Anatomy, Physiology & Healing
The skin is the largest organ of the body. The skin functions to protect from external elements, examples are:
Prevents the absorption of harmful substances
Helps regulate body temperature
Acts as a barrier to keep out infection
Melanin in the skin protects us from the harmful effects of UV light
Provides a waterproof coating that prevents us from becoming dehydrated
Provides an energy reserve in the form of stored fat
The skin covers the entire surface of the body and weighs approximately one-ninth of one’s total body weight. It is thinnest on the eyelids and thickest on the soles of the feet. The thickness of the skin can affect its color. For example, thin skin will look pinker as the blood in the subcutaneous tissue will show through. Whereas thicker skin, such as on the soles of the feet, tend to look yellow. The skin varies in color due to age, race inherited factors and external factors such as climate. There are also medical reasons for skin color variations, such as rashes where the skin will be red, heart or lung conditions turning the skin blue, or jaundice which will yellow the skin.
The skin is continually shedding and renewing itself. The outer skin plays a major role in maintaining body temperature and in protecting the body from harm. People feel sensations such as pain or heat because of sensors in the skin that transmit messages to the brain.
With age and sun damage, the skin will lose some of its elasticity due to lack of collagen, at which time wrinkles will appear. The skin secretes an oily substance known as 'sebum' that will help to maintain the skin's suppleness, although there are no sebaceous glands on the palms of the hand or soles of the feet.
The skin also secretes sweat, usually the result of temperature changes – this is known as insensible perspiration. Sweat can also be due to fear or nervousness – this is known as sensible perspiration. This last form is produced by apocrine sweat glands.
The skin is made up of three layers called:
• Subcutaneous Epidermis
The epidermis is the upper portion of the skin and consists of five layers:
Image of 5 layers of skin
Horny layer (stratum corneum)
The outermost layer of the stratum corneum is mostly dead, microscopically scaled and tightly packed cells, having an appearance of shingles on a rooftop. This layer acts as one of the principal defenses of the body against injury, invasion of bacteria, and acts as a waterproof covering for the skin.
Many outside influences can increase the keratinization; friction, chafing, and ultraviolet radiation (UVR) are all examples.
Because UVR stimulates melanogenesis (formation of the pigment melanin), more keratinocytes will be produced to pick up the melanosomes created by the melanocyte. The keratinocyte and the pigment granule melanin both play a major role in the skin barrier defense systems.
Ethnically darker skin, which evolved to withstand strong UV light, has a thicker stratum corneum than Caucasian skin. It takes about 3 weeks for the epidermal cells to reach the stratum corneum from the stratum germinativum. The cells are then shed through a process called desquamation.
Clear layer (stratum lucidum)
This layer is only found in thicker areas of the skin such as the palms of the hands or the soles of the feet.
The stratum lucidum is found below the horny layer and consists of dead keratinized cells without a nucleus. The cells are transparent, which allows the passage of sunlight into the deeper layers.
Granular layer (stratum granulosum)
Keratin granules appear in cells. These cells contain granules of ‘keratohylain,’ which hardens to form keratin protein. In this layer the cells begin to die. The cells have granules within them caused by the nuclei breaking up.
Prickle cell layer (stratum spinosum)
It is the spinosum layer where the keratinization process begins, while the hardening of the interior of the cells is continuous; the keratinocyte is interacting with the surrounding melanocytes.
The melanosome (now known as the pigment melanin) becomes part of the keratinocyte. It will settle over the nucleus area of the keratinocytes (cell protection), which will then move upward to the stratum corneum and desquamation.
When the skin is exposed to UV from the sun or artificial sources, an increase in these events occur, causing an increase in the number of keratinocytes and an increase in the number of melanosomes; this culminates in increased melanin transfer to keratinocytes. Melanosomes are made up of cells, which have a spikey surface to connect with surrounding cells. This is the layer that begins to synthesize keratin. In this layer the cells are living. Pigment granules called melanin may be found here.
Basal layer (stratum germinativum)
The basal layer is responsible for cellular regeneration.
These are column-shaped cells responsible for producing new epidermal cells. Cells divide and move up to higher layers. The remaining cells divide to fill the gaps. This process of cell division is caused by mitosis.
