The benefits of quitting smoking on the skin

Finn GOTTRUP and his colleagues measured the effect of smoking cessation on the epidermal healing of a wound and collagenase, the enzyme that breaks down collagen. To do this, skin fluid samples were taken from 48 smokers (aged 33, smoking 20 packs per day) and 30 people who had never smoked, and the epidermis was excised. Transepidermal water loss (TEWL) was measured after two, four and seven days, which increases during an injury, and decreases during the healing process. Subsequently, the smokers were randomly divided between continuous smoking or withdrawal with a nicotine patch. The sequence was repeated after 4, 8 and 12 weeks, and the levels of matrix metalloproteinase MMP-8 and MMP-1, and neutrophils in the fluid were evaluated by an immuno-enzymatic test.

One week after the injury, the TEWL (Transepidermal Water Loss) showed no significant difference between smokers and abstainers, respectively 17.20 g/cm2 per hour and 18.95 g/cm2 per hour. However, individuals who had never smoked showed a TEWL of 13.89 g/cm2 per hour. Consequently, the healing progression of abstaining smokers was similar to that of smokers and significantly slower than that of individuals who had never smoked.

However, in smokers, the level of MMP-8 was 36.4 ng/mL, compared to 15.2 ng/mL in those who had never smoked. The level of MMP-8 in abstinent smokers was 21.2 ng/mL, after four weeks of cessation. Therefore, the MMP-8 level in abstinent smokers was almost half that of smokers and was not significantly different from those who had never smoked. MMP-1 was not affected by smoking and abstinence. After abstinence, the number of neutrophils in the blood significantly decreased to the level of those who had never smoked. The correlation between MMP-8 and the neutrophil count is significant. Indeed, neutrophils produce MMP-8.

What are the mechanisms involved?

These results suggest a long-term impairment of healing in smokers, but a potential reversibility of extracellular matrix degradation four weeks after smoking cessation. Indeed, MMP-8 is a collagenase that limits the rate of degradation of fibrillar collagen I and III and is primarily released by polymorphonuclear neutrophils. Additionally, it is expressed by epidermal keratinocytes during healing. Type I collagen is abundant in the skin and scar tissue.

As an enzyme that breaks down collagen I, MMP-8 could potentially be involved in the tissue rupture mechanism as observed in smokers. It can be hypothesised that quitting smoking leads to a decrease in collagen degradation, and therefore a certain restoration of skin elasticity through the reduction of neutrophil levels and consequently MMP-8, but the effects on healing could be permanent.

Once again, additional studies may shed light on these results.