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I am unaware that osteoblasts take some sort of cues from osteoclastic activity.

My rather simplistic understanding of why osteroporosis occurs is that post-menopausal women produce significantly reduced estrogen, which is the main engine driving osteoblastic (bone-building) activity. Meanwhile, osteoclasts continue unimpeded and outperform osteoblasts; the result is a loss of bone density because bone resorption outruns bone formation.

I simply do not understand the logic of suppressing 'remodeling' and that that might somehow lead to reducing fracture risk. You might preserve bone mass but is it of sufficient quality to prevent fractures?

In his book, McCormick likes CTX in the range 100-375 and P1NP in the range of 30-50.

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Replies to "I am unaware that osteoblasts take some sort of cues from osteoclastic activity. My rather simplistic..."

@rjd
Yes, osteoblasts do take cues from osteoclast activity via “coupled remodeling.” When osteoclasts resorb bone, they release signals that help recruit and activate osteoblasts to rebuild at the same site. This process ensures that bone formation is closely linked to bone resorption, maintaining skeletal integrity:
https://pmc.ncbi.nlm.nih.gov/articles/PMC3899560/
You summarized postmenopausal bone loss due to estrogen deficiency really well. From what I’ve read, estrogen seems to act more as a regulator that maintains the balance between bone formation and resorption, rather than as a direct “engine” driving osteoblast activity.

I share your skepticism about fracture reduction resulting from suppressing remodeling by bisphosphonates. Clinical trials have, however, shown a reduction in fracture risk, especially in the first 3–5 years, likely because bisphosphonates preserve existing trabecular connectivity and slow the rate of resorption, hence helping maintain bone density. With available anabolic therapies nowadays, the approach of repeated use of an anabolic agent followed by antiresorptive therapy is now evidence-based, increasingly recommended, and reflected in some updated clinical guidelines. Hopefully, this represents a better long-term management strategy.