Androgens and the skeleton.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanism-based reasoning and animal experiments with no new human data.
What was done
This is a narrative review examining the biological mechanisms by which androgens and estrogens regulate bone remodeling, longitudinal endochondral growth, and radial bone growth, drawing on physiological principles and mouse experimental models.
What was found
The abstract reports no quantitative figures or statistical data, describing physiological mechanisms qualitatively: - Sex steroid deficiency accelerates bone remodeling by extending osteoclast lifespan and shortening osteoblast lifespan, whereas androgen and estrogen administration preserves cancellous bone mass regardless of age or sex. - Androgens stimulate endochondral bone formation at puberty onset and mediate epiphyseal closure at puberty completion via aromatization into estrogens acting through estrogen receptor alpha (ER alpha). - Androgens promote periosteal radial bone growth, while estrogens restrict it. - Mouse data indicate radial bone expansion under androgen control relies on both androgen receptors (AR) and ER alpha pathways, whereas ER beta limits growth in females without affecting male bone size.
Why it matters
It outlines how androgens help protect skeletal integrity in men by preserving cancellous bone architecture and driving cortical bone expansion through AR and ER alpha pathways.
Limits
The abstract contains no quantitative metrics, human trial data, sample sizes, or systematic search methodology, and relies in part on mouse models to infer receptor mechanisms.
Cited by
- supports Pre-pubertal castration of males prevents epiphyseal growth plates from fully closing and leads to osteoporosis due to the lack of aromatization of testosterone to estrogen.