40
THOMAS S. ARGYRIS
epithelial tumors (Levi-Montalcini, 1958). In damage, the tissue response
is much more specific. Another major difference between the growthpromoting effects of damage and those of tumors is that damage initiates
cell proliferation of tissues that are refractile to the growth-promoting
effects of tumors, such as liver, kidney, and resting hair follicles (T. S.
Argyris and B. F. Argyris, 1959; Argyris and Trimble, 1964b; Kollar,
1963). Therefore, it would seem that growth-promoting substances from
tumors are different from those released by damage. What the molecular
basis is for the difference between tumor growth-promoting substances
and those involved in damage is another problem for the future.
In the beginning of this review it was pointed out that damage initiates
a very complex growth syndrome. It involves proliferation and enlargement of the cells of the epidermis and hair follicles, and proliferation of
the connective tissue. It involves cell differentiation, as in the synthesis of
collagen and other kinds of intercellular substances. It involves migration
of epithelial and connective tissue cells to resurface the wound and to fill
in the gap. This catalog of events hardly exhausts the list of those occurring. Abercrombie (1957) has called this kind of growth, or growth
syndrome, episodic growth. Episodic growth induced by damage involves
also a considerable amount of degrowth or remolding due to a considerable extent to cell death, as is seen in the loss of connective tissue in scar
formation. Thus the adult organism uses the basic tools of embryonic development, that is, cell proliferation, differentiation, movement, and death,
to produce the growth necessary for wound healing, just as the embryo
uses these tools to accomplish development. An important problem for
the future will be to learn if the mechanisms by which the basic tools of
cell differentiation, proliferation, movement, and death, used in the adult
for wound healing, are the same as those used in the embryo for development.
VI. Summary
Damage to the skin initiates a complex growth syndrome. The epidermal cells undergo hyperplasia and hypertrophy. The hair follicles immediately adjacent to the wound lose their sebaceous glands and are
transformed into hyperplastic cords of enlarged cells. Hair follicles distant from the wound are stimulated to grow normally. The loose areolar
connective tissue in the subcutis and beneath the panniculus carnosus
proliferates and becomes the chief source of the granulation tissue.
The stimulation of growth of each of the tissues of the skin is probably
THOMAS S. ARGYRIS
epithelial tumors (Levi-Montalcini, 1958). In damage, the tissue response
is much more specific. Another major difference between the growthpromoting effects of damage and those of tumors is that damage initiates
cell proliferation of tissues that are refractile to the growth-promoting
effects of tumors, such as liver, kidney, and resting hair follicles (T. S.
Argyris and B. F. Argyris, 1959; Argyris and Trimble, 1964b; Kollar,
1963). Therefore, it would seem that growth-promoting substances from
tumors are different from those released by damage. What the molecular
basis is for the difference between tumor growth-promoting substances
and those involved in damage is another problem for the future.
In the beginning of this review it was pointed out that damage initiates
a very complex growth syndrome. It involves proliferation and enlargement of the cells of the epidermis and hair follicles, and proliferation of
the connective tissue. It involves cell differentiation, as in the synthesis of
collagen and other kinds of intercellular substances. It involves migration
of epithelial and connective tissue cells to resurface the wound and to fill
in the gap. This catalog of events hardly exhausts the list of those occurring. Abercrombie (1957) has called this kind of growth, or growth
syndrome, episodic growth. Episodic growth induced by damage involves
also a considerable amount of degrowth or remolding due to a considerable extent to cell death, as is seen in the loss of connective tissue in scar
formation. Thus the adult organism uses the basic tools of embryonic development, that is, cell proliferation, differentiation, movement, and death,
to produce the growth necessary for wound healing, just as the embryo
uses these tools to accomplish development. An important problem for
the future will be to learn if the mechanisms by which the basic tools of
cell differentiation, proliferation, movement, and death, used in the adult
for wound healing, are the same as those used in the embryo for development.
VI. Summary
Damage to the skin initiates a complex growth syndrome. The epidermal cells undergo hyperplasia and hypertrophy. The hair follicles immediately adjacent to the wound lose their sebaceous glands and are
transformed into hyperplastic cords of enlarged cells. Hair follicles distant from the wound are stimulated to grow normally. The loose areolar
connective tissue in the subcutis and beneath the panniculus carnosus
proliferates and becomes the chief source of the granulation tissue.
The stimulation of growth of each of the tissues of the skin is probably