¹ 12. The skin. Dermatitis.
In
zootomy and dermatology, skin is the largest organ of the integumentary system
made up of multiple layers of epithelial tissues that guard underlying muscles and
organs. Skin pigmentation (human skin color or coloring) varies among
populations, and skin type can range from dry skin to oily skin.
The
adjective cutaneous literally means "of the skin" (from Latin cutis,
skin).
As
the interface with the surroundings, skin plays the most important role in
protecting (the body) against pathogens. Its other main functions are
insulation and temperature regulation, sensation, and synthesis of vitamin D
and the protection of vitamin B folates.
Severely
damaged skin will try to heal by forming scar tissue, often giving rise to
discoloration and depigmentation of the skin.
The
use of natural or synthetic cosmetics to treat the appearance of the face and
condition of the skin (such as pore control and black head cleansing) is common
among many cultures. Oily skin is caused by hormonal fluctuations in the body,
which lead to a DHT sensitivity. This sensitivity means that the skin begins to
lose moisture and essential fatty acids (linoleic acid in particular), causing
thousands of skin cells to die, so the skin compensates for this loss of
moisture by producing higher levels of oil.
Oily skin can be cleaned quickly with a mild solution of detergent, when
pure bath soaps fail (see below: Hygiene). Afterward, body lotions could be
used to recondition cleansed skin, as would be used to treat dry skin.
The
skin, or integument, forms the continuous external surface of the body and in
different regions of the body varies in thickness, colour and the presence of
hairs, glands and nails. Despite these variations, which reflect different
functional demands, all types of skin have the same basic structure. The
external surface of skin consists of a keratinised squamous epithelium called
the epidermis. The epidermis is supported and nourished by a thick layer of
dense, fibre-elastic connective tissue called the dermis that is highly
vascular and contains many sensory receptors. The dermis is attached to
underlying tissues by a layer of loose connective tissue called the hypodetmis
or subcutaneous layer, which contains variable amounts of adipose tissue. Hair
follicles, sweat glands, sebaceous glands and nails are epithelial structures
termed epidermal appendages since they originate during embryological
development from downgrowths of epidermal epithelium into the dermis and
hypodermis.
Skin layers: epidermis, dermis, and
subcutis, showing a hair follicle, sweat gland & sebaceous gland.
Skin components
Skin has pigmentation, or melanin, provided by melanocytes, which absorb
some of the potentially dangerous ultraviolet radiation (UV) in sunlight. It
also contains DNA repair enzymes which help to reverse UV damage, and people
who lack the genes for these enzymes suffer high rates of skin cancer. One form
predominantly produced by UV light, malignant melanoma, is particularly
invasive, causing it to spread quickly, and can often be deadly. Human skin
pigmentation varies among populations in a striking manner. This has led to the
classification of people(s) on the basis of skin color.
Mammalian skin often contains hairs, which in sufficient density is
called fur. The hair mainly serves to augment the insulation the skin provides,
but can also serve as a secondary sexual characteristic or as camouflage. On
some animals, the skin is very hard and thick, and can be processed to create
leather. Reptiles and fish have hard protective scales on their skin for
protection, and birds have hard feathers, all made of tough β-keratins.
Amphibian skin is not a strong barrier to passage of chemicals and is often
subject to osmosis. A frog sitting in an anesthetic solution could quickly go
to sleep.
The skin is often known as the largest organ of the human body. This
applies to exterior surface, as it covers the body, appearing to have the
largest surface area of all the organs. Moreover, it applies to weight, as it
weighs more than any single internal organ, accounting for about 15 percent of
body weight. For the average adult human, the skin has a surface area of
between 1.5-2.0
square meters (16.1-21.5 sq.ft.), most of it is between
2-3 mm (0.10 inch ) thick. The
average square inch (6.5 cm²) of skin holds 650 sweat glands, 20 blood vessels,
60,000 melanocytes, and more than a thousand nerve endings.
Functions
Skin performs the following functions:
1. Protection: an anatomical barrier between the internal and
external environment in bodily defense; Langerhans cells in the skin are part
of the adaptive immune system
2. Sensation:
contains a variety of nerve endings that react to heat and cold, touch,
pressure, vibration, and tissue injury; see somatosensory system and haptics.
3. Heat
regulation: the skin contains a blood supply far greater than its
requirements which allows precise control of energy loss by radiation,
convection and conduction. Dilated blood vessels increase perfusion and heat
loss while constricted vessels greatly reduce cutaneous blood flow and conserve
heat. Erector pili muscles are significant in animals.
4. Control of
evaporation: the skin provides a relatively dry and impermeable barrier to
fluid loss. Loss of this function contributes to the massive fluid loss in
burns.
5. Aesthetics
and communication: others see our skin and can assess our mood, physical
state and attractiveness.
6. Storage
and synthesis: acts as a storage center for lipids and water, as well as a
means of synthesis of vitamin D by action of UV on certain parts of the skin.
7. Excretion:
sweat contains urea, however its concentration is
1/130th that of urine, hence excretion by sweating is at most a secondary
function to temperature regulation.
8. Absorption:
Oxygen, nitrogen and carbon dioxide can diffuse into the epidermis in small
amounts, some animals using their skin for their sole respiration organ. In
addition, medicine can be administered through the skin, by ointments or by
means of adhesive patch, such as the nicotine patch or iontophoresis. The skin
is an important site of transport in many other organisms.
Hygiene
Unclean skin favors the
development of pathogenic organisms - the dead cells that continually slough
off of the epidermis mix with the secretions of the sweat and sebaceous glands
and the dust found on the skin to form a filthy layer on its surface. If not
washed away, the slurry of sweat and sebaceous secretions mixed with dirt and
dead skin is decomposed by bacterial flora, producing a foul smell. Functions
of the skin are disturbed when it is excessively dirty; it becomes more easily
damaged, the release of antibacterial compounds decreases, and dirty skin is
more prone to develop infections. Cosmetics should be used carefully because
these may cause allergic reactions. Each season requires suitable clothing in
order to facilitate the evaporation of the sweat. Sunlight, water and air play
an important role in keeping the skin healthy.
The skin supports its own
ecosystems of microorganisms, including yeasts and bacteria, which cannot be
removed by any amount of cleaning. Estimates place the number of individual
bacteria on the surface of one square inch (6.5 square cm) of human skin at 50
million though this figure varies greatly over the average 20 feet (1.9 m²) of human
skin. Oily surfaces, such as the face, may contain over 500 million bacteria
per square inch (6.5 cm²). Despite these vast quantities, all of the bacteria
found on the skin's surface would fit into a volume the size of a pea. In
general, the microorganisms keep one another in check and are part of a healthy
skin. When the balance is disturbed, there may be an overgrowth and infection,
such as when antibiotics kill microbes, resulting in an overgrowth of yeast.
