Androgens and estrogens in skeletal sexual dimorphism.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic, animal model, and imaging literature.
PubMed 24385015 · doi:10.4103/1008-682X.122356
What was done
This narrative review summarizes literature regarding the roles of androgens and estrogens in male bone homeostasis, skeletal sexual dimorphism, and osteoporosis. It reviews bone tissue endocrinology (including local conversion of testosterone via aromatase and 5α-reductase), microarchitectural imaging via high-resolution peripheral computed tomography, and cell-specific Cre/LoxP knockout mouse studies evaluating androgen and estrogen receptor functions across osteoblasts, osteoclasts, and osteocytes.
What was found
The abstract reports no numerical data. It notes that sex steroids influence male peak bone mass and cortical versus trabecular bone turnover, and that sex steroid deficiency impacts skeletal homeostasis through direct nuclear receptor actions as well as pleiotropic interactions with IGF-1, inflammatory signaling, oxidative stress, mechanical loading adaptation, and central nervous system pathways.
Why it matters
The review synthesizes compartment- and cell-specific mechanisms of sex steroid action, clarifying structural and endocrine pathways underlying male osteoporosis and bone strength.
Limits
As a narrative review, it lacks a systematic search protocol and risk-of-bias assessment. No quantitative metrics or effect sizes are provided in the abstract, and substantial mechanistic conclusions rely on knockout mouse models rather than human clinical trials.
Cited by
- supports The male biological form is characterized by greater bone density, more fast-twitch muscle fibers, and higher levels of testosterone compared to females.