yeah, so? receptor binding is irrelevant without ligand availability. the question isn't whether DHT can bind mandibular AR, it is whether DHT is present in sufficient conc. at mandibular osteoblasts to meaningfully participate in receptor occupancy.
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the periosteum itself lacks the enzymatic activity that converts T to DHT.
and the studies showing DHT increases cortical thickness are predominantly ex vivo or rodent models using supraphysiological concentrations that bear no relationship to human endogenous physiology.
what?
the 5ART2D male in one study had normal T levels, near zero DHT throughout entire life, fully functional androgen receptors.
3/4 patients had completely normal BMD. 4th had osteopenia or whatever, can't remember.
also, the estrogen-bone relationship is mediated via completely different receptors (ER alpha, ER beta) and a different mechanism (anti-resorptive via osteoclast apoptosis). DHT doesn't share this mechanism nigga, why are you comparing them?
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if DHT was needed for bone density, a suppression like this would cause bone loss. it didn't.
the skeleton requires T and E for maintenance. T acts directly on osteoblasts via AR and indirectly via aromatization to estradiol.
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shush.
true, but irrelevant.
the real question is: which isoform and at what level?
the Notelovitz review explicitly states that periosteal cells dont have 5AR activity. periosteal apposition is the mechanism by which mandibular widening and angular development takes place. presence of 5AR elsewhere, like trabecular osteoblasts, is irrelevant here.