Layers and Sub-Layers of the Skin

May 24, 2019

The skin is composed of two main layers. The epidermis is the outer layer which comes into contact with the external environment. It is considerably thinner than the dermis, approximately 10% of total skin thickness. The dermis is the powerhouse of the skin, providing the supportive structures to allow the epidermis to function.

Ninety percent of epidermal cells are keratinocytes which are thought of as the building blocks of the epidermis. shown here are the three layers of the skin.


The epidermis, which forms the top layer of skin, is constantly shedding millions of dead cells. It is estimated that normal skin sheds at a rate of a million cells every 40 minutes (Hinchcliffe et al., 1999) which equates to around 18 kg over a lifetime (Marieb and Hoehn, 2007). This process of skin cell shedding is known as desquamation. As skin cells are shed, new cells are constantly pushing up from underneath to replace them. If cells develop too quickly, the skin becomes piled up and thickened (as in skin diseases such as psoriasis) and if too slowly, the skin will be thin and atrophied (as occurs in old age). The normal transit time for epidermal cells (i.e. the time they take to move from the bottom layer of the epidermis to the top layer) is around 35 days. Epidermal thickness varies over the surface of the skin and can be thought of as either ‘thick’ skin or ‘thin’ skin. Thick skin occurs on the palms and soles and has neither hair follicles nor sebaceous glands but does have sweat glands. In these areas, the epidermis is between 400 and 600 μm. Thin skin, which covers the rest of the body, has hair follicles, sebaceous glands and sweat glands and is between 75 and 150 μm thick.

Ninety percent of epidermal cells are keratinocytes which are thought of as the building blocks of the epidermis. They start off as actively dividing cells and by the time they reach the skin surface they are anucleate bundles of keratin known as corneocytes. Keratin is synthesised within the keratinocytes from amino acids, particularly cysteine which allows for disulphide bond cross-linking which gives added strength to the skin. This is particularly predominant in hair and nails. Keratin is the same basic building block that is found in hair and nails in humans and horns, claws, hoofs and feathers in animals and birds.

Other epidermal cells include melanocytes (around 8% of total number of cells) and Langerhans cells.

Sub-layers of our Epidermis

Basal layer

Also known as the stratum basale or stratum germinativum, this is a single layer of columnar-shaped keratinocytes, some of which are stem cells undergoing constant cell division to produce new keratinocytes (Tortora and Derrickson, 2006). Each active basal cell divides every 4 days to produce daughter cells which then go on to differentiate and mature. These basal cells are ‘power-houses’ of activity containing various cellular structures which allow them to replicate effectively. Each cell has a large nucleus made up of cytoplasm containing ribosomes, which are attached to rough endoplasmic reticulum, a small Golgi complex and a few mitochondria The basal layer also includes the melanocytes, responsible for producing melanin which gives colour to skin and hair and protection from ultraviolet (UV) radiation. The production of melanin is under genetic control and is regulated by melanocyte stimulating hormone (MSH) secreted from the anterior lobe of the pituitary gland. Clinically, it is interesting to note that MSH is very similar in structure to adrenocorticotrophic hormone (ACTH). People with increased ACTH secretion, for example in Addison’s disease, show increased pigmentation in sun-exposed sites and where they experience mild trauma (Hinchcliffe et al., 1999) because ACTH acts as MSH.

The production of melanin occurs within organelles known as melanosomes, in the cytoplasm of the melanocytes. Within these melanosomes, the amino acid tyrosine is converted into melanin in the presence of the enzyme tyrosinase. From here it is transferred into the cytoplasm of the surrounding keratinocytes. Variations in hair pigment are caused by biochemical differences in the melanin produced in blondes, brunettes and redheads. The racial differences in skin pigment can be explained by the fact that in Caucasians, melanosomes are grouped in complexes which degenerate as the keratinocytes move towards the surface of the skin. In darker-skinned people the skin contains the same number of melanocytes, but the melanosomes are larger, remain separate and persist throughout the thickness of the epidermis (Graham-Brown and Burns, 1996). The quantity of melanin found in keratinocytes depends to a large extent on genetic make-up and the environment, that is how much UV exposure someone is subjected to.

