|Themes: Aesthetic Mesotherapy, Controversies in Aesthetic Medicine, Combination Therapy.
The majority of modalities used for skin rejuvenation incorporate the wound healing process. Conventional wisdom has leaned towards more is best. The biggest challenge is finding the balance between the degrees of injury (acceptable downtime) and effectiveness (best outcome). Darker skin types limit aggressive treatments. Ablative treatments, e.g. laser resurfacing and deep peeling, while aesthetically effective, may cause epidermal thinning, papillary dermis fibrosis and cicatricial healing. Fractional treatments minimize this effect, but there is still up to 20% coagulation of tissue and the ensuing necrosis stimulates cicatricial healing. Medical needling does exactly the opposite, which is ideal.
Preservation of the epidermis maintains environmental protection and minimizes downtime. There are no reported post treatment pigmentation issues, even with sun exposure. The procedure breaks down scar tissue, allowing reorganization. It can be performed on most areas of the body by individuals with minimal skills and requires minimal capital outlay.
Percutaneous collagen induction uses thousands of tiny needle pricks into the upper dermis to trigger the wound healing cascade. The upregulation of TGF-B3 through this process is thought to be the reason for natural collagen regeneration following needling, as opposed to scar collagen secondary to TGF-B1 and B2 associated with thermal injury.
Understanding the predictable phases of wound healing dictates optimum timing for treatment and modalities to obtain greatest success. Prolonging the inflammatory phase (day 1-5) will result in more growth factors. Photomodulation and lymph drainage are valuable from day 2-14 and then cosmetic rolling combined with Sonophoresis and micro-current are beneficial to assist maximum delivery of nutrients to cells. Collagenase peaks at around day 14 to reorganize collagen fibrils, converting collagen 3 to collagen 1 and it therefore makes no sense to reinjure the skin more frequently than every 30 days.
Collagen synthesis requires Vitamin A (e.g. Retinyl Palmitate, Retinyl Acetate, Retinol or Tretinoin), Vitamin C (e.g. Magnesium Ascorbyl Phosphate, L-Ascorbic Acid), key amino acids (proline & glycine), bioflavonoids, growth factors, selenium, silicon allied with magnesium and calcium, copper peptides, zinc and iron (co-factors), hormones and essential fatty acids (for cell function and membranes). Stem cell products and platelet rich therapy hold enormous promise.
Does depth of injury matter?
To gain some insight, a retrospective study on 44 patients was done using data from Visia Skin Analysis to provide objective numbers. While there are many variables (age, lifestyle, compliance, active ingredients and dose applied topically, duration of treatment etc.) the positive findings are encouraging in that they were obtained, for the most part, under least favorable conditions (compliance).
Methods: Measurements for brown spots, pores, wrinkles, evenness and UV spots were used to determine effectiveness of products alone vs. the use of rollers with 0.2 mm, 0.3 mm, 0.5 mm, 1 mm and 2 mm long needles combined with products.
Editors note: This article was originally published back in 2004, and since that time there has been increasing controversy of both the dangers associated with use and the questionable professional ethics of beauty therapists/aestheticians providing sun bed facilities. With the emergence of new sunbed (Or Solarium) standards in many parts of the world, we thought it would be a good idea to review and update the article.
While tanning booths and sunbeds are a popular revenue earner in many beauty salons, little thought is given to the damage they can cause to the cells of the skin through prolonged or unsupervised use.
The negative effects of UVA from the sunbed will often require remedial treatments that will cost far more than the cost of the sunbed tan did.
While it is true that the UVR spectrum of most sun beds does not cause erythema, there is still damage being caused at a cellular level, and for some individuals this can lead to melanomas and skin cancers.
In the US, the FDA warns that some tanning operators may claim that UVA sunlamps and sunbeds are safer than the sun and UVB lamps. This is not true. In fact, exposure to the UV radiation from sunlamps adds to the total amount of UV radiation you get from the sun during your lifetime, further increasing your risk of cancer.
Such was the concern; the American Medical Association (AMA) passed a resolution in 1994 calling for a ban of the use of suntan parlour equipment for non-medical purposes. U.S Dermatologists have also urged the FDA to take action to discourage use of suntan parlours and suntan beds.
