Abstract

This study is intended to examine the effect of hypothyroidism and thyroxin replacement on axial and appendicular skeletal growth, growth plate thickness and to observe associated microscopic changes within the growth plates. Experimental albino rats were developed with carbimazole and carbimazole plus thyroxin. Animals were administered with these drugs throughout pregnancy (prenatally) and for a period of six weeks, postnatally. At the end of the experiment the animals were sacrificed, measured and processed to demonstrate the bony and cartilaginous parts. Ulna and tibia of both sides were removed and processed for light microscopy and growth plate measurement. At the end of the experiment, reduction in the crown rump length was observed in the carbimazole treated animals. It was 8.77%, 13.26% and 7.25% in the prenatal, two weeks and six weeks age group animals respectively. In carbimazole plus thyroxin treated animals, this reduction was 3.22%, 2.94% and 3.42%, when compared to their age matched controls. Reduction in the thickness of the Epiphyseal growth plate (EGP) was 16.89% and 12.80% in the ulna of the two and six weeks age group and 18.06 % and 15.65% in the tibia of the these animals respectively. The carbimazole plus thyroxin treated animals showed an increase in the thickness of EGP as compared to their age-matched controls though the crown rump length of these animals was less than the controls. Prenatally treated hypothyroid rats showed disrupted growth plates without any well-formed microscopic zones. The results of this study showed that the pre and postnatally, carbimazole induced hypothyroidism and its replacement therapy affected the axial and appendicular skeletal growth. Proximal limb bones of the prenatally induced hypothyroid animals showed the greatest skeletal change in this study.

Highlights

  • Growth is a continuous biologic process influenced by genetic, nutritional, environmental, and hormonal factors. [1] Thyroid hormones exert an important effect on growth and differentiation of tissues in many mammalian species. [2] Euthyroid status is essential for normal skeletal development and adult bone maintenance. [3, 4] Hypothyroidism in children causes growth arrest, delayed bone maturation, and epiphyseal dysgenesis

  • Decrease in the CROWN RUMP LENGTH (CRL) in the pups born to Carbimazole treated mothers was approximately 8.77%, statistically highly significant (P

  • Decrease in the CRL noted in the Carbimazole treated animals was approximately 13.27%, statistically highly significant (P

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Summary

Introduction

Growth is a continuous biologic process influenced by genetic, nutritional, environmental, and hormonal factors. [1] Thyroid hormones exert an important effect on growth and differentiation of tissues in many mammalian species. [2] Euthyroid status is essential for normal skeletal development and adult bone maintenance. [3, 4] Hypothyroidism in children causes growth arrest, delayed bone maturation, and epiphyseal dysgenesis. [1] Thyroid hormones exert an important effect on growth and differentiation of tissues in many mammalian species. Does the maternal hypothalamicpituitary-thyroid (HPT) axis undergo a series of adjustments, the fetus develops its own HPT axis and the placenta plays an active role in iodide and T4 transport and metabolism. [7] In normal pregnant women, the thyroid gland maintains a euthyroid state with only minor fluctuations in serum T4 and TSH. Thyroid hormone of the embryo and fetus are required for development, considering the maternal hormone crosses placenta very limitedly. [9] Contrary to this belief, some of the newer animal studies have reported that thyroid hormone crosses the placenta in a more liberal manner and that the maternal T4 does reach the fetus. Thyroid hormone of the embryo and fetus are required for development, considering the maternal hormone crosses placenta very limitedly. [9] Contrary to this belief, some of the newer animal studies have reported that thyroid hormone crosses the placenta in a more liberal manner and that the maternal T4 does reach the fetus. [10]

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