WEll as id hope you already know CB25, the epiphyseal growth plates undergo 2 processes which result in increased longitudinal growth.
The first is Chondrogenesis, the formation of cartilage which occurs throughout the layers of the growth plate (germative, proliferative, hypertrophic, calcification) via chondrocytes.
The second is Osteogenesis, the conversion of that cartilage to bone by the osteo-cells.
You stop growing as a result of osteogenesis outdoing chondrogenesis resulting in entire calcification of the growth plate.
You need to research a disease called Gigantism. Its a disease in which supraphysiological height and size is acheived in a growing adolescent, mainly as a result of excess GH exposure, excess GHRH stimulation, or in even rarer cases, a mutation of the aromatase enzyme gene, or the esstrogen receptor-alpha mutation. Estrogen-receptor-alpha is the estrogen receptor in the growth plates thats reponsible to ultimately leading to epiphyseal fusion via the aromatised estrogen from natural testosterone.
By blocking the aromatase enzyme via an anti-aromatase such as Letrozole or Aromasin, you can recreate the same form of gigantism as that seen in both estrogen receptor alpha mutation and aromatase enzyme gene mutation. Except you can stop it anytime you want, and proceed with it anytime you want, simply by taking or not taking the anti-aromatase agent.
Most of my research is confined to University publishings and such, so I cant provide a severe amount of data via the internet, but heres some basic stuff.
http://www.swmed.edu/home_pages/news/estrogen.htm
http://www.docguide.com/dg.nsf/Print...2564D0006E361C
Novel treatment of delayed male puberty with aromatase inhibitors.
Dunkel L, Wickman S.
University of Helsinki, Hospital for Children and Adolescents, Finland.
[email protected]
BACKGROUND: As the evidence for the role of oestrogens in epiphyseal closure appears unequivocal, we hypothesized that boys with constitutional delay of puberty would attain greater adult height if oestrogen action was suppressed. METHODS: We conducted a randomized, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone plus placebo or testosterone plus a potent fourth-generation aromatase inhibitor, letrozole. FINDINGS: Letrozole effectively inhibited oestrogen synthesis. The 17beta-oestradiol concentrations increased in the untreated group and in the testosterone/placebo-treated group, but in the testosterone/letrozole-treated group no such increase was observed until letrozole treatment was discontinued. Testosterone concentrations were threefold higher in the testosterone/letrozole-treated group than in the other groups. Within 18 months, bone age had advanced by 1.1 +/- 0.3 years in the untreated group and by 1.7 +/- 0.3 years in the testosterone/placebo-treated group, but only by 0.9 +/- 0.2 years in the testosterone/letrozole-treated group (p = 0.02 between treatment groups). Predicted adult height did not change significantly in the untreated group and in the testosterone/placebo-treated group, whereas in the testosterone/letrozole-treated group the increase was 5.1 +/- 1.2 cm (p = 0.004). CONCLUSIONS: Our findings suggest that, if oestrogen action is inhibited in growing adolescents, adult height will increase. This observation provides a rationale for studies aimed at delaying bone maturation in several growth disorders. Copyright 2002 S. Karger AG, Basel
Long term treatment with low dose testosterone in constitutional delay of growth and puberty: effect on bone age maturation and pubertal progression.
Bergada I, Bergada C.
Hospital de Ninos R. Gutierrez, Division of Endocrinology, Buenos Aires, Argentina.
We compared the effects of long term low dose treatment with testosterone on pubertal growth and sexual development in boys with constitutional delay of growth and puberty (CDGP). We treated 24 boys with intramuscular monthly injections with low dose testosterone enanthate (33-50 mg) for 20 months, at a chronological age of 14.5 +/- 1.0 years and SDS height of -3.31 and compared their response to a group of 14 control boys. Treated patients showed an earlier and significant increase in height velocity compared to controls, 10.1 vs 4.0 cm/year, while the latter group showed their growth spurt twelve months later. Both groups showed an initial acceleration in bone age without impairment of predicted adult height. During the first 12 months of treatment the increment of testicular volume in the treated patients was slightly slower than controls; however the earlier the puberty, the slower the testicular increment compared to controls. We conclude that treatment of boys with constitutional delay of growth with low dose testosterone is effective in improving their height velocity without impairment of predicted final height. Progression of testicular volume during treatment in some patients is more delayed; however, after treatment it increased normally.