As the new cells are produced, they push older cells above them towards the surface of the skin – until they finally reach the horny layer. It takes 3 – 6 weeks for the skin cells to be pushed up from the basal layer to the horny layer.
The Stratum Germinativum or Basal Cell Layer is located at the Dermal Epidermal Junction (Basal Lamina) that separates the Epidermis from the Dermis.
The formation of the pigment melanin begins in the basal cell layer by the melanocyte cell, giving the skin protection against harmful ultraviolet rays.
This zone in the epidermis contains two other important cells – Langerhan and Melanocyte cells.
Langerhan cells absorb and remove foreign bodies that enter the skin. They move out of the epidermis and into the dermis below, and then finally enter the lymph system – the body’s waste disposal system.
Melanocyte cells are responsible for the production of melanin in the skin. These protect the other epidermal cells from the harmful effects of UV. Melanin helps determine one’s skin color; the more melanin present, the darker one’s skin tone.
The dermis lies below the epidermis and connects with the basal layer. It is often described as the “true skin” that is responsible for the strength and elasticity of the skin. It contains lots of specialized cells and structures, including nerves, blood vessels, glands and hair follicles.
It consists of two layers: Papillary layer and Reticular layer
This is the upper section and contains small tubes called capillaries, which carry blood and lymph. It also has nerve endings. This layer provides nutrients for living layers of the epidermis. It contains a thin arrangement of collagen fiber.
Lying directly beneath the basal layer of the epidermis and the dermal/epidermal junction, the papillary layer contains small cone shaped projections called papillae point that point upward into the epidermis.
This is one of the most active layers in the skin and contains the following structures within its network:
• Loose connective tissue fibers collagen and elastin (areolar)
• Interstitial glycosaminoglycans gel
• Defense cells, mast cells, phagocytes and white blood cells
• Fibroblasts and Fibrocytes (a small interactive form of fibroblast)
Below the papillary layer is the reticular layer. This is denser and consists of dense irregular connective tissue (collagen and elastin), which differs from loose connective tissue of the papillary layer.
Elastic fibers allow stretching and can recoil to their original length, preventing damage to the tissue. Collagen fibers form 75% and elastin form 4% of the connective tissue. Reticulin fibers ensure stability between the dermis and the epidermis. Fibroblasts and mast cells are found in this layer.
The reticular layer consists of two types of protein:
Elastin fibers which give the skin its elasticity
Collagen fibers which give the skin its strength
These fibers are held in a gel-like substance called ‘ground substance’. The collagen and elastin fibers form a strong network which gives a youthful appearance.
As we age, these fibers in the skin begin to harden and fragment; the network starts to break down and the skin starts to lose its elasticity and show visible signs of aging. Blood circulation to the skin declines; nutrients do not reach the surface, resulting in sallow skin. The fatty layer beneath the skin grows thinner, so one appears concaved as the bone structure is more prominent. The reticular layer is vital to the skin’s health and appearance and so it is essential to maintain to prevent signs of aging.
Subcutaneous Epidermis Layer
The subcutaneous layer is situated below the dermis. It consists of adipose tissue (fat) and areolar tissue. The adipose tissue helps to protect the body against injury and acts as an insulating layer against heat loss, helping to keep the body warm. The areolar tissue contains elastic fibers, making this layer elastic and flexible. Muscle is situated below the subcutaneous layer and is attached to bone.
The subcutaneous layer is borderline between the deepest layer and the reticular above, and is often indistinct.
The subcutaneous is made up of adipose tissue (fat cells) and loose connective tissue (areolar) because it is so rich in blood vessels, lymphatic vessels and nerve fibers.
Fibroblasts and fibrocytes (immature fibroblasts) are the cells responsible for lying down and maintaining the extracellular matrix in both the papillary and the reticular layers of the dermis.
The glycosaminoglycans (GAG’s) make up a proportion of the extracellular fluid of the dermis. They are made by the fibroblast and made up of Hyaluronic acid, Heparan sulfate, Heparin and Dermatan sulfate.
The GAG’s retain water and form a gel substance through which ions, hormones and nutrients can freely move.
A main component of this gel is hyaluronic acid, which is a large polysaccharide made of glucuronic acid and glucosamine that attract water and is increased in tissues under repair or growth.
The importance of the fibroblasts cannot be overestimated.
