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.

CHEMICAL SKIN PEEL - patient instructions

Skin peeling involves an application of a chemical solution to sun-damaged, unevenly pigmented, and finely wrinkled facial areas. The procedure is meant to diminish imperfections by peeling away the skin's top layers. It has proven to be a very popular nonsurgical cosmetic procedure. Chemical peels vary according to their specific ingredients and their strength. Depth of peeling action may also depend on factors such as how long solutions remain on the skin and whether they are lightly applied, or more heavily or vigorously applied.

A chemical peel is typically done in an office-based procedure room or outpatient surgical or aesthetic facility. Before the procedure,  the skin specialist will clean your face and might cover your eyes with ointment, gauze, tape or goggles. He or she might also protect your hair. The specialist will select the best chemical or chemical mix for the individual patient. 

Pain relief isn't typically needed for a light chemical peel.

If you're having a medium chemical peel, you might have the option of taking a sedative and a painkiller.If you're having a deep chemical peel, your doctor will likely numb your skin with a local anesthetic and give you a sedative or use regional anesthesia — which numbs a certain part of your body.

A solution is applied using a sponge, cotton pad, cotton swab or brush to the areas to be treated (or the entire face, avoiding the eyes, brows and lips). Generally, the most superficial peels are those using alpha hydroxy acids (AHA), such as glycolic, lactic or fruit acid. Various concentrations of an AHA may be applied weekly or at longer intervals to obtain the best result. A trichloroacetic acid (TCA) peel is stronger, and has a greater depth of peel compared to AHA's.

AHA:

• No anesthesia or sedation is needed, and the patient will feel only a mild tingling or stinging sensation when the solution is applied.
• Sometimes a single treatment will give skin a healthier, radiant look.
• No downtime - patient can immediately resume normal activities.
• Can be mixed with a facial cream or wash in milder concentrations as part of a daily skin-care regimen.

TCA:

• TCA is especially effective in treating darker-skinned patients.
• Can possibly be used to achieve some effects of a deep peel, depending on the concentration and manner of application.
• Generally shorter recovery time than with a deep (phenol) peel.

Both:

• Short, safe procedure.
• No covering or after-peel ointment is necessary.
• Other Considerations:

During the procedure

During a light chemical peel:

• A brush, cotton ball, gauze or sponge will be used to apply a chemical solution typically containing glycolic acid or salicylic acid. The treated skin will begin to whiten.
• You might feel mild stinging while the chemical solution is on your skin — up to 10 minutes.
• At the end the skin specialist will apply a neutralizing solution or wash treated skin to remove the chemical solution.

During a medium chemical peel:

• Your doctor will use a cotton-tipped applicator or gauze to apply a chemical solution containing trichloroacetic acid, sometimes in combination with glycolic acid. The treated skin will begin to whiten.
• After a few minutes, your doctor will apply cool compresses to soothe treated skin. You might also be given a hand-held fan to cool your skin. No neutralizing solution is needed, however.
• You might feel stinging and burning for up to 20 minutes.

During a deep chemical peel:

• You'll be given intravenous (IV) fluids and your heart rate will be closely monitored.
• Your doctor will use a cotton-tipped applicator to apply carbolic acid (phenol) to your skin. Treated skin will begin to turn white or gray.
• To limit your exposure to phenol, your doctor will do the procedure in portions at 10- to 20-minute intervals. A full-facial procedure might take 60 to 90 minutes.

After the procedure

After a chemical peel of any depth, follow your doctor's directions for cleansing, moisturizing and applying protective ointments to your skin.
After a light chemical peel, treated skin will be red, dry and mildly irritated — although these effects might be less noticeable with each repeat treatment. Your doctor might apply a protective ointment, such as petroleum jelly, to soothe the area. In some cases, a crust might form over treated skin as it begins to heal.
Treated areas develop new skin about three to seven days after a light chemical peel. New skin might temporarily be lighter or darker than normal.
After a medium chemical peel, treated skin will be red, tight and swollen. You'll feel stinging. Your doctor might apply a protective ointment, such as petroleum jelly, to soothe the area. Use ice packs for comfort and sleep in a semi-reclined position to reduce swelling.
You'll likely schedule a checkup 24 hours after treatment and another checkup two to three days after treatment so that your doctor can monitor healing.
As swelling decreases, treated skin will begin to form a crust and might darken or develop brown blotches. Treated areas develop new skin about five to seven days after a medium chemical peel, but redness might last for months.
After a deep chemical peel, you'll experience severe redness and swelling. You'll also feel burning and throbbing, and your eyelids might swell shut. Your doctor will apply a watertight dressing containing zinc oxide to treated skin. He or she might also prescribe painkillers. Sleep in a semi-reclined position to reduce swelling.
You'll likely schedule a checkup 24 or 48 hours after treatment so that your doctor can remove the dressing and clear away any yellowish liquid oozing from treated skin.
Treated areas will develop new skin within about two weeks after a deep chemical peel, although cysts or white spots might appear for several weeks and redness might last for months. Treated skin might become darker or lighter than normal or lose the ability to tan.
You might prefer to remain at home while you're healing from a chemical peel. Once new skin completely covers the treated area, you can use cosmetics to conceal any redness.