Oxandrolone therapy in constitutionally delayed growth and puberty. Bio-Technology General Corporation Cooperative Study Group.
Wilson DM, McCauley E, Brown DR, Dudley R.
Department of Pediatrics, Stanford University, California, USA.
BACKGROUND. Male adolescents with constitutional delay of growth and puberty may have significant psychosocial difficulties related to their sexual immaturity and short stature. The purpose of this study was to test the hypothesis that 1 year of oxandrolone therapy would increase growth velocity and thereby improve psychosocial functioning in boys with constitutional delay of growth and pubertal development. METHODS. Forty boys (ages 11 to 14.7 years) with delayed pubertal development and short stature were recruited from the pediatric endocrine clinics of 14 medical centers. The boys were randomized using a block design stratified for age to receive either oxandrolone (0.1 mg/kg daily for 1 year) or an identical-appearing placebo tablet, using a double-masked design. RESULTS. Growth velocity in the oxandrolone-treated boys was significantly greater than in the control boys (9.5 vs 6.8 cm/y). Likewise, the mean height SD score increased 0.41 in the oxandrolone group, whereas it decreased 0.03 in the control group. Those in the oxandrolone group gained 2.4 kg more than those in the placebo group. Mean predicted adult heights did not change in either group. The mean rates of pubertal progression were equivalent in both groups. Self-image (Piers-Harris Self Concept Scale) and social competence (Child Behavior Profile) were normal at baseline in both groups and did not change significantly over the course of the study in either group. No complications of oxandrolone therapy were identified. CONCLUSIONS. This randomized, placebo-controlled trial demonstrates that low-dose oxandrolone can increase both height and weight velocity in boys with delayed puberty safely. Under the conditions of this study, however, the increased growth velocity in the oxandrolone-treated boys was not associated with a greater improvement in psychosocial status compared with the control boys.
Circulating levels of IGF-1 directly regulate bone growth and density.
Yakar S, Rosen CJ, Beamer WG, Ackert-Bicknell CL, Wu Y, Liu JL, Ooi GT, Setser J, Frystyk J, Boisclair YR, LeRoith D.
Section on Cellular and Molecular Physiology, Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, Maryland 20892, USA.
IGF-1 is a growth-promoting polypeptide that is essential for normal growth and development. In serum, the majority of the IGFs exist in a 150-kDa complex including the IGF molecule, IGF binding protein 3 (IGFBP-3), and the acid labile subunit (ALS). This complex prolongs the half-life of serum IGFs and facilitates their endocrine actions. Liver IGF-1-deficient (LID) mice and ALS knockout (ALSKO) mice exhibited relatively normal growth and development, despite having 75% and 65% reductions in serum IGF-1 levels, respectively. Double gene disrupted mice were generated by crossing LID+ALSKO mice. These mice exhibited further reductions in serum IGF-1 levels and a significant reduction in linear growth. The proximal growth plates of the tibiae of LID+ALSKO mice were smaller in total height as well as in the height of the proliferative and hypertrophic zones of chondrocytes. There was also a 10% decrease in bone mineral density and a greater than 35% decrease in periosteal circumference and cortical thickness in these mice. IGF-1 treatment for 4 weeks restored the total height of the proximal growth plate of the tibia. Thus, the double gene disruption LID+ALSKO mouse model demonstrates that a threshold concentration of circulating IGF-1 is necessary for normal bone growth and suggests that IGF-1, IGFBP-3, and ALS play a prominent role in the pathophysiology of osteoporosis.