Blog - Pastiche Training

The importance of Photo type & Risk Assessment

Mon, 21 Oct 2019 08:30:00 GMT

There have recently been several web forum and group discussions about photo type and relevance to skin analysis, and during these discussions there appeared to be for some participants, a rudimentary understanding of the importance of this characteristic in professional skin analysis. The purpose of this primer is to provide a good base of understanding. FBH

A key area of discussion should be about Skin Colour Terminology; and that we should clarify the reference to a skin colour and the burn time category within which it lays, by using the modern terminology of ‘photo type’ and risk. With the mixed ethnicities of today, the older Fitzpatrick Skin Types (Scale 1 to 6) terminology of skin colour analysis; although a good starting point, is no longer adequately applicative.

Differences in each tone of skin colour can be seen more obviously in the Fitzpatrick Skin Type Scale of 4 to 6, and those differences associated with the genetics of hemisphere. (Location)
The closer to the equator, the darker the skin tone and when moving further north or away from the equator, the skin tone becomes lighter.

There was a controversy at the time that the Fitzpatrick Skin Type Scale was published in 1975 because still at that time there were light and dark skin tones within each race and the scale was considered too narrow to be useful. [1] However, that been said, the Fitzpatrick Skin Type Scale has been used ever since by the medical and cosmetic industries.
Nowadays there are many misunderstandings with the term ‘skin type’ used today; those of you trained in the Pastiche Method of skin analysis were taught that ‘skin type’ is a reference to the intrinsic skin groups of lipid dry, oily and diffused redness.
For others, the term ‘skin type’ often still refers to the original Fitzpatrick classification of skin colour; and today older medical professionals still make the reference of Fitzpatrick skin type or just skin type.
During the 1990’s the use of the Fitzpatrick Skin Type Scale was revised; however although the Scale was a good reference for the skins burn time, it did not give any indication of the skins ability to accumulate melanin and change colour (tan). Nor did it indicate the risk for skin cancer or post inflammatory hyperpigmentation.

I use the very large continent India as a perfect example of this phenomenon. Therefore, because there are light and dark skin tones within each of the original Fitzpatrick Skin Type Scale, I have always recommended that each of the 6 types used in the scale is further broken down into a low, medium and high in order to add a higher resolution, or accuracy. This Photo Type Scale would be similar to the original von Luschan’s scale of 36 tones, but not so extensive. [2,3]
One of the reasons I did not allocate skin’s that I was analysing in to one of the 6 Fitzpatrick categories was that my skin diagnostic devices that measure melanin density in the skin were telling me that there were more variables in tone to allocate to a single type. In fact, some Skins that would normally be classified as one Fitzpatrick type could have fitted in to 9-sub tones according to the measurement scale. The diagram below illustrates the relationship. For example how would you accurately classify skin’s with readings of 23-25 or 32 to 35 on a conventional Fitzpatrick scale?

Understanding Skin response to UVR is important and separated into two categories;
The first category is the term Minimal Erythema Dose ; (acronym one MED). One MED was the point of reference used to describe the minimal exposure time to UVR to create visible redness (erythema) or for a skin colour to burn. It is commonly used today as an indication of a sunscreen’s Sun Protection Factor also known as the SPF.

The other category is the Minimal Melanogenic Dose , (acronym MMD). We refer to MMD as the skin’s ability to tan or the epidermis’s ability to accumulate melanin. MMD is usually determined several days after UV exposure (immediate pigment darkening) and when a change in skin colour occurs several days later between exposed and non-exposed skin. (Delayed pigment darkening). MMD is the terminology used when describing the melanocytes ability to protect skin, and it has been proven that even the fairest skin can accumulate melanin within the epidermis over a period of a summer.

Understanding how skin responds to UVR exposure has high priority in the skin treatment professions today as is the correct terminology that enables us all to communicate at one level. To clarify and avoid misunderstanding, I suggest that the term Photo Type Scale becomes the standard reference as a way to classify the typical response of different colours of skin to ultraviolet exposure.

The Photo Type Scale can also indicate skin risk; this risk may be a genetic predisposition for skin cancer especially for those skins that carry the red hair gene. (MC1R) (Melanocortin 1 receptor)

Red hair appears most commonly in people with two copies of a recessive allele (Ref-4) on chromosome 16 which produces an altered version of the MC1R protein. The MC1R recessive variant gene that gives people red hair and non-tanning skin is also associated with freckles though it is not uncommon to see a redhead without freckles. Eighty percent of redheads have an MC1R gene variant, and the prevalence of these alleles is highest in Scotland and Ireland. (5)

Alternatively, the Photo Type Scale can indicate risk for post inflammatory hyperpigmentation, which affects photo types 4 to 6. The genetic risk for keloid scarring may also be summarized if the photo type was found to be in the 5 – 6 group.

Information gathered during the consultation can provide you with the genetic data to determine a skin that is at risk for either skin disorder. With the mixed ethnicities of this millennium, it is not always apparent that skin has the red hair gene and patients, or clients may not know their genetic heritage; It is important to know or determine this if the Photo Type is a high 3 or low 4.

Diagnostic equipment is available now that help to determine photo type and measure accumulated melanin with great accuracy. [6] The modern, LED black light scanners show the hidden Ephelides (Freckles) that are an indicator of the red hair gene. [7] If the genetic history of a client shows a combination of the ability to tan and the red hair gene, (which is not uncommon among those of a photo type 3 and 4) it should be considered high risk for skin cancer and post inflammatory hyperpigmentation.

Because the ability to tan often means that the skin can tolerate a longer period of unprotected UV exposure, this combination of genes could culminate into skin cancer and pigmentation as the melanocyte and keratinocyte cells age and intrinsic antioxidant defense systems decline.

It was during my years as an Electrologist that I found that some of the lower Photo Types were prone to post inflammatory hyperpigmentation (PIH), not just the photo types 4 to 6 as indicated by the training of the day. It was after reviewing clients genetic history many years later that I attributed this susceptibility to PIH to the fact that many of my clients had mixed ethnicity’s and that their visible skin colour was not a reliable indication of their ‘risk’ for pigmentation.
This is another reason why the genetic heritage on both sides of the family tree is vitally important during a consultation.

The MMD was also a factor because if a skin measured as photo type 3 without sun exposure, I observed that the same skin could accumulate melanin and measure as a Photo Type 4 by the end of summer; thereby increasing the risk of post inflammatory hyperpigmentation during the wound healing process of electrolysis.

The modalities of intense pulsed light and laser commonly used for hair reduction and skin rejuvenation are taught with the emphasis on being mindful of accumulated melanin between treatments. Melanin measurements using equipment such as the CK SPA 99 [6] during the consultation and before each treatment ensure that an IPL/Laser devices fluence can be altered to accommodate any melanin increase or if appropriate, for treatment to be postponed.

It was these experiences over time that prompted me to create a Photo Type Scale table that included the skin risk for modalities such as electrolysis, intense pulsed light, laser or collagen induction therapy. Today, this chart is used by educators and skin treatment professionals worldwide as a clinical reference tool. [8] See below.

References for this article

1. https://en.wikipedia.org/wiki/Color_terminology_for_race
2. “Felix von Luschan Skin Color chart” by C Burnett
3. https://en.wikipedia.org/wiki/Felix_von_Luschan
4. https://en.wikipedia.org/wiki/Allele
5. https://en.wikipedia.org/wiki/Red_hai r
6. SPA 99 Skin pigmentation/Erythema measuring device
7. http://ww w.sylton.com/observ-
8. The A-Z of understanding pigmentation

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Is Hair Care Affecting Your Skin Health?

Mon, 21 Oct 2019 08:28:00 GMT

It’s Ironic that many people spend a lot of time and money on skin care products for their sensitive, reactive skin, but don’t consider that same amount of money, care, and thought be given to the shampoo, conditioner, and colour frequently applied to their scalp and hair.

As professional skin treatment therapists, could we be doing more to educate them? FBH

The core principle of treating sensitive, reactive skins (such as eczema, psoriasis, or dermatitis) is by Corneotherapy techniques and skin care products. We use these products because the ingredients are more physiologically compatible with the skin.

Imagine if they were to apply this same principle to their scalp and hair care products. What difference would it make?

We need to understand that the scalp is a continuation of facial skin, and is made up of the same type of epidermal cells (known as Corneocytes) as the face.

These Corneocytes are a large part of skin barrier defence systems, designed to protect the inner epidermis and dermis from the environment.
Hair is specialized epithelial cells that are “hard” keratin proteins called Trichocyte keratins that could classify as a ‘barrier defence system.’ As hair too plays a role in protection against friction, bacteria, and temperature control similar to skin.

Having established the link between epidermal cells and hair cells it stands to reason that hair and scalp should be given the same care and attention when it comes to formulating ‘personal care’ products.

Consider the action of cleansing facial skin with shampoo; it is not something that many would ever consider.

However, every time hair is washed, the scalp skin is subjected to surfactants that were designed for hair; not skin.

If your facial skin had issues with ‘barrier disorders’ such as eczema, psoriasis, or dermatitis and classified as ‘high risk’ (sensitive), then so will your scalp skin, and should be given the same consideration as facial skin.

Skin, Scalp, and Hair also become compromised with barrier defence disorders through medical conditions such as cancer and associated treatments such as chemotherapy. Hair loss is accepted and classified as a standard result of chemotherapy, but very little thought given to the condition of the scalp hidden under a scarf or hair piece.