Finally, the epidermis contains specialised cells called Merkell cells. At the interface of the epidermis and dermis, the flattened process of a sensory neuron comes into contact with the tactile disc of the Merkell cells thus detecting certain aspects of touch and sensation.

Prickle cell layer

As keratinocytes mature and differentiate, they go through the transition to the prickle cell layer where the cells become interlocked by a network of desmosomes. Desmosomes are designed specifically to hold cells together and as such are important structures which give the resilience to the skin. They consist of a plaque on either side of the plasma membrane (where a plaque is a dense layer of protein). On one side of this plaque, extending into the intracellular space, are glycoproteins known as cadherins which attach to one another. On the other side of the plaque, filaments consisting of keratin (known as tonofilaments), stretch from one side of the cell to the other where they attach to other desmosomes. This provides the cell with structural stability. The cells in this layer are so called because when they are fixed and observed under microscope, the cells pull slightly away from each other so that the desmosomes can be seen stretching across the intracellular space giving the cells a prickle-like appearance.

The prickle cell layer of the epidermis is between 8 and 10 layers thick. Keratohyalin granules are present in the keratinocytes and they contain a substance which combines with intermediate filaments of the cytoskeleton converting them to keratin; these also contribute to the resilience of the skin. Also in this section of the skin, lipid-filled membrane coating bodies start to develop.

Langerhans cells are present in the prickle layer. These cells are highly specialised dendritic cells which are an important part of the immune system, located within the skin. They are called dendritic cells because the surface membrane is folded in a similar way to the dendrites of the nervous system. This is so that the Langerhans cells can have maximum surface area to allow interaction with other cells. As immature cells, they are highly endocytotic (i.e. their plasma membrane invaginates producing an intracellular vesicle which surrounds the ingested material). However, as the Langerhans cells differentiate they have an increased capacity to migrate to T-cell areas and to function as antigen-presenting cells (Roitt and Delves, 2001). Mature Langerhans cells are covered in molecules known as major histocompatibility complex molecules, class II. These are adept at presenting the pieces of antigen protein to T-cells, which are then destroyed (Lydyard et al., 2000).

What is the Granular layer?

Also called the stratum granulosum, this is the part of the epidermis where there is high lysosomal activity. Lysosomes are organelles which contain enzymes that digest the cell contents causing the cell nuclei to disintegrate. At this stage the keratohyalin granules become more prominent within the cell and the lipid-filled membrane coating vesicles, which have been produced in both the granular and prickle cell layers, start to undergo exocytosis extruding the glycolipid over the keratinocyte membranes, thus helping to lubricate and waterproof the skin. These lipids include 40% ceramides, the rest being comprised of fatty acids, cholesterol and cholesterol sulphate. Langerhans cells continue to be present in the granular layer.

The Skin’s Horny layer

The horny layer or stratum corneum is the outer layer that interfaces with the environment. It is vital that it is capable of keeping out unwanted allergens and pathogens and retaining moisture by preventing water loss by evaporation. The cells of this outer layer are fibrous, tough bundles of keratin known as corneocytes. Filaggrin, a protein, which is also seen in the cells at this point, binds with keratin to help provide an effective skin barrier. Recent research has shown that the correct functioning of filaggrin is essential for effective barrier function of the skin. Examining the genetic make-up of people who suffer from icthyosis and atopic eczema shows loss of function mutations for filaggrin which may explain why the barrier function is compromised in these individuals (Hoffjan and Stemmler, 2007).