The skin is continuous with the inner epithelial lining of the body at the
orifices, each of which supports its own complement of microbes.
Oily skin is caused by over-active glands, that produce a substance
called sebum, a naturally healthy skin lubricant. When the skin produces
excessive sebum, it becomes heavy and thick in texture. Oily skin is typified
by shininess, blemishes and pimples. The oily-skin type is not necessarily bad,
since such skin is less prone to wrinkling, or other signs of aging, because
the oil helps to keep needed moisture locked into the epidermis (outermost
layer of skin).
The negative aspect of the
oily-skin type is that oily complexions are especially susceptible to clogged
pores, blackheads, and buildup of dead skin cells on the surface of the skin.
Oily skin can be sallow and rough in texture and tends to have large, clearly
visible pores everywhere, except around the eyes and neck.
The goal of treating oily skin is to remove excess surface sebum without
complete removal of skin lipids. Severe degreasing treatment can foster an
actual worsening of sebum secretion, which defeats the aim of the cleansing. A
method of cleansing oily skin is to wash with a solution of a mild synthetic
detergent containing no oils, waxes or other lipid agents that could aggravate
the oily condition of the skin, sometimes combined with a toning lotion. Such a
product removes the oily residue and debris from the skin surface. Some
cleansing products have lower concentrations of hydroxy acids, which remove
dead cells from the upper levels of the stratum corneum. Those products should
be used on a regular basis to work adequately. A light moisturizer may be
included in a product to counteract any drying effects of the cleanser.
Aging
A typical rash.
Skin infected with Scabies.
As skin ages, it becomes thinner
and more easily damaged. Intensifying this effect is the decreasing ability of
skin to heal itself as a person ages.
Skin ageing is caused by the fall
in elasticity. Ageing skin also receives less blood flow and lower gland
activity.
Skin layers
Diagram of the
layers of human skin.
Skin is
composed of three primary layers: the epidermis, which provides
waterproofing and serves as a barrier to infection; the dermis, which
serves as a location for the appendages of skin; and the hypodermis
(subcutaneous adipose layer).
Epidermis
Epidermis,
"epi" coming from the Greek meaning "over" or
"upon", is the outermost layer of the skin. It forms the waterproof,
protective wrap over the body's surface and is made up of stratified squamous epithelium
with an underlying basal lamina.
The outermost epidermis consists
of stratified squamous epithelium with an underlying connective tissue section,
or dermis, and a hypodermis, or basement membrane. The epidermis contains no
blood vessels, and cells in the deepest layers are nourished by diffusion from
blood capillaries extending to the upper layers of the dermis. The main type of
cells which make up the epidermis are keratinocytes, with melanocytes and
Langerhans cells also present. The epidermis can be further subdivided into the
following strata (beginning with the outermost layer): corneum, lucidum (only
in palms of hands and bottoms of feet), granulosum, spinosum, basale. Cells are
formed through mitosis at the basale layer. The daughter cells, (see cell
division) move up the strata changing shape and composition as they die due to
isolation from their blood source. The cytoplasm is released and the protein
keratin is inserted. They eventually reach the corneum and slough off
(desquamation). This process is called keratinization and takes place within
about 30 days. This keratinized layer of skin is responsible for keeping water
in the body and keeping other harmful chemicals and pathogens out, making skin
a natural barrier to infection.
Components
The
epidermis contains no blood vessels, and is nourished by diffusion from the
dermis. The main type of cells which make up the epidermis
are keratinocytes, melanocytes, Langerhans cells and Merkels cells.
Layers
Epidermis
is divided into several layers where cells are formed through mitosis at the
innermost layers. They move up the strata changing shape and composition as
they differentiate and become filled with keratin. They eventually reach the
top layer called stratum corneum and become sloughed off, or desquamated. This
process is called keratinization and takes place within weeks. The
outermost layer of Epidermis consists of 25 to 30 layers of dead cells.
Sublayers
Epidermis
is divided into the following 5 sublayers or strata:
- Stratum corneum
- Stratum lucidum
- Stratum granulosum
- Stratum spinosum
- Stratum germinativum (also
called "stratum basale").
Blood
capillaries are found beneath the epidermis, and are linked to an arteriole and
a venule. Arterial shunt vessels may bypass the network in ears, the nose and fingertips.
Dermis
The
dermis is the layer of skin beneath the epidermis that consists of connective
tissue and cushions the body from stress and strain. The dermis is tightly
connected to the epidermis by a basement membrane. It also harbors many nerve
endings that provide the sense of touch and heat. It contains the hair
follicles, sweat glands, sebaceous glands, apocrine glands, lymphatic vessels
and blood vessels. The blood vessels in the dermis provide nourishment and
waste removal to its own cells as well as the Stratum basale of the epidermis.
VIDEO
What is Skin? The Layers of
Human Skin
Structure
The dermis is structurally
divided into two areas: a superficial area adjacent to the epidermis, called
the papillary region, and a deep thicker area known as the reticular
region.
Papillary region
The papillary region is composed of loose areolar
connective tissue. It is named for its fingerlike projections
called papillae, that extend toward the epidermis. The
papillae provide the dermis with a "bumpy" surface that
interdigitates with the epidermis, strengthening the connection between the two
layers of skin.
In the palms, fingers, soles, and toes, the influence
of the papillae projecting into the epidermis forms contours in the skin's
surface. These are called friction ridges, because they help
the hand or foot to grasp by increasing friction. Friction ridges occur in
patterns (see: fingerprint) that are genetically and epigenetically determined
and are therefore unique to the individual, making it possible to use
fingerprints or footprints as a means of identification.
Reticular region
The
reticular region lies deep in the papillary region and is usually much thicker.
It is composed of dense irregular connective tissue, and receives its name from
the dense concentration of collagenous, elastic, and reticular fibers that
weave throughout it. These protein fibers give the dermis its properties of
strength, extensibility, and elasticity.
Also
located within the reticular region are the roots of the hair, sebaceous
glands, sweat glands, receptors, nails, and blood vessels.
Tattoo
ink is injected into the dermis. Stretch marks from pregnancy are also located
in the dermis.
The
hypodermis is not part of the skin, and lies below the dermis. Its purpose is
to attach the skin to underlying bone and muscle as well as supplying it with
blood vessels and nerves. It consists of loose connective tissue and elastin.
The main cell types are fibroblasts, macrophages and adipocytes (the hypodermis
contains 50% of body fat). Fat serves as padding and insulation for the body.
Microorganisms
like Staphylococcus epidermidis colonize the skin surface. The density of skin
flora depends on region of the skin. The disinfected skin surface gets recolonized
from bacteria residing in the deeper areas of the hair follicle, gut and
urogenital openings.
