ACNE - the treatment protocol

PURIFYING LINE

Acne is a very common and widespread skin disease that does not only affect teenagers but also adults. All the same, its visible nature causes a psychological (self-image) and psychosocial (quality of life) impact, the consequences of which can be extremely embarrassing.

A TAILORED TREATMENT: THE KEY TO SUCCESS!

LONGIDERM combines a PURIFYING CONCEPT in a special range containing active ingredients from natural and chemical origin. They target the causes of acne and reduce imperfections in oily and acne-prone skin.

Different steps are described:

1. CLEANSE WITH THE PURIFYING FOAM

INDICATION:

This light and easy-to-apply purifying foam ensures a daily cleansing of oily and acne-prone skin. It offers a complete system that penetrates the pores and prevents sebum from accumulating. It removes impurities and dead cells and leaves the skin looking healthier and clearer.

RESULTS & ACTIVE INGREDIENTS:

• - SALIX ALBA soothes irritations and induces a keratolytic effect that unclogs pores.
• - ROSMARIN EXTRACT refreshes the skin, helps control the growth of micro-organisms and strengthens the skin’s natural defence mechanism thanks to its antioxidant properties.
• - AZELAIC ACID is a multifunctional ingredient that acts on hyperseborrhea and balances the production and secretion of sebum thanks to its keratolytic and sebo-regulating properties. This acid has moisturising, anti-inflammatory and brightening effects.
• - ARGININ deeply purifies the skin, soothes and stimulates cellular metabolism.
• - CAPRYLOYL GLYCINE is a sebo-regulating agent that cleanses the skin while keeping it moisturised. It acts against the proliferation of micro-organisms.

 This foam is available in a 100 ml foam dispenser.

2. PURIFY WITH THE PURIFYING LOTION

INDICATION:

This lotion with toning, astringent and soothing properties completes the daily cleansing of oily and acne-prone skin. It tightens the pores and leaves the skin looking clearer and healthier. It also induces a keratolytic effect in order to avoid the skin conditions caused by the association of sebum and impurities.

RESULTS & ACTIVE INGREDIENTS:

• - ALCOHOL refreshes, degreases and disinfects the skin.
• - AZELAIC ACID acts on hyperseborrhea and balances the production and secretion of sebum. It improves the skin’s moisture, suppleness and complexion.
• - SALICYLIC ACID is an antibacterial and anti-inflammatory agent that prevents the growth of micro-organisms and keeps the skin moisturised. It supports the skin’s defence mechanism thanks to its antiradical properties.
• - SALIX ALBA soothes irritations and normalises keratinisation. It prevents dead cells and impurities from accumulating and clogging pores.
• - ARGININE deeply purifies the skin, soothes and stimulates cellular metabolism.
• - VITAMIN C is an antioxidant that helps to scavenge free radicals, encourages collagen synthesis and optimizes cell renewal.

This lotion is available in a 100 ml spray.

3. TARGET WITH THE PURIFYING SERUM

INDICATION:

This non-greasy serum is a LOCAL intensive care meant to correct skin breakouts and accelerate their resorption.

RESULTS & ACTIVE INGREDIENTS:

• - the “MULTI-ACID” COMPLEX acts synergistically to efficiently remove impurities and prevent sebum from accumulating. In this complex:

1. SALIX ALBA tightens pores, moisturizes and reduces skin discomfort.
2. GLYCOLIC ACID softens the skin and stimulates its exfoliation. Dead cells are eliminated more easily. It has regenerating and restructuring properties while stimulating cellular renewal and collagen production.
3. SHIKIMIC ACID has a sebo-normalizing and exfoliating action. This anti-inflammatory agent helps to prevent the proliferation of micro-organisms.
4. AZELAIC ACID regulates sebum secretion and prevents pores from clogging. It has anti- inflammatory effects and scavenges free radicals. The brightening action leaves the skin looking radiant.
5. MANDELIC ACID reduces inflammation, redness and pigment spots. This moisturiser and exfoliant helps to remove dead cells from the skin surface and in this way stimulates cell renewal.
6. ARGININE deeply purifies the skin; soothes and stimulates cellular metabolism.