Because immune systems deteriorate during treatments such as chemotherapy, the purer a formulation can be, the better the end product will be.

It is challenging in the formulating of hair care products today to access ingredients suitable for scalp and hair care product that have a high content of plant origin surfactants; with many of those plants used for the ingredients being certified organic.

If you or your clients suffer from eczema, psoriasis, or dermatitis then consider that the hair care products you are using may not be helping the condition.

You ideally should be seeking a well-balanced skin care formulation for scalp skin, and hair care, and a natural, allergy certified hair care formulation that will not compromise the immune system during illness or allergy or deteriorate the barrier defence systems of scalp skin, or hair.

If you are providing professional serviced in clinic for people with sensitive or reactive skins, perhaps you could be offering them a solution for their hair at the same time you prescribe your take home skin care.

Why risk the client inadvertently undoing all the good work you’ve done on their skin when you can provide a complete package?

Consider it extending the principles of Corneotherapy to the scalp and hair. FBH

Dermatological, Cosmeceutical and Corneotherapy: The difference explained

Mon, 21 Oct 2019 08:27:00 GMT

Dermatological, Cosmeceutical and Corneotherapy:
The difference explained

There is perhaps equal measures of misunderstanding and misconception regarding the grades of skincare products, particularly when the formulations approach dermatological effects.
This is not helped when new marketing terms are invented to imply performance. In this article we will look at the definition of the two main classes of products that straddle the border between cosmetic and medicinal and their use in Corneotherapy.
This article is a distillation and compilation of information sourced from colleagues who share my passion for sharing knowledge. FBH

Cosmeceuticals: Cosmetic ingredients with pharmaceutical effects
The cosmetic industry uses the word Cosmeceuticals to refer to cosmetic products that have medicinal or drug-like benefits.
The term has been around for over 15 years, and is one of the new terms that is part of the new terms that evoke curiosity and encourage trial purchase of products. The terms “medical cosmetics”, “cosmedics” and “medicosmetics” are similarly circulated.
When these terms are borrowed or re-engineered from medicine or pharmacy language, you can be sure that the public will become interested in any new product that uses these expressions.

The terms dermatocosmetics, dermaceuticals, skinceuticals and cosmeceuticals were created specifically for this reason. If a manufacturer or marketer goes further and gets endorsement from individuals with the title Dr in their name, then this garnishes the brand name to reference a medical or scientific background. A scientific sounding name and a medical connection can almost guarantee excellent sales in many markets.

Let us be clear however: the term cosmeceuticals does not appear in the European Cosmetic Directive, nor is recognised by the American FDA.

Regardless of it’s legal status or recognition, it makes sense to define the term, particularly if a certain level of quality and performance is associated with it. So when can we, or should we speak of a cosmetic ingredient that has a pharmaceutical effect, AKA Cosmeceutical?

These are the recognized criteria:

1. The ingredient should not be listed among the banned substances in the European Cosmetic Directive.

2. Will not have any systemic effects. Example: Hormones are banned in cosmetics.

3. The active agent needs to be capable of penetrating into the skin barrier and further permeating into the epidermis as the target destination.

4. The destination (cell, tissue, blood vessel, enzyme, receptor, etc) and the triggered, intervened or inhibited biochemical process there should be proven both in vitro and in vivo.

5. The externally visible and advertised effect has to be clinically evident, statistically proven, reproducible and significant.

6. The product safety of the substance (about its toxic profile according to the requirements of the EU Cosmetic Directive) has to be documented in the safety report.
7. The ingredient will be a pharmaceutically active agent that improves and stabilises the condition of the skin and eliminates skin disorders.
8. Pharmaceutical claims such as skin healing, acne treatment, inhibition of fibrinolysis and antimycotic effects, etc, are not permitted for marketing and promotional purposes; even if they are evident with the use in cosmetic formulations.

If the criteria mentioned above strictly interpreted, many highly praised and modern cosmeceuticals would just fall through the cracks– either as a single substance or in a preparation combined with other substances.

As this type of formulation is not designed to act on the skin’s surface but destined to be effective in the deeper layers of the skin, cosmeceuticals should in principle be free of any counterproductive additives. Consequently, the inclusion of fragrance and allergenic preservatives do not fit the true concept of a cosmeceutical.
Equally; so as to avoid a washout of active agents and skin lipid components, non-degradable emulsifiers would be taboo in the case of products to treat skin barrier disorders.
With cornification disorders such as acne, the use of paraffin oils, and comedogenic hydrocarbons in a formulation does not correspond with cosmeceutical principles. While lipids should be avoided in formulations designed for perioral dermatitis, minor doses are allowed with rosacea.

In summary, the matrix of a true cosmeceutical formulation should guarantee an excellent ease of use, correspond with the physiology of the skin, be free of unnecessary additives and avoid adverse side-effects.

It can be said that these are the same, albeit often disregarded claims that are used for topical pharmaceuticals; a fact that has contributed to the creation and justification of cosmeceuticals.

It can be concluded that while cosmeceutical products have fewer restrictions regarding the selection of their matrix components, they are in no way inferior to pharmaceuticals.

While European skin care manufacturers have to comply with the EU Cosmetic Directive, in the US and different countries of South East Asia particular products, such as sun protection products, fall within the definition of “medical skincare”. These products are submitted to a separate, complex and costly registration process. The authorities in charge also routinely control the content of UV filters.

The close monitoring results from the fact that damage to the skin can still occur when application dosages are disregarded and consumers rely on the information on the labels.

Dermatological: Cosmetics with dermatology affect
The term “dermatological cosmetics” already suggests the combination of dermatology and skin care, but what does dermatological cosmetics actually mean? What is the difference between dermatological and conventional cosmetics?
Based on a current examples, the concepts of dermatological skin and beauty care and their compatibility with existing laws and regulations can be described by the following:
The term “dermatological” is not a cosmetic treatment or activity that is comparable to the medical treatment provided by the dermatologist and consequently prohibited by law for use by cosmeticians, aestheticians, beauty therapists and skin treatment therapists.
The term “Dermatological” in connection with “dermatological cosmetics” however, represents a quality feature and describes a cosmetic treatment adapted to the physiological needs of an individual skin. (Cosmetics with dermatology affect).

For that reason, skin care concepts based on the types of creams used in dermatology (by a dermatologist) are finding their way in to cosmetic skin treatments (By appropriately trained skin treatment specialists) that are designed for intense skin care programs as well as supportive prevention strategies. This type of approach is gaining more and more importance in today’s world where skin barrier disorders are becoming more common.

These dermatological types of creams are known as Derma Membrane Structure (DMS), and can fulfil both the dermatological and supportive prevention requirements for skin, and as the name suggests, DMS creams are designed to be compatible to the physiological properties of the skin.

Skin treatment therapists use them as a base cream to apply separately (as a moisturiser) or in combination with cosmetically active agents, while dermatologists and pharmacists utilize them as a pure base cream for prescriptions, either individually or in combination with pharmaceutically active agents. From a chemistry point of view, the criteria for dermatological cosmetics are that they are free of non-physiological emulsifiers, preservatives, mineral oils, perfumes, dyes and additives. When we consider at the ingredients used in conventional cosmetics (INCI), these important criteria that make dermatological cosmetics true to their name cannot be ignored or taken for granted.

We have learnt in previous publications and education that the many emulsifiers that are not physiologically compatible to the skin can cause neurodermatitis and similar barrier disorders. As a matter of principle, any cosmetics designed from a dermatological approach should therefore be free of these emulsifiers. High concentrations of mineral oils and silicones in formulations may also impede the natural regeneration of the skin; studies of renowned scientists have proven this. Fragrances are mentioned as the number one sensitising substance in cosmetics today; and as with preservatives, individuals with a very sensitive or even pre-damaged skin are mostly affected.

The manufacturing costs of products free of preservatives and fragrance usually exceed the costs of producing conventionally preserved and fragrance-containing products simply because they must use much higher quality raw materials for manufacture. This is particularly apparent in water based creams, that require different ingredients and in particular, unscented raw materials. Due to these aspects and the ever rising costs of today, many manufacturers with a history of conventional formulations have too many cost barriers to allow them to produce an uncompromisingly dermatological product range. Consequently they are not as common as they could- or should be.

Unfortunately, the properties of the substances which show counterproductive effects after long-term treatment (and therefore should be avoided), are predominantly cited in dermatological spheres but far less frequently in cosmetic literature. The reason for this is obvious; for cosmetics marketers this type of information is “inconvenient” for unconditional acceptance of their products.

Dermatology deals with the needs of the skin itself. In all dictionaries and encyclopaedias the term “derma “directly refers to “skin” with dermatology explicitly and exclusively signifying skin science.
Consequently, another feature of dermatological cosmetics is a potential supportive care and prevention of skin disorders or even diseases. In this case, special emphasis is given on skin protection as described in the European guidelines which consequently results in additional quality features such as:

Skin-identical or skin-related components.
Creams with a physical structure identical to the membrane-like composition of the skin barrier layers.

Cosmetic dermatology or dermatological cosmetics complements the fields of both conventional medicine and traditional cosmetics/ skin care while extending their field of activity.
Aestheticians, skin treatment therapists, dermatologists and pharmacists with foresight already have realised customers needs, and are now expanding their range of services appropriately.
As a result, more and more therapists are seeking information on dermatology; while dermatologists who deal with cosmetics and pharmacists are improving their sales competence in Dermatics and cosmetics.

