Mode of action

For silicone, several mechanisms of action have been proposed in relation to scar management. Some of the most relevant medical studies are discussing the following aspects:

Release of low molecular weight silicone [1]

Study content: An in-vitro release of low-molecular-weight silicone fluid from a Silicone Gel was most likely responsible for its efficacy.

Note: There have been studies both in favour and against these findings probably due to the fact that different silicone formulations (e.g. sheets, oil or gel) have slightly different properties.

Acts at the “Stratum Corneum” reducing evaporation [2]

Study content: Results from the study suggest that silicone induces mild hydration of the Stratum Corneum (SC) especially after its repeated treatments. It seems to keep the SC in an adequately but not over-hydrated condition, preventing the development of hydration dermatitis.

The precise mechanism by which the silicone prevents the excessive hydration of the SC is still not clear from the results of the present study. However, we think that silicone produces a situation in which it acts as if it were a part of the underlying SC, protecting the skin surface from various external stimuli that increase pruritus and the consequent inadvertent scratching of the scars without perturbing the SC function.

Static electricity on silicone helps in the alignment of collagen deposition [3]

Study content: Silicone occlusive sheeting (SOS) in the management of hypertrophic and keloid scarring, including the possible mode of action of silicone, by static electricity.

Note: The passage of static electricity over a prolonged period of time may be the critical factor in scar inhibition. It is postulated that over a period of weeks to months the resulting electrical field may have some inhibitory effect on the scar tissue.

Positive influence on overproduction of growth factors [4]

Study content: The effect of Silicone Gel on basic fibroblast growth factor levels in fibroblast cell culture.

Conclusions: These results suggest that Silicone Gel is responsible for increased bFGF levels in normal and foetal dermal fibroblasts. We postulate that Silicone Gel treats and prevents hypertrophic scar tissue, which contains histologically normal fibroblasts, by modulating expression of growth factors such as bFGF. Our data support the hypothesis that substances that favourably influence wound healing do so by correcting a deficiency or overabundance of the growth factors that orchestrate the tissue repair process.

Normal and foetal fibroblasts exhibit higher levels of bFGF when exposed to Silicone Gel. The increase in bFGF level associated with silicone treatment of normal fibroblasts, which are found in normal and hypertrophic scar tissue; suggests a possible mechanism of action for the clinically observed response of hypertrophic scar tissue to Silicone Gel normal and foetal fibroblasts exhibit higher levels of bFGF when exposed to Silicone Gel. The increase in bFGF level associated with silicone treatment of normal fibroblasts, which are found in normal and hypertrophic scar tissue; suggests a possible mechanism of action for the clinically observed response of hypertrophic scar tissue to Silicone Gel. An increase in bFGF concentration would result in a reduction of collagen proliferation.

General Conclusions:

The exact mechanism of action by which Silicone Gel works is still unknown. Many have agreed that it acts at the stratum corneum, which reduces evaporation and restore homeostasis. Therefore it reduces mast cell activity, oedema, vasodilatation, and excessive extra cellular matrix formation.[5]

The release of low molecular weight silicone particles has been debated by many investigators but experts continue to believe that there may be a chemical effect.

A group of publications have demonstrated the in-vitro, positive effect of silicone over growth factors and collagen concentration.

It is possible that not one but several of these mechanisms are involved in the positive effect of silicone over scar tissue formation.

 

References

  • Quinn KJ. et al. Burns 1985;12:102–108
  • Suetake T et al. Br J Plast Surg 2000;53:503-507
  • Hirshowitz B et al. Plast Reconstr Surg 1998;101:1173-1183
  • Hanasono MM et al. Arch Facial Plast Surg 2004;6:88-93
  • Chan KY et al. Plast Reconstr Surg 2005;116(4):1013-1020
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