A New Breakthrough in the cause of Rosacea!
Acne rosacea appears to be caused by an overly zealous innate immune response and not by bacteria.
Dr Richard L. Gallo, M.D., Ph.D., of the University of California in San Diego has made some interesting discoveries....
This new information means that we now need to explain to clients that acne rosacea, or "adult" acne, may be caused by an overabundance of naturally occurring Anti-microbial proteins (peptides) in skin, and not, as previously thought, by the bacteria responsible for causing acne vulgaris the P.acnes bacteria.- Editor
What are antimicrobial peptides? (AMPs)
Antimicrobial peptides (AMPs) are ancient components of the innate immunity. These molecules interact with and rapidly inactivate infectious agents by a mechanism, which is generally mediated by disruption of the integrity of the microbial membranes.
In mammals, AMPs are synthesized and secreted in those tissues that are exposed to environmental microbes, such as skin and mucosal epithelia, where they provide an immediate-early defence against infection.
The protection effected by locally synthesized peptides is reinforced
by systemically derived AMPs, which are stored in the granules of phagocytes (Langerhans cell) and are released on demand at sites of microbial invasion.
Most AMPs are members of the defensin and of the cathelicidinpeptide families. Accumulating evidence indicates that members of both families act not only as innate microbicidal agents, but can mediate a range of other biological effects and the movement of inflammatory and immune cells, re-epithelialization of healing skin, induction of angiogenesis, apoptosis of transformed and immune cells.
The Antimicrobial Protein called Cathelicidin Peptides
Cathelicidins are positively charged Anti Microbial Peptides, which can react with the negatively charged surface of microbes (such as bacteria, viruses and yeast) and destroy these organisms. Cathelicidins are produced by keratinocytes, neutrophils and mast cells.
They are found in sweat and saliva; attract neutrophils, mast cells, monocytes and T cells; and increase angiogenesis, keratinocyte proliferation, and synthesis of extracellular matrix.
Cathelicidin Peptides are activated by serine protease enzymes (stratum corneum tryptic enzyme) through cleavage into smaller peptides and a cathelin peptide.
The link to Rosacea
It has been recently discovered that clients with Rosacea have abnormally high levels of Cathelicidin, these levels combined with associated higher levels of serine protease activity results in the generation of pro-inflammatory forms of the antimicrobial peptide, which in turn cause an inflammatory skin response. Cathelicidin messenger RNA was also evident in rosacea skin by in situ hybridization in contrast to normal epidermis where cathelicidin mRNA is hardly detectable.
Cathelicidin peptides can promote changes in tissue similar to those seen with rosacea, in addition individuals with other inflammatory diseases like psoriasis also expressed more cathelicidin than normal facial skin. Together, the evidence suggests that too much stratum corneum tryptic enzyme and too much cathelicidin leads to the abnormal peptides that cause the symptoms of these skin disorders.
Finding that rosacea is caused by what Dr. Gallo called a "trifecta of unfortunate factors," points to new avenues of research into inflammatory diseases, the authors reported online in Nature Medicine. "Influencing the balance of antimicrobial peptides, and their post-secretory processing, provides an opportunity for designing more effective therapy and reveals the potential for the involvement of proteolysis and cathelicidin expression in other inflammatory disorders," they wrote.
The original study and research was undertaken by Richard L. Gallo, M.D., Ph.D., of the University of California in San Diego, and colleagues with support from the National Institutes of Health, the National Rosacea Society.
2008 Virtual Beauty Corporation
Call the appearance of dimpled skin what you will or even, as some do refuse to acknowledge that there is such a concern as Cellulite/ Orange Peel skin The appearance of the body skin is usually of great concern and one of the main reasons for clients to seek body treatment in salon.
So what is cellulite/orange peel skin and can we, as skin care therapists do anything about it?
This is usually a female concern. On average, women have 35 billion fat cells compared to 28 billion for men. What aggravates orange peel skin? Highly refined foods, fizzy drinks, alcohol, coffee, smoking, sedentary lifestyle, hormones. A lot of these factors are more within the clients control so thorough consultation is important and the client needs to have realistic expectations. There is no recognised origin or single cause of cellulite, but a range of predisposing factors.
These may initiate, worsen and perpetuate a cellulite process, mainly in women. The involvement of estrogens is evident, as demonstrated by the emergence and/or presence of cellulite in times of hormonal changes (the problem often starts after puberty and worsens during pregnancy or estrogen therapy during the menopause).
Including sex, race, fatty tissue distribution and characteristics of the hormone receptors on the affected cells.
