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23 The control of growth
Alberts, B., Bray, D., Lewis, J., Raff, M., Roberts, K., and Watson, J .D. (1994). Molecular biology of the cell, (3rd edn), Chapters 17,21, and 22. Garland, New York.
Campbell, E. J. M., Dickinson, C. J. , Slater, J. D. H., Edwards, C. R. W., and Sikora, E. K. (ed.) (1984). Clinical physiology, (5th edn), Chapter 9. Blackwell Scientific, Oxford.
Laycock, J. F. and Wise, P. H. (1996). Essential endocrinology, (3rd edn), Chapter 13. Oxford University Press, Oxford.
Luskey, K. L. (1992). Growth and development. In Textbook of endocrine physiology, (2nd edn), (ed. J. E. Griffin and S. R. Ojeda), Chapter 11. Oxford University Press. Oxford.
Tanner, J. M. (1989). Foetus into man, (2nd edn). Castlemead, London.
Each statement is either true or false. The answers are given below.
1. Relating to growth:
a. The adolescent growth spurt occurs, on average, earlier
in boys than in girls;
b. Long bones increase in length by interstitial growth of
the epiphyseal plate cartilage;
c. Bone mass starts to fall after puberty;
d. Lymphoid tissue mass is greater at age 6 than at age
e. The adolescent growth spurt is absent in pituitary
2. Concerning the physiology of bone:
a. The shaft of a long bone is called the diaphysis;
b. The organic matrix of bone is secreted by chondro-
c. Dividing cartilage cells are situated in the marrow
cavity of long bones;
d. Bone remodeling is a function of osteoblasts and
e. The long bones develop from fibrous connective tissue;
f. Most bones are formed by endochondral ossification of a
hyaline cartilage model;
g. The principal inorganic components of bone are
calcium and phosphates.
3. The endocrine control of growth:
a. Bone growth during fetal life is controlled primarily by
b. Growth hormone secretion is stimulated by IGF-1;
c. An excess of vitamin D causes rickets;
d. Parathyroid hormone is required for normal osteoblastic
e. The sex steroids are chiefly responsible for closure of the
4. Concerning the control of cell population size:
a. Liver cells respond to loss of liver tissue by increasing
their rate of division;
b. Nerve is a regenerarive tissue;
c. Oncogenes protect normal cells from transformation
into cancer cells;
d. Cells from a malignant neoplasm are less well-
differentiated than normal cells.
1. The adolescent growth spurt occurs on average about
2 years earlier in girls than boys. It is not seen in GH-
deficient pituitary dwarves unless treated with exogenous
hormone. Bones grow by the addition of new cartilage at
the epiphyses, which later becomes ossified. Bone mass
remains virtually stable after puberty, beginning to fall
from around the age of 40. Lymphoid tissue has a greater
total mass in children, falling to adult levels after puberty.
2. The organic matrix of bone (osteoid) is secreted by
osteoblasts. The dividing cartilage cells are situated in the
inner regions of the epiphyseal junction. Bone remodeling
involves the resorption of old bone by osteoclasts and the
accretion of new bone which is dependent on osteoblastic
activity. The flat bones, for example of the skull, develop
from fibrous connective tissue. The long bones, like most of
the skeleton, develop by endochondral ossification of a carti
lage model. Complex crystals of calcium phosphate (hydrox-
yapatite) are the principal inorganic components of bone.
3. During fetal life the principal hormonal regulator of skele
tal growth and development is thought to be thyroxine.
GH stimulates the synthesis and secretion of the IGFs.
Rickets is caused by vitamin D deficiency. Normal circu
lating levels of PTH are required for osteoblastic activity
and the secretion of osteoid. Estrogens and androgens,
secreted in large amounts at puberty, bring about closure
of the epiphyses.
4. Liver cells increase their mitotic activity following loss or damage to liver tissue. In this way large amounts of liver tissue may be regenerated. Nervous tissue does not regenerate significantly. Nerve cells stop dividing during
infancy. Oncogenes are thought to be responsible for the genetic transformations leading to certain cancers. Malignant cancer cells show a loss of differentiation.
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