They are involved in normal growth, healing, wound repair and the day-to-day physiological activities of every tissue and
organ in the body.
Fibroblasts synthesize connective tissue fibers, including collagen and elastin fibers, as well as glycosaminoglycans and glycoproteins.
For the manufacture of collagen, the fibroblast first produces pro-collagen. This is produced in the rough endoplasmic reticulum, which is then in Golgi bodies from which arise secretory vesicles. These will then discharge the pro-collagen into tropocollagen, which then combines with other tropocollagen to form the collagen fibrils. Trauma from Plasma Energy stimulates the fibroblast to produce collagen and elastin.
The same as collagen, elastin is present in many structures in the body, not just in the skin. Elastin makes up only around 3% of the skin, whereas collagen makes up 70% of the dry mass of skin. Degradation of elastin fibers is associated with UV exposure. Elastosis is one of the key features of photo-aged skin.
The fact that new elastin fibers are not produced is a challenge in the aesthetic industry.
Collagen is an abundant protein that is the main component of connective tissue and is found in fibrous tissue like the skin, tendons, ligaments, cartilage, bones, corneas and blood vessels.
There are 28 collagen subtypes, 11 of which are in the dermis of the skin.
Types of Collagen
The basal lamina serves as a structural support for tissues and as a permeable barrier to regulate movement of both cell and molecules.
The dermal-epidermal junction contains type IV collagen, laminin and highly specialized type VII collagen.
During wound healing, type III collagen appears in the wound about four days after the injury. Wound collagen, or type III, is immature collagen tissue and does not provide a great deal of tensile strength. It is initially deposited in the wound in a random fashion.
It takes approximately three months for type III collagen to mature into type I collagen.
As skin ages, reactive oxygen species (associated with many aspects of aging) lead to increased production of the enzyme collagenase, which breaks down collagen. Then fibroblasts (the critical players in firm, healthy skin), lose their normal stretched state. They collapse, and more break-down enzymes are produced. People in their 80s have four times more broken collagen than people in their 20s.
Immune functions of the skin:
Langerhan cells are ‘guard’ cells, found in the Stratum Filamentosum (Spinosum) but start in the dermis. They move across the skin and are stimulated to action by the entry of foreign materials, acting as macrophages to engulf bacteria.
If someone has a bad immune system, any micro-wound treatment will not be as effective. Make sure this is explained to clients.
There are 6 basic skin types. However, a person’s facial skin can vary at different times during their life due to illness or hormonal imbalance.
Caused by under or inactive oil glands that do not produce enough sebum to keep the skin naturally hydrated. It usually has a dull appearance, feels dry and itchy and is sometimes sensitive.
Caused by glands that produce too much sebum, resulting in skin that appears shiny and has large open pores. Oily skin types are prone to develop comedones (blackheads) and acne. However, oily skin typically remains younger looking and suppler over time than other skin types.
Can be dry, normal or oily. Characterized by their delicacy. Sensitive skin frequently reacts adversely to environmental conditions and often requires special treatment to remain in good condition.
Produces sebum at a moderate rate, resulting in a balanced state. Looks consistently plump, moist and vibrant.
Most common skin-type. Frequently characterized by an oily T-Zone that covers the forehead, nose and chin; whilst the skin around the cheeks, eyes and mouth is normal to dry.
Mature skin becomes dry as sebaceous glands become less active. Skin loses elasticity – fine lines and wrinkles appear. Skin appears thinner with broken capillaries, especially on the cheek area and around the nose. Facial contours become slack as muscle tone is reduced. Blood circulation becomes poor which interferes with skin nutrition, making it appear sallow. Due to decrease in metabolic rate, waste products are not removed as quickly, leading to puffiness of the skin.
The Fitzpatrick scale (also Fitzpatrick skin typing test; or Fitzpatrick phototyping scale) is a numerical classification schema for human skin color. It was developed in 1975 by Thomas B. Fitzpatrick as a way to estimate the response of different types of skin to ultraviolet (UV) light.