Dermopharmacy, cosmetic medicine, cosmeceuticals are the key words of today which refer to the fact that there is no longer a clear dividing line between skin care, prevention,and treatment. Furthermore, many of the substances are used as cosmetically and dermatologically active agents.
Two example of this are Urea and D-panthenol. Urea is an ingredient used in cosmetic formulations for dry, stressed skin and in dermatology in creams for the treatment of neurodermatitis. D-panthenol supports the regeneration of the skin in cosmetic applications and is used to accelerate healing in dermatology.

Corneotherapy : The link between cosmetics and dermatology
Corneotherapy with Dermatological cosmetics takes the science of cosmeceuticals one step further, and is rapidly becoming recognised as the modality that provides the link between dermatology and cosmetics. (Dermatological)
In this context, we can reasonably and correctly title the formulations used in true Corneotherapy as Corneotherapeutic.
Corneotherapy can be described as a modality or methodology that focuses on ameliorating (restructuring) the stratum corneum without using any pharmaceutical agents. Corneotherapy uses dermatological cosmetics based on the dermatological types of creams known as Derma Membrane Structure to obtain it’s efficacy.

The key feature of Corneotherapy is that the primary task of any formulation or treatment is to correct or create homeostasis in the skin so that it will then effect it’s own repair.
This is particularly significant with the increasing number of skin conditions related to, or exacerbated by barrier disorders of various types.
Without discussing the complicated biophysical processes in detail, in summary, it may be said that corneotherapy aims at a recovery of the stratum corneum and above all, that it improves the skin barrier function and consequently the homeostasis of the skin.

Corneotherapy is known for it’s signature outside-in therapy approach, whereas “outside” is the stratum corneum and “in” are the therapeutic effects starting in the stratum corneum and working their way into the deeper skin layers.
In contrast, there is conventional inside-out therapy where a pharmaceutical agent will inhibit inflammatory processes in the skin or influence the immune system while only having secondary effects on the stratum corneum (“out”). This comparison clearly shows the potential significance of an adjuvant care of the stratum corneum, even in combination with a conventional therapies.
In order for the outside-in therapy approach to work with minimum side effects, the formulations used must follow the same strict criteria as dermatological products. This would exclude many of the cosmeceuticals currently available because of their unnecessary additives and non physiological ingredients.

It is well established that a healthy and properly functioning skin barrier inhibits pathogenic germs, such as Staphylococcus aureus that is widely found in cases of atopic dermatitis, from penetrating into the epidermis. A disordered stratum corneum, however, tends to support recurrences. This example shows the importance of avoiding counterproductive effects of skin care that has not been created with skin barrier health in mind.

It has been known for quite some time, that skin cleanser components such as sodium lauryl sulfate (SDS) may cause major skin irritations by firstly damaging the barrier function and subsequently causing cellular reactions.

Furthermore, a SDS damaged skin barrier enables sensitizing substances that are used to preserve and fragrance skin care products, to easily penetrate the skin. Interestingly, SDS is widely used as a standard irritant in dermatological research.

One of the major advantages of corneotherapy using dermatological cosmetics is that it is largely free of side effects in comparison with a treatment with topical pharmaceuticals.
Preventively applied corneotherapy may well extend the intervals between occurrences and reduce; or even avoid the application of conventional dermatic products.
A precondition for successful corneotherapy, however, is a precise diagnosis of the skin and relevant conditions, and the application of expertise regarding the structure of skin care products and their components.
Besides the above mentioned moisturizing substances, lipids, and filming agents, ceramides, as well as amides play a significant role in the selection of components.

Despite the effectiveness of Corneotherapy in the treating of many skin barrier related conditions and beyond, there is only hope that it will (despite its relatively unspectacular procedures compared with conventional treatments) may soon gain acceptance.

Compilation, translation and editing by Florence Barrett-Hill.

References
1. Dr Hans Lautenschläger; Dermatological cosmetics – linking cosmetics and medicine published in Kosmetische Praxis 2005 (5), 12-14 http://www.dermaviduals.com/english/publications/products/dermatological-cosmetics-linking-cosmetics-and-medicine.html
2. Dr Hans Lautenschläger; Highly effective – Cosmeceuticals- published in medical Beauty Forum 2014 (4), 16-18
3. Lautenschläger H, The history and current aspects of corneotherapy, IV. International Symposium on Aesthetic Medicine, Moscow, April 19-20th, 2005
4. Friberg SE et al., Water permeation of reaggregated stratum corneum with model lipids, J Invest Dermatol 1990;94:377-380
5. Lübbe J, Secondary infections in patients with atopic dermatitis, American Journal of Clinical Dermatology 2003;4(9):641-654

Addendum;
The United States (US) and European Union (EU) both work to ensure the safety of cosmetics for consumers through rigorous regulation.
The 27 European Union Member States have transposed the European Union Cosmetics Directive, enacted in 1976, into national law. Each Member State has health authorities that then regulate cosmetics within their respective national boundaries according to the law.
In the United States, the cosmetics industry is regulated by the U.S. Food and Drug Administration (FDA) which has been granted broad regulatory authority under the Federal Food, Drug, and Cosmetic Act, enacted in 1938.
See more at: http://www.cosmeticsinfo.org/

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Understanding Dermal Pigmentation

Mon, 21 Oct 2019 08:26:00 GMT

Commonly misunderstood within the skin treatment /specialist professions, is the term Dermal Pigmentation, and it is appropriate that some clarity and thought to the subject be considered.

I have already published the basics on the topic of melanogenesis and want to reiterate that the formation of skin pigment is an Epidermal event NOT Dermal, and the melanocyte began its life during the embryonic stage at the neural crest. During those formative months the melanocyte move will move to those areas of the body where pigment is found.

There are 120 genes involved in this cell movement, and consequently the potential for 120 reasons why something could go wrong. An example of something going wrong is the development of a birthmark.

The melanocyte is genetically programmed before it leaves the neural crest, and it is this programming that determines the colour of the hair, skin, and eyes. Another fact for you to remember is that although we talk about melanocytes as one cell, there are several genres of that cell. For example, the melanocyte that colours our hair does not require exposure to UVR, unlike the cell that colours skin, which does.

Melanocytes will eventually settle in the lowest region of the epidermis (basal layer), just above the dermal-epidermal junction that separates the epidermis from the dermis. Typically, about one in every ten cells in this layer is a melanocyte, with a ratio of one melanocyte to thirty keratinocytes, which is the predominant cell of the epidermis. The association of melanocyte and keratinocyte have been called the “epidermal melanin unit”.

Defining Dermal Pigmentation

This discussion is about Dermal Pigment and I want to be very clear that the type of pigment I am referring to is NOT pigmented lesions such as simple congenital pigmented naevi , which in the simplest terms be referred to as birthmarks or moles AND are beyond our scope of practise. (Naevi (US English: nevi) are congenital or acquired growths or pigmented blemishes on the skin; birthmarks or moles. As examples, moles are melanocytic naevi).

Congenital melanocytic naevi are caused by localised genetic abnormalities resulting in the proliferation of melanocytes.

This abnormal proliferation is thought to occur between the 5th and 24th weeks of gestation. If proliferation starts early in development, giant and medium-sized congenital melanocytic naevi are formed. Smaller congenital melanocytic naevi are formed later in development after the melanoblasts (immature melanocytes) have migrated from the neural crest to the skin.
(Thanks to www.dermnetnz.org/topics/congenital-melanocytic-naevi/ )

Dermal Pigmentation: How do we analyse it? Can we analyse it?

That is the question. To begin, we must have a short refresher on the areas of the epidermis and dermis that will be involved in the answer.
It is now established that if the PAR2 receptor within the keratinocyte cell membrane does not receive the melanosome, then it may become part of extracellular space, and be placed into the Dermal-Epidermal Junction. (DEJ) Read more here.

What is the Dermal Epidermal Junction?

(Basement membrane zone)
The Dermal-Epidermal Junction (DEJ) is comprised of three layers and made up of connective tissue that has many pockets and channels throughout (Like a sea sponge).

The connective tissue of the DEJ allows for the plasma containing nutrients, hormones, and oxygen seep up into the cell producing layers of the epidermis, and of course, permit the dispersion of waste back to the Lymphatic System within the dermis. Structures of the DEJ derive their origin from both the epidermis and dermis; The Lamina Lucida is on the epidermal side of the DEJ and primarily of epidermal origin, Lamina Densa in the middle and Fibro-reticular Lamina or Sub Lamina Densa is on the Dermal border of the junction. Keratinocytes are anchored into the Lamina Lucida by Hemidesmosomes , and the Dermis secured into the Fibro-reticular lamina by collagen type V11 anchoring fibrils of dermal origin.

The DEJ provides strength and integrity to both the epidermis and dermis and can withstand many of the tearing forces that skin undergoes on a daily basis.

Another contributor to the strength of the DEJ is the Rete Peg (Rete Ridges/Papillae) finger-like projections into the epidermis.

The Rete Pegs allow a greater amount of plasma containing nutrients, hormones, oxygen into the cell producing layers of the epidermis, by increasing the surface area of the epidermis.

I want you to note that the Rete Pegs go both up into the epidermis and down into the dermis. Rete Pegs flatten with age; reducing surface area and the amount the plasma seepage into the epidermis.

What does this have to do with dermal pigmentation?

There are three points that must be understood.

1. It is into the Lamina Lucia that pigment carrying melanosomes become located if not received by the keratinocyte; accruing for many years in this location before it becomes visible at the surface- slowly building up in the small pockets and channels of the DEJ’s layers.