In many sun tanning clinics, there is a degree of consultation with the client regarding the suitability of a particular skin type for specific frequency/duration of treatments, however in some clinics it is just a "pay and self-serve use" approach.
(This is more prevalent in Hairdressing salons than Aesthetics and beauty clinics)
While sunbed clinic operators who do provide a consultation and believe they may be providing a safe service for their clients, there is an important factor to consider:
With the mixed ethnicity of many people, it is difficult to gauge the risk of using the sunbeds by simply observing the colour of their skin. Mixed genetic pools will often disguise or alter the REAL Fitzpatrick rating for the particular skin colour and therefore the risk. Without some way to measure the melanin content to calculate the risk, how can we be sure we will not have a time bomb on our hands? (My own skin is a perfect example of this) Although melanin measuring devices have been around for over ten years, a majority of operators choose not to use them. (Or don't think they need to)
In many countries, health authorities provide guidelines for the use of artificial sun tanning devices, (Such as this example from the UK) however with the emergence of more and more artificial UV related issues, (Including death) there are likely to be more stringent regulations on the horizon.
UVA is the silent killer of cells
Skin is a potential target of oxidative injury because it is continuously exposed to visible light, ultra violet irradiation and oxygen, all critical for the maintenance of cellular life.
Skin is the bodys first line of barrier defence, and as part of the skin structure there are numerous other types of barrier defence system designed to protect those structures themselves.
It is well accepted that alterations in skin lipids due to exposure to UVR result in membrane damage. The major reactive species that can initiate lipid peroxidation is the hydroxyl radical OH. Damages of the membrane function are associated with a variety of harmful skin alterations.
UVR leads to erythema, chronic exposure leads to acceleration of the skin aging process and increased risk of skin cancer development over time.
Sun light components responsible for photo aging are wavelength region arbitrarily defined as UVB, which is in the range of 290 to 320 nm. UVB light normally penetrates the epidermis.
UVA is in the range 320 to 400nm (also called long and short UVA respectively, or UVA 1 & UVA 2) and is considered less damaging at a given dose or irradiation, however it penetrates much more deeply into the skin and has a greater effect on dermal tissue.
UVA is the primary wavelength used in sun beds because it causes the tanning reaction both the immediate tanning and immediate pigment darkening reaction. (IPD) and the delayed tanning reaction, or new melanogenisis.
UVA can also evoke the sunburn reaction, but the erythema or sunburn producing capacity of UVA is very weak, but the long term deleterious effects on the skin and accelerating skin aging are high.
Although UVA radiation causes less erythema than UVB, it is becoming increasingly clear that this spectrum of sunlight is insidious and cannot be disregarded.
UVA Skin Cell Damage
- Damage to melanocytes caused by DNA damage
- Vit C oxidization
- Impair Vitamin A receptors within cell membranes
- Excess keratinisation
- DNA damage and inhibition of DNA synthesis
- Depletion of epidermal Langerhans cells reducing skin barrier defence
- Increase in matrix metalloproteinases (MMPs) cause damage to collagen and elastin fibres
- Damage to cell membranes through lipid peroxidation
- Increase in free radicals
UVA induced photosensitivity
What is not well know is that UVA is the portion of the UV spectrum most often associated with photosensitivity resulting from drugs and disease.
Sunbed clients taking certain prescription drugs can unknowingly increase their reaction to ultraviolet radiation. These drugs may not make them noticeably sensitive to sunlight, but they may make them very sensitive to the intense ultraviolet radiation in a tanning booth.
In the US, the FDA has published a list of medications that increased sensitivity to light (HHS Publication FDA 91-8280).
These drugs include, but are not limited to:
- Some antibiotics
- Some high blood pressure medications
- Some tranquilizers
- Some birth control pills
- Some oral diabetes medications
A final word...
If you have a sun bed in your clinic & believe you are a Professional skin treatment therapist, think again!
A TAN IS A SCAR! This statement should be enough to stop skin treatment therapists offering the service of sunbeds in clinics.
It is well known that treatments for the ageing skin are a large part of the services offered by a beauty salon. Treatments for skin lightening, wrinkles, resurfacing, muscle atrophy and more, so why offer a service that is going accelerate all of these conditions?
In the eyes of consumer protection agencies it could be considered professional negligence.