This serum is available in a 15ml bottle.

4. MOISTURISE WITH THE HYDRA-PURIFYING CREAM AND/OR THE HYDRA-PURIFYING CREAM +

INDICATION:

The action to be taken facing acne is to moisturise the skin instead of drying it up. LONGIDERM has developed a light care (HYDRA-PURIFYING CREAM) to be used morning and evening and a more intensive care (HYDRA-PURIFYNG CREAM +) to be used at night in presence of severe acne. Both are indicated to moisturise, balance and correct oily and acne-prone skin.

RESULTS & ACTIVE INGREDIENTS:

• - AZELAIC ACID gently cleanses the epidermis and compensates for the irritating and drying effects of anti-acne treatments. It normalises sebum secretion rates significantly. Moreover, it has a brightening and toning action.
• - SALIX ALBA soothes irritations, regulates sebum production and normalises keratinisation.
• - SALICYLIC ACID is known for its antibacterial and anti-inflammatory properties that help eliminate and prevent pimples and skin imperfections.
• - Its MOISTURISING, ANTIOXIDANT and ANTI-AGING ingredients restore the moisture level of the skin, enhance its barrier function and induce an anti-aging effect to fight the signs of skin aging.

Both creams are available in a 30 ml “Airless”.

HYALURONIC ACID in a cosmetic formulation

The skin matrix is one of the most important structures in the skin. It is what would remain if you took the skin (the fibrous middle layer of the skin) and removed all cells from it. It is responsible for structural integrity, mechanical resilience, stability and many other properties of the skin. The degradation of the skin matrix and the loss of its fullness plays an important role in the development of wrinkles and other signs of skin aging. The best known components of the skin matrix are structural proteins (notably collagen and elastin), which are vital to skin health and youthfullness. However, during aging these proteins are lacking and the dermis is loosing its volume. Wrinkles become obvious and a dermal laxity results in the appearence of more marked skin grooves. In addition to the framework of structural proteins, the skin matrix also needs appropriate filling, which provide mechanical cushioning, hold moisture, enhance barrier function, and so forth. The principal skin matrix fillers are glycans, a class of glucose-based polymers that includes glycosoaminoglycans and proteoglycans. As far as skin rejuvenation is concerned, the most important glycan may be hyaluronic acid (a.k.a. hyaluronan, hyaluronate or HA).

THE STRUCTURE

Hyaluronic acid is a bio-polymer whose unit consits of D-Glucuronic acid and N-Acetyl Glucosamine. Hyaluronic acid chains can be up to 25,000 units long or even longer; their molecular weight ranging from about 5,000 to 20,000,000 Da.

Hyaluronic acid is synthesized by the enzymes called hyaluronan synthases. Humans have at least three types of hyaluronic acid synthases: HAS1, HAS2, and HAS3. HAS1 and HAS2 synthases produce high molecular weight HA whereas HAS3 produces low molecular weight HA. Hyaluronic acid is degraded by the enzymes called hyaluronidases, of which there also appear to be several types.

THE IMPORTANCE in the SKIN PHYSIOLOGY

Hyaluronic acid has many functions throughout the body, especially in the connective tissue. In the skin, some of its known roles are the following:

• Holding moisture


• Increasing viscosity and reducing permeability of extracellular fluid


• Contributing to mechanical resilience and suppleness of the skin


• Regulation of tissues repair


• Regulation of movement and proliferation of cells


• Regulation of immune and inflammatory responses

The physiological effect of hyaluronic acid largely depends on the size (molecular weight) of its chains. In particular, relatively small HA molecules (weighing less than about 20,000 Da) appear to trigger the early phases of wound healing, including activation of various types of immune cells and inflammatory responses. In tissue injury there is an increased degradation of extracellular matrix (and HA in particular). These degradation fragments (i.e. small size HA fragments) act as indicators of injury and trigger wound healing. On the other hand, large HA molecules appear to suppress local immune response and inflammation. By the similar logic, the predominance of large HA molecules sends a signal that the skin is intact and defense and/or repair are not required. This is why in the LONGIDERM formulation most of the products have medium to large chains. In special LONGIDERM formulations HA small chain are used as a carrier for other molecules such as peptides.

