GROWTH INDUCED BY DAMAGE
37
healing and compensatory hypertrophy, it is instructive to review some
of the principal characteristics of both of these types of induced growth
because it may help us to predict if the triggers are the same in both
cases.
Both wound healing and compensatory hypertrophy have in common
the loss of a portion of an organ or tissue. Usually the loss of mass in
wound healing is confined to a small area, whereas the loss of mass in
compensatory hypertrophy involves the loss of a larger portion of an
organ. There are exceptions to this generalization, as in the case of
chemical damage of the liver, e.g., with carbon tetrachloride, where the
damage is spread throughout the entire liver. The removal of a portion
of an organ or one of a pair of bilateral organs is usually not accompanied
with much damage to the organ concerned. This is especially obvious in
the best studied cases of compensatory hypertrophy, in the liver and
kidney, where the removal of a liver lobe or of one kidney is attended
with little or no damage to the organ. However, in many other cases,
such as in partial thyroidectomy and pancreatectomy the organ is
damaged. The relationship of this damage-induced growth, associated
with the removal of a portion of an organ, to the compensatory response
has never been critically evaluated. It is assumed to be unimportant.
Damage-induced growth differs from compensatory hypertrophy in
that damage induces a large amount of overgrowth of the tissues surrounding the damaged area. This overgrowth is especially obvious in
wound healing in the skin where the epidermal and adjacent hair follicle
cells undergo considerable proliferation, resulting in a thick mass of
epithelium. Overgrowth in wound healing is also obvious in the amount
of granulation tissue formed. It is in such excess that a considerable
amount of degrowth occurs (Abercrombie, 1957).
A corollary to the fact that growth is excessive after damage is that
damage-induced growth is not as adaptive as that of compensatory hypertrophy. If it were, so much overshoot in tissue growth would probably
not be seen. The excessive proliferation of the surrounding epithelium
and connective tissue is an indication of this. Moreover, the stimulation
of hair growth surrounding the wound has little obvious adaptive value.
This is even more glaring when we realize that the hair follicles are
dragged into the wound, break up, and form keratinized cysts (Argyris,
1956a). Similarly, the proliferation of the connective tissue around a
regenerating nerve seems to have little adaptive value (Abercrombie and
Santler, 1957). In contrast, there is little overgrowth in compensatory
hypertrophy (Abercrombie, 1957; Harkness, 1957).
37
healing and compensatory hypertrophy, it is instructive to review some
of the principal characteristics of both of these types of induced growth
because it may help us to predict if the triggers are the same in both
cases.
Both wound healing and compensatory hypertrophy have in common
the loss of a portion of an organ or tissue. Usually the loss of mass in
wound healing is confined to a small area, whereas the loss of mass in
compensatory hypertrophy involves the loss of a larger portion of an
organ. There are exceptions to this generalization, as in the case of
chemical damage of the liver, e.g., with carbon tetrachloride, where the
damage is spread throughout the entire liver. The removal of a portion
of an organ or one of a pair of bilateral organs is usually not accompanied
with much damage to the organ concerned. This is especially obvious in
the best studied cases of compensatory hypertrophy, in the liver and
kidney, where the removal of a liver lobe or of one kidney is attended
with little or no damage to the organ. However, in many other cases,
such as in partial thyroidectomy and pancreatectomy the organ is
damaged. The relationship of this damage-induced growth, associated
with the removal of a portion of an organ, to the compensatory response
has never been critically evaluated. It is assumed to be unimportant.
Damage-induced growth differs from compensatory hypertrophy in
that damage induces a large amount of overgrowth of the tissues surrounding the damaged area. This overgrowth is especially obvious in
wound healing in the skin where the epidermal and adjacent hair follicle
cells undergo considerable proliferation, resulting in a thick mass of
epithelium. Overgrowth in wound healing is also obvious in the amount
of granulation tissue formed. It is in such excess that a considerable
amount of degrowth occurs (Abercrombie, 1957).
A corollary to the fact that growth is excessive after damage is that
damage-induced growth is not as adaptive as that of compensatory hypertrophy. If it were, so much overshoot in tissue growth would probably
not be seen. The excessive proliferation of the surrounding epithelium
and connective tissue is an indication of this. Moreover, the stimulation
of hair growth surrounding the wound has little obvious adaptive value.
This is even more glaring when we realize that the hair follicles are
dragged into the wound, break up, and form keratinized cysts (Argyris,
1956a). Similarly, the proliferation of the connective tissue around a
regenerating nerve seems to have little adaptive value (Abercrombie and
Santler, 1957). In contrast, there is little overgrowth in compensatory
hypertrophy (Abercrombie, 1957; Harkness, 1957).