In part I chapter 1 a description is given of the dermal wound heating process focussing on collagen metabolism in healing wounds. Although scar tissue is relatively inert there is, ciuring a relatively long period varying from one to several years, a higher level of collagen metabolism within the scar tissue than in the intact skin surrounding the wound. This makes it possible for the scar tissue to remodel and adapt to what-ever mechanical requirements there are.
Chapter 2 gives a survey of what is known from literature on the sub-ject of the influence of mechanical forces on collagen formation in scar tissue. Experiments have shown that mechanical forces are decisive for collagen fibre orientation in scar tissue. It was also found that with rats and rabbits the tensile strength of wounds increases with an increase of tension on wound edges. It is not known whether the amount of collagen in experimental wounds is also influenced by heightened tension on wound edges. After that the clinical data on the influence of mechanical forces on scar tissue were examined. Although no systematic study of this was found in literature, clinically it has long been accepted that the tension on wound edges is one of the causes of hypertrophic scars. Outside pressure applied for a long period of time may cause a diminution in hypertrophic scars.
In chapter 3 the possibilities are discussed of influencing collagen metabolism in scar tissue. Corticosteroids (triamcinolon) applied locally seem to go some way towards pharmacological control of the growth of scar tissue. Hypertrophic scars nevertheless remain relatively resistant to therapy. The operating surgeon will as far as possible have to eliminate factors that contrihute towards the formation of hypertrophic scars. Tension on wound edges is one of those factors.
1n order to obtain more insight in the role of tension on wound edges for the formation of hypertrophic scars an experiment on pigs was carried out. The experiment examined what would be the influence on collagen metabolism in a healing wound of increased tension on the wound edges. For this purpose eight pigs were anaesthetized and in their flanks experimental wounds were made. Tension on the wound edges was obtained by excising a strip of skin 1 cm wide.
In similar places on the other f1ank control wounds werc made. These were just incisions of the same length. Each time two experimental and two control wounds were made and for each pig this procedure was repeated six times at intervals of two weeks. When the pigs were sacrificed the wounds were 2 – 4 - 6 - 8 - 10 and 12 weeks old. Examination of the wounds consisted of determining the breaking strength and strain of a 1 cm wide strip of scar, the amount of neutral salt soluble, acid soluble and insoluble collagen per gram scar tissue and histological assessment of the wounds.
There was a tendency towards lower rates in the total amount of collagen per gram scar tissue in experimental wounds than in control wounds (P < 5%). On macroscopic inspection no clear difference was found between experimental and control wounds, so that it may be assumed that tension on wound edges in pigs is not a stimulus towards ac-accumulation of collagen in scar tissue. This is in contradiction with what was expected as in humans the clinical experience exists that tension on wound edges is often the cause of scar hypertrophy. The salt soluble collagen fraction represents newly formed collagen. The fact that there was a tendency towards higher neutral salt soluble collagen fractions in experimental wounds then in control wounds (P < 5%) is an indication that the collagen synthesis was higher in experimental wounds. The total amount of new formed collagen in the scars did not increase. So it may be assumed that the collagen degradation in experimental wounds was increased as well. Hence the collagen metabolism in scar tissue of pigs is determined among other things by tension on wound edges du-ring the first postoperative months (remodeling phase).
Experimental wounds showed a clear tendency towards higher breaking strength than control wounds (P < 5%). No difference was detected for strain.
No histological difference was found between experimental and control wounds as regards the micro-architecture of the collagen tissue as assessed by normal light microscopy, polarized light microscopy and differential-interference contrast microscopy. The difference in breaking strength between experimental and control wounds without difference in micro-architecture of the collagen tissue and without increase in the amount of collagen may therefore be explained as a qualitative and/or quantitative change in the molecular cross-linking mechanism affected by increased tension on the wound edges.