Hyaluronic acid and aging

The skin content of hyaluronic acid decreases with age. This contributes to the loss of moisture and the skin becomes thinner and less full. The loss of HA may also impair the skin's ability to repair itself and possibly affects the synthesis and deposition pattern of other skin matrix components.

Topical hyaluronic acid

Topical hyaluronic acid can be formulated in form of gels and serums. HA can provide effective skin surface moisturizing and can be combined with other ingredients. 

HA can penetrate into the dermis if the molecule is small enough.  Medium-to-large size HA molecules (perhaps with molecular weight above 20,000 Da) will not penetrate sufficiently to have an impact on the skin matrix. However, small size HA (5,000 - 20,000 Da) may penetrate into the dermis in significant amounts. The effect on the matrix is controversial. Assuming small size HA molecules penetrate into the dermis, they are likely to trigger some elements of the wound healing response (as we discussed above), such as immune activation, inflammation, cell division, blood vessel growth, new skin matrix synthesis and so forth. The net effect might be either matrix degradation and accelerated skin aging or matrix remodeling and improved skin texture. 

Inhibiting the degradation of hyaluronic acid

If stimulating HA synthesis is problematic or insufficient, an alternative could be to inhibit its degradation by blocking the enzyme hyaluronidase. Escin, a saponin extracted from horse chestnut is one of these actives. In a few clinical trials, it was shown to strengthen veins and improve venous insufficiency, presumably via inhibiting hyaluronidase and elastase in vein walls. It may (or may not) be able to inhibit these matrix-degrading enzymes in the skin. The other candidate, surprisingly, is a variant of a well-known skin care ingredient ascorbyl palmitate. Its isomer L-Ascorbic Acid 6-Hexadecanoate was shown to inhibit hyaluronidase in some species, including mammals. 

SERUM HYDROCAPTEUR LONGIDERM

The SERUM HYDROCAPTEUR of LONGIDERM is based on science. One of the major players in the serum is the NDGA. This why I will spend a whole page on its function.

Nordihydroguaiaretic acid (NDGA) is a potent antioxidant compoundand LOX inhibitor found in the long-lived creosote bush. It is believed that NDGA reduces cell damage by free radicals, so under the free-radical theory of aging, could be responsible for the bush's long life.

Lipoxygenases (LOX) belong to a heterogenous family of lipid-peroxidizing enzymes and are involved in the biosynthesis of mediators of inflammation. Based on their regiospecificity during interaction with substrates, LOX have been classified as 5-, 8-, 12-, and 15-LOX. They insert oxygen at carbon 5, 8, 12 or 15 of arachidonic acid, forming 5S-, 8S-, 12S-, or 15S-hydroperoxyeicosatetraenoic acid (5-, 8-, 12-, or 15-HPETE). HPETEs can be further reduced by glutathione peroxidase to the hydroxy forms (5-, 8-, 12-, 15-HETE), respectively. 5-LOX is a dioxygenase that catalyzes the incorporation of molecular oxygen into arachidonic acid (oxygenase activity), producing HPETE and then forms the unstable epoxide LTA4 (LTA4 synthase activity). This is followed by the insertion of molecular oxygen at position C5, converting LTA4 to either 5(S)-hydroxy-6-trans-8, 11, 14-cis-eicosatetranoic acid (5-HETE) or leukotrienes. Hydrolytic attack of LTA4 by leukotriene A4 hydrolase yields LTB4, a potent neutrophil chemoattractant and stimulator of leukocyte adhesion to endothelial cells. LTA4 can be conjugated with glutathione to form LTC4 by the action of LTC4 synthase. 5-LOX pathway has been implicated in the development and progression of human cancers. Hence, 5-LOX inhibitors have been sought for their chemopreventive effects. Inhibition of 5-LOX activity is shown to block prostate cancer cell proliferation. 12-LOX exists in three distinct forms: the leukocyte-type, the platelet-type, and the epidermal form. The platelettype 12-LOX converts arachidonic acid to 12-(S)-HETE. The leukocyte-type 12-LOX metabolizes arachidonic acid or linoleic acid to either 12(S)-HETE or 15(S)-HETE. The epidermal form of 12-LOX converts arachidonic acid to 12-HETE and 15-HETE. 12-LOX has been shown to be involved in both cancer cell proliferation and survival. Inhibition of 12-LOX blocks cell proliferation and induces apoptosis in carcinosarcoma cells. 8-LOX is expressed in the skin after irritation or treatment with tumor promoters. Compared with other LOX enzymes, 8-LOX has received little attention for its role in carcinogenesis and cancer growth. 15-LOX exists as two isozymes, 15-LOX-1 and 15-LOX-2. It converts arachidonic acid to 15-HPETE which is then reduced by glutathione peroxidase to 15-HETE. The preferred substrate for 15-LOX-1 and 15-LOX-2 are linoleic acid and arachidonic acid, respectively. The 15- LOX-1 product, 13-S-HODE, is reported to enhance cell proliferation and potentiate the mitogenic response to EGF in different cell types. 