Less than ideal habits, with abundance of carbohydrates or fat; salt excess and low water intake produce liquid retention (oedema).
Sedentary life worsens the problem because muscles get reduced, local fat accumulations appear, muscle flaccidity increases, and blood circulation is altered. Tight clothes, inadequately supportive shoes, or extended periods of time in the same position also impacts circulation.
Tobacco alters microcirculation, alcohol augments lipogenesis and some medications also contribute to the development of cellulite.
The Why & How
Not only do men have less fat cells they have another difference!
In women, fat cells are organised in cylindrical chambers by surrounding (inflexible) connective tissue. In men, fat cells are organised as smaller diagonal units, this diagonal construction allows for increase of fat cell size without the rippling that occurs on skin with cylindrical fat cells.
Fat cells swell, and capillary walls become excessively permeable slows circulation which leads to slow
lymphatics and slow removal of excess fluids. Adipose cells cluster and are further bound by collagen which further impedes blood flow, connective strands stiffen, pulling down on anchor points giving the orange peel effect. So you can see the problem is not just a matter of fat but a problem with connective tissue, lymphatics, diet etc so needs a multi pronged attack.
Making the grade
When looking at cellulite/orange peel skin in clinic we need to have a grading system:
Stage One: No visible dimpling, some excess fluid apparent. The patient observes only minor symptoms. Thickening of the areolar stratum (the outermost layer of the adipose tissue, which is in contact with dermis), increased capillary permeability,uneven size of adipocytes and micro hemorrhages can be observed. It is a short lasting stage not usually observable to the naked eye.
Stage Two: Excess fluid, jiggly appearance to skin. No dimpling when standing or lying down. Dimples visible when pressed/pinched. The vascular problem worsens. Paleness, lower temperature and decreased elasticity. Minimal alterations appear on the skin surface. Hyperplasia and hypertrophy of the adipocytes and fibres in the area of capillary dilation, micro hemorrhages and thickening of the capillary basal membrane are observed.
Stage Three: Larger areas of excess fluid. Orange peel appearance becomes more evident. Visible dimpling when standing, disappears when lying down. Minor pitting and indurations. Orange peel looking skin is observed. At the histological level, the adipocytes gather into capsules to form micro nodules under the dermal connective tissue. Sclerosis of the small arteries inner layer. If treatment is not applied at this stage, the problem tends to become chronic.
Stage Four: Cottage cheese appearance. Multiple visible lumps under skin. Visible pitting when standing and lying down. Moderate to severe dimpling. Implantation of cellulite is already definitive and the aesthetic alteration is important and observable. The most visible nodules are already palpable, can sometimes be painful.
Stage Five: mattress like appearance. Large, multiple hardened lumps under skin surface (macro nodules) Tender when touched (nerve compression) Major pitting and induration.
Once we have established the severity of the concern before we start any treatment/recommend any lifestyle changes/ recommend any product we need to remind ourselves of what is actually occurring within the cells/systems- which cells and processes are we dealing with and formulate the best way to deal with the malfunction of these systems.
Adipocytes come from stem cells, which are also able to produce other cell types such as muscle-cells or osteoblasts. When differentiated to pre-adipocytes, they can stay in that state or they can differentiate to mature adipocytes.
Differentiated adipocytes lose their ability to divide. However, they have a very long half-life and the ability to store increasing amounts of lipids!!
Adipogenesis is the differentiation process by which pre-adipocyte cells end up as mature adipocytes. Adipocytes are specialised cells regulating the amount of stored fat in the adipose tissue through the basic mechanisms of lipolysis and lipogenesis.
Lipolysis is a catabolic pathway, whereby stored triglycerides (TG) yield free fatty acids (FFA) and glycerol. This pathway is activated as the organism demands energy, which is produced by the subsequent oxidation of FFAs. The activating stimulus is mediated by hormones involving the cyclic AMP pathway such as glucagon and adrenaline.
The lipolysis process starts when these hormones increase cyclic adenosin 3-5monophosphate (cAMP) levels, which induces PKA (Protein kinase A) to phosphorilate a serine on the hormone sensitive lipase (HSL) thus activating it.
Opposite to lipolysis, the lipogenesis process is aimed at storing energy, in the form of TG, into the adipocyte. In this case, the FFAs re-esterify to yield TG. Notice that synthesis of TG requires glycerol phosphate, while lipolysis yields glycerol. Since no glycerol kinase is present in the adipocytes, the occurrence of lipogenesis requires glucose intake, since glucose can be transformed into glycerol phosphate.
