Stretch marks: prevent and reduce them

To segment the sale of the cosmetic, it is aimed at specific imperfections. Wrinkles, skin spots, signs of aging on the face. Cellulite, localized fat deposits, stretch marks on the body.
– Stretch marks: let’s see them
– Treatments for stretch marks
For various reasons, treatments to reduce stretch marks have a very limited impact on the market even if some cosmetics, such as Bio-Oil have had great success in sales by specifically associating themselves with this imperfection.
The fact that there are relatively few cosmetics intended for the treatment of stretch marks is not due specifically to the lack of evidence on their effectiveness, in fact cosmetics against cellulite or localized adiposity are not much more credible. The limited supply is probably conditioned not only by the scarce effectiveness, but also by the limited extent of the imperfection that generally involves a lower consumption of the product.
Stretch marks: let’s see them
Stretch marks, in the Latinorum medicale called “striae” , are permanent signs of the skin whose prevalence varies between 20% and 70%, manifesting themselves mainly in young women and subject to rapid increases in body mass. They appear in different circumstances (physiological, pathological, iatrogenic 1) and affect the dermal structure up to the reticular dermis. The cause has not been well identified, mainly affecting a young, female population, in areas stressed by repeated movements or subject to significant increases in mass with consequent extension of the skin. They occur above all in certain areas, normally disposing along precise lines that suggest they are related to a mechanical distension, such as the tearing of a fabric perpendicular to the forces that stimulate it, hence the name of “ striae distensae “. The skin is mostly less compact, of less volume, slightly depressed and without glands, hence the name of ” striae atrophicans (atrophic)”, with a lighter color, hence the name of ” striae albae”. The complex of skin marks is very similar to the outcomes of a scar. Stretch marks are formed and evolve through different phases and in many cases the initial phase seems associated with an inflamed state, recognizable by a characteristic darker, red color ( striae rubrae ) but which can modulate from cerulean to purple up to an intense brown ( striae nigrae ). It is not proven that the red or pink coloration of the early phase is always due to an inflammatory condition since it can also depend only on the greater transparency of the skin subject to distension. While lasting and indelible, they can spontaneously shrink and regress.
A certain affinity with scars and the positive correlation with some pathologies (Cushing and Marfan syndrome) suggest the contribution of genetic, biochemical-hormonal and mechanical factors. The histological appearance of stretch marks varies according to the evolutionary phase. The epidermis, in the early phase ( striae rubrae ), appears practically normal. Only later does it become atrophic, reducing its thickness and smoothing itself (clearer and shinier appearance) until the papillary design completely disappears. In the dermis, the main histological changes occur in all its components: cellular, intercellular and fibrous (collagen and elastin).
While in the skin the structures and fibrous septae, both of collagen and of elastin, have a chaotic arrangement, tendentially trabecular, in the stretch marks, as in the scars a substantial alignment is detected, resulting in tendency perpendicular to the length of the stretch mark and, above all, as in the scars, parallel to the dermo-epidermal junction and to the surface of the skin.
The dermis is thinned, its thickness may be less than half of the contiguous one not subject to stretch mark. In the initial phase ( striae rubrae ) a modest perivascular infiltrate, predominantly lympho-monocytic, an increase in Langherans cells was detected. There are some mast cells that appear degranulated while the fibroblasts are in the quiescent phase. In the late stage ( striae albae) cellular alterations and cellular infiltrate regress, with evident signs of normalization of both fibroblasts and mast cells. Collagen fibers appear altered both in the initial and late stages: there are aspects of fragmentation and thinning which then tend to regress, but a constant feature is their arrangement parallel to the dermo-epidermal junction in the papillary dermis. In the deep dermis the collagen bundles appear compacted, as if by reduction of the intercellular substance. Even the elastic fibers, in early lesions, are characterized by various alterations, such as breaks, curling, elongation and especially thinning, especially in the central area of ​​the lesion; instead they tend to appear thickened in late lesions, i.e. in the scarring phase, and to assume aspects of normality, albeit with a different architecture and greater alignment. Even the elastic component, such as collagen, in practice undergoes a regenerative process, giving the lesion characteristics similar to those of scar tissue.
Treatments
Stretch mark is a manifestation of very specific changes in the skin tissues due to various factors that are not yet well understood.
It cannot be reduced or eliminated without “restructuring” the architecture of the dermis as well, restoring conditions similar to those of normal skin.
For this reason, topical treatments and remedies to reduce stretch marks in the late phase ( striae albae ) are lacking not only in terms of evidence of results, but also in the rationale why these results should be there. The situation is better for stretch marks treated in the initial phase, striae rubrae , or for preventive treatments.
Although stretch marks are essentially an aesthetic problem that has little impact on both health and social relationships, there are many medical or scientific publications (but many should be considered pseudo-medical and pseudoscientific) that discuss how to prevent, treat or reduce them. Some of the treatments suggested to reduce stretch marks are similar to those used in the treatment of scars.