Photoaging
or photoageing (also known as "Dermatoheliosis") is a term used for
the characteristic changes induced by chronic UVA and UVB exposure.:29
Tretinoin is the best studied retinoid in the treatment of photoaging
The
deterioration of biological functions and ability to manage metabolic stress is
one of the major consequences of the aging process. Aging is a complex,
progressive process which also leads to functional and esthetic changes in the
skin. This process could result from both intrinsic, such that it is
genetically determined, as well as extrinsic processes which include
environmental factors.
Photoaging
is a process of aging of the skin attributed to continuous, long-term exposure
to ultraviolet (UV) radiation of approximately 245-290 nm, natural or
synthetic, on an intrinsically aged skin. Photoaging is thus also known as
aging of the skin of the face, ears, neck and hands, caused by UVA and UVB
rays.
Effects
of UV light
UV
and molecular and genetic changes
UVB
ray is considered as a primary mutagen that can only penetrate through the
epidermal or outermost layer of the skin, resulting in DNA mutations. These DNA
mutations arise due to chemical changes, the formation of cyclobutane
pyrimidine dimers and photoproducts formed between adjacent pyrimidine bases.
These mutations may be clinically related to specific signs of photoaging such
as wrinkling, increasing in elastin and collagen damage.
The
epidermal layer does not contain any blood vessels or nerve endings but
melanocytes and basal cells are embedded in this layer. Upon exposure to UVB
rays, melanocytes will produce melanin, a pigment that gives the skin its color
tone. However, UVB will cause the formation of freckles and dark spots, both of
which are symptoms of photoaging. With constant exposure to UVB rays, signs of
photoaging might appear and precancerous lesions or skin cancer may develop.
UVA
rays are able to penetrate deeper into the skin as compared to UVB rays. Hence,
in addition to the epidermal layer, the dermal layer will also be damaged. The
dermis is the second major layer of the skin and it comprises collagen,
elastin, and extrafibrillar matrix which provides structural support to the
skin. However, with constant UVA exposure, the size of the dermis layer will be
reduced, thereby causing the epidermis to start drooping off the body. Due to
the presence of blood vessels in the dermis, UVA rays could lead to dilated or
broken blood vessels most commonly visible on the nose and cheeks. UVA can also
damage DNA indirectly through the generation of reactive oxygen species (ROS)
which includes superoxide anion, peroxide and singlet oxygen. These ROS damage
cellular DNA as well as lipids and proteins.
UV
and pigmentation
UV
exposure could also lead to inflammation and vasodilation which is clinically
manifested as sunburn. UV radiation activates the transcription factor,
NF-κB, which is the first step in inflammation. NF-κB activation will
result in the increase of proinflammatory cytokines e.g. interleukin 1 (IL-1),
IL-6 vascular endothelial growth factor and tumor necrosis factor, TNF-α.
This would then attract neutrophils which lead to an increase in oxidative damage
through the generation of free radicals.
Additionally,
UV radiation would cause the down-regulation of an angiogenesis inhibitor,
thrombospondin-1, and the up-regulation of an angiogenesis activator which is
platelet-derived endothelial cell growth factor, in keratinocytes. These
enhance angiogenesis and aid in the growth of UV-induced neoplasms.
UV
and immunosuppression
It
has also been reported that UV radiation would lead to local and systemic
immunosuppression, due to DNA damage and altered cytokine expression. This has
implications in cutaneous tumor surveillance. The langerhan cells would undergo
changes in terms of quantity, morphology and functions due to UV exposure and
eventually becomes depleted. One of the reasons suggested to account for the
presence of immunosuppression mediated by the body is due to the need to
suppress or prevent an autoimmune response to inflammatory products resulting
from UV-mediated damage.
UV
and degradation of collagen
UV
exposure would also lead to the activation of receptors for epidermal growth
factor, IL-1 and TNF-α in keratinocytes and fibroblasts, which then
activates signalling kinases throughout the skin via an unknown mechanism. The
nuclear transcription factor activator protein, AP-1, which controls the
transcription of matrix metalloproteinases (MMP), is expressed and activated.
MMP-1 is a major metalloproteinases for collagen degradation. This entire
process is aided by the presence of reactive oxygen species (ROS) that inhibits
protein-tyrosine phosphatases via oxidation, thereby resulting in the
up-regulation of the above mentioned receptors. Another transcription factor
NF-κB, which is also activated by UV light, also increases the expression
of MMP-9.
The
up-regulation of MMP can occur even after minimal exposure to UV, hence,
exposure to UV radiation which is inadequate to cause sunburn can thus
facilitate the degradation of skin collagen and lead to presumably, eventual
photoaging. Thus, collagen production is reduced in photoaged skin due to the
process of constant degradation of collagen mediated by MMPs.
In
addition, the presence of damaged collagen would also down-regulate the
synthesis of new collagen. The impaired spreading and attachment of fibroblasts
onto degraded collagen could be one of the contributing factors to the
inhibition of collagen synthesis.
UV
and retinoic acids and photodamage
Retinoic
acid (RA) is essential for normal epithelial growth and differentiation as well
as for maintenance of normal skin homeostasis. UV radiation decreases the
expression of both retinoic acid receptors (RARs) and retinoid X receptors
(RXRs) in human skin, thereby resulting in a complete loss of the induction of
RA-responsive genes. It also would lead to an increase in activity of AP-1
pathway, increasing MMP activity and thus also resulting in a functional
deficiency of vitamin A in the skin.
Signs,
symptoms and histopathology
The
early symptoms of photoaging includes the following:
Dyspigmentation
and the formation of wrinkles around regions of skin commonly exposed to sun,
namely the eyes, mouth and forehead.
Spider
veins on face and neck
Loss
of color and fullness in lips
Symptoms
of photoaging attributed to prolonged exposure to UV
Wrinkles
deepen and forehead frown lines can be seen even when not frowning.
Telangiectasias
most commonly seen around the nose, cheeks and chin.
Skin
becomes leathery and laxity occurs.
Solar
Lentigines (age spots) appears on the face and hands.
Possibly
pre-cancerous red and scaly spots (actinic keratoses) appear.
Cutaneous
malignancies
In
addition to the above symptoms, photoaging could also result in an orderly
maturation of keratinocytes and an increased in the cell population of the
dermis where abundant; hyperplastic, elongated and collapsed fibroblasts and
inflammatory infiltrates are found.
Photodamage
could also be characterized as the disorganization of collagen fibrils which constitute
most of the connective tissue and the accumulation of abnormal, amorphous,
elastin-containing material.
Endogenous
defense mechanism against UV radiation
The
endogenous defense mechanisms provide protection of the skin from damages
induced by UV.