The necessary FFAs for lipogenesis usually come in the bloodstream from the diet. However, they can also be synthesised from glucose entering into the adipocyte, with the participation of the enzyme FAS (Fatty Acid Synthase) in a process called lipogenesis de novo.
Solution in summary
So, how do we utilise this information and what responsibility does it confer upon our client, and how does it relate to treatment of our clients? You need to examine your treatment formula for three particular capabilities (and emphasise to the client her part in the process too) Your product supplier should be able to explain to you how their actives work on the following processes:
Adipogenesis inhibition - PREVENTION
Slows down capability of lipid storage (inhibiting those adipocytes from continuing to expand in size)
PREVENTION - Clients responsibility= Diet, EFAs, Water intake
Lipolysis activation - TREATMENT -
Elimination of already accumulated fat (minimising of adipocyte size)
TREATMENT - Clients responsibility= Exercise, EFAs, Water intake
Lipogenesis inhibition -KEEP-FIT
Avoids creation of new lipid deposits (inhibits differenciation from pre adipocyte to adipocyte)
KEEP FIT - Clients responsibility= Diet, Exercise, EFAs, Water intake
You must emphasise to your client that treatment of cellulite/orange peel skin takes commitment and that a lot of the responsibility for long term success rests with her.
As a therapist you need to look for ingredients and treatment modalities that target other factors also (apart from solely lipid storage in adipose tissue) such as actives/modalities that focus on improving blood circulation or skin refirming properties.
Remember to nourish the skin adequately (from the inside with diet/supplements) as well as supplying topically the gold standard for healthy looking skin Vitamins A, C E and a full brigade of Antioxidants.
Michelle Woodyard is an ITEC & NaSA qualified professional therapist/educator with over 16 years experience. With eight of those years as a business owner, Michelle intimately understands what level of expertise is required to keep ahead of the competition. Since moving in to roles as a technical representative and educator for leading skin care companies, Michelle, the eternal scholar has grown both her own knowledge and that of her clients. I love the industry, am excited to see all the changes occurring and to be involved with many inspiring salon owners and staff
2008 Virtual Beauty Corporation
Have you observed at the end of a long treatment program for pigmentation that some pigment just does not respond to treatment? The frustration, disappointment and dashed expectation experienced by both client and therapist cannot be described.
The pigmented anomalies you are observing are not pigmented lesions caused by melanin, but a colored anomaly that has a similar appearance: Lipofuscins.
Initial analysis is not easy; they will however, not always follow the normal pattern of pigmentation. They are often linked to trauma like surgery, over use of sun beds and chemical burns, and will be found in most Fitzpatrick skin tones, with a greater predominance in the Fitzpatrick 3 & 4 category.
The lesion will not respond to IPL because the chromophore is in fact not melanin.
I have observed this type of pigmented lesion for many years not fully understanding what it was, but I had however linked part of the cells & systems involved and affected to other similar skin conditions.
An example is the type of pigment that occurs from bruising or damage involving the vascular system, and I think the best example of this pigmentation is the lesion often seen after scelotherapy or the removal of varicose veins. To see this pigment at a cellular level will help you choose a more appropriate treatment option.
Cells and systems involved with the formation of Lipofuscins
Lipofuscin is a yellow-brown pigmented waste material deposited in many nerve and skin cells, where it
is believed to interfere with cellular metabolism. Lipofuscin is made up of cross-linked, peroxidized lipids and cross-linked proteins (Glycation). Lipofuscin deposits in skin are easily misdiagnosed as solar lentigines.
Lipofuscin remains after the breakdown and absorption of damaged blood cells and understandably, these deposits of lipofuscin debris increase with aging. They can be found in deep organ tissues as well as in skin tissue. Lipofuscin is merely a sign that other deleterious reactions have already taken place.
For example; free radicals and toxic aldehydes may react with the cross-linked proteins, causing damage and leaving lipofuscin as a superfluous by-product.
I believe the terminology peroxidized lipids also requires further discussion because Lipofuscins can begin at this point also.
Lipid peroxidation refers to the oxidative degradation of lipids. It is the process whereby free radicals `steal' electrons from the lipids in cell membranes, resulting in cell damage.
This process proceeds by a free radical chain reaction mechanism. It most often affects polyunsaturated fatty acids like phospholipids, because they contain multiple double bonds in between which lie methylene -CH2- groups that are especially reactive hydrogen.
Living organisms have evolved different molecules that catch free radicals and protect the cell membrane, one of which is alpha-tochopherol also known as vitamin E.