Various reviews and meta-analyzes of these publications have concluded that research on the effectiveness of stretch mark treatments suffers from significant methodological deficiencies, draws controversial conclusions, obtains inconclusive results, and proposes implausible rationale.
For some time, the positive correlation with Cushing’s and Marfan’s disease and negative in pregnant women with Ehlers-Danlos syndrome, have associated the onset of stretch marks with the cortisol content and an “imbalance” in the protein components: fillagrin , collagen, elastin. But a precise causal mechanism has not been identified. What underlies the appearance of stretch marks seems to be a qualitative-quantitative modification of collagen and elastin, which would lead to an altered molecular structure of the fibers with consequent variation in the architecture of the dermis.
Since the causes are not clear, it is difficult to understand how to prevent or reduce these structural changes in the skin.
In short, there is a lot of talk about it, but a “first choice” treatment that gives a high probability of success has not yet been identified.
Many cosmetic brands have focused on the confused concept of “elasticizing the skin”.
They are mostly cosmetics formulated in emulsion for the body with botanical extracts: Centella asiatica (see: Trofolastin – Clarins – Bepanthenol) or with flavonoids and tannins (see: Rilastin – Phytolastil by Lierac – Somatoline) of which some in vitro tests would show an alleged effectiveness.
The root “lastil” often appears in the name of the product or ingredient, which suggests the elasticity of the skin or elastin.
Some are unbalanced with less plausible claims such as: stimulating the production of elastin and collagen, reducing elastosis, etc.
Apart from the teratogenic risk in pregnant women, another active ingredient proposed in the dermatological field for the topical treatment of stretch marks is Tretinoin.
The effectiveness of the various active ingredients proposed, generally supported only by some in vitro tests, is highly questionable and always assuming that the products contain adequate concentrations, no one sensibly explains how they could “restructure” an already formed stretch mark.
The current trend is therefore to sell products to “prevent” the formation of stretch marks, given the relative result obtained with a good systematic massage.
Even in the prevention of stretch marks, the evidence that massage with a specific oil or with a specific active is more effective than any product to be massaged is scarce and not very credible. One gets the impression that it is the mechanical and “plastic” action of the massage and the “manipulation” of the stretch mark associated with an increase in skin hydration that produces some relative results.
The approach is different, with some success on stretch marks, especially in the initial phase, of the treatments that involve a “limited damage” which is followed by the normal repairing processes of the skin. A good example is the chemical peel. It can be made with both cosmetic acids and trichloroacetic acid or other dermatological peelings. The chemical peel on stretch marks presumably acts with mechanisms similar to those that lead to a partial restructuring of the dermis in wrinkles. The always relative effectiveness of peeling is also confirmed with mechanical peeling techniques, typically with dermabrasion.
Among other things, they are treatments that can produce a slight increase in pigmentation, which, although it is normally considered an adverse reaction of almost all chemical peels if you are subsequently exposed to UV, in the case of white and shiny stretch marks it helps to reduce the evidence. However, this technique introduces the risk, difficult to control, of producing more unsightly spots than the stretch mark itself. The possibility of partially masking the striae albaeacting above all on pigmentation, it has been proven with controversial results both with self-tanning products and with resorcinol-based peels. Some research has tested only exposure to UVB sources focused in the stretch mark area, with partial results but suggesting potential developments. The results with the use of photodynamic therapies with the interaction between light and photosensitizing agents are more interesting.
Still in the field of “limited damage” we can consider treatments such as microperforation (needling or laser fraxel) in addition to laser resurfacing which seem to give encouraging results.
The rationale supporting treatments with radiofrequency or with lower power density light (pulsed light, IPL, Laser or Led) is different. Excluding the effect of any ultraviolet rays and the interaction with any photosensitizing active, these are techniques that would act only as a function of the heat induced by the radiation.
Not reaching the levels of heat that lead to necrosis and vaporization of superficial tissues, as in resurfacing, at low levels a sort of biostimulation is hypothesized, while at higher levels of energy density, the tissues reach 60 ° C for a time sufficient, biochemical reactions are also hypothesized, breaking of cross-links in long protein chains, formation of HSP ( Heat shock protein) of which, however, it is not clear whether they interfere positively or negatively in any “reparative” processes of the stretch mark.
Even if not practiced, specific surgical actions are possible aimed at reducing the imperfection. While the surgical perforation of the stretch mark can now be easily replaced by needling or fraxel, the partial subcision has given conflicting results in the face of particularly high risks of adverse reactions.
However invasive and with questionable results some treatments proposed with subcutaneous injections of hyaluronic acid, collagen, autologous plasma enriched with piastine, cortisone or other presumed active.
Rodolfo Baraldini

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