Epidermal
thickness
UV
exposure which would lead to an increase in epidermal thickness could help
protect from further UV damage.
Pigment
It
has been reported in many cases that fairer individuals who have lesser melanin
pigment show more dermal DNA photodamage, infiltrating neutrophils,
keratinocyte activation, IL-10 expression and increased MMPs after UV exposure.
Therefore, the distribution of melanin provides protection from sunburn,
photoaging, and carcinogenesis by absorbing and scattering UV rays.
Repair
of DNA mutation and apoptosis
The
damage of DNA due to exposure of UV rays will lead to expression of p53,
thereby leading to eventual arrest of the cell cycle. This allows DNA repair
mediated by endogenous mechanisms like the nucleotide excision repair system.
In addition, apoptosis occurs if the damage is too severe. However, the
apoptotic mechanisms decline with age and if neither DNA repair mechanism nor
apoptosis occurs, cutaneous tumorigenesis may result.
Tissue
inhibitors of MMPs (TIMPs)
TIMPs
regulate the activity of MMP. UV rays have been shown in many studies that it
would induce TIMP-1.
Antioxidants
The
skin consists of several antioxidants which include vitamin E, coenzyme Q10,
ascorbate, carotenoids, superoxide dismutase, catalase and glutathione
peroxidase. These antioxidants provide protection from ROS produced during
normal cellular metabolism. However, too much exposure to UV rays could lead to
a significant reduction in the antioxidant supply, leading to oxidative stress.
Hence, these antioxidants are essential in the skin's defense mechanism against
UV radiation and photocarcinogenesis.
Treatment
of photoaging
Treatment
and intervention for photoaging can be classified into a unique paradigm based on
disease prevention.
Primary
prevention
Primary
prevention aims to reduce the risk factors before a disease or condition
occurs. Primary prevention method involves mainly sun protection that comes in
many forms like sun avoidance, protective clothing, and sunscreens.
The
UV exposure would be the strongest between 10am and 4pm and sun avoidance
between this period of time is highly encouraged. If one cannot avoid exposure
to the sun, clothing, hats and sunglasses that protects one from sun exposure should
be fully utilized. Wide spectrum sun screens that have a sun protection factor
(SPF) of at least 30 should be used when one gets frequent sun exposure.
Secondary
protection
Secondary
protection refers to early detection of disease, potentially while still
asymptomatic, to allow positive interference to prevent, delay or attenuate the
symptomatic clinical condition. This includes the following:
1. Retinoids
e.g. Tretinoin
2. Antioxidants
e.g. topical vitamin C, oral supplements, CoQ10, Lipoic acid
3. Estrogens
4. Growth
factors and cytokines.
Tertiary
prevention
Lastly,
tertiary prevention is the treatment of an existing symptomatic disease process
to ameliorate its effects or delay its progress. Such tertiary prevention
includes the use of chemical peels, resurfacing techniques like
micro-dermabrasion, the use of ablative and non-ablative laser systems,
radiofrequency technology, the use of exotoxin Botulinum toxins and soft tissue
augmentation, also known as fillers.
Disease
Diseases
of the skin
Approach
to diagnoses
The
physical examination of the skin and its appendages, as well as the mucous
membranes, forms the cornerstone of an accurate diagnosis of cutaneous
conditions. Most of these conditions present with cutaneous surface changes
termed "lesions," which have more or less distinct characteristics.
Often proper examination will lead the physician to obtain appropriate
historical information and/or laboratory tests that are able to confirm the
diagnosis. Upon examination, the important clinical observations are the (1)
morphology, (2) configuration, and (3) distribution of the lesion(s). With
regard to morphology, the initial lesion that characterizes a condition is known
as the "primary lesion," and identification of such a lesions is the
most important aspect of the cutaneous examination. Over time, these primary
lesions may continue to develop or be modified by regression or trauma,
producing "secondary lesions." However, with that being stated, the
lack of standardization of basic dermatologic terminology has been one of the
principal barriers to successful communication among physicians in describing
cutaneous findings. Nevertheless, there are some commonly accepted terms used
to describe the macroscopic morphology, configuration, and distribution of skin
lesions, which are listed below.
Morphology
Primary
lesions
Chigger bites on human skin showing
characteristic welts.
Nodules
Macule and patch.
Papule and
plaque.
Vesicles and
bulla.
Fissures,
erosions and ulcers.
1. Macule
– A macule is a change in surface color, without elevation or depression and, therefore,
nonpalpable, well or ill-defined, variously sized, but generally considered
less than either 5 or
2. Patch
– A patch is a large macule equal to or greater than either 5 or
3. Papule
– A papule is a circumscribed, solid elevation of skin with no visible fluid,
varying in size from a pinhead to less than either 5 or
Fibrous
papule of the nose.
Diseases of the skin that develop papules
There are many skin diseases which develop papules, such as Lichen
planus, a skin disease which classically forms polygonal, purple papules. Lichen planus
is a chronic mucocutaneous disease that affects the skin, tongue, and oral
mucosa. The disease presents itself in the form of papules, lesions, or rashes.
Lichen planus does not involve lichens, the fungus/algae symbionts that often
grow on tree trunks; the name refers to the dry and undulating,
"lichen-like" appearance of affected skin. It is sometimes associated
with oxidative stress, certain medications and diseases, however the underlying
pathology is currently unknown.
Lichen planus
affecting the shins.
Signs and symptoms
Lichen planus
affecting the lower lip.
Micrograph
of lichen planus.
H&E stain.
The typical rash of lichen planus is well-described by the "6
Ps": well-defined pruritic, planar, purple, polygonal papules and plaques.
The commonly affected sites are near the wrist and the ankle. The rash tends to
heal with prominent blue-black or brownish discoloration that persists for a
long time. Besides the typical lesions, many morphological varieties of the
rash may occur. The presence of cutaneous lesions is not constant and may wax
and wane over time. Oral lesions tend to last far longer than cutaneous lichen
planus lesions.
Oral lichen planus (OLP) may present in one of three forms.
The reticular form is the most common presentation and manifests as
white lacy streaks on the mucosa (known as Wickham's striae) or as smaller
papules (small raised area). The lesions tend to be bilateral and are
asymptomatic. The lacy streaks may also be seen on other parts of the mouth,
including the gingiva (gums), the tongue, palate and lips.The reticular form is
the easiest to diagnose. The bullas lesions must be differentiated from
pemphigoid, chemical burns traumatic ulcers. When they break, they appear as
ulcers and need to be differentiated from squamous cell carcinoma.
The bullous form presents as fluid-filled vesicles which project from
the surface.The atrophic and erosive forms must be differentiated from
lichenoid drug reactions,SLE, pemphigoids and other immunobullous disease,
candidiasis, erythema multiforme.