For these reasons NDGA could play an important role in the prevention of skin cancer. This theory was confirmed by Pupe et al. UVB irradiation on keratinocytes induced induced tumor necrosis factor and this can be induced by reactive oxygen species. NDGA could inhibit the formation of TNF - alpha. The importance of LOX products in the oxdative metabolism is illustrated in the article. NDGA plays a protective effect in the UVB damage. It inhibits the UVB induced TNF mRNA expression.

An important article about the subject on UVB and ROS you find the abstract below. It was published in Photochemistry and Photobiology, 2003, 78(1): 68–74

Induction of Tumor Necrosis Factor–a by UVB:A Role for Reactive Oxygen Intermediates and Eicosanoids

Annemie Pupe, Hugo Degreef and Marjan Garmyn

Department of Dermatology, Katholieke Universiteit Leuven, Leuven, Belgium

ABSTRACT

UVB irradiation induces nuclear factor–jB (NF-jB) activation, tumor necrosis factor–a (TNF-a) expression and reactive oxygen intermediates (ROI) in keratinocytes. We investigated whether ROI play a role in UVB-induced TNF-a mRNA expression. The antioxidants N-acetyl cysteine, NAC, epigallocathin gallate, EGCG, butylated hydroxyanisole (BHA) and vitamin C could reduce UVB-induced TNF-a mRNA levels to various degrees; vitamin E (a-tocopherol) had no effect. BHA was the most potent inhibitor. The oxidant tertiary butylated hydroperoxide could effectively induce TNF-a mRNA expression.

Nordihydroguaiaretic acid (NDGA) and MK-886, inhibitors of lipoxygenase (LOX), and indometacin and quinacrine, inhibitors of cyclooxygenase (COX) and phospholipase A2, respectively, could also reduce UVB-induced TNF-a mRNA expression. Inhibition by NDGA was in concordance with the results for BHA. NDGA, indometacin, quinacrine and BHA could also effectively inhibit the inhibitor of NF-jB degradation, thereby maintaining NF-jB inactivity. In conclusion, we show that ROI are implicated in the induction of TNF-a mRNA by UVB and that not all antioxidants are equally effective inhibitors. COX products and more importantly LOX products, which themselves are products of an oxidative metabolism, are the main ROI implicated in this induction of TNF-a expression by UVB probably via activation of NF-jB.

LIPO HA peeling of LONGIDERM

Superficial peelings have been used to correct skin imperfections and encourage epidermal renewal. This peeling is very usefull due its chemical modification on the salicylic acid molecule. Doctors love to use this peeling in acne patients, since it gives perfect results. 

The LIPO-HA peeling, based on an upgraded salicylic acid, is a chemical exfoliant which is efficient, easy to use and takes about 15 minutes to complete. It has been developed to treat acne and seborrheic prone skin, irregular pigmentation, skin imperfections, dull skin, wrinkles and fine lines, chronological and/or actinic aging (photo-aging), as well as superficial and acne scars.

This solution has few or no side effects and allows the skin to recover its youthful and radiant complexion. It can be suggested as a skin care treatment, observing at least 8 to 12 days between each session.  An average of 4 to 5 sessions will be required for an optimal result. In order to optimize and extend the effects of the LIPO-HA, it is advised to use the skin care products of LONGIDERM because of their high concentration of active substances in their cosmeceutical formula.