Skin Fitz Type I
People with skin type I are usually pale, blonde or red hair, freckled with blue eyes and likely to experience severe sun damage from ultra-violet exposure. They usually burn easily, without ever having a tan. This skin type is believed to be highly susceptible to premature aging and skin cancers (including melanoma, the deadliest type of skin cancer) and one is therefore advised to take extreme care, and use sunscreen and other measures as protection against harmful UV rays since extreme sun exposure can result in serious damage, premature aging and skin cancers such as squamous cell carcinoma SCC, Basal cell Carcinoma BCC and Melanoma.
The Role of Pheomelanin:
It has been recognized that the type of melanin that blondes and redheads have –pheomelanin - seems to be important in skin cancer risk. This type of melanin acts as a co-conspirator in causing a person to be more at-risk for developing skin cancer. In other words, this type of melanin that causes blonde and red hair increases the risk for cell death such as seen in sunburn. Melanin filters out UV radiation, but it also actually increases the UV harmful effects and causes cell death, particularly when the melanin is the kind found in light hair or skin. Pheomelanin acts with the sun's UV rays to increase sun damage. Pheomelanin or red melanin can vary widely, depending on whether ancestors were Irish, Swedish or Dutch, and some of these variations are known to be associated with greater risk for skin cancer.
Skin Type I individuals are conducive to the usual aesthetic treatments and most treatments can safely be done without the danger of adverse side effects such as hyper- or hypopigmentation occurring.
Skin Fitz Type II
People with Skin Type II are usually fair with blue eyes, light or fair skin. They manage to get a light tan with repeated exposure to sun but have a high risk for skin cancer (including melanoma, the deadliest type of skin cancer). These skin types are therefore advised to take extreme care, use sunscreen and protect themselves from harmful UV rays as extreme sun exposure can result in serious damage, premature aging and skin cancers such as squamous cell carcinoma SCC, Basal cell Carcinoma BCC and Melanoma.
Skin Type II individuals are conducive to the usual aesthetic treatments and most treatments can safely be done without the danger of adverse side effects such as hyper- or hypopigmentation occurring.
Skin Fitz Type III
People with skin type III have sensitive skin and although their skin is still white, it is slightly darker than those with skin types I and II. Their skin sometimes burns and may tan to a light bronze, but their risk for skin cancer remains higher than average. Skin Type III individuals are also susceptible to basal cell carcinoma and squamous cell carcinoma. These skin types are therefore advised to take care, use sunscreen and protect themselves from harmful UV rays as extreme sun exposure can result in serious damage, premature aging and as mentioned earlier, life threatening skin cancers, including melanoma.
Skin Type III individuals are conducive to the usual aesthetic treatments and most treatments can safely be done without the danger of adverse side effects such as hyper- or hypopigmentation occurring.
Skin Fitz Type IV
People with skin type IV have dark hair and light Mediterranean, olive looking skin – beige with light brown tint. They typically tan with ease and seldom get burned. Their risk to develop skin cancer is less than those with skin types I-III, but still present. They should therefore still take care, use sunscreen and protect themselves from harmful UV rays as extreme sun exposure can result in serious damage, uneven skin tone, premature aging and possible skin cancers.
Skin type IV can be prone to an overactive production of melanin following sun exposure, which can result in the uneven pigmentation of melasma especially if they are on hormonal therapy such as the oral contraceptive or during pregnancy.
Those with a higher level of skin type such as skin type IV -can be prone to an overactive production of melanin following certain light and laser skin rejuvenation treatments or laser hair removal and thus proper preparation of the skin and sun avoidance is recommended prior to aesthetic treatments such as laser / light and peels. This can help prevent permanent discoloration or scarring of the skin. This is the last type of client that is an ideal candidate for this procedure.
Skin Fitz Type V
People with skin type V have an olive or dark skin tone. This includes light-skinned African-Americans, Indians and those of Middle Eastern descent. They tan easily and very rarely burn. Although skin cancer is not common among people with this skin type, they should still take the necessary precaution to protect their skin against skin cancer. Individuals with this skin type should still protect themselves from the sun as chronic sun exposure leads to uneven skin tone and pigmentation.
Skin Type V also reacts differently and at times more severely to common conditions such as acne, eczema, dermatitis, psoriasis and seborrheic dermatitis (dandruff) which can lead to potential problems with pigmentation, or uneven darkening or lightening of skin color as the formation of melanin is a dynamic process and responds to various stimuli. Thus, the skin is more reactive to an injury, which can lead to dark marks called Post-inflammatory Hyperpigmentation PIH. PIH may take years to fade thus wearing a sunscreen is essential to prevent PIH. This skin type can also produce less pigmentation called Hypopigmentation or lightened areas, after a burn or other injury.