The legal implications abound.
Note: In March 2008, Australian authorities introduced new regulations for operators of sunbed and solarium clinics. The regulations raised the minimum age for users from 15 to 18-years-old.
The regulations will also prohibit solarium use for people with fair skin. Under the new laws the frequency and duration of solarium sessions will also be limited.
|Florence Barrett-Hill is Australasias leading independent beauty therapy technical educator, therapist, researcher and author who has vast experience covering all aspects of professional beauty therapy and paramedical skin care.
Florence has over 30 years of experience and holds over a dozen diplomas and international qualifications covering every aspect of modern skin treatment therapy. Her ground-breaking book "Advanced Skin Analysis" has received critical acclaim worldwide and is a standard text in many beauty therapy schools and colleges.
Florence is the director of Pastiche Resources, an international post graduate education service provider. Pastiche offer training programs covering a myriad of technical subjects internationally.
2004 Virtual Beauty Corp
I have a concern; and that is, we are observing an epidemic of over-exfoliation in the beauty therapy industry.
It is the lets peel it mind set that so many therapists have as a first choice treatment modality that is my greatest concern.
An epidemic of over-exfoliation
This has came about from the advent of glycolic peels in the early nineties, and progressed on through to now, with Microdermabrasion machines, enzymes and acids galore to choose from.
It is as if the industry has forgotten that one of the ethics of the beauty therapy profession is to preserve the integrity of the epidermis at all times. Have we also forgotten that the epidermis, a major line of skin barrier defence contains many intricate systems that work in synergy with one another to protect the body?
Each day the skin suffers multiple attacks, whether physical or mechanical, from undesirable microorganisms or the sun.
It withstands these with very sophisticated detection, protection and defence systems in the epidermis and dermis. In addition to its protective function the skin also has a metabolic function, and a sensory function. Finally, it must maintain its integrity by repairing itself.
To carry out its protective task, the skin must be a resistant and impermeable barrier. This role falls in large part on the epidermis, directly Impermeable.... but not impenetrable
The keratinocyte is a hydrophobic cell with a lifecycle is around 10-15 days from mitosis to arriving in the stratum corneum layer as a corneocyte; it will then take around 3-5 days to desquamate.
All other cells of the epidermis have a lifecycle of 28-30 days.
It is the superficial layer of the skin (stratum corneum), which makes the skin impermeable and hydrophobic, protecting the underlying dermis and subcutaneous layers. This layer also resists chemical attacks, thanks to the corneocytes filled with the hard insoluble protein keratin the lipid cement (bilayers) and corneo-desmosome, which ensures cohesion between the corneocytes, and therefore impermeability.
The first line of "skin barrier defence"
Skin is covered by the acid mantle (pH between 4 and 5.5). This is the hydrolipidic film which has all the prope
rties required to prevent non-resident bacteria from developing and maintain the skin's barrier. It is composed of a mixture of sweat, sebum and lipids to which antibiotic peptides are added called defensins and dermcidins synthesised by the sweat glands. The horny layer is not a sterile place and numerous resident bacteria (1012 bacteria/m2) are sheltered there and prosper in the inter-corneocytic spaces.
Normal skin flora; are microbes, mostly bacteria, that live symbiotically in and on the body with, usually, no harmful effects to us. Three species of bacteria are particularly well adapted to withstand the acid environment and antibiotic peptides: Staphylococcus, Propionibacterium and Corynebacterium. The microflora of the acid mantle is an important part of human skin contributing to its function and activities. The various resident species are of an advantage in most cases but under some circumstances and with some groups of people the skin microflora is involved in minor to major pathological processes, e.g. acne.
Maintaining the physiological pH of the skin is essential to avoid the proliferation of pathogens and an excess or lack of hygiene upsets the equilibrium of this cutaneous flora.
Hydrolipidic Film (acid mantle) also maintains hydration; Free water from the dermis continually crosses the epidermis by capillarity and evaporates from the surface of the skin, known as the Trans Epidermal Water Loss, or TEWL (on average 9g/m2of skin per hour). In addition to creating an environment for the skin flora to reside, the hydrolipidic film (acid mantle) plays the important role of maintaining epidermal hydration by slowing down transdermal water loss (TEWL). Plus creating a physical barrier to friction and movement.
