration dependent) manner, and that alterations in GH signalling might underlie osteopenic phenotypes induced by mechanical unloading (i.e.that GH pathways are involved in bone's mechanostat). If that is actually the case, please introduce and clarify for the reader so we can follow your logic.