2. UVR stimulates melanogenesis , but also has a negative deteriorating effect of the connective tissue such as Collagen Type 1 of the dermis; by the increase in Collagenase Enzymes via UVA. (Matrix metalloproteinase enzyme MMP).
The increase in Collagenase (MMP1) linked to actinic ageing, is deterioration of connective tissue. Connective tissue supports all appendages within the dermis, such as the capillaries within the Rete Pegs/Papillary layer, and of course, the dermis supports the epidermis. This loss of support induces angiogenesis resulting in increased inflammation, erythema and vascular matting. Also, and it is important to note that when the supporting connective tissue of the DEJ deteriorates, accumulated pigment granules may filter down into the dermis.

3. Genetics contribute to dermal pigmentation because the skins that are in a high photo type 3 through to photoype 6 are high risk for pigmentation, vitiligo and keloid scarring. Each photo type comes with a risk; be it skin cancer or pigmentation. Any of the skin conditions that have a propensity towards post inflammatory hyperpigmentation will be compounded by the higher photo type. See risk analysis matrix below.

So what sort of pigmented skin condition do we look for where these indications have occurred?

An anomaly could be called Dermal Pigmentation if there is a combination of genetics, high melanin and high vascular/erythema readings because connective tissue is involved at two levels: the DEJ and the supporting Connective tissue of the dermis.

If there have been years of accumulated melanin within the DEJ, it is logical to assume that a correspondently large amount of connective tissue damage has also accrued.

Weakening the connective tissue support (superficial fascia septa) of the microcapillaries and triggering inflammation and angiogenesis, which increases localised vascular matting and erythema. The vascular damage is always behind or adjacent a pigmented lesion so therefore not always visible, diagnostic equipment can give you this information enabling you to make correct modality choices.

There are some skin diagnostic devices available that have the ability to measure both melanin and erythema levels accurately.
It has been my experience that whenever I have received high melanin readings, I got correspondingly high erythema readings.
I began to ascertain over the years and included in my classes that whenever you get high melanin readings, you always get correspondingly greater erythema, especially with MSH Cascade (Melasma).

MSH Cascade (Melasma) Butterfly pattern of pigmentation

Part of the reason dermal pigmentation is so difficult to resolve with clinical services directly linked to the length of time the pigment has been visible and how long the leading cause was involved in the formation.
For example, if the cause of MSH Cascade was found to be many years of oral contraception medication and sun exposure you could assume that dermal pigmentation was a result. If this is combined with photo type 4 to 6, then the chances are compounded. If however, the MSH Cascade pattern of pigmentation was linked to pregnancy and care was taken to avoid sun exposure during and post pregnancy, the pigmentation may resolve with careful treatment and sun protection over time.

Post Inflammatory Hyperpigmentation

This skin condition is an example of a predisposition towards pigmentation because of genetics, combined with inflammation and UV exposure during the wound healing processes.
The injury could be an insect bite, excema and photosensitising medication such as steroid creams, or acne all resulting in Post Inflammatory Hyperpigmentation.

Solar Lentigines

Solar lentigines, arise in middle age and also result from extensive sun exposure. They are most often found on the halo of the face and backs of hands. Lentigines tend to persist for long periods and don’t disappear in the winter (though they may fade). The correct term for a single lesion is solar or actinic lentigo.
I very often call this anomaly pre-solar keratosis and always have them checked for squamous cell carcinoma or basal cell carcinoma. Lentigines are common in those with fair skin but are also frequently seen in those who tan easily or have naturally dark skin.

Diagnostic equipment will not do a skin analysis for you.

However, their use confirms your analysis or raises a question in your mind that makes you investigate further.
There has been discussion over the years of being able to discern dermal pigmentation under woods light mode. However, myself personally won’t make the assumption that I can discern the difference and prefer to use the comparatives I have given you above.

Diagnostic equipment comes in many forms, and most use a variety of light modes (or sources) and magnification.
The examples in this article are imaging from the Pastiche PDM device, Canfield’s Visia and Sylton’s Observ.

Using these light modes teaches you to notice that some anomalies look the same.
This image barely shows any visible pigmentation, but does indicate thin skin density and diffused redness.

When the same image is viewed under True UV it shows that pigmentation has similar colours to thin skin density and diffused redness.
It is only with practice and continually comparing back to the Daylight mode do you start to see the differences.

To help communicate your analysis to clients, one of the newer light based diagnostic modes known as predictive or complexion analysis is particularly useful. An example is shown below.

We see here the small regular pattern of ephelides confirming that there may be red hair in the genetic history.

Red hair appears most commonly in people with two copies of a recessive allele on chromosome 16 which produces an altered version of the MC1R receptor (Melanocortin 1 receptor), increasing the risk for skin cancer.

To summarize

I have listed three indications that can be referred to as Dermal Pigmentation.

1. MSH Cascade (Compounded Melasma) Butterfly pattern of pigmentation

2. Post Inflammatory Hyperpigmentation

3. Solar Lentigines

The objective of this blog is to once again raise the awareness of teachers, educational bodies, distributors and therapists within the medical and skin treatment industry of how teaching incorrect or redundant information results in a knowledge base that has no relevance to the times.
All three of these conditions are difficult to resolve and this challenge should be your indication to consider Dermal Pigmentation may be what you are analyzing. Use diagnostic equipment that measures both melanin and erythema to confirm your analysis; if both numbers are high in comparison to other reference numbers, chances are you have Dermal Pigmentation. FBH

Want to learn more about pigmentation? Enrol for our A-Z of pigmentation course at the link here.

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Broken capillaries: fact or fiction?

Mon, 21 Oct 2019 08:25:00 GMT

Broken capillaries: fact or fiction?

The objective of this blog is to raise the awareness of teachers, educational bodies, and distributors to the medical and skin treatment industry of how teaching incorrect, superseded
or redundant information results in a knowledge base that has no relevance to the current times.

The old language of ‘broken capillaries’ being the one most often used regarding education for the modalities available for treating vascular disorders is an excellent example, so let’s review the physiology of the circulatory system and find out why the term ‘broken capillaries” should be relegated to the past.

The body has two parallel circulations: vascular, and the less conspicuous lymph circulation, the latter working in synergy with the circulatory system. The circulatory system is continuous; with no beginning or end and a heart, pump to drive it, whereas the lymphatic system has “dead end” capillaries and no heart pump.

There are several vital functions that the circulatory system plays in the health and wellbeing of skin; these functions most often work in synergy with the lymphatic system.
The first important role of the circulatory system is the transportation of materials such as blood cells, hormones, nutrients, oxygen and waste to and from all cells of the body.

Secondly, by working in synergy the circulatory system along with the lymphatic system, keep all fluids in the body constant, and includes the transport of specialized cells such as T lymphocytes and macrophages of the immune system. Finally, the extensive network of capillaries also functions to control the cutaneous blood flow, in response to the bodies’ temperature control requirements, stabilizing pH and maintain homeostasis. In other words, very significant.

“Skin colour is a site of response.” A change in skin colour is a site of response to some other event. You have been taught to use skin colour to diagnose some skin conditions such as couperose, telangiectasia and lipid peroxidation.

The network of capillaries in the neck and facial area of the skin is much denser than the torso or limbs. As a result, the face and neck are one of the first areas of the body to show a colour variation due to a shift in blood flow, pressure or lack of oxygen. This colour change reflects an alteration to homeostasis and the bodies wellbeing or health.

Unlike the arteries and veins, capillaries are fragile and are only one endothelial cell thick, and so small that blood cells can only pass through them in single file.

Capillary cells have the ability to regenerate from pre-existing blood vessels; this process is called angiogenesis. Angiogenesis occurs in the healthy body for healing wounds, and for restoring blood flow to tissues after injury or trauma.

How do endothelial cells do this?
Each endothelial cell is programmed to mend or create a new capillary (Rebudding) if any injury, break or tumor occurs, ensuring that there is no interruption of blood flow and the circulatory system remains continuous.

Angiogenesis occurs in the early phases of wound healing, repair or replacement of the vascular system. (The Lag or Proliferative phase: 3-5 days)

The re-activated endothelial cells produce enzymes from the Matrix Metalloproteinase family and release them into the surrounding tissue.
Along with these enzymes are the growth factors that stimulate the endothelial cell to multiply.
These enzymes break down surrounding extracellular tissue, making space to permit the migration of the endothelial cells.

As they migrate into the surrounding tissues, the activated cells begin to divide, rapidly organizing into the hollow tubes (Rebudding) that gradually evolve into a mature network of blood vessels.
As a result of the newly formed capillaries, an increase in the vascular network may appear as telangiectasia or couperose.

If there were a break in the circulatory system, blood cells, hormones, nutrients, and oxygen would fail to reach cell producing layers of skin or tissue, and cellular necrosis or tissue death results.
There can be an increase in vascular matting or vascular threading due to angiogenesis, but there are no broken capillaries.
It is because of angiogenesis, that the term “broken capillary” is incorrect and misleading when discussing vascular skin conditions or disorders with patients or clients.

What are spider naevi; how do they form?
Spider naevi result at any age, even children can develop them as a result of running a high temperature, or they appear across the décolletage of menopausal women and are an indicator of extra oestrogen or a result of an injury.

Developed by centrally dilated arteriole from which numerous small capillaries radiate, that resemble the legs of a spider, which how the lesion came by the name, ‘spider naevi.’