The horny layer contains a number of substances known as natural moisturising factors (NMF). These substances which include lactic acid, pyrrolidonecarboxylic acid and urea are water loving. They attract and hold water thus helping to maintain the hydration of the horny layer. Around 15% of the stratum corneum is water, if this falls below 10% the skin will become dry. The lipids, which were produced in the prickle and granular layers, continue to be present in the horny layer. They form what is known as a lipid bilayer which helps to further fortify the barrier function of the skin. In order to ensure the effective barrier function of the skin, all these mechanisms need to be in place.…

Dermis: The Skin Powerhouse and its Function in the Health of Your Skin

May 24, 2019

A diagram of human Skin. With its layers and sub-layers

Lying between the epidermis and the subcutaneous fat, the dermis is the support system for the epidermis, providing it with nutrients and oxygen and removing waste products. It consists largely of connective tissue.

Connective tissue consists of a ground substance with protein fibres distributed throughout it. The ground substance contains water and a mixture of large organic molecules which are a combination of polysaccharides (complex carbohydrates) and proteins. The most common type of polysaccharides in connective tissue is glycosaminoglycans (GAGS). These help to trap moisture, making the ground substance more jelly-like and viscous. GAGS include hyaluronic acid which binds cells together, lubricates joints and shapes the eyeball.

This ground substance plays an important role in providing bulk for the dermis which acts as a shock absorber and a lubricant between the collagen and elastin (protein) fibres when the skin moves. Due to its high viscosity, hormones, waste products and nutrients may pass through it; however, it is difficult for bacteria to move through.

The protein component of the dermis is largely made up of collagen

and elastin. Fibroblasts, which are found extensively throughout the dermis, are responsible for the production of collagen and elastin. The fibres that make up collagen are tough and resist stretching but they are flexible and as such they give structural strength to the skin. Bundles of collagen lie parallel to one another throughout the dermis forming cleavage or tension lines (Figure 2.5). Surgical incisions that are made parallel to these lines are much less likely to gape and will heal more effectively, than those that are made across tension lines. Collagen also has a strong water binding capability helping to maintain hydration in the dermis. Twenty-five percent of the body’s protein is collagen.


Elastic fibres, which are thinner than the collagenous fibres, are made of a stretchy, coiled protein called elastin. These springy fibres allow the skin to return to its normal shape after being stretched.

The dermis also contains tissue mast cells containing vasoactive chemicals (e.g. histamine); these are involved in moderating the immune and inflammatory responses in the skin and are found near hair fo

llicles and blood vessels. Macrophages and histocytes are also present, which are phagocytic and engulf particulate matter. Blood vessels and cutaneous lymphatics run through the dermis, as do a number of nerve bundles and sensory receptors.

There are two distinct layers to the dermis, the papillary and the reticular.

At the interface with the epidermis, the papillary layer is approximately 1/5th of the total thickness of the dermis. It is the less dense of the two layers and contains thin elastic fibres. It also carries the blood vessels and nerve endings that supply the epidermis. This layer is thrown into ‘peg like’ projections known as dermal papillae which interlock with the rete pegs of the epidermis. Some of the dermal papillae contain capillary loops and others contain nerve endings and touch receptors such as Meissner’s corpuscles. The human fingerprint, unique to each of us, is created by dermal papillae lying on dermal ridges, thus producing epidermal ridges that create a print when in contact with a surface. Usefully, the epidermal ridges on palms and soles increase friction and allow for a better grip.

The denser reticular layer makes up the bulk of the dermis. It is packed with collagen and coarse elastic fibres that give the dermis its strength and flexibility.

Is there Ethnic differences in skin structure?

There is little consensus about differences in skin structure between ethnic groups. It is commonly thought that Afro-Caribbean skin is drier than Caucasian skin. Researchers differ in their views on this. Authorities agreed, however, that there was no difference in the water content of the epidermis. One explanation as to why it is commonly thought that black skin is drier than white skin is that when skin cells shed, they are more noticeable against black skin than white, giving an ‘ashy’ tone to the skin. What does seem to be true is that desquamation is greater in black skin than white skin (up to 2.5 times).