Sentries lying in wait
The skin has a very elaborate defence system, where different types of cells act together or successively.
Langerhans cells (LCs), which are dendritic cells originating from the bone marrow, then by T-lymphocytes and macrophages. (See wound healing article) LCs: located above the basal layer, are large cells with long, branching extensions or dendrites. Some of these reach the dermo-epidermal junction; others come close to the stratum corneum.
The close relationship between LCs and KCs through the LCs dendrites; together they form a genuine immuno-competent epidermal unit. Although LCs make up only 2 to 4% of epidermal cells by number, they represent more than 25% of the skin barrier defence of the epidermis.
Langerhans cells are responsible for immune response against an antigen applied locally to the skin.
If an antigen penetrates and crosses the horny layer, these cells take charge of it and leave the epidermis. Within less than 6 hours they may be found in dermal lymphatic vessels where they pass the antigen to T-lymphocytes Real killer cells, the T-lymphocytes release the immunological cascade reaction to eliminate the antigen and keep it in the "immunological memory".
If the same antigen again penetrates the epidermis, even years later, it will be immediately recognised and the immunological reaction will be more rapid and effective. If the antigen however manages to cross this first line of defence, the macrophages of the dermis detect it and eliminate it.
This duo is complemented by the keratinocytes, which, in the case of an infection, produce more cytokine IL1, which stimulates T-lymphocyte activity.
Unless you wanted to create an inflammatory response why would you compromise the integrity of the skin by continually removing the first lines of skin barrier defence?
Therapists often complain that their clients strip the skin to the point where it is red, sensitised and aggressed. So why as professional therapists, are we doing the same to our clients skin?
We know the removal of the acid mantle on a daily basis through harsh alkaline washes and toners will lead to an imbalance of the micro flora.Many skin care lines over used by clients, lead to an underlying sensitivity and an impaired acid mantle. The associated dryness that comes from this action exacerbates the blocking of the pilosebaceous duct, thus accelerating a micro-comedone problem.
The machines, acids and enzymes that are being unthinkingly used by therapists are having the same result.
Yes, exfoliation of the skin is an important step in cleansing the face and body. It can remove the dead skin cells that may have accumulated on the top layer of the epidermis. However, why did the skin accumulate dead skin cells in the first place? This is a question that the therapist often never asks herself and one she should before embarking on a treatment program.
But general exfoliation is not my concern; it is the almost continual ablative removal of the epidermis that is being practised in the beauty therapy industry, which inspired me to write this article. The overuse of professional peels and accompanying modalities for peeling, and the belief that continual peeling or abrading the skin will be the answer to wrinkles, pigmentation and acne.
When the causes of these skin conditions often have nothing to do with the build up of dead skin cells on the skin surface. In addition no further support or treatment is offered after the peeling program, no concern for the inflammatory response caused or healing required completing the treatment.
That old fashioned glycolic creams for continual home care are all thats being offered to the client.
Skin conditions like pigmentation and ageing make up a large part of our clients concerns. The actives required to make changes to these skin conditions are often in the vitamin and coenzyme families.
The area of the epidermis and dermis to be affected by these actives is below the granular layer and dermal epidermal junction.
This is where a peeling modality comes into play, as a tool for the penetration of the active required to make the change to the skin cell. Not the answer but a tool.
Peeling is half the answer:
Removal of the upper layers of the epidermis includes many cells; in addition to this removal, a certain amount of trauma occurs within the dermis. This will involve fibroblast stimulation, increased blood circulation and the dermal reserve (glycosaminoglycans) is stimulated to react to this trauma, resulting in a plumper dermis.
There are many cell and support systems involved in this trauma, protease enzymes will be needed to address the removal of dead and unwanted protein, which will assist the formation of new proteins collagen and elastin. A well functioning lymphatic system plays a very big supporting role in these protease enzymes and all of the dermal action.
Before embarking on a treatment course, ensure that all backup systems are well functioning and that a good antioxidant and repair skin treatment program is in place.
Just to name a few of the actives available to skin treatment therapists of the new millennium, this will involve actives like Vitamins A,C&E, Essential Fatty Acids, Amino Acids and the antioxidants alpha lipoic acid and carnosine for protease enzymes.
2003 Virtual Beauty Corporation
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