XXY - Tall

	tall
	It is common for XXYs to have long bone growth of the arms and legs when compared to the trunk. This is due to the epiphyseal openings near the joints remaining open longer than is typical. One major factor in the closing of the epiphyseal plate is when testosterone reaches the desired adult levels. Insufficient testosterone in the body of an XXY therefore often prompts the epiphyseal plate to stay open longer than average and to promote long bone growth in the limbs and extremities. Too much testosterone supplementation at too young of an age can close the plates prematurely and cause short stature. Young XXY children (especially from the ages of 4-7) may also be taller than average. Whether this will have any effect on final height is unknown. However, "it is not known whether the chromosomal defect in Klinefelter syndrome (XXY) has an effect on bone density independent of gonadal steroid deficiency. There are data to suggest, however, that the characteristic long bone abnormality, with increased lower body segment, is present before puberty and therefore is probably attributable to the underlying genetic defect rather than androgen deficiency." ("Hormonal Determinants and Disorders of Peak Bone Mass in Children"; The Journal of Clinical Endocrinology & Metabolism Vol. 85, No.11; Leslie A. Soyka, Wesley P. Fairfield, and Anne Klibanski). Further research has resulted in the discovery of a gene that regulates growth and final stature. Each sex chromosome carries this gene, and since XXYs have three sex chromosomes, we get three doses of this gene. The gene was first found during a search for the cause of short stature in women with Turner syndrome, in which there is loss of genetic material from the X chromosome, and explains why Turner syndrome causes individuals to be short. Iannotti JP. University of Pennsylvania School of Medicine, Philadelphia. Orthop Clin North Am. 21(1):1-17, 1990 Jan. The growth plate is made of cartilaginous, bony, and fibrous components, which act together to achieve longitudinal bone growth. The unique metabolism of the growth plate is a result of its unique microcirculation and extracellular microenvironment. The growth plate chondrocytes are responsive to both mechanical and hormonal stimuli, which can alter their normal function. Pathologic states result from environmental, hormonal, nutritional, and genetic factors. [References: 155] Back Top

tall

It is common for XXYs to have long bone growth of the arms and legs when compared to the trunk. This is due to the epiphyseal openings near the joints remaining open longer than is typical. One major factor in the closing of the epiphyseal plate is when testosterone reaches the desired adult levels. Insufficient testosterone in the body of an XXY therefore often prompts the epiphyseal plate to stay open longer than average and to promote long bone growth in the limbs and extremities. Too much testosterone supplementation at too young of an age can close the plates prematurely and cause short stature.

Young XXY children (especially from the ages of 4-7) may also be taller than average. Whether this will have any effect on final height is unknown. However, "it is not known whether the chromosomal defect in Klinefelter syndrome (XXY) has an effect on bone density independent of gonadal steroid deficiency. There are data to suggest, however, that the characteristic long bone abnormality, with increased lower body segment, is present before puberty and therefore is probably attributable to the underlying genetic defect rather than androgen deficiency." ("Hormonal Determinants and Disorders of Peak Bone Mass in Children"; The Journal of Clinical Endocrinology & Metabolism Vol. 85, No.11; Leslie A. Soyka, Wesley P. Fairfield, and Anne Klibanski).

Further research has resulted in the discovery of a gene that regulates growth and final stature. Each sex chromosome carries this gene, and since XXYs have three sex chromosomes, we get three doses of this gene. The gene was first found during a search for the cause of short stature in women with Turner syndrome, in which there is loss of genetic material from the X chromosome, and explains why Turner syndrome causes individuals to be short.

Iannotti JP.
University of Pennsylvania School of Medicine, Philadelphia. Orthop Clin North Am. 21(1):1-17, 1990 Jan.

The growth plate is made of cartilaginous, bony, and fibrous components, which act together to achieve longitudinal bone growth. The unique metabolism of the growth plate is a result of its unique microcirculation and extracellular microenvironment. The growth plate chondrocytes are responsive to both mechanical and hormonal stimuli, which can alter their normal function. Pathologic states result from environmental, hormonal, nutritional, and genetic factors. [References: 155]

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