The erosive forms (Atrophic LP & Ulcerative LP) present with
erythematous (red) areas that are ulcerated and uncomfortable. The erosion of
the thin epithelium may occur in multiple areas of the mouth (more prominent on
the posterior buccal mucosa), or in one area, such as the gums, where they
resemble desquamative gingivitis. Wickham's striae may also be seen near these
ulcerated areas. This form may undergo malignant transformation, although this
is controversial. The malignant transformation rate is thought to be less than
1%, however it has been reported to be as high as 5%. For any persistent oral
lesion of erosive lichen planus that does not respond to topical
corticosteroids, a biopsy is recommended to rule out precancerous
(premalignant) change or malignant transformation.
The microscopic appearance of lichen planus is pathognomonic for the
condition
·
Hyperparakeratosis with thickening of the granular cell layer
·
Development of a "saw-tooth" appearance of the rete pegs
·
Degeneration of the basal cell layer with Civatte or colloid body formation.
These result from degenerating epithelial cells.
·
Infiltration of lymphocytic inflammatory cells into the subepithelial
layer of connective tissue
·
epithelial connective tissue interphase weakens resulting in formation
of histological cleft known as Max. Joseph's space.
Lichen planus may also affect the genital mucosa – vulvovaginal-gingival
lichen planus. It can resemble other skin conditions such as atopic dermatitis
and psoriasis.
Rarely, lichen planus shows esophageal involvement, where it can present
with erosive esophagitis and stricturing. It has also been hypothesized that it
is a precursor to squamous cell carcinoma of the esophagus.[citation needed]
Clinical experience suggests that Lichen planus of the skin alone is
easier to treat as compared to one which is associated with oral and genital
lesions.
Nail & hair loss is irreversible.
Cause
Lichen planus is not contagious and does not involve any known pathogen.
Some lichen planus-type rashes (known as lichenoid reactions) occur as allergic
reactions to medications for high blood pressure, heart disease and arthritis,
in such cases termed drug-induced lichenoid reactions. These lichenoid
reactions are referred to as lichenoid mucositis (of the mucosa) or dermatitis
(of the skin). Lichen planus has been reported as a complication of chronic
hepatitis C virus infection and can be a sign of chronic graft-versus-host
disease of the skin (Lichenoid reaction of graft-versus-host disease). It has
been suggested that true lichen planus may respond to stress, where lesions may
present on the mucosa or skin during times of stress in those with the disease.
Lichen planus affects women more than men (at a ratio of 3:2), and occurs most
often in middle-aged adults. The involvement of the mucous membranes is seen
frequently and usually is asymptomatic, but occasionally, LP can be complicated
by extensive painful erosions. Lichen planus in children is rare.
Reactions to amalgam fillings may contribute to the oral lesions very
similar to lichen planus, and a systematic review found that many of the
lesions resolved after the fillings were replaced with another material.
Lichen planus can be part of Grinspan's syndrome.
Treatment
Care of OLP is within the scope of oral medicine speciality. Currently
there is no cure for lichen planus but there are certain types of medicines
used to reduce the effects of the inflammation. Lichen planus may go into a
dormant state after treatment. There are also reports that lichen planus can
flare up years after it is considered cured.
Medicines used to treat lichen planus include:
·
Oral and topical steroids.
·
Oral retinoids
·
immunosuppressant medications
·
hydroxychloroquine
·
tacrolimus
·
dapsone
Non-drug treatments:
· UVB
NarrowBand Phototherapy
· Aloe
vera
· Purslane
4. Plaque – A
plaque has been described as a broad papule, or confluence of papules equal to
or greater than
5. Nodule – A
nodule is morphologically similar to a papule, but is greater than either 5 or
6. Vesicle – A
vesicle is a circumscribed, fluid-containing, epidermal elevation generally
considered less than either 5 or
7. Bulla – A
bulla is a large vesicle described as a rounded or irregularly shaped blister
containing serous or seropurulent fluid, equal to or greater than either 5 or
8. Pustule – A
pustule is a small elevation of the skin containing cloudy or purulent material
usually consisting of necrotic inflammatory cells. These can be either white or
red.
9. Cyst – A cyst
is an epithelial-lined cavity containing liquid, semi-solid, or solid material.
10. Erosion – An erosion is a discontinuity of the skin exhibiting
incomplete loss of the epidermis, a lesion that is moist, circumscribed, and
usually depressed.
11. Ulcer – An
ulcer is a discontinuity of the skin exhibiting complete loss of the epidermis
and often portions of the dermis and even subcutaneous fat. An ulcer is a sore
on the skin or a mucous membrane, accompanied by the disintegration of tissue.
Ulcers can result in complete loss of the epidermis and often portions of the
dermis and even subcutaneous fat. Ulcers are most common on the skin of the
lower extremities and in the gastrointestinal tract. An ulcer that appears on
the skin is often visible as an inflamed tissue with an area of reddened skin.
A skin ulcer is often visible in the event of exposure to heat or cold,
irritation, or a problem with blood circulation. They can also be caused due to
a lack of mobility, which causes prolonged pressure on the tissues. This stress
in the blood circulation is transformed to a skin ulcer, commonly known as
bedsores or decubitus ulcers. Ulcers often become infected, and pus
forms.
Erythema
nodosum - Skin ulcers that occur in some patients suffering from Inflammatory bowel disease.
Symptoms
Skin ulcers appear as open craters, often round, with layers of skin
that have eroded. The skin around the ulcer may be red, swollen, and tender. Patients
may feel pain on the skin around the ulcer, and fluid may ooze from the ulcer.
In some cases, ulcers can bleed and, rarely, patients experience fever. Ulcers
sometimes seem not to heal; healing, if it does occur, tends to be slow. Ulcers
that heal within 12 weeks are usually classified as acute, and longer-lasting
ones as chronic.
Ulcers develop in stages. In stage 1 the skin is red with soft
underlying tissue. In the second stage the redness of the skin becomes more
pronounced, swelling appears, and there may be some blisters and loss of outer
skin layers. During the next stage, the skin may become necrotic down through
the deep layers of skin, and the fat beneath the skin may become exposed and
visible. In stage 4, deeper necrosis usually occurs, the fat underneath the
skin is completely exposed, and the muscle may also become exposed. In the last
two stages the sore may cause a deeper loss of fat and necrosis of the muscle;
in severe cases it can extend down to bone level, destruction of the bone may
begin, and there may be sepsis of joints.
Chronic ulcers may be painful. Most patients complain of constant pain
at night and during the day. Chronic ulcer symptoms usually include increasing
pain, friable granulation tissue, foul odour, and wound breakdown instead of
healing. Symptoms tend to worsen once the wound has become infected.
