However, raw EGF thus manufactured is easily broken down by certain enzymes that abound in chronic wounds. This is why gels with such unmodified EGF do not really heal chronic wounds such as bed sores or diabetic feet ulcers.

Moreover, the release of unmodified EGF from these gels into the wounds cannot be controlled. Most of it is released in an initial burst and then it is all diffused. Binding EGF to other molecules like collagen can slow down that diffusion. This may keep the EGF in situ so it can work on EGF receptors that are found on cell surfaces.

When EGF docks on EGF-specific receptors, it causes the latter to send the right signals to the insides of cells. These signals then trigger off certain well regulated cellular processes.

The reason scientists strive for a better EGF gel is that chronic ulcers are almost impossible to heal. In the bedridden, such as stroke patients, bedsores can lead to tissue death and thence blood poisoning, which can kill. Then there are foot ulcers which account for more hospitalisations than any other diabetic complication.

While using EGF gels for chronic ulcers seems eminently reasonable, stimulating EGF receptors unnecessarily - in the hope of stemming skin ageing, say - seems unwise for two reasons.