Arterioles are the connection between larger arteries and the smaller capillaries that bring plasma containing hormones, blood cells, oxygen and nutrients to cell producing layers such as the papillary layer of the dermis and basal cell layer of the epidermis.

A junction called a precapillary sphincter which controls the blood flow to the capillary might have lost the ability to control blood flow due to injury, inflammation or deteriorating supporting connective tissue.
As a result, blood seeps into a small area of surround connective tissue creating the spider appearance.

To summarize: What I hope you have gained from this information is updated knowledge regarding apparent vascular anomalies, and that that the terminology you use into the future is factual, ‘time current’ and professional. FBH

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Ageing skins, comedones and other keratolytic disorders

Mon, 21 Oct 2019 08:23:00 GMT

Why do many ageing skins develop comedones and other keratolytic disorders?
There is now universal agreement that free radicals are involved in the physical, biochemical, and pathological changes associated with aging. Oxidative damage to proteins, lipids, and DNA accumulates and increases with age, and is associated with age-related skin conditions, disorders and diseases.

In mature skins, and those that have had extensive sun exposure over 60 plus years; senile comedones can appear in the oddest of places. An example is the eyelid area that we can see here.
It is important to understand that this type of lesion does not get categorized into ‘non-inflammatory acne. Despite the fact it is a comedone, it is best practice to classify it into Aging Keratolytic Skin Conditions.
What causes an aging skin to show a variety of skin conditions that it has never suffered from at any previous age? Well, the answer to this question is cellular age. Ageing cells can be under the heading of two of categories: Mitochondrial Ageing or Cellular Senescence.

What is a Mitochondria?
Mitochondria play a significant role in the generation of energy for creating whatever that cell was designed to make. All cells of the human body have many Mitochondria.
Having established Mitochondria are organelles within cells that take nutrients and break them down and creates energy-rich molecules for the cell,(ATP) we need to recognize that as Mitochondria generate the energy that our cells require for creation; that this energy causes the Reactive Oxygen Species (ROS) of free radical to be produced, Oxidative stress is created as a side effect of this energy creation.

To prevent the damage from ROS, cells possess several antioxidant enzymes such as Superoxide Dismutase’s (SOD), Mn SOD and Cu/Zn SOD, Catalase, and Glutathione Peroxidase, which are located in the mitochondria or the intracellular fluid (Cytosol).

Occasionally, these antioxidant mechanisms fail, or the balance between antioxidants and ROS are disrupted because of either depletion of antioxidants or accumulation of ROS. Higher production of ROS in the body may change DNA structure, resulting in modification of proteins and lipids, activation of several stress-induced transcription factors, and production of pro-inflammatory and anti-inflammatory cytokines (Cell signalling).

The ageing antioxidant defense systems and cellular organelles; Mitochondria Ageing-Mitochondria DNA Damage-Cellular Senescence
Under normal conditions, cells can remove or detoxify the ROS to lower levels by using antioxidants and thereby maintain balance. In an ageing cell, these built-in antioxidant defense systems decline to result in oxidative stress. The subsequent lipid peroxidation causes the dysfunction of a cell’s lipids, nucleus, and mitochondria energy production and creation.

To compound the cellular dysfunction, a decline in mitochondrial respiratory function along with an insufficient supply of energy can significantly increase mitochondrial free radical production (Van Houten et al., 2006; Lee et al., 2007). Increased oxidative damage may enhance inflammatory responses and alter cellular functions resulting in the many of the skin conditions seen on senior skins, such as Senile Comedones, Seborrheic Keratosis and Skin Cancer.

Depending on the age of the client the level of deterioration could be M/DNA damage, M/DNA ageing or Cellular Senescence.

Ageing sebaceous gland cells and keratinocytes with deteriorating supporting connective tissue combine to create the perfect environment for senile comedones.
Both the sebaceous gland cell (sebocyte) and keratinocyte will have a slower cell turnover (mitosis) and poor quality secretions (Ceramides of the multilamellar lipids and Triglycerides of the sebum) due to dysfunction of the cell’s lipids, nucleus, and mitochondria energy production.

In addition to slow cell turnover, the keratinocyte fails to complete the cornified cell envelope compaction process and corneocyte formation, resulting in an increase in the ratio of fragile, immature cornified cells and reduced stratum corneum cohesion.
This failure to compact leads to a dramatic increase in scaling and a compaction of multiple layers of sheets of unseparated corneocytes and blocked pilosebaceous ducts; all of which will contribute to the formation of a senile comedone. See this video of the lifecycle of the keratinocyte to learn more about the cornification process.

Other than the physical changes that come about with cellular ageing, there is the nutritional changes that occur as part of the ageing process.
This is a difficulty in the absorption of nutrients that have an antioxidant profile; as well as those essential lipids such as Omega 3 needed for cell membrane health, the multilamellar lipids and acid mantle formation.

The elderly should also be encouraged to consume a diet rich in antioxidants as there is evidence that such a diet especially in combination with a healthy life style can lower the rate of all-causes and cause-speciﬁc skin disorders.

There is now universal agreement that free radicals are involved in the physical, biochemical, and pathological changes associated with aging. Oxidative damage to proteins, lipids, and DNA accumulates and increases with age, and is associated with age-related skin conditions, disorders and diseases. This is supported by the fact that in elderly subjects a higher daily intake of fruits and vegetables is associated with an improved antioxidant status compared to subjects consuming diets poor in fruits and vegetables.

To summarize the key points so as to ascertain why maturing skins get comedones and other keratolytic disorders:

1. Cellular age and mitochondria age or damage: Cellular memory and energy are compromised

2. Slow cell turnover of keratinocyte and sebocyte: Slower differentiation cycles reduce barrier defense

3. Incomplete corneocyte compaction by the keratinocyte: Cornified cell envelope formation is incomplete resulting in fragile immature cornified cells that will reduce skin barrier defense and aggravate the desquamation process of the corneocyte.

4. Incomplete desquamation of corneocyte: Corneocyte fails to desquamate from within the pilo sebaceous duct and from the skin surface.

5. Poor quality and quantity of sebum created by the sebocyte: Reduced cellular memory, oxidative stress and nutrition will result in reduced sebum Q&Q.

6. Declining built in cellular defense systems: Declining protection against ROS will accelerate declining mitochondria memory and energy production. Accelerating lipid peroxidation.

7. Antioxidant nutrition compromised: Reduced replacement of nutrients and co factors required for cell health.

8. Increase in reactive oxygen species of radical (ROS): Increased ROS combined with declining antioxidant nutrition will compound all points 1 to 7.

Interested in learning more about this topic? We have an accredited course awarded 5 CPD credits for your vocational development. Details are here.

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New procedures for old Treatments

Mon, 21 Oct 2019 08:17:00 GMT

Some 15 years after I originally wrote this article, I still come across therapists and aestheticians practicing somewhat “outdated” techniques and procedures related to the humble application of the mask. I’ve revived it once more; as both a reminder and a wake-up call to the educators who are still teaching largely obsolete practices.

The treatment procedures of many skin conditions involving the use of masks require urgent revision in order for many therapists to obtain the best from new formulations and modern treatment philosophies.
Although formulations have changed over the years, facial techniques and procedures have not always kept pace. Techniques of the 70s and 80s are still in use with these more modern products, and many Aesthetic and Beauty Therapy Schools still continue to teach old philosophies today.

In many cases, both time and money is being wasted, and the continuing combination of this old thinking and modern product results in the therapists credibility being questioned. One of the most practical and rewarding changes the therapist can make to treatment procedures relates to the massage and mask aspects of her facial practices.
The mask is perhaps the most important stage of any facial treatment, as they are designed to provide one of a number of therapeutic actions. Unfortunately, it is possible to reduce or in worst cases negate the effects of some masks by performing the massage at the incorrect time during the procedure.

The practice of massaging before the application of masks is an area where changes in product formulation may contraindicate this procedure.

Generally massage mediums are carrier oils combined with essential oils or water in oil based creams. The action of these substances is primarily lubrication and occlusion. The massage oil seals the skin and slows the trans-dermal water flow. Conversely, many of the formulations commonly used throughout the facial procedure to effect saturation and hydration are all water based.

The laws of physics and chemistry tell us that water will not penetrate an oil saturated skin, yet many therapists still attempt to infuse their water based masks through oil. Although the skin is thoroughly wiped dry after the massage, there is always sufficient residual oil embedded in the skin to retard the absorption of water based substances.

The answer to this problem is simple, and only involves the relocation of the massage stage of the treatment to follow the mask.
This change is really common sense when looking at the beneficial effects objectively.

After the application of all water-based creams, ampoules and masks, the therapist then massages with the medium of her choice. This is usually oil with essential oils or a water & oil based cream with therapeutic qualities.
In addition to locking in all the therapeutic properties of the water-based substances previously applied, the massage is a pleasant relaxing way to conclude the treatment.
Post mask massage philosophy is not new, as many leading manufacturers have recognized it as a professional practice for years.

Interestingly, no therapist, beauty therapy tutor, supplier or rep who advocated the massage before mask procedure could offer a valid theory to substantiate the method when asked why. “That’s the way I was taught” and “It relaxes the client” were the most common responses.
Inexplicably, many schools still teach this old method without regard to the type of active ingredients being used even though it is becoming more questionable. This is a typical example of Rote Learning misapplied.