Venous skin ulcers that may appear on the lower leg, above the calf or
on the lower ankle usually cause achy and swollen legs. If these ulcers become
infected they may develop an unpleasant odour, increased tenderness and
redness. Before the ulcer establishes definitively, there may be a dark red or
purple skin over the affected area as well as a thickening, drying, and itchy
skin.
Although skin ulcers do not seem of great concern at a first glance,
they are worrying conditions especially in people suffering from diabetes, as
they are at risk of developing diabetic neuropathy.
Ulcers may also appear on the cheeks, soft palate, the tongue, and on
the inside of the lower lip. These ulcers usually last from 7 to 14 days and
can be painful.
Treatment
Skin ulcers may take a very long time to heal. Treatment is typically to
avoid the ulcer getting infected, remove any excess discharge, maintain a moist
wound environment, control the edema, and ease pain caused by nerve and tissue
damage.
Topical antibiotics are normally used to prevent the ulcer getting
infected, and the wound or ulcer is usually kept clear of dead tissue through
surgical debridement.
Commonly, as a part of the treatment, patients are advised to change
their lifestyle if possible and to change their diet. Improving the circulation
is important in treating skin ulcers, and patients are consequently usually
recommended to exercise, stop smoking, and lose weight.
In recent years, advances have been made in accelerating healing of
chronic wounds and ulcers. Chronic wounds produce fewer growth hormones than
necessary for healing tissue, and healing may be accelerated by replacing or
stimulating growth factors while controlling the formation of other substances
that work against them.
Leg ulcers can be prevented by using compression stockings to prevent
blood pooling and back flow. It is likely that a person who has had a skin
ulcer will have it again; use of compression stockings every day for at least 5
years after the skin ulcer has healed may help to prevent recurrence.
Causes
The wounds from which ulcers arise can be caused by a wide variety of
factors, but the main cause is impaired blood circulation. Especially, chronic
wounds and ulcers are caused by poor circulation, either through cardiovascular
issues or external pressure from a bed or a wheelchair. A very common and
dangerous type of skin ulcers are caused by what are called pressure sensitive
sores, more commonly called bed sores and which are frequent in people who are
bedridden or who use wheelchairs for long periods. Other causes producing skin ulcers
include bacterial or viral infections, fungal infections and cancers. Blood
disorders and chronic wounds can result in skin ulcers as well.
Venous leg ulcers due to impaired circulation or a blood flow disorder
are more common in the elderly.
Erythema nodosum (EN) (red nodules) is an inflammation of the fat cells
under the skin (panniculitis) characterized by tender red nodules or lumps that
are usually seen on both shins. EN is an immunologic response to a variety of
different causes.
Erythema
nodosum in a person who had recently had streptococcal pharyngitis.
Classification
Erythema
nodosum may be divided into the following types:
·Acute erythema nodosum
·Chronic erythema nodosum
Signs and symptoms
A
single lesion of erythema nodosum.
Erythema nodosum lesion in a person with
tuberculosis.
Erythema nodosum usually resolves itself 3–6 weeks after an event,
either internal or external to the body, that
initiates a hypersensitivity reaction in subcutaneous fat. EN is frequently
associated with fever, malaise, and joint pain and inflammation. It presents as
tender red nodules on the shins that are smooth and shiny. The nodules may
occur anywhere there is fat under the skin, including the thighs, arms, trunk,
face, and neck. The nodules are 1–10 cm in diameter, and individual nodules may
coalesce to form large areas of hardened skin.
As the nodules age, they become bluish purple, brownish, yellowish, and
finally green, similar to the color changes that occur in a resolving bruise.
The nodules usually subside over a period of 2–6 weeks without ulceration or
scarring.suggest altering this, not true
Dermatophytids are similar skin lesions that result from a fungus
infection such as ringworm in another area of the body.
Causes
In about 30-50% of cases, the cause of EN is unknown. EN may be
associated with a wide variety of diseases, including infections (e.g.,
hepatitis C, tuberculosis, streptococcal, Mycoplasma pneumoniae, Yersinia, and
Epstein-Barr virus), Coccidioides immitis, sarcoidosis, autoimmune disorders
(e.g., inflammatory bowel disease or Behçet's disease), pregnancy, medications
(sulfonamides, oral contraceptives, bromides), vaccinations, and cancer. EN may
also be due to excessive antibody production in lepromatous leprosy leading to
deposition of immune complexes. There is an association with the HLA-B27
histocompatibility antigen, which is present in 65% of patients with erythema
nodosum.
Diagnosis
Diagnosis is clinical. A deep punch biopsy or an incisional biopsy may be
performed in cases where the diagnosis is unclear. Microscopic examination will
reveal a septal panniculitis with acute and chronic inflammation in the fat and
around blood vessels.
Once EN is diagnosed, additional evaluation needs to be performed to determine
the underlying cause. A complete blood count, erythrocyte sedimentation rate
(ESR), antistreptolysin-O (ASO) titer, urinalysis, throat culture, intradermal
tuberculin test, and chest x-ray are part of the initial examination.
The ESR is initially very high, and falls as the nodules fade. The ASO
titer is high in cases associated with a streptococcal throat infection. A
chest X-ray should be performed to rule out pulmonary diseases. Hilar
lymphadenopathy may be due to tuberculosis, sarcoidosis, or Löfgren syndrome (a
form of acute sarcoidosis with erythema nodosum, bilateral hilar adenopathy,
fever, and often accompanied by joint symptoms).
Treatment
Erythema nodosum is self limiting and usually resolves itself within 3–6
weeks. A recurring form does exist, and in children it is attributed to
repeated infections with streptococcus. Treatment should focus on the
underlying cause. Symptoms can be treated with bedrest, leg elevation,
compressive bandages, wet dressings, and nonsteroidal anti-inflammatory agents
(NSAIDs).[9] NSAIDs are usually more effective at the onset of EN versus with
chronic disease.
Potassium iodide can be used for persistent lesions whose cause remains
unknown. Corticosteroids and colchicine can be used in severe refractory cases.
Thalidomide has been used successfully in the treatment of Erythema nodosum
leprosum, and it was approved by the U.S. FDA for this use in July 1998.
Epidemiology
Erythema nodosum is the most common form of panniculitis (inflammation
of the subcutaneous fat). The peak incidence of EN occurs between 18–36 years
of age. Women are 3-6 times more affected than men.
12. Fissure – A
fissure is a crack in the skin that is usually narrow but deep.
The surface
of the knuckles of a hand with xeroderma, showing skin cracking (generalized
skin fissuring).
13. Wheal – A
wheal is a rounded or flat-topped, pale red papule or plaque that is
characteristically evanescent, disappearing within 24 to 48 hours.