There is debate, also, around whether black skin has a higher pH than white skin. One suggested mechanism for a higher skin pH in people with black skin is that they have more active apocrine glands, the secretions from these may explain a more acidic skin pH.

Whilst keloid scarring occurs in all racial groups, it is more common in those of Afro- Caribbean descent. Afro-Caribbean men are more likely to suffer from ingrown hairs following shaving. The hair follicle is curved and as the hair (which has been made pointy by shaving) grows, it is more likely to grow back into the skin, thus causing an inflammatory reaction; this may be misdiagnosed as acne. It is known as pseudofolliculitis barbae. Post-inflammatory and/or post-traumatic hyperpigmentation is more commonly seen in darker skins. This will usually fade, but may be the source of considerable concern.…

Skin Diagnostic Aids Used in Clinical Practice

May 23, 2019

It is also known as dermoscopy. This technique refers to the examination of the skin using skin surface microscopy. A dermatoscope (or dermoscope) is a device used for the examination of cutaneous lesions. It has a hand-held device with a magnifier with either cross-polarized or non-polarized light or a liquid medium of oil between the instrument and the skin to illuminate a lesion without glare from reflected light. The device is useful for examining pigmented lesions such as naevi and potential malignant lesions such as melanomas. There are specific dermoscopic patterns that aid in the diagnosis of the following pigmented skin lesions such as melanomas, moles (benign melanocytic naevi), freckles (lentigos), atypical naevi, seborrhoeic keratosis and pigmented basal cell carcinomas. Evidence suggests that while dermatoscopy improves the diagnostic accuracy for melanoma compared to the unaided eye, it requires sufficient training and is not recommended for untrained users.

Wood’s light

Wood’s light is a lamp emitting long-wave UVA used to examine pigmentary changes in the skin and fluorescent infections. This ultraviolet light source is used to screen for the fungal infection, tinea capitis; however, only certain species fluoresce (green) (Microsporum canis and Μ. audouinii). Other uses include highlighting patches of pityriasis versicolor caused by Pityrosorum yeast which fluoresces yellow; erythrasma, a bacterial infection affecting the skin folds, caused by Corynebacterium fluoresces green and vitiligo which delineates patches which can be otherwise missed.


Mycology can be used to identify superficial fungal infections including yeasts (candidiasis and pityriasis versicolor), dermatophytes (ringworm/ tinea – tinea unguium) or moulds (e.g. Scopulariopsis) using scales scraped from the edge of a scaly lesion, nails using a blunt instrument such as blunt scalpel blade or blunt edge of a stitch cutter. Scrapings of scale should be taken from the leading edge of the rash (as this is where active spores are most likely to be found) after the skin has been cleaned with alcohol, such as surgical spirit or 70% alcohol. This minimises contamination and is an aid to microscopy if greasy ointments or powders have been applied. Samples can be collected on kits providing black paper envelopes (e.g. Dermapak), which can be easily transferred to the lab. It is essential to have an adequate sample and provide full clinical details if the test is to be successful; whilst the precise quantity is difficult to quantify, as a general rule it is worth including as much material as possible so that full laboratory investigations can be carried out. It is always useful to have enough skin or nail to repeat the culture if necessary. Sample the discoloured, dystrophic or brittle parts of the nail only, gently digging as far back as possible from the distal part of the nail. For dermatophyte infections, samples should be taken from the distal nail and from debris under the nail (subungual debris). For superficial onychomycosis, the scraping should be from the nail surface and for Candida infections (e.g. a chronic paronychia) a swab should be taken from the proximal nail fold.

Hair can be plucked from the affected area with forceps; the infected hairs come out easily. The scalp may then be scraped with a blunt scalpel. Preferably, the sample should include hair stubs, the contents of plugged follicles and skin scales. Hair cut with a scissors is unsatisfactory as the focus of infection is usually below or near the surface of the scalp.