It makes sense that with the plethora of new, more effective cosmetic formulations, those old methods do not work and challenge our credibility must be discarded. This is especially relevant with the new ionisable actives and the increased use of sonophoresis. One has to ask: why would you want to decrease the effectivness of the procedure and waste the investment of these great devices?

We must make a concerted effort to re-educate ourselves, only by recognizing and discarding this old thinking can we go forward to make significant changes in a clients skin condition, enjoy professional success and greater job satisfaction. FBH

This article was originally published in www.beautymagonline.com in 2001

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The Importance of the Skin Surface Microflora

Mon, 21 Oct 2019 08:15:00 GMT

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Environmental Defense Treatments for Summer

Mon, 21 Oct 2019 08:13:00 GMT

In an earlier one of my ‘Flo says’ publications,
we talked about hydration treatments and mentioned a little about how the relevant ambient humidity can affect the results of a treatment. I often
say in class that you have to think like a ‘weather presenter’ and consider if the treatment is seasonally appropriate or if the correct procedure
has been chosen for the client’s living, working or play environment.

The mind-set of thinking that a ‘Hydration treatment because it’s summer’ is a good idea may be entirely inappropriate for a summer clinical service
as these treatments can often over hydrate in conditions of high humidity.

What should you be thinking of as a suitable treatment for the summer? What environmental conditions prevail the most often? UVR is usually the first
thing that comes to mind for most of you, however, along with that thought you should be thinking ‘free radicals and oxidative stress and the resulting
lipid peroxidation.’

Oxidative Stress

Oxidative stress is the loss of both oil and water soluble antioxidants within the immediate environment around the protective membrane.

Examples of these are vitamin E, thioctic acid (alpha lipoic acid), omega’s 3 & 6, (in the form of essential fatty acids), vitamin A, (in the form
of retinyl palmitate and beta-carotene) and vitamin C. Although vitamin E abounds in quantity, it is a very poor antioxidant and can only neutralise
a small number of free radicals before becoming inactive. Vitamin E is reactivated by vitamin C and therefore without vitamin C, the cell has lost
an important antioxidant (Vit E) leaving it susceptible to oxidative stress.

This compounded loss of vitamin E then leads on to lipid peroxidation, which is a deterioration of the phospholipids that make up 45% of the cell.

Including antioxidants into your facial treatment

So how do you change a hydration treatment into one that protects the skin from the environment? What actives do you require to make a difference?

Think free radicals and the ensuing oxidative stress and lipid peroxidation that follows.

What actives commonly negate the action of a radical? Of course, it is the antioxidant and flavonoids group.

The relative importance and interactions between different antioxidants is a complex area, with the various metabolites and enzyme systems having
synergistic and interdependent effects on one another.

The action of one antioxidant may depend on the proper function of other members of the antioxidant system, and the amount of protection provided
by any one antioxidant, therefore, depends on its concentration, its reactivity towards the particular reactive oxygen species being considered, and
the status of the antioxidants with which it interacts.

There are two main groups of antioxidants:

(Hydrophilic) water soluble or (Hydrophobic) oil-soluble, and in general, the following principles apply:

• Water-soluble antioxidants react with oxidants in the cell, (Intracellular) and outside the cell (extracellular).

• Lipid-soluble antioxidants protect cell membranes from lipid peroxidation and work in synergy with the water-soluble group.

Not all enzymes, proteins, vitamins, and metabolites can be used as actives in cosmetic chemistry. However, what should be understood is what specific
cells of various systems require to function efficiently. This knowledge will help choose an antioxidant most effective for a particular condition.

ACE Vitamins

The ACE Vitamins are always the first to come to mind when thinking about protecting a skin from oxidative stress. Environmental Defense treatments
could use these vitamins as serums under masks or may even be the mask itself, all would offer good repair and protection.

Botanicals

Others available are the botanicals as antioxidants. Many if not most of the antioxidants used in the cosmetic industry come from botanical origins
and categorising the actions of botanical antioxidant is difficult because they are too many to mention. However, most botanical antioxidants can be
classified into one of the three categories; flavonoids, carotenoids, and polypheols.

Flavonoids/Bioflavonoids

Flavonoids possess a polyphenolic structure that accounts for their antioxidant, UV protectant, and metal chelation abilities. Bioflavonoids work
with other antioxidants to offer a system of protection. Numerous studies have shown their unique role in protecting vitamin C from oxidation in the
body, thereby allowing the body to reap more benefits from vitamin C.

Polyphenols as antioxidants

Polyphenols compose the largest category of botanical antioxidants.

The most widely used commercialised polyphenol antioxidants are:

• Epigallocatechin gallate (EGCG) (from greeen & white tea)

• Ferulic Acid

• Caffeic acid

• Resveratrol

• Rosmarinic acid (rosemary)

• Hypericin (St. John’s wort)

• Ellagic acid (pomegranate fruit)

• Chlorogenic acid (blueberry leaf)

• Oleuropein (olive leaf)

Xanthones as antioxidants

Xanthones exhibit strong antioxidant activity, and are thought to be more potent than both vitamin C and vitamin E.

Often referred to as the “Super Antioxidants”, Xanthones have been found to support and enhance the body’s immune system.

They are heat stable molecules and unlike proteins, won’t denature or lose their structure when heated.

This property should make them a useful addition to sun protection and other formulations exposed to radiant heat.

Carotenoids

In addition to ßeta-carotene, lutein, lycopene and astaxanthin, there are also the colourless carotenoids; phytoene and phytofluene from algae and
tomato sources that are also UV protectants and antioxidants.

Writing the treatment program:

The outline that follows is for a compromised skin that is high risk for pigmentation. This means I am following the protocols for a sensitive skin.

After the usual preparatory phase of cleanse and balancing the acid mantle with your post cleanser lotion, apply the antioxidant serums of your choice.

Just remember that if you have chosen a Vitamin C it is best to use an encapsulated sodium ascorbyl phosphate or ascorbyl tetraisopalmitate. (Oil
soluble vit C)

Do not use ascorbic acid it is too acidic and will cause the high risk skin to sting.

Now apply a layer of cream suitable for lipid dryness or compromised skin. Then apply the mask, preferably a paraplastic mask that will infuse the
actives and cream by the occlusive properties of the mask. Peel off the mask after 20 minutes and then massage with a cream or oil that also has an
antioxidant profile.

Complete your treatment with an oil soluble antioxidant and with
a sun protection product if it has been a day time appointment. Of course if the treatment has been performed during the evening, finish with a layer
of oil soluble antioxidant serums and night cream.

Why do I finish this treatment with an oil soluble antioxidant?

Using the principle that oil sits on top of water, it is logical to assume that after the completion of the facial massage which had been done with
an oil based cream or massage oil, that to apply a water based serum would be a waste of time. Why? Simple physics. Because a water based serum would
be unable to penetrate the oil that has been massaged into the skin for preceding 20 minutes.

The other reason is that an oil soluble antioxidant will not oxidise as quickly and the benefits of the environmental defense treatment is extended.

I know you will now reconsider what the new summer treatment protocols will be and that you will offer your clients a treatment that is of benefit
to the skin – not one that is just about hydration and relaxation. FBH

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The Skin Diagnostician: A 21st Century occupation

Mon, 21 Oct 2019 08:12:00 GMT

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The new season: Where have the customers gone?

Mon, 21 Oct 2019 08:11:00 GMT

Beginning business and trading for the New Year comes with challenges and without planning, you may find holes develop in your customer record system. Many things should be done at this time of the year especially if there is ‘down time’ not used wisely. How long has it been since you looked at your client record system (or cards if you still have them) and sorted them into their respective genre` of treatment, and then put them into active and inactive client records?

Sorting treatment type is straight forward to some degree. However, many clients have multiple services within one appointment so how do you define that into categories? The general rule is to sort that type of customer record into the treatment category that takes the most time. IE Facial, half wax and lash tint. The facial takes the most appointment time so that would be the type of organisation.

You then arrange each category into active and inactive files. So what do I mean by inactive? I would consider a year inactive if you have not seen a client for 12 months then it logical they are inactive. However, it is deciding what you would consider the minimum inactive status to be, that is going to be your starting point, and it could be different for each category. However, let us generalise for the sake of this conversation and say six months is the chosen inactive status.

The inactive clients are the ones that slip through the system cracks or loopholes as I call them and if you do not actively seek them out you may find that you are close to getting “traded in” for a more dynamic clinic.

So now you have sorted you client records how big is the inactive pile compared to the active? I am hoping for your sake that the inactive pile is the smallest if it is the other way round it may be time for some serious planning and changing of your ways.

So what are we going to do with these inactive files? We are going to read all of them and ask some questions.

Dear Mrs xxxxx

We offer you ourcompliments and wish to remind you that your Annual Skin Analysis appointment with our Skin Diagnostician is now due.

The policy of our practice is that prevention is better than cure and therefore in the interests of your skin health we urge you contact us and schedule an appointment. Please note that if there are any problems with your skin the earlier, it is treated, the easier and less costly it will be to rectify.

Please telephone, email or text to schedule your appointment.

Our receptionist will reply with confirmation.

Kind regards

The Skin Solutions Clinc Team

Marketing to those inactive clients will need to be subtle there could be many personal reasons why a client has not returned to you. However, the longer you leave it to contact the customer the more complicated it becomes.

Because the long term goal of any business owner is to one day, sell their company, keeping a client card ‘active’ is a way of ensuring the equity in your business is maintained.

The client card that is active is what amounts to ‘good will’ proving that your clinic is active and viable and worth purchasing.