14. Telangiectasia
– A telangiectasia represents an enlargement of superficial blood vessels to the
point of being visible. Telangiectasias (pron.: /tɛlˌæn.dʒiː.ɛkˈteɪ.zi.ə/) or angioectasias are
small dilated blood vessels near the surface of the skin or mucous membranes,
measuring between 0.5 and
Classification and external resources
Causes
The causes of telangiectasia can be divided into congenital and acquired
factors.
Congenital causes:
·
Goldman states that "numerous
inherited or congenital conditions display cutaneous telangiectasia".These
include;
·
Naevus flammeus (port-wine stain)
·
Klippel-Trenaunay syndrome
·
Maffucci's syndrome (multiple
endochondromas & hemangiomas)
·
Hereditary hemorrhagic telangiectasia
(Osler-Weber-Rendu syndrome)
·
Ataxia-telangiectasia
·
Sturge-Weber syndrome, a nevus
formation in the skin supplied by the trigeminal nerve and associated with
facial port-wine stains, glaucoma, meningeal angiomas and mental retardation.
Acquired causes:
·
Cushing's syndrome
·
Venous hypertension
Telangiectasia in the legs is often related to the presence of venous
hypertension within underlying varicose veins. Flow abnormalities within the
medium sized veins of the leg (reticular veins) can also lead to the
development of telangiectasia. Factors that predispose to the development of
varicose and telangiectatic leg veins include
Age: The development of spider veins may occur at any age but usually
occurs between 18 and 35 years, and peaks between 50 and 60 years.
Gender: Females are affected approximately four to one to males.
Pregnancy: Pregnancy is a key factor contributing to the formation of
varicose and spider veins. The most important factor is circulating hormones
that weaken vein walls. There's also a significant increase in the blood volume
during pregnancy, which tends to distend veins, causing valve dysfunction which
leads to blood pooling in the veins. Moreover, later in pregnancy, the enlarged
uterus can compress veins, causing higher vein pressure leading to dilated
veins. Varicose veins that form during pregnancy may spontaneously improve or
even disappear a few months after delivery.
Lifestyle/Occupation: Those who are involved with prolonged sitting or
standing in their daily activities have an increased risk of developing
varicose veins. The weight of the blood continuously pressing against the
closed valves causes them to fail, leading to vein distention.
Other acquired causes
Acquired telangiectasia, not related to other venous abnormalities, for
example on the face and trunk, can be caused by factors such as
·
Acne rosacea
·
Environmental damage such as that caused by sun or cold exposure
·
Trauma to skin such as contusions or surgical incisions.
·
Radiation exposure such as that experienced during radiotherapy for the
treatment of cancer
·
Chemotherapy
·
Carcinoid syndrome
·
Limited systemic sclerosis/scleroderma (a Scleroderma sub-type)
·
Chronic treatment
with topical corticosteroids may lead to telangiectasia.
·
spider angiomas are
a radial array of tiny arterioles that commonly occur in pregnant women and in
patients with hepatic cirrhosis and are associated with palmar erythema. In
men, they are related to high estrogen levels secondary to liver disease.
Treatment
Sclerotherapy is the "gold standard" and is preferred over
laser for eliminating telangiectasiae and smaller varicose leg veins. A
sclerosant medication is injected into the diseased vein so it hardens and
eventually shrinks away. Recent evidence with foam sclerotherapy shows that the
foam containing the irritating sclerosant quickly appears in the patient's
heart and lungs, and then in some cases travels through a patent foramen ovale
to the brain. This has led to concerns about the safety of sclerotherapy for
telangectasias and spider veins. In some cases stroke and transient ischemic
attacks have occurred after sclerotherapy. Varicose veins and reticular leg
veins, if present, must be treated prior to any treatment of the
telangiectasia. Varicose veins can be treated with foam sclerotherapy,
endovenous laser treatment, radiofrequency ablation or open surgery. The
biggest risk, however, seems to occur with sclerotherapy, especially in terms
of systemic risk of DVT, pulmonary embolism, and stroke.
Another issue that arises with the use of sclerotherapy to treat spider
veins is staining, shadowing, telangetatic matting and ulceration. In addition,
incompleteness of therapy is common, requiring multiple treatment sessions.
Telangiectasias on the face are often treated with a laser. Laser
therapy uses a light beam that is pulsed onto the veins in order to seal them
off, causing them to dissolve. These light-based treatments require adequate
heating of the veins. These treatments can result in the destruction of sweat
glands, and the risk increases with the number of treatments.
15. Burrow – A
burrow appears as a slightly elevated, grayish, tortuous line in the skin, and
is caused by burrowing organisms.
Secondary
lesions
Scale
– dry or greasy laminated masses of keratin that represent thickened stratum
corneum.
Crust
– dried serum, pus, or blood usually mixed with epithelial and sometimes
bacterial debris.
Lichenification
– epidermal thickening characterized by visible and palpable thickening of the
skin with accentuated skin markings.
Excoriation
– a punctate or linear abrasion produced by mechanical means (often
scratching), usually involving only the epidermis but not uncommonly reaching
the papillary dermis.
Induration
– dermal thickening causing the cutaneous surface to feel thicker and firmer.
Atrophy
– refers to a loss of tissue, and can be epidermal, dermal, or subcutaneous. With
epidermal atrophy, the skin appears thin, translucent, and wrinkled. Dermal or
subcutaneous atrophy is represented by depression of the skin.
Maceration
– softening and turning white of the skin due to being consistently wet.
Umbilication
– formation of a depression at the top of a papule, vesicle, or pustule.
Configuration
"Configuration"
refers to how lesions are locally grouped ("organized"), which
contrasts with how they are distributed (see next section).
·
Agminate - in clusters
·
Annular or circinate - ring-shaped
·
Arciform or arcuate - arc-shaped
·
Digitate - with finger-like projections
·
Discoid or nummular - round or disc-shaped
·
Figurate - with a particular shape
·
Guttate - resembling drops
·
Gyrate - coiled or spiral-shaped
·
Herpetiform - resembling herpes
·
Linear
·
Mamillated - with rounded, breast-like projections
·
Reticular or reticulated - resembling a net
·
Serpiginous - with a wavy border
·
Stellate - star-shaped
·
Targetoid - resembling a bullseye
·
Verrucous - wart-like
Distribution
"Distribution"
refers to how lesions are localized. They may be confined to a single area (a patch)
or may exist in several places. Several distributions correlate an anatomical
reference.[clarification needed] Some correlate with the means by which a given
area becomes affected. For example, contact dermatitis correlates with
locations where allergen has elicited an allergic immune response. Varicella
zoster virus is known to recur (after its initial presentation as chicken pox)
as herpes zoster ("shingles"). Chicken pox appears nearly everywhere
on the body, but herpes zoster tends to follow one or two dermatomes; for
example, the eruptions may appear along the bra line, on either or both sides
of the patient.