Where diagnosis is unclear but there is a differential diagnosis, an ellipse of skin can be taken through the edge of a lesion. There is a need to ensure that normal and abnormal skin (epidermis, dermis and fat) are included in the sample. Incisional, excisional and punch biopsies may be taken. Punch biopsies provide only limited sample, which may be inadequate for histological examination. Typically, the punch biopsy includes the full thickness skin and subcutaneous fat in the diagnosis of skin diseases. A round-shaped knife ranging in size from 1–8 mm is taken. The smaller size punch (1 mm) helps to minimise bleeding and assists in the vhealing of the wound without stitching. To diagnose many inflammatory skin conditions, the common punch size used is the 3.5- or 4-mm punch.


The source of bacteria can be determined by swabbing a fluid sample pustules, vesicles, erosions and ulcers.

Patch testing

It is a technique used to diagnose contact allergic dermatitis based on the principle of delayed hypersensitivity (an immune response). Evidence of contact allergy is derived from a patient history (such as occupation), clinical examination and patch testing. The aim of the patch test is to ascertain allergic contact dermatitis by aiming to reproduce a rash on a small controlled area of skin using standardised batches or trays of allergens (termed batteries) or those commonly used at work or home. Standard batteries of substances (now often pre-prepared) are comprised of patches made up of Finn chambers and hypoallergenic tape that are applied to the patient’s upper back; they should incorporate probable (standard battery) and possible substances (e.g. occupational specific) based on their history. The results are read at two stages, 48 hours and 72 hours; this timing sequence is related to the type IV hypersensitivity reaction, which is a delayed immune response. Care is needed to avoid misleading results from contact irritants that are distinct from hypersensitivity reactions. Differentiation is not always easy, however, the use of standard allergens and rigorous technique are required.…

Understanding and Describing Skin Lesions and Rashes

May 23, 2019

Dyshidrotic Dermatitis On Hands

With the very high number of skin health and skin disease conditions, it is particularly useful to be able to understand and systematically describe the different features and observable patterns of the underlying skin lesion or rash. Documenting the appearance of a lesion or rash can be challenging given their pattern of distribution and the sublety of their surface features. As such, it is necessary to gain familiarity with the typical types of lesions seen and rash patterns; these are introduced below.

What are Rashes

A rash is a change in the colour or texture of the skin and as such reflects the nature and pattern of a collection of individual lesions.

Owing to the wide-ranging nature of lesions, it is helpful to understand their different types. A useful distinction is also made of primary and secondary lesions. Primary lesions are caused directly by the skin disease process; this includes macules, papules, nodules, plaques, wheals, vesicles, bulla, pustules and cysts. Secondary lesions refer to the consequences of the skin disease process; these include scale, crust, fissures, lichenification, erosion, ulcers, excoriation, scar and atrophy.

Guidance on describing skin lesions.

1. Look first to identify:

a. Sites involved: specify body area
b. Number of lesions: single, multiple
c. Distribution: includes symmetrical or not, localisedor generalised
d. Arrangement: includes discrete, coalescing,disseminated, linear, annular

2. Feel the lesions by:

a. Surface palpation: with finger tips – smooth,uneven, rough
b. Deep palpation: by squeezing between finger and thumb – soft, firm, hard

3. Describe a typical lesion using the following headings:

a. Type of lesion
b. Surface features
c. Colour, including erythematous or non-erythematous
d. Border of rash/lesion: well/poorly defined or an accentuated edge
e. Size and shape of individual lesion: includes round, irregular, serpiginous

Normal Skin Health Changes From Infancy to Early Childhood

May 23, 2019

Here are a number of skin changes in the early months which can be considered ‘normal’ that do not usually require any intervention except reassurance. The terms may be a little strange but please bear with science, they have a very strange way of naming things.


These are tiny white spots which appear over the nose and face of babies; they are common. Their formation is probably related to the stimulus of the sebaceous glands which become temporarily blocked. There is no need to squeeze them as they will resolve of their own accord. The sebaceous glands become small and inactive soon after birth and as they do the milia resolve. The sebaceous glands remain inactive until puberty.

