This post will be more informative in nature. I had typed the term “estrogen bone growth” into google and one of the first ranked links was to this article written on pubmed entitled “Hormonal Regulation Of Longitudinal Bone Growth.”
The abstract is below. The article was found from PubMEd located HERE and the most important parts were highlighted.
Eur J Clin Nutr. 1994 Feb;48 Suppl 1:S150-8; discussion S158-60.
Hormonal regulation of longitudinal bone growth.
Department of Orthopedics (Hand Surgery), Sahlgren’s Hospital, Sweden.
The regulation of postnatal somatic growth is complex. Genetic, nutritional factors and hormones exert regulatory functions. Hormones that have an established role in the regulation include growth hormone (GH), thyroid hormone and sex steroids. GH promotes mainly the growth of the long bones in terms of final height, while the action of the sex steroids and thyroid hormone is less well known. Longitudinal bone growth is the result of chondrocyte proliferation and subsequent endochondral ossification in the epiphyseal growth-plates. The growth-plate is a cartilaginous template that is located between the epiphysis and the metaphysis of the long bones. GH and insulin-like growth factor-I (IGF-I) have different target cells in the epiphyseal growth-plate. GH stimulates the slowly dividing prechondrocytes in the germinative cell layer while IGF-I promotes the clonal expansion in the proliferative cell layer of a GH primed cell. Thyroid hormone blocks the clonal expansion and stimulates chondrocyte maturation. IGF-I mRNA is primarily regulated by GH, and IGF-I is produced in several tissues such as the liver, muscle, fat and epiphyseal growth plates. However, IGF-I mRNA is also increased during compensatory growth of heart and kidneys and by estrogen in the Fallopian tube in the rat. Nutrition, i.e. energy from fat and carbohydrates and proteins, also influences the final height, but the cellular mechanism of action is not known. The aim of this article is to review hormonal action on longitudinal bone growth.
Me: It is too bad that I can’t pay for a way to read the entire article. The thing I took away from the abstract was that the Gh and the IGF-1 have different target cells in the growth plates. The GH stimulates the prechondrocytes in the germinative cell layer while the IGF-1 promotes the clonal expansion in the proliferative cell layes of a GH primed cell. So, the Gh starts the chondrocytes out by getting ready and the IGF-1 helps the cells divide and multiply. This shows that both the GH and the IGF-1 are both needed to get the plates to proliferate and grow thicker from cell multiplication.
As stated very clearly, the thyroid hormone (which one it is is not revealed in the abstract) causes the clonal expansion (aka cell division and growth) to be blocked and causes the chondrocytes to grow old. This suggests that if I can just figure out which thyroid hormone is causing the blocking of cell division and cell senescence, we can find another way to slow down the growth plate decrease and maturation process.