@hopefullibrarian
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362945/
" More importantly, the robust anabolic effect of treatment is limited to the first few months of therapy, curtailing the progressive, large increases in bone mass. Perhaps a strategy can be identified whereby patients can experience the anabolic effects of romosozumab on multiple occasions with a limited interval or the use of alternate drugs between courses."

Other studies I emailed to myself! There are probably more on my email....
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8567484/
https://pubmed.ncbi.nlm.nih.gov/32777516/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8085670/
others w/out links

In summary, our studies extend previous studies and reveal novel information on the effects of sclerostin deficiency in bone and sclerostin-depleting treatments on hematopoietic stem cells. Our data indicate that SOST depletion and Sost deficiency not only affects B cell development in the BM relatively early, but also creates an inflammatory bone marrow microenvironment that may become more severe over time. Investigation of the changes in the bone marrow architecture, including alterations in vasculature function and quality, proportions of arterioles and sinusoidal vessels, and local oxygen tension [67,101,102,103], may provide evidence for the specific cell-extrinsic mechanisms that drive the promotion of myelopoiesis in the Sost−/− mice and Scl-Ab-treated mice. In future studies, it would be interesting to investigate the localization of HSC in the Sost−/− bone marrow endosteal and sinusoidal niches, and quantify if specialized niches that promote myeloid differentiation or recruitment are increased [104]. Studies to test possible combinational therapy of Scl-Ab with IL-1 antagonists or TNFα blockade to control myeloid skewing are another potential area of further investigation. The information provided by our studies may be useful in monitoring humans treated with romosozumab for changes in immune cell frequencies, chronic inflammation, and signs of anemia, such that treatments for osteoporosis can be modified to address these hematopoietic changes.

and

Recent findings: Changes in sclerostin levels affect distinct niches within the bone marrow that support hematopoietic stem cells and B cell development. Sclerostin's regulation of adipogenesis could also be important for immune cell maintenance with age. Surprisingly, B cell development in the bone marrow is influenced by Sost produced by mesenchymal stem cells and osteoblasts, but not by osteocytes. Additionally, extramedullary hematopoiesis in the spleen and increased pro-inflammatory cytokine levels in the bone marrow are observed in global Sost-/- mice. In addition to changes in bone marrow density, sclerostin depletion affects B lymphopoiesis and myelopoiesis, as well as other changes within the bone marrow cavity that could affect hematopoiesis. It is therefore important to monitor for hematopoietic changes in patients receiving sclerostin-depleting therapies.

Finally

"The study will investigate if it is possible to maximize the effect of romosozumab by giving it in 2 periods of 6 months interrupted by zoledronate for 12 months compared to romosozumab for 12 months uninterrupted followed by zoledronate for 12 months. The investigators will also evaluate if 6 months of romosozumab followed by 18 months of zoledronate is non-inferior to the standard regimen of romosozumab for 12 months followed by zoledronate for 12 months."
Links (both are about the same study):
https://ctv.veeva.com/study/the-optimised-use-of-romozosumab-study
https://classic.clinicaltrials.gov/ct2/show/NCT06059222