Primary Osteoporosis Induced by Androgen and Estrogen Deficiency: The Molecular and Cellular Perspective on Pathophysiological Mechanisms and Treatments.
Level 5 - mechanism / opinion, no new human data
Narrative review describing cellular mechanisms and treatment pathways without original empirical data or systematic review methodology.
PubMed 39596206 · doi:10.3390/ijms252212139
What was done
This is a narrative review summarizing the molecular and cellular pathophysiological mechanisms of primary osteoporosis driven by estrogen and androgen deficiency. The authors describe classical genomic and non-genomic signaling pathways of sex hormone receptors, bone remodeling dynamics, and current pharmacological and non-pharmacological therapeutic strategies.
What was found
The abstract reports no quantitative data or empirical findings. It outlines that estrogen promotes osteoprotegerin production to inhibit RANKL-mediated osteoclastogenesis and supports osteoblast survival via Wnt signaling. Estrogen deficiency increases pro-inflammatory cytokines (IL-1, IL-6, TNF-α) and RANKL. Androgens modulate bone metabolism directly through androgen receptors and via aromatization to estrogen. The review also summarizes current therapies (bisphosphonates, teriparatide, RANKL inhibitors, sclerostin inhibitors, SERMs, calcitonin, nutrition, and exercise) and highlights non-genomic/ligand-independent receptor signaling as potential targets for safer drug design.
Why it matters
It provides a synthesized overview of sex hormone signaling in bone turnover, illustrating how dissecting genomic versus non-genomic receptor actions could help develop bone-protective agents that bypass the adverse effects of traditional hormone replacement therapies.
Limits
The abstract provides no original empirical data, quantitative effect estimates, or systematic literature search methodology. Discussion of clinical efficacy, fracture reduction rates, and drug-specific adverse event profiles is not quantitatively detailed.
Cited by
- supports Estrogen loss induces interleukin-6 (IL-6), which promotes the development of osteoporosis.