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Daisy17, hi. One way of knowing is by the way the medications work. Most of the medications block cell that dissolve defective bone. Bisphosphonates attach to the bone preventing these osteoclastic cells from attaching causing the death. Prolia stops these cells from developing fully and Evenity blocks a protein necessary for their production. The pth 1-34 medications increase the production of both types of cells the osteoclasts that dissolve older and damaged bone and the osteoblasts the cells that produce new bone.
Then there are the warnings on all the other meds about osteonecrosis and atypical fractures. In a sense all of the clinical trials signal issues about bone quality except Forteo and Tymlos.
There are actual studies about bone quality. https://www.healio.com/news/endocrinology/20220726/2-years-of-teriparatide-restores-bone-quality-to-premenopausal-levels estores%20bone%20mineral%20quality,that%20of%20healthy%20premenopausal%20women.%E2%80%9D
There are other less accessible studies, animal studies and pathological studies. https://journals.plos.org/plosone/articleid=10.1371/journal.pone.0229820
Not to obscure your point about how ephemeral these bones are. It may become more common to stay on Forteo or Tymlos now that the restrictions have been removed.

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Replies to "Daisy17, hi. One way of knowing is by the way the medications work. Most of the..."

@gently Greatly apreciate the time you put into research and sharing it with us.. My endo has mentioned that he wanted me to go on yourvipath after tymlos . Your mentioning of the pth -34 medication caused me to look up yorvipath and this too is a pth-34 med used for hypoparathyroidism. My parathyroid was snagged during thryroidectomy and my hypocalcimia has been controlled by oral meds. The thought of shooting myself with yet another drug has been unsettling. Looking up on google:
PTH (1-34) primarily stimulates bone formation by directly acting on osteoblasts through the PTH receptor 1 (PTHR1), activating cAMP/PKA signaling pathways. It increases the proliferation and differentiation of osteoprogenitor cells, promotes osteoblast survival, and upregulates osteogenic genes like RUNX2 and collagen I. Intermittent administration leads to anabolic (bone-building) effects, while continuous administration promotes a catabolic (bone-breakdown) effect.