There is a greater risk of keloid (raised, often large scars) development because darker skin has a better bed of collagen. Studies suggest that the fibroblasts which make collagen, are larger and more numerous and active. Damage to darker skin is therefore associated with a greater incidence of keloids and hypertrophic scars. These clients are not candidates for this procedure.
Skin Fitz Type VI
People with skin type VI have a dark skin color and are usually of African descent. Their skin rarely burns and although skin cancer is not common among people with this skin type, they should still take the necessary precaution to protect their skin against skin cancer, namely wear sunscreen with an SPF higher than 15 and seek the shade between 10am and 4pm. Individuals with this skin type should protect themselves from the sun as chronic sun exposure leads to uneven skin tone and pigmentation.
Acral lentiginous melanoma, a very virulent form of the disease, is more common among darker-skinned people. These melanomas tend to appear on parts of the body not often exposed to the sun, and often remain undetected until after the cancer has spread. Individuals should therefore check their skin regularly from head-to-toe and pay careful attention to any suspicious growths, especially on the palms, soles of the feet and on mucous membranes.
Skin type VI also reacts differently and at times more severely to common conditions such as acne, eczema, dermatitis, psoriasis and seborrheic dermatitis (dandruff) which can lead to potential problems with pigmentation, or uneven darkening or lightening of skin color as he formation of melanin is a dynamic process and responds to various stimuli. Thus, the skin is more reactive to an insult, which can lead to dark marks called Post-inflammatory Hyperpigmentation PIH. PIH may take years to fade, thus wearing a sunscreen daily is essential to prevent PIH. This skin type can also produce less pigmentation called Hypopigmentation or lightened areas, after a burn or other injury.
There is a greater risk of keloid (raised, often large scars) development because darker skin has a better bed of collagen. Studies suggest that the fibroblasts which make collagen, are larger and more numerous and active. Damage to darker skin is therefore associated with a greater incidence of keloids and hypertrophic scars.
(phase 1-5 day)
The moment the skin tissue is damaged, mast cells in the tissue release histamine to trigger the inflammatory response. At the same time, the capillaries and arterioles begin dilating and release blood plasma into the area as part of the inflammatory response to injury.
The plasma contains nutrients, oxygen, antibodies and white blood cells to help flush away any foreign matter from the area. After the initial rush of the inflammatory response, leucocytes and the later arriving macrophages, remove the dead tissue and foreign material, then fibrin lay down and the tissue is dissolved.
Fibroblastic phase (5-28 days). Also, the Regenerative phase
Once the wound is ready to move into the regenerative phase, a sequence of events occurs called “collagen synthesis”. Collagen, however, cannot be synthesized in the abundance of oxygen and nutrients, and if the blood supply has been damaged, it will need to be replaced.
New Collagen Production
To produce new collagen tissue, the fibroblasts that are found in low numbers in the dermis proliferate and migrate to the base of the wound with the help of growth factors and a very important glycoprotein called fibronectin.
Fibronectin acts as a conduit for fibroblasts, and it binds both the wound and the fibroblast together to allow the fibroblast to stay in place (the fibronectin) and take up residence in the wound.
Once in the wound, fibroblasts begin to synthesize collagen fibers and produce fibronectin, and GAGs like hyaluronic acid. This dermal remodeling will continue for up to two years from the original injury, with this time varying based on the individual and their age. Unfortunately, the scar is rarely as strong as the tissue it replaced.
Post Inflammatory Hyperpigmentation
History can include infestation, allergic reactions, mechanical injuries (picking acne lesions) or reactions to medications, phototoxic eruptions, burns, bruising and inflammatory skin diseases from eczema/dermatitis family.
This type of pigmentation can darken with exposure to UV light and with the use of various chemicals and medications, such as tetracycline, bleomycin, doxorubicin, 5-fluorouracil, busulfan, arsenicals, silver, gold, anti-malarial drugs, hormones and clofazimine.