Mongolian blue spot

These are also relatively common in babies of Indo-Asian or Afro-Caribbean origin and occur in over 90% of children of Mongolian extraction. They consist of a blue grey patch on the skin which often occurs on the sacrum but can occur anywhere on the body. The skin surface is normal. The cause is thought to be elongated melanocyte precursor cells in the dermis. They can be mistaken as trauma from non-accidental injury, so should be documented in the notes. For most children these patches will fade as they get older, some however will persist into adulthood.

Benign acquired melanocytic lesions

Both freckles and lentigo can be described as benign acquired melanocytic lesions. Freckles are areas of skin where melanocytes are seen to be more active than in neighbouring areas. As a result, small (less than 5 mm in diameter), flat areas of pigmentation appear, generally scattered over the face, neck and arms, appearing in a variety of shades depending on the individual and the time of the year (darker in summer). Lentigo (plural being lentigenes) are also flat and a similar variety of sizes as the freckles, but they do not vary with sun exposure. Unlike freckles where there is no increase in the number of melanocytes, in lentigo there are.

Congenital melanocytic naevi

These lesions may be small or giant and occur in approximately 1% of births. The surface of the lesion may be smooth or rough and warty; there may be one or more hair follicles in the lesion. Giant congenital melanocytic naevi (those that cover a large area of the body and may be accompanied by thousands of smaller lesions) are associated with malignant melanomas and parents will need careful counselling about what action to take. Sometimes, the lesions are too large to consider surgical excision and grafting.

Vascular naevi

Vascular naevi are caused by dilated and tortuous, but otherwise normal blood vessels. Where capillary vessels are involved, a superficial or deep type may be described.

The superficial capillary naevi are caused by abnormal dilated vessels in the superficial dermis leading to salmon-coloured patches often on the face that will fade quite quickly. They are relatively common, occurring in approximately 50% of all neonates. The deeper capillary naevi are known as ‘port wine stains’, and because the vascular abnormality extends deeper into the dermis, these do not resolve and may even extend throughout life. The colour of the patches varies from pale pinkish red to dark purple; the colours will deepen with age. These changes can be associated with intracranial vascular changes and neurological pathology, so any child with a facial port wine stain should be investigated.

Arterial naevi

Otherwise known as superficial angiomatous naevi or strawberry birth marks, these occur in around 10% of children by the age of 1. Commonly, they start growing within a few days to a few weeks of birth and are usually relatively soft and irregular in outline. Sometimes there is a deeper component to these naevi where the subcutis is involved, in these instances the changes may lead to a distortion of normal anatomy. Growth of the lesion usually stops at around 6 months and resolution is usually spontaneous and complete, although if the lesion was particularly large, lose skin or atrophy may be left. The following rule of thumb is usually quite accurate:

Forty percent are gone by the age of 4 years; 50% by 5 years; 60% by 6 years; 70% by 7 years; 80% by 8 years and 90% by 9 years. (Graham-Brown and Bourke, 1998).

If the lesion interferes with feeding, breathing or sight, treatment may be recommended. For smaller areas, this is likely to be a steroid injection, but other options may be necessary including laser therapy. These types of naevi usually occur on the head, neck, buttocks or perineal areas. If they are associated with the lower back, sacrum or buttocks, a scan is usually recommended to exclude problems of tethering of the spinal cord.

Physiological jaundice (icterus neonatorum)

At about 2 days of age, parents may notice that their newborn is a yellowish colour. This is quite normal and results from the breakdown of the excess red blood cells that the child needed when they were in utero. As the child breaths following delivery, it no longer has any need of these red blood cells, so they break down leading to high serum bilirubin levels and the consequent yellow colour. This type of jaundice should not be confused with pathologic jaundice which occurs within 24 hours of birth and may be indicative of ABO or rhesus incompatibilities.…