MELANOMA - screening is the best prevention

The incidence of melanoma increases during the last decade. This is the reason why I am discussing the ABCDE rules of a melanoma.

Melanoma is a kind of skin cancer so common and obvious at the same time that doctors encourage self-detection. The detection is based on the mnemonic ABCDE:

• Asymmetry of the spot.
• Border: irregular.
• Color: varies.
• Diameter: large.
• Evolution of the spot.

The tests is simple, it’s tempting to try to design the overall aspect of the lesion :

Asymmetry: one half unlike the other half.

Border: Irregular, scalloped or poorly defined border.

Color:  Most normal moles are uniform in color. But varied shades of brown, tan, or black may be a sign of melanoma.

Diameter: a mole smaller than a pencil eraser is probably not cancerous.

Finally, the evolution of the spot: “the change of a spot may indicate that the lesion is becoming malignant”.

Do this test on regular basis,  and if you have any questions ask your skin specialist. This can be a live saver ...

General information on melanoma you will find here.

In our lab we developed the SERUM HYDROCAPTEUR of Longiderm where the NDGA plays a major role in the prevention of skin cancer.

Free Radicals

What are free radicals and how do they affect the condition of my skin?
Free radicals are created as an essential part of life when energy produced in the cells. During this process, free radicals are produced that are highly charged oxygen molecules and are harmful to the skin and the body in general. They are usually neutralized by antioxidants like vitamins C, E, etc. However, when the body is overwhelmed by free radicals, they overcome the antioxidants available, which may lead to wrinkling on the skin and may also be associated with precancerous and cancerous skin legions. The most common causes of free radicals are excess sun, smoking, stress and obesity. The best way to fight free radicals is with natural antioxidants, as well as topical antioxidant creams or lotions. The LONGIDERM Team worked on these subject.

Free radicals can steal an electron and break down another biomolecule such as loose proteins, sugars, fatty acids, etc. that are NOT part of a larger chemical structure. In these cases the free radical does little damage. If a free radical steals an electron from one of the proteins that is contained in a strand of collagen (rather than a loose protein), it causes a change in the chemical structure of the collagen at that point and causes a break in the collagen strand. This is damage. Once a bundle of collagen has multiple points of damage which occurs over years, the strand of collagen becomes dysfunctional and loses its elastic quality. The skin begins to sag. Over time free radical damage happens to the various components of the body and this damage is progressive.

Free radicals chip away at cell walls, molecule by molecule, making holes. The cells leak and lose their chemical balances. Subsequent free radicals are able to chip away at DNA, making cells dysfunctional. If this damage affects cellular DNA, the cell may malfunction and this is what happens cell by cell over the lifetime of a human being, ultimately causing entire organs to malfunction, because their cells malfunction. If the DNA of basal keratinocytes, for example, are damaged the cells may become dysfunctional and the basal cells will reproduce cells that are equally as damaged and dysfunctional, resulting in the aging and dysfunction of the skin and its various components. Aging is simply the progression of damage, caused by free radicals.

More about the LONGIDERM ultrasound:

Ultrasound (sonophoresis, phonophoresis and ultraphonophoresis) is a technique for increasing the skin permeation of ingredients using ultrasound as a physical force. It is a combination of ultrasound therapy with topical delivery of actives to achieve elevated concentrations of the molecules at selected sites in the skin. In this technique, the ingredients of the selected serum or gel are used to transfers ultrasonic energy from the device to the skin. The gel or serum is the coupling medium. Application of ultrasound enhances skin permeability. The mechanism of transdermal skin permeation involves disruption of the stratum corneum lipids, thus allowing the drug to pass through the skin. A corresponding reduction in skin resistance was observed due to cavitation, microstreaming and heat generation.

Key Points

• Ultrasound enhance the absorption of actives when the formulation is applied to the skin
• Absorption of actives increased with longer exposure time and eventually use of an occlusive dressing.

OTHER CLINICAL EFFECTS of ULTRASOUND :

- Stimulation of collagen and elastin fibre synthesis.
- Reduction wrinkles and fine lines.
- Reduction of pigmental changes and eliminationof comedomes.
- Helps to control and prevent acne. Fades acne scars.
- Facilitates the elimination of toxins and metabolites.
- Provides a lymphatic drainage.