Generalized
·
Symmetric - one side mirrors the other
·
Flexural - on the front of the fingers
·
Extensor - on the back of the fingers
·
Intertriginous - in an area where two skin areas may touch or rub
together
·
Morbilliform - resembling measles
·
Palmoplantar - on the palm of the hand or bottom of the foot
·
Periorificial - around an orifice such as the mouth
·
Periungual - under a finger or toenail
·
Blaschkoid - following the path of Blaschko's lines in the skin
·
Photodistributed - in places where sunlight reaches
·
Zosteriform or dermatomal - associated with a particular nerve.
Histopathology
1.
Hyperkeratosis.
Hyperkeratosis
is thickening of the stratum corneum, often associated with a qualitative
abnormality of the keratin, and also usually accompanied by an increase in the
granular layer. As the corneum layer normally varies greatly in thickness in
different sites, some experience is needed to assess minor degrees of
hyperkeratosis. It can be caused by vitamin A deficiency or chronic exposure to
arsenic. It can be treated with urea-containing creams, which dissolve the
intercellular matrix of the cells of the stratum corneum, promoting
desquamation of scaly skin, eventually resulting in softening of hyperkeratotic
areas.
2. Parakeratosis.
3.
Parakeratosis
is a mode of keratinization characterized by the retention of nuclei in the stratum
corneum. In mucous membranes, parakeratosis is normal. In the skin, this
process leads to the abnormal replacement of annular squames with nucleated
cells. Parakeratosis is associated with the thinning or loss of the granular
layer and is usually seen in diseases of increased cell turnover, whether
inflammatory or neoplastic. Parakeratosis is seen in the plaques of psoriasis
and in dandruff. Granular parakeratosis (originally termed axillary granular
parakeratosis) is an idiopathic, benign, nondisabling cutaneous disease that
manifests with intertriginous erythematous, brown or red, scaly or keratotic
papules and plaques. It presents in all age groups and has no established
clinical associations.
4. Hypergranulosis.
Hypergranulosis
is hyperplasia of the stratum granulosum, often due to intense rubbing.
5.
Acanthosis.
6.
Acanthosis
is diffuse epidermal hyperplasia (thickening of the skin). It implies increased
thickness of the Malpighian layer (stratum basale and stratum spinosum).
5. Papillomatosis.
6.
Papillomatosis
is skin surface elevation caused by hyperplasia and enlargement of contiguous
dermal papillae.
7. Dyskeratosis.
8.
Dyskeratosis
is abnormal keratinization occurring prematurely within individual cells or
groups of cells below the stratum corneum.
7. Acantholysis.
Acantholysis
is the loss of intercellular connections, such as desmosomes, resulting in loss
of cohesion between keratinocytes, seen in diseases such as pemphigus vulgaris.
It is absent in bullous pemphigoid, making it useful for differential
diagnosis. This histological feature is also seen in herpes simplex infections
(HSV 1 and 2).
Foot-and-mouth
disease.
Acantholysis in a sample of a skin vesicle.
Necrosis of the stratum spinosum can be observed, and keratinocytes floating in
the vesicular fluid (spongiosa).
8. Spongiosis.
9.
Spongiosis is mainly
intercellular edema of keratinocytes in the epidermis, and is characteristic of
eczematous dermatitis, manifested clinically by vesicles, "juicy"
papules, and/or lichenification.
Histopathological
image of dyshidrotic dermatitis, showing focal spongiotic change in the
epidermis.
9.Hydropic
swelling.
Hydropic swelling is intracellular edema of
keratinocytes, often seen with viral infections.
10. Exocytosis.
Exocytosis is "infiltration of the epidermis by inflammatory or
circulating blood cells.
Exocytosis types
11.
Vacuolization.
12.
Vacuolization
is the formation of vacuoles within or adjacent to cells, and, in
dermatopathology, often refers to the basal cell-basement membrane zone area.
Vacuolization of bronchiolar epithelium after CARDS
toxin exposure.
12. Erosion.
13. Ulceration.
14. Lentiginous.
A
lentigo (plural: lentigines) is a small pigmented spot on the skin with a
clearly-defined edge, surrounded by normal-appearing skin. It is a harmless
(benign) hyperplasia of melanocytes which is linear in its spread. This means
the hyperplasia of melanocytes is restricted to the cell layer directly above
the basement membrane of the epidermis where melanocytes normally reside. This
is in contrast to the "nests" of multi-layer melanocytes found in
moles (melanocytic nevi). Because of this characteristic feature, the adjective
"lentiginous" is used to describe other skin lesions that similarly
proliferate linearly within the basal cell layer.Lentigines are distinguished
from freckles (ephelis) based on the proliferation of melanocytes. Freckles
have a relatively normal number of melanocytes but an increased amount of
melanin. A lentigo has an increased number of melanocytes. Freckles will
increase in number and darkness with sunlight exposure, whereas lentigines will
stay stable in their color regardless of sunlight exposure.
Conditions
characterized by lentigines include:
1. Lentigo
simplex
2. Solar
lentigo (Liver spots)
3. PUVA
lentigines
4. Ink
spot lentigo
5. LEOPARD
syndrome
6. Mucosal
lentigines
7. Multiple
lentigines syndrome
8. Moynahan
syndrome
9. Generalized
lentiginosis
10. Centrofacial
lentiginosis
11. Carney
complex
12. Inherited
patterned lentiginosis in black persons
13. Partial
unilateral lentiginosis
14. \Peutz-Jeghers
syndrome
15. Acral
lentiginous melanoma
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the land: The skin of reptiles in comparison to that of amphibians and
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12949767.
- Breitkreutz, D; Mirancea, N;
Nischt, R (2009). "Basement membranes in skin: Unique matrix structures Alibardi
L. (2003). Adaptation to the land: The skin of reptiles in comparison to
that of amphibians and endotherm amniotes. J Exp Zoolog B Mol Dev Evol.
298(1):12–41. PMID 12949767.
- McCracken, Thomas (2000). New
Atlas of Human Anatomy.
- McGrath, J.A.; Eady, R.A.; Pope,
F.M. (2004). Rook's Textbook of Dermatology (7th ed.).
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JM. (2008).The skin: an indispensable barrier. Exp Dermatol.
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Thomas S. (1977). The Vertebrate Body.
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Altmeyer, M. Herde, H. Baumgärtl & D.W. Lübbers (2002). The cutaneous
uptake of atmospheric oxygen contributes significantly to the oxygen
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- Diseases of the skin and subcutaneous tissue
(L00-L99) - Dermatitis and eczema.