Osteoporosis Due to Hormone Imbalance: An Overview of the Effects of Estrogen Deficiency and Glucocorticoid Overuse on Bone Turnover.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing molecular mechanisms without original human data or systematic methodology
PubMed 35163300 · doi:10.3390/ijms23031376
What was done
This narrative review summarizes literature regarding the molecular mechanisms of action, risk factors, and pharmacological management of estrogen deficiency-related osteoporosis (EDOP) and glucocorticoid-induced osteoporosis (GIOP).
What was found
The abstract provides no quantitative data or numerical findings. It outlines that estrogen normally upregulates osteoprotegerin (OPG), suppresses RANKL, and promotes osteogenesis via Wnt/β-catenin and BMP pathways, while its deficiency elevates pro-inflammatory cytokines (IL-1, IL-6, TNF) and accelerates bone resorption. Conversely, glucocorticoid excess disrupts BMP and Wnt signaling, shifts mesenchymal stem cell differentiation from osteoblasts to adipocytes, raises the RANKL/OPG ratio, and triggers osteoblast and osteocyte apoptosis.
Why it matters
It highlights how distinct cellular and molecular etiologies distinguish postmenopausal bone loss from steroid-induced bone demineralization, framing the mechanistic rationale for targeted therapeutic strategies.
Limits
The paper is a narrative review without a systematic search methodology, meta-analytic pooling, risk-of-bias evaluation, or new empirical clinical data.
Cited by
- supports Estrogen is osteoprotective, so postmenopausal decreases in estrogen increase bone resorption and osteoporosis risk.