Indication:

Superficial chemical peeling with desquamating properties for professional use meant for the correction of skin imperfections such as dull skin, uneven complexion, acne-prone skin, irregular texture and surface. The lipophilic derivative of salicylic acid in its formula develops an affinity with the lipids of the stratum corneum.

It is important to know that this modified salycylic molecule is very strong, since it is 7 times more lipophyl than a classical salicylic acid.

Use:

The LIPO-HA peeling is formulated on an alcohol base and can be used, if wanted, without neutralization. Before any use, read the instructions for use carefully and analyse the contraindications.

How Do Lipo-HA LONGIPEEL Work?

This Beta hydroxy acid peels work by breaking the bonds that hold dead skin cells in place. This allows the cells to be easily removed leaving behind healthier, newer looking skin. One advantage of this peeling is that the anti-inflammatory properties of  the modified salicylic acid helps to prevent problems such as irritation occurring after the treatment. In addition this modified salicylic acid, unlike alpha hydroxy acids are very soluble in lipids (fats and oils) so these types of chemical peels are more effective if you have an oily skin. They can penetrate oily skin better to clean the pores more effectively and remove accumulated sebum and cell debris. This makes them especially effective for people who suffer from acne. Salicylic acid chemical peels are also a better choice for people with sensitive skin than alpha hydroxy peels such as glycolic acid. 

What to Expect During and After  a LONGIPEEL procedure?

Before the peel solution is applied the skin is prepared by thoroughly cleaning with the DERMO NETTOYANT DOUCEUR. Protect the sensitive area with vaseline as shown in the picture.

During the peel the eyes are well protected, this to avoid any products coming in contact with the eye mucosa. After this step a PEEL-PRIMER solution is applied. The LONGIPEEL solution is applied to the skin and left for between 10 and 15 minutes. Different layers can be applied. 

You can neutralize the peeling with the NEUTRALIZER.  

Cold compresses or a mild cream, EPI-CONFORT or lotion may be applied to help ease any irritation.

 Your skin may be slightly red and flaky after the procedure. The top layer of the skin will gradually fall off over the next few days allowing new skin to appear. It is important to use sunscreen after a chemical peel as exposure to the sun can cause further irritation and side effects. Smoking is also discouraged for the same reasons. You will be given instructions on how to care for your skin following the chemical peel by your dermatologist or skin expert.

Results after 2 sessions of lipo HA 15 %: 

You will find more information on their website www.dermalliance.eu

This LIPO-HA 5%, 10% & 15% peeling is available in a packaging of 2 vials containing each 6.5ml.

LED FUNDAMENTALS

Light therapy is one of the oldest therapeutic modalities used to treat various health conditions in history. Sunlight benefits in treating some skin diseases have been exploited for more than thousands of years in ancient Egypt, India, and China. Solar radiation therapy was later rediscovered by Niels Ryberg Finsen, a Danish physician and scientist who won in 1903 the Nobel Prize in Physiology or Medicine in recognition of his contribution to the treatment of diseases, notably lupus vulgaris and open skin tuberculosis. Phototherapy involving the use of an artificial irradiation source was born.

It was only many years later that light therapeutic benefits were uncovered again using other segments of the electromagnetic spectrum (EMS) with visible and near-infrared wavelengths. In the late 1960s, Endre Mester, a Hungarian physician, began a series of experiments on the carcinogenic potential of lasers by using a low-powered ruby laser (694 nm) on mice. To everybody surprise, the laser did not cause any cancer but improved the hair growth. This was the first demonstration of “photobiostimulation” with low-level laser therapy (LLLT), thereby opening a new applications for medical science. This lead him to conduct other studies provided support for the efficacy of red light on wound healing. Since then, medical treatment with coherent light sources (lasers) and noncoherent light (light-emitting diodes, LEDs) has expanded.

