Colette Hourseau

Ageing and hair cycles

The phototrichogram is a non‐invasive technique by which, on the same precise area of the scalp, each individual hair may be identified, and its current growth phase established. This technique was used to study the duration of hair cycles in 10 male subjects, balding and non‐balding, by observations at monthly intervals over a period of 8‐14 years. The accumulated data served to characterize the effects of ageing in these subjects: a reduction in the duration of hair growth and in the diameter of hair shafts, most evident in the thickest hairs, and a prolongation of the interval separating the loss of a hair in telogen and the emergence of a replacement hair in anagen. These various aspects of ageing of scalp hair contribute to its progressive overall impoverishment. They resemble those observed in the course of male‐pattern balding, although their development is less marked.

Hair cycle and alopecia.

Male pattern alopecia is the outcome of profound modifications in the duration, succession and frequency of hair cycles. These phenomena were studied by phototrichogram in 10 male subjects, with or without alopecia, over a period of 15 years. Almost 10,000 hair cycles were accounted for, yielding a detailed picture of the alopecia condition: (1) A decrease in the duration of anagen for a certain proportion of hairs, a proportion which increases in size, the more advanced the alopecia; the result of this premature transformation from anagen to telogen is an increase in the rate of hair loss. (2) A parallel decline in hair diameter. (3) Longer latency periods between the fall of a hair and the onset of regrowth, leading to a reduction in the number of hairs present on the scalp surface. The shorter finer hairs are absent more frequently and absent for longer periods and this contributes to the effect of alopecia.

MEXORYL SX : A BROAD ABSORPTION UVA FILTER PROTECTS HUMAN SKIN FROM THE EFFECTS OF REPEATED SUBERYTHEMAL DOSES OF UVA

There is now considerable evidence that chronic UVA exposure induces damage in animal and human skin; however, little is known about UVA protection of human skin. The aim of this study is to evaluate the efficacy of Mexoryl SX, a broad UVA absorber (lamada max = 345 nm) against UVA-induced changes in human skin. The regimen of UVA exposure (13 weeks with increasing suberythemal doses) induces intense pigmentation with no erythema. Skin hydration and elasticity decrease, whereas total skin thickness, assessed by echography, remains unchanged. Irradiated epidermis reveals a significant thickening of the stratum corneum, an absence of hyperplasia and an increase in the expression of the protective iron-storage protein ferritin. No significant alterations are seen using antisera against type IV collagen or laminin, suggesting that the dermal-epidermal junction (DEJ) is mainly preserved. In dermis, enhanced expression of tenascin is seen just below the DEJ but type I procollagen, which is localized at the same site, is unaltered. Although we are unable to visualize any changes in elastic network organization using Luna staining or specific antiserum directed against human elastin, we notice an increased deposition of lysozyme or alpha-1 antitrypsin on elastin fibres. Mexoryl SX (5%) efficiently prevents these alterations. Thus, these results suggest that UVA photoprotection can prevent early putative alterations leading to photoageing.

Accumulated p53 protein and UVA protection level of sunscreens

Nuclear p53 expression is a sensitive parameter for the detection of ultraviolet (UV)‐induced skin damage, and it has been used as an endpoint to evaluate the effectiveness of sunscreens. In this study, we compared the protection provided by two sunscreens having identical sun protection factors (SPF) but different UVA protection factors (UVA‐PF) measured by the persistent pigment darkening method (PPD). The SPF of the sunscreens was 7 and the UVA‐PF were respectively 7 and 3. Nuclear p53 protein was quantified in human skin biopsies treated with sunscreens and exposed 8 times to 5 MED of solar simulated radiation (SSR). The results showed that both sunscreens offered only partial protection against the increased expression of nuclear p53 protein induced by repetitive SSR exposures. However, a significantly lower level of p53‐positive cells was found in areas protected with the sunscreen having the higher UVA‐PF compared to the other sunscreen protected areas. In order to verify whether the difference in efficacy of these products was due to the difference in UVA absorption capacity, we quantified epidermal p53 protein accumulation after 8 exposures to either UVA (320–400 nm) or UVA1 (340–400 nm). We showed that as with SSR, repetitive exposures to 12.5 and 25 J/cm2 of UVA or UVA1 induced a significant increase in p53‐positive cells in the human epidermis. These results confirmed that SPF determined on the basis of an acute erythemal reaction does not predict the level of protection against cumulative damage. They also showed that the protection provided by two sunscreens with different UVA protection factors is different (based on nuclear p53 protein accumulation), and that the PPD method can distinguish varying levels of sunscreen efficacy against UVA‐induced cell damage.