2
THOMAS S. ARGYRIS
inhibitor may not be the intiating step responsible for the stimulation of
growth in wound healing. The evidence for the release of stimulators, or
for sublethal intracellular damage, as the stimulus mechanism for
damage-induced growth will also be discussed. Evidence will be presented
that suggests that the mechanism involved in the initiation of growth in
compensatory hypertrophy may not be the same as that in wound healing.
It will be recommended that the loss of inhibitor and other hypotheses
should be maintained and used as a system of multiple hypotheses upon
which to base future experiments.
II. Nature of the Tissue Response to Damage
A. Introduction
We shall discuss primarily the proliferative response of the skin tissues
to a cut, but the principles apply to the proliferative response of almost
any tissue to damage.
Damage results in a proliferative response by all the competent tissues
surrounding the wound. If the damage is severe enough and/or our
instruments sensitive enough, we can also detect that damage produces
systemic effects that are not growth-promoting in the usual sense of the
word. In this review we shall not discuss the nongrowth-promoting
systemic effects produced by damage. Good reviews on this subject are
abundant (Arey, 1936; Moore, 1956; Slome, 1961; Stoner, 1960; Williamson, 1957). Nor shall we consider in detail the proliferative response of
each tissue surrounding the wound. We shall describe the proliferative
events only in so far as they are necessary for us to discuss the mechanism
by which growth might be induced by damage. (For details of the
response of skin and other organs to damage, many reviews are available,
see for example, Abercrombie, 1957; Arey, 1936; Argyris, 1964; Bullough,
1962, 1965; Cameron, 1952, 1955; Johnson and McMinn, 1960; Montagna
and Billingham, 1964; Needham, 1960; Russell and Billingham, 1962;
Stoner, 1960; Washburn, 1960; Wright, 1958.)
B. The Response of the Skin Tissues to Damage
1. The Response of the
Epidermis
Damage results in the thickening of the epidermis adjacent to the
wound (Fig. 1). This thickening owes to both cellular proliferation and
enlargement (Arey, 1936; Allgower, 1956; Argyris, 1954, 1956a; Argyris
and Bell, 1959; Bullough and Laurence, 1960a; Johnson and McMinn,
THOMAS S. ARGYRIS
inhibitor may not be the intiating step responsible for the stimulation of
growth in wound healing. The evidence for the release of stimulators, or
for sublethal intracellular damage, as the stimulus mechanism for
damage-induced growth will also be discussed. Evidence will be presented
that suggests that the mechanism involved in the initiation of growth in
compensatory hypertrophy may not be the same as that in wound healing.
It will be recommended that the loss of inhibitor and other hypotheses
should be maintained and used as a system of multiple hypotheses upon
which to base future experiments.
II. Nature of the Tissue Response to Damage
A. Introduction
We shall discuss primarily the proliferative response of the skin tissues
to a cut, but the principles apply to the proliferative response of almost
any tissue to damage.
Damage results in a proliferative response by all the competent tissues
surrounding the wound. If the damage is severe enough and/or our
instruments sensitive enough, we can also detect that damage produces
systemic effects that are not growth-promoting in the usual sense of the
word. In this review we shall not discuss the nongrowth-promoting
systemic effects produced by damage. Good reviews on this subject are
abundant (Arey, 1936; Moore, 1956; Slome, 1961; Stoner, 1960; Williamson, 1957). Nor shall we consider in detail the proliferative response of
each tissue surrounding the wound. We shall describe the proliferative
events only in so far as they are necessary for us to discuss the mechanism
by which growth might be induced by damage. (For details of the
response of skin and other organs to damage, many reviews are available,
see for example, Abercrombie, 1957; Arey, 1936; Argyris, 1964; Bullough,
1962, 1965; Cameron, 1952, 1955; Johnson and McMinn, 1960; Montagna
and Billingham, 1964; Needham, 1960; Russell and Billingham, 1962;
Stoner, 1960; Washburn, 1960; Wright, 1958.)
B. The Response of the Skin Tissues to Damage
1. The Response of the
Epidermis
Damage results in the thickening of the epidermis adjacent to the
wound (Fig. 1). This thickening owes to both cellular proliferation and
enlargement (Arey, 1936; Allgower, 1956; Argyris, 1954, 1956a; Argyris
and Bell, 1959; Bullough and Laurence, 1960a; Johnson and McMinn,