LED photobiomodulation is the latest category of nonthermal light therapies to find its way to the dermatologic armamentarium. Initial work in this area was mainly developed by National Aeronautics and Space Administration (NASA). NASA research came about as a result of the effects noted when light of a specific wavelength was shown to accelerate plant growth. Because of the deficient level of wound healing experienced by astronauts in zero-gravity space conditions and Navy Seals in submarines under high atmospheric pressure, NASA investigated the use of LED therapy in wound healing and obtained positive results. This research has continued and innovative and powerful LEDs are now used for a variety of conditions ranging from cosmetic indications to skin cancer treatment (as a photodynamic therapy light source).

THE TECHNOLOGY

A light-emitting diode (LED) is complex semiconductor light source that convert electrical current into incoherent narrow spectrum light. LEDs are used as indicator lamps in many devices and are increasingly used for other lighting. Appearing as practical electronic components in 1962, early LEDs emitted low-intensity red light, but modern versions are available across the visible, ultraviolet and infrared wavelengths, with very high brightness.

When a light-emitting diode is switched on, electrons are able to recombine with electron holes within the device, releasing energy in the form of phatons. This effect is called electroluminescence and  the color of the light (corresponding to the energy of the photon) is determined by the energy gap of the semiconductor. An LED is often small in area (less than 1 mm²), and integrated optical components may be used to shape its raduiation patern. LEDs present many advantages over incandescent light sources including lower energy consumption, longer lifetime, improved physical robustness, smaller size, and faster switching.

To understand why a LED emmit a certain wavelight it is necessary to analyse it’s components: The LED consists of a chip of semiconducting material doped with impurities to create a p-n junction. As in other diodes, current flows easily from the p-side, or andode, to the n-side, or cathode, but not in the reverse direction. Charge-carriers—electrones and holes—flow into the junction from electrodes with different voltages. When an electron meets a hole, it falls into a lower energy level, and releases energy in the form of a photon.

The wavelength of the light emitted, and thus its color depends on the band gap energy of the materials forming the p-n junction. Infrared and red devices are made with gallenium arsenide. Advances in materials have enabled making devices with ever-shorter wavelengths, emitting light in a variety of colors.

CUTANEOUS SQUAMOUS CELL CARCINOMA

Cutaneous squamous cell carcinoma (SCC) is the most common cancer arising from malignant proliferation of the keratinocytes of the epidermis. Treatment of cutaneous SCC is always indicated since progression of the tumor may lead to very extensive local tissue destruction or metastasis resulting in significant morbidity or death. Early treatment provides the best opportunity to cure cutaneous SCC.

In contrast to basal cell carcinoma (BCC), which rarely metastasizes, around 2 to 5 percent of cutaneous SCCs metastasize to regional lymph nodes or more distant sites. The approach to treatment is dependent upon the presence or absence of tumor features and patient characteristics that are predicted for an increased risk for aggressive tumor behavior. Cutaneous SCCs that do not have high-risk features have low frequencies of recurrence and metastasis. The histology will gave the most valuable information.

Histologically, it arises from the uncontrolled multiplication of cells of epithelium, or cells showing particular cytological or tissue architectural characteristics of squamous cell differentiation, such as the presence of keratin, tonofilament bundles, or desmosomes, structures involved in cell-to-cell adhesion.

All squamous cell carcinoma lesions are thought to begin via the repeated, uncontrolled division of cancer stem cells of epithelial lineage or characteristics. Accumulation of these cancer cells causes a microscopic focus of abnormal cells that are, at least initially, locally confined within the specific tissue in which the progenitor cell resided. This condition is called squamous cell carcinoma in situ, and it is diagnosed when the tumor has not yet penetrated the basement membrane or other delimiting structure to invade adjacent tissues. Once the lesion has grown and progressed to the point where it has breached, penetrated, and infiltrated adjacent structures, it is referred to as "invasive" squamous cell carcinoma. Once a carcinoma becomes invasive, it is able to spread to other organs and cause a metastasis, or "secondary tumor", to form.

Most squamous cell carcinomas result from prolonged exposure to ultraviolet (UV) radiation, either from sunlight or from tanning beds or lamps. Avoiding UV light as much as possible is the best protection against all types of skin cancer. Sunscreen is an important part of a sun safety program, but by itself doesn't completely prevent squamous cell carcinoma or other types of skin cancer.