Ahmed R.G., 2018. Maternal thyroid dysfunctions and neonatal bone maldevelopment. American Research Journal of Endocrinology 2(1), 1-6. (original) (raw)

Thyroid hormones (THs) play an essential role during the fetal and neonatal development, particularly the normal growth of bone cells. THs also induce the cellular proliferation of cartilage growth in the epiphyseal plate of long bones by stimulation the release of growth hormone (GH) and IGF (insulin-growth factor). In addition, thyroid receptors (TRs; α and β) were found in chondrocytes, growth plat, and osteoblasts. It has also been revealed that triiodothyronine (T3) can activate the terminal differentiation of growth plate chondrocytes, osteoclastic growth and the osteoblasts process. On the other hand, the maternal hypothyroidism delayed the body growth and ossification in rat. In addition, hypothyroidism can reduce the bone turnover, osteoclast bone reabsorption, osteoblast formation, and remodeling process. Alternatively, the hyperthyroidism can accelerate the development of skeletal bones and premature closure of the epiphyseal growth plates (EGPs), and subsequent diminish the longitudinal bone growth. During the early childhood, severe hyperthyroidism can induce the premature fusion of the sutures of the skull and craniosynostosis. More importantly, the disturbances in the TRα1 or TRβ can perturb and delay the development of epiphyseal growth plates and the ossification process. Thus, the maternal thyroid disorders may alter the general skeletal features during the prenatal and postnatal development. Additional examinations are desired to identify the gene expression and signaling of THs-bone axis during the development. Also, several experimental studies are required to test whether T3 can act directly or indirectly in osteoclasts.

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