So today when you have ‘down time’ instead of cleaning out the cupboards, clean out your filing system.

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Why Burn time decreases as skin ages

Mon, 21 Oct 2019 08:10:00 GMT

Observation of skin over 35 years has shown me that the original burn time that a skin could tolerate when young becomes shorter with age, along with less tolerance to heat. Older skin also displays a greater predisposition to post inflammatory hyperpigmentation after an injury, even if in the lower Photo type scale. The colour tone of skin is divided into 6 categories as an assessment of the response of skin to sun exposure. This is known as the Photo type scale, or Fitzpatrick Skin Type and was first developed in 1975.

Later in the 1990’s the Fitzpatrick Skin Type Scale was updated and although the Scale was a good reference for the skins burn time, it did not give any indication of the skins ability to accumulate melanin and change colour (tan).

Nor did it indicate the risk for skin cancer or post inflammatory hyperpigmentation, however this scale is used as a point reference for this discussion.

Why does skin burn time decrease with age?
The turnover and regeneration of cells change as skin ages. Based on the strength of genetic heritage these changes accelerate and compound the amount of oxidative stress each skin cell is exposed to by the living and working environment of the individual.Cells have different stem cell resources and regeneration cycles, for example, the melanocyte cell has no stem cell resource and very few regeneration cycles, most of which are completed by the age of eighteen.The melanocyte resides in the basal layer resting on the lamina lucida of the dermojunction and is considered the 5th in line of epidermal barrier defence. A dendritic cell, the melanocyte works in synergy with the ascending keratinocyte in the spinosum layer by passing melanin carrying melanosomes. So there are two cells involved in the melanogenesis of an ageing skin.

Here are some considerations of why skin burn time decreases with age.
1. No stem cell resource to draw on as melanocytes age, and documented that skin loses a minimum of 10% functioning melanocytes every 10 years from the age of 35.

2. The remaining melanocytes have little if any regeneration cycles.

3. Mitochondrial DNA ageing (MDNA) and Cellular Senescence of both melanocytes and keratinocytes mean inefficient cellular function and epidermal barrier defence formation.

4. MDNA ageing or Senescence Melanocyteshave a reduced production of melanosomes and poor quality and quantity in the percentage of melanin granules produced. This reduced production may be due to incorrect endoplasmic reticulum folding during the melanosome/melanin formation.

5. Cellular antioxidant defence systems decline with age, causing greater intracellular oxidation, cellular stress, and inflammation.

6. Dendrites become shorter as the melanocytes age, making it difficult to place melanosomes and pigment evenly throughout the spinosum layer, thereby reducing the epidermal barrier defence.

7. Essential fatty acid deficiency due to poor absorption of nutrients is common among ageing clients andcontributes to the malfunctioning dendrites of melanocytes and keratinocyte plasma membranes.

8. Any changes to the strength and function of the keratinocyte reduce all levels of epidermal barrier defence such as cell envelope formation, corneocyte compaction and resulting stratum corneum density.

9. Calcium levels required for corneocyte compaction decline with age, affecting stratum corneum density and strength.

10. Atrophy of the spinosum layer is also a contributing factor in the inefficient placement of melanin.

Conclusion:

1. Discuss all of the above considerations with your ageing patients or clients, perhaps even include some information in your next newsletter.

2. Discuss with the patient or client the importance of increasing the SPF factor of sun protection product to be higher than previously used and to use protective clothing such as broad brim hats, long sleeves dresses or shirts, longer skirts, and pants or leggings.

3. Include antioxidant protection for application under the sun protection product and after sun exposure.

4. Offer Environmental Defense facials over the summer period.

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Pigmentation: Melanosome Transfer to Keratinocyte

Mon, 21 Oct 2019 08:09:00 GMT

There is always a discussion about the skin condition pigmentation as being one of the most challenging skin conditions to successfully treat. What we learn in our base training is simple and does not cover what is truly a very complex process…

However it is enough knowledge to know that there are many things that can go wrong, and that lateral thought must be applied to this skin condition.

A number of updates regarding the relationship between melanocyte to keratinocyte have been recently published in medical and dermatology journals.

This knowledge changes our view on how pigment is transferred across to the keratinocyte, a long debated discussion point amongst professionals.
Learning that the keratinocyte has a receptor within the cell membrane for receiving melanosomes reinforces my belief that unless the cell membrane is viable, flexable and permeable these receptors may not function efficiently.

Melanosome transfer: some new information.

The protease-activated receptor 2 (PAR 2) regulates pigmentation via keratinocyte-melanocyte interactions:

The protease-activated receptor 2 (PAR 2) regulates pigmentation via keratinocyte-melanocyte interactions. THis PAR-2 is expressed by keratinocytes, but not in melanocytes. This new knowledge changes the dynamics of how we thought in the past.

PAR-2 controls melanosomes ingestion and phagocytosis by keratinocytes and exerts a regulatory role in skin pigmentation. Modulation of PAR-2 activity can enhance or decrease melanosomes transfer and affects pigmentation only when there is keratinocyte-melanocyte contact. This new information supports the phagocytosis theory.
Protease-activated receptor (PARs) expressed in multiple types of cells and tissues are involved in growth and development, mitogenesis, (Mitogenesis is the triggering of mitosis), typically via a mitogen. Inﬂammatory response regulation, malignant transformation, vascular tonus, and blood pressure regulation.

There isanother resident cell of the basal layer that would have the PAR 2 receptor for melanosomes – the basal cell keratinocyte (Mother cell).This cell does not ascend or differentiate as does the daughter keratinocyte cell. The basal cell keratinocyte is attached to the dermal-epidermal junction by keratin filaments called hemidesmosomes (Half a desmosome). Lamina Densa and Lamina Lucida of the dermojunction are thinner under the melanocytes and melanocytes are not connected to the dermojunction with hemidesmosomes. It is now knownthat the melanocyte does not have the PAR2 receptor, so cannot be influenced by misplaced melanosomes as we thought in the past.

So what becomes of the misplaced melanosomes if they are not picked up (phagocytized) by the ascending keratinocyte?

Accumulated pigment within the dermo junction:

Melanosomes can become deposited in the pockets and channels of connective tissue that makes up the Dermojunction.Here it can accumulate for many years before being visually seen as pigmentation.

Then, of course in later life, if the dermojunction deteriorates that accumulated pigment may become part of the dermis. Here it should be picked up by melanophages. (Note word should ).

CORNEOTHERAPY: The practice of repairing the epidermis first. IE: Working from the top downwards should establish a healthier spinosum layer giving a denser structure, and this should prevent melanosomes depositing in the dermojunction and basal layer cells.

Should we call pigment that has accumulated in the dermojunction ‘dermal pigmentation’? It depends on your personal view and which book you have read; let’s look at some facts. The dermojunction (basement membrane) is important for epidermal/dermal commmuniction and for skin homeostasis.

The skin consists of two main layers, epidermis and dermis, separated by the dermal-epidermal junction (dermojunction). Epidermal-dermal communication through the dermojunction is important for skin homeostasis. The basement membrane contains specialized structures, called the anchoring complex, which ensure the stability of connection and communication between these two tissue compartments. The junction serves the following functions: (1) epidermal-dermal adherence, (2) mechanical support for the epidermis, and (3) a barrier to the exchange of cells and of some large molecules across the junction.

The proteins within the anchoring complex provide links to the intracellular cytoskeletal keratins in keratinocytes (hemidesmosomes) into the lamina lucida, making it primarily of epidermal origin.

The lamina densa composed of (1) type IV collagen, (2) anchoring fibrils made of type VII collagen, and (3) dermal microfibrils makes the lamina densa of dermal origin. An intact basement membrane at the epidermal-dermal junction is essential to stability of the skin. If melanosomes/pigment accumulate into the lamina lucida, one could say that it is still epidermal pigmentation, however if the dermojunction becomes unviable and this residing pigment becomes part of the papillary layer, it is dermal pigmentation.

However, do we have all the answers? No, melanogenesis is a complicated process about which we are continually learning. Just try to think logically about structure and function of the skin and avoid following the “marketing” rabbit hole. (Bunny trail)

Melanosome transfer: some new information.

The protease-activated receptor 2 (PAR 2) regulates pigmentation via keratinocyte-melanocyte interactions:

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The Three R’s of Corneotherapy

Mon, 21 Oct 2019 08:07:00 GMT

Repair, Replenish, Regenerate. These three Rs should be second nature to every esthetician/beauty therapist and form the foundation of effective Corneotherapy, but they have also been abused extensively for retail marketing purposes. Learn how to use these three Rs as a methodology of thinking that will truly separate Corneotherapy from the domestic retail market.

The Three Rs of Corneotherapy: Repair, Replenish, Regenerate

Consider Corneotherapy the pathway to sustainable skin health, and the pathway that will care for the skin throughout the client’s lifetime.

Learning the three Rs at school was always taught from the first day of attendance. Those lessons of reading, writing and arithmetic have stayed with you all of your lives, and you use them daily.

Learning the three Rs of Corneotherapy/Skin therapy should be taught from the first day of attendance at any school for estheticians irrespective of country, and as professionals we should use them daily.

Repair : is the first lesson. All clients that attend a clinic have arrived because of skin concern; this concern may be for discoloration, redness, pustules or comedones, dryness or wrinkles. These are all indications of compromised skin , and one where the keratinocyte has not completed the differentiation cycle efficiently enough to form the first three lines of skin barrier defence. These are the acid mantle, stratum corneum, and the multilamellar lipid structure (Bilayers). Without these three lines of skin barrier defense, the inner world of the epidermis and dermis is open to the extremes of the outer environments that contain allergens and pathogens.