What must be remembered is that Vitamin E is not a very efficient anti-oxidant and can only neutralise small amounts of free radicals before it becomes inactive.
For this vital resident antioxidant to be continually effective within a cell membrane Vitamin C must be available, because Vitamin C will reactivate Vitamin E
so it may continue the antioxidant process.
I think this really reinforces the synergy of cells and systems and one must always be aware of what works with what, so that the complete story is understood.
Understanding that the health of a cell membrane is imperative to skin health may seem a little fundamental, however a cell can only perform and make what it was genetically designed to do, if it itself is in good health.
A cell membrane is a complicated and intricate eco system that requires better understanding if one is to embark on treatment programs that may improve skin appearance.
Cell health has to always be part of the preparatrory phase of the treatment program otherwise very limited results will occur.
Now that you have a better understanding of the cause and effect of Lipofuscin, let us turn our minds to treatment.
Cell preparation will be a basic part of dispersing this anomaly, and the client will have to make a commitment to cell nutrition to obtain the best result. The daily topical application of actives and weekly salon treatments will be the basis of this treatment program.
It has been proven that some remedies and actives do exist. They will not be prevalent in products just yet, but some innovative formulators have sourced and include these actives into modern skin lightening ranges. In doing so they have covered their bases in the treatment of all pigmented anomalies. This has come about from the understanding that Lipofuscins are not easily discernable from melanin based pigmented lesions like solar lentigines, and the Lipofuscin lesion does have a UVR exposure element in its formation.
Lipofuscin treatment actives
You will be seeking formulations with the following active ingredients:
DMaE, or dimethylaminoethanol. This naturally occurring substance has been shown to help cells rid themselves of lipofuscin, while allowing them to retain useful nutrients. DMaE also helps strengthen cell walls, resulting in better skin tone and elasticity.
Alpha Lipoic Acid: another naturally occurring antioxidant that has the benefit of being both water and oil soluble. This enables the antioxidant to have a effect both inside & outside the cell and the cell membrane. From a formulators point of view this is an added advantage. If something can applied to skin that the cells and systems already recognise there is less chance of an adverse inflammatory response occurring within skin.
Retinyl palmitate, of the vitamin A family is now well known to have nothing but positive effects on skin cells. This vitamin works in synergy with Vit C & Vit E so is part of the triangle of antioxidants that will benefit lipofuscin lesions. Of course even the simple beta carotene that is so undermined as an antioxidant would have to be considered of benefit to this condition, my main reason for this is that an antioxidant it can quench vast numbers of free radicals, is stable in formulations and will sit happily alongside most other actives.
Vitamin E (Tocopherols): Due to its multifunctional abilities and roles in skincare, Vit E is one of the most valuable of all the vitamins. Naturally occurring vitamin E is responsible for the protection and maintenance of the lipids and lipoproteins in the cell membranes of the heart, muscles and blood vessels. It also assists the skins water binding ability. These properties help maintain healthy connective tissue and epidermis. The vitamin has shown proven biological activity as an anti-oxidant, anti-inflammatory and free radical scavenger, making Vitamin E a necessary part of any anti-ageing formula.
It is important to remember that the effects of Vitamin E is assisted by Vitamin C: When Vit E has had a neutralising effect on a free radical it becomes inactive. Vitamin C reactivates Vit E to continue working as an antioxidant, completing the triangle of these cellular antioxidants.
Essential Fatty Acids: EFA's are often referred to as Vitamin F, and consist principally of unsaturated linoleic, linolenic and arachidonic acids. Deficiency of essential fatty acids lead to abnormally enhanced transdermal water transport in addition to dryness, scaly skin.Essential fatty acids (EFA's) form the basic building blocks of body fats, biological membranes and prostaglandins. Any deficiency of the essential fatty acids will lead to a reduction in the formation of prostaglandins, eventually resulting in compromised cell membranes.
Correctly identifying Lipofuscin before treating with conventional pigment modalities will mean the chances of making a difference will be greater.
The quest for the achievement of the perfect skin goes on, repair of damaged proteins being the greatest challenge. The race is on and with every year that passes more and more weapons to treat the damaged ageing skin are being developed.
I do however believe that prevention is easier than cure; and you the skin treatment therapist can easily achieve this by giving preventative protocols and products to young clients and by raising early awareness of the effects that nutrition, environment and genetics can have on skin cells.
By offering anti-ageing treatments clients during their 20's, and by continuing your own education you will be in a position to offer effective long term solutions to clients and keep them for a longer period of time.
2006 Virtual Beauty Corporation