Dermal pigmentation caused by trauma:
A combination of the inflammatory response and ultraviolet causes the inflammation to disrupt the basal cell layer, a combination of melanin pigment being released and subsequently trapped by macrophages in the papillary layer. Once the wound healing has completed and the junction repaired the melanin pigment granules caught within the dermal layer have no way of escape and thus a more difficult type of pigment granule to eliminate.
Post-Inflammatory Hyperpigmentation is a darkening of skin that is the result of acne scarring or skin injury due to the inflammatory response in skin. The cells associated with melanin production are closely linked with the skin immune system cells; meaning one cannot be stimulated without the other being stimulated.
Post inflammatory hyperpigmentation can be seen after endogenous or exogenous inflammatory conditions. Essentially any disease with cutaneous inflammation can potentially result in post inflammatory hyperpigmentation in individuals capable of producing melanin.
Several skin disorders such as acne, atopic dermatitis, allergic contact dermatitis, incontinent pigment, lichen planus, lupus erythematosus, and morphea have post inflammatory hyperpigmentation as a predominant feature. Exogenous stimuli, both physical and chemical, can cause injury to the skin followed by PIH. These include mechanical trauma, ionizing and nonionizing radiation, heat, contact dermatitis, and phototoxic reaction.
Optimal treatment for PIH includes prevention of further pigment deposition and clearing of the deposited pigment. Chemical peels work best when used in combination with topical bleaching regimens. Laser therapy should be used with extreme caution and care. Given the propensity of darker-skin types to develop post inflammatory hyperpigmentation, superficial peels work best, while minimizing complications.
Tyrosinase inhibitors, such as Vitamin C, arbutin, kojic acid and mulberry, have been favored for their ability to inhibit melanin by targeting the tyrosinase enzyme, which covers the amino acid phenylalanine into the melanin precursors.
Effective topical vitamins include niacinamide and several forms of vitamin C, including L-ascorbic acid, magnesium ascorbyl phosphate (MAP) and tetrahexyldecyl ascorbate, an oil soluble version.
In addition to having a direct skin-lightening effect, Vitamin C can help protect against sun damage by neutralizing free radicals that contribute to hyperpigmentation. Studies have shown that Vitamin C and E in combination can improve the efficacy of sunscreen. A great all-around skin vitamin, Vitamin A helps pigmentation problems by treating slight discoloration and evening skin tone. Vitamin A can be taken orally as well as applied topically in the form of a retinol cream or other retinol.
If a client suffers from PIH they need to be using a tyrosine inhibitor one-two weeks before treatment to avoid further PIH.
Day 1. The Swelling peaks the day following the treatment. Some clients might find it harder to open their eyes as soon as they get up in the morning on the first day following the eye treatment. Gradually, throughout the day the swelling will subside slightly. Discomfort, pain and slight discharge can occur, but this is normal.
Day 2. The swelling is the same or slightly less than the previous day (Day 1). The swelling peaks soon after waking up and subsides slightly throughout the day. Sometimes swelling also spreads to the lower eye-bags even if no plasma aesthetic treatment was carried out on the lower eyelids, this is normal because the upper eyelid communicates with the lower eyelid and some fluid inside the upper eyelid can spread to the eye bags. This is normal, and this undesired swelling of the lower eyelid will subside over the following days.
Day 3. The swelling should start to subside noticeably and the spots where plasma arc was applied will start turning into scabs. The scabs must not be picked and should fall off on their own accord. The discomfort experienced during day1 and day 2 should have subsided dramatically. No further pain should be experienced on the third day following the treatment. For those people who experience eye-bag swelling, this should still be present during the third day.
Day 4. No discomfort or pain should be felt fourth following the treatment. Some residual minor swelling can still be on the upper eyelids.
Day 5. Most swelling should have subsided, and some scabs may still be present. The minor swelling on the eye bags should have almost subsided.
Day 6. The scabs should have started to fall off. In most cases during Day 6 people will struggle to tell whether any aesthetic treatment has ever been performed.
Day 7. Almost all scabs should have fallen off. At this point, it is ok to start to apply makeup as usual.
Week 2. The area, although it has healed, may feel more tender and look pinker than usual and people may experience a stinging sensation while applying creams or washing normally.
Week 3 and 4. They still may be slightly tender and pinker than the rest of the area.
Month 2. Tenderness should have subsided, and the area should have fully blended with the surrounding skin.