Consider the analogy of a house with holes in the roof, the inner part of the house is open to the extremes of the environment and becomes damp and mouldy, creating an unhealthy ecosystem for the residents. When thinking of a compromised skin in these terms it immediately becomes apparent and logical that by repairing the outer defense and structural components of the epidermis, the inner world will return to homeostasis and calm.

Nutrients supplied topically and nutritionally will ensure a healthy and viable cell membrane

Replenish: is the second lesson. Nutrients supplied topically and nutritionally will ensure a healthy and viable cell membrane, with effective active and passive transfer of oxygen, hormones, nutrients, and elimination of waste.

The extracellular environment must be optimally functional, because it is here where anti-oxidants and extracellular fluid abound protecting the cell from the outside. Also, the intracellular environment must be protected and nourished, this will ensure that the built-in defense systems and the energy creation of the cell, function correctly.

Regenerate : is the third lesson. Once the epidermal cells have been repaired and replenished, you can consider moving down to the dermis.

Here you need to consider what it is that requires your attention. Normally this will mean rebuilding the loose connective tissue that makes up the rete pegs, papillary layer and the superficial fascia septa that support all appendages of the dermis.

Dermal treatment modalities must preserve all of the work you have done to the cell producing layers of the epidermis and not cause disruption or inflammation of the innate immune system.

The target cell, of course, is the fibroblast, and you again must consider what this cell requires for building the connective tissue collagen.

Usually, vitamin C is the first active that comes to mind when thinking of what the fibroblast requires for collagen synthesis and, of course, the supporting glycosaminoglycan such as hyaluronic acid, and glucosamine.

Vitamin A in all its forms and amino acids such as proline and lysine.

The three Rs have been used in many different ways for marketing products to this industry for years. However, I want them used as a methodology of thinking that will separate this industry from the domestic retail market, multi-level marketing products and those companies that have only entered this industry for a quick dollar and want to sell you something.

Consider Corneotherapy the pathway to sustainable skin health and the pathway that will care for the skin throughout the client’s lifetime.

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Epidermal Turnover: The 30 day Myth?

Mon, 21 Oct 2019 08:06:00 GMT

There are two Questions I am often asked during my seminars that deserve an airing: If the epidermis is renewed every 30 days, why don’t I have a beautiful and perfect new skin every month? And if every pigment carrying Melanosome is transferred to a keratinocyte, and every keratinocyte ultimately desquamates in 30 days, why do I have pigmentation?

The reason for these questions arising is due to a combination of prior learning and the amount of literature written about epidermal cell turnover giving the impression that a new epidermis is the end result of the 30-day cell turnover. Where did the original idea that every cell of the epidermis turns over in 30 days come from?

The generic statement epidermal cell turn over in 30 days is used in most beauty therapy and dermatological literature. At one time, the amount of research done on the epidermis may have justified this claim, but with the vast knowledge we have today, the statement is somewhat misleading.

This means that a fundamental mistake in the understanding of the cells of the epidermis is continuing to occur and that basic beauty therapy training that still teaches this presumption is flawed. This means going back to the beginning for new thinking to be put in place.

There are a number of key cells in the epidermis, each with a different function and vastly different lifecycles. Up to 20% of these cells do not desquamate at the end of their life, so to lump them all in to the 30 day scenario is both incorrect and fosters a lack of understanding.

The earliest reference I have relating to the physics of what goes on in the epidermis is dated 1986 and is a paper that was published in a journal for cosmetic chemists and formulators.

This paper was the first I had read that gave a detailed account of the keratinocyte lifecycle and differentiation.
It was for me revolutionary, thought provoking and an eye opener. Even after fully understanding that the keratinocyte had a lifecycle of 8-10days from mitosis to arriving in the stratum corneum, I never really appreciated the significance and made the connection.
It was much later when further research led me to pursue more knowledge about the melanocyte that I discovered that the keratinocyte and melanocyte were very different but worked in synergy with one another.
I discovered that the keratinocyte has an unlimited stem cell resource, along with a short and eventful lifecycle that ultimately ended in desquamation. Conversely, the melanocyte lives for years, is slow cycling and has no major stem cell resource to draw on if destroyed.
It immediately becomes obvious that these two cells are physically dissimilar and have very different lifecycles. One has a lifecycle of 10 days and the other years, however they both reside in the epidermis and work in synergy to build an important part of the skin barrier defense system.

There are still a number of other epidermal cells to discuss during the course of this article, but at this point I ask you; with this information about the Melanocyte and keratinocyte, how can the epidermal cell turn over in 30 days statement be substantiated, and do you believe it now?

Let us review a short-list of the resident cells of the epidermis, along with a brief breakdown of the role that each plays, and their individual lifecycles.
The skin has a very elaborate defense system, where different types of cells act together or successively. Besides the keratinocyte, there are three types of specialised cells in the epidermis.
The melanocyte produces pigment (melanin), the Langerhans’ cell is the frontline defence of the immune system in the skin, and the Merkel’s cell’s that serve as mechano-receptor and are involved in the function of touch.

Keratinocyte

The keratinocyte is the predominant cell of the epidermis and accounts for 70 to 80% of the cellular population.
Keratinocytes are programmed to undergo cell death, this process is known as apoptosis, with a life of around 8 to 10 days from mitosis to arriving in the stratum corneum, depending on age and environment.

It is a hydrophobic cell and is responsible for generating and maintaining the skins barrier function. It has an unlimited stem cell resource that is situated in the bulge area of the hair follicle and deep rete pegs.

Langerhans cell

Another cell that is involved in epidermal protection is the Langerhans cell, which are dendritic cells originating from the bone marrow. Langerhans dendrites will shorten with old age and are susceptible to UVR, chemical and water burns which ultimately cause a cell migration from the epidermis.

These cells are easily replenished from bone marrow when required, providing the epidermal environment is intact/healed. They represent around 2-5% of the epidermal population, but because of their dendritic nature, have the ability to protect up to 25% of skin barrier defence.
The function of these cells is to detect any foreign bodies (antigens) that have penetrated the epidermis, capturing intruders and then carrying them to the lymph nodes in the dermis, where they are presented to the lymphocytes. A cellular type of immune response is then triggered, neutralising and finally eliminating the antigen. The nature of the Langerhans cell means that this too will have a longer life than 30 days.

Merkel cells

Merkel cells are non-dendritic non-keratinocytic epithelial cells located primarily in or near the basal layer of the epidermis. Merkel cells are commonly found in innervated clusters around hair follicles.

Merkel cells account for 6-10% of the cells in the epidermis, and are situated between the keratinocytes in the basal layer. They will remain in contact with a nerve ending.
They serve as mechano-receptors and are involved in the function of touch. They detect vibrations, pressure, touch etc, which are transmitted via a network of fibres to the brain as a stream of nerve impulses. These impulses will result in a sensation.
The origin of Merkel cells is uncertain because they share both epidermal and neuroendocrine features, however they too will be long living cells.

Melanocyte: long lived and slow cycling.

Formed at the neural crest during the embryonic stage, as the foetus develops the melanocyte will start migrating away from the neural crest and travel through the body until arriving in various parts of the body where pigment is normally found, like the epidermis, hair and eyes. They will eventually settle in the lower region of the epidermis the basal layer.

Around one in every ten cells in this layer is a melanocyte; they are a stable, slow cycling and long-lived cell, with no major stem cell resource. Melanocytes are dendritic cells, and it is estimated that each melanocyte makes contact through the dendrites with about 35 keratinocytes.

Their function is to produce melanin, the pigment that gives the skin its colour, and to transfer it to the surrounding keratinocytes by means of cytoplasmic processes. The keratinocyte will ultimately carry the pigment to the skin surface and desquamate.

Summary

So what have we learnt? Well we certainly learnt that the 4 major cells of the epidermis all have different origins and life cycles. We also know that the keratinocyte is the one cell that has the shortest life and an ulimited stem cell resource. The Langerhans cell is also replaced from the bone marrow when required, however the melanocyte is long-lived and slow cycling with no major stem cell resource to repair or replace.
The Merkels cell is still under investigation, but could be placed within the nervous system cell family, which are slow to heal and repair, and definitely not turning over in 30 days.
Not one cell in the epidermis individually has a 30-day life cycle. In reality, they all have different lifecycles and most interestingly; they all work in synergy with the keratinocyte.

To further the perception of beauty therapists as skin professionals, our basic training and literature must be based on current facts, and not the misconceptions of previous and obsolete knowledge. Only then will we be treated with the respect we deserve.

If you wish to challenge yourself, I want you to think about my second question.
“If every pigment carrying Melanosome is transferred to a keratinocyte, and every keratinocyte ultimately desquamates in 30 days, why do I have pigmentation?”

References:

[1] K D Marenus, PhD, Functional Ultrastructure of the Epidermis Cosmetic & Toiletries, vol 99, 52, 1984.

[2] Martin M Rieger, PhD, Keratinocyte Function Cosmetic & Toiletries, vol 107, 35-40 1992

[3] Jean L Bolognia & Seth J Orlow, Melanocyte Biology Pigmentary Disorders. Page 44.

[4] Derek R Highley, PhD, The Epidermal Keratinization Process vol 99, 60-61

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