skin pigmentation + hari disorder

7/27/2019 skin pigmentation + hari disorder

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Dr. H.W. WONG

DermatoVenereology dept.

Medical Faculty, UKRIDA

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Human skin color is mainly determined bymelanin pigments (contribute the most),carotene and hemoglobin.

Racial differences in skin color result fromdifferences in the kinds and amounts ofmelanin.

There are 6 Skin types in the human skin

according Fitzpatrick, Type 1( white, Walespeople), up to Type 6 ( Black, Negro)

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When carotene, a precursor of vitamin A, istaken into the body, it accumulates in thehorny cell layer and subcutaneous fat layer,resulting in yellowish skin color (carotinoid

pigmentation).

Dermal deposition of extrinsic substancescan caused also by tattooing or injury.

Abnormalities of the blood vessels andhemoglobin may also cause changes in skincolor.

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Most diseases of abnormal pigmentation arecaused by elevated or reduced melanincontent; the disorders involving skin colortend to be congenital or to be caused by

autoimmune reaction or sun exposure.

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1. Oculocutaneous albinism (OCA)1) OCA1

2) OCA23) OCA34) OCA4

5) Hermansky-Pudlak syndrome (HPS)6) Chdiak-Higashi syndrome (CHS)

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2. Vitiligo vulgaris3. Piebaldism4. Sutton nevus5. Vogt-Koyanagi-Harada disease6. Senile leukoderma

7. Nevus depigmentosus8. Leukoderma pseudosyphiliticum

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1. Ephelides2. Melasma3. Riehls melanosis4. Friction melanosis5. Dyschromatosis symmetrica

hereditaria6. Senile lentigo

7. Addisons disease8. Pigmentatio petaloides actinica9. Erythema dyschromicum perstans

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1. Carotenemia

2. Argyria3. Tattoos

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1. Oculocutaneous albinism (OCA) Synonym: Congenital albinism There is congenital abnormality in

melanin synthesis absent from birth. All types are autosomal recessive. Patients tend to be prone to skincancer, from high photosensitivity tosunlight.

Sunscreen is essential

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Oculocutaneous albinism (OCA) isclassified by the causative genes intoOCA1, OCA2, OCA3 and OCA4

It is also seen as a symptom ofhereditary diseases includingHermansky-Pudlak syndrome and

Chdiak-Higashi syndrome

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Melanocytes are normal in numberand size; however, immaturemelanosomes (stage I, II and III) are

observed by electron microscopy In Chdiak-Higashi syndrome, giantlysosomes are detected in the skin,

leukocytes and other organs

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Use of sunscreen is essential frombirth, in order to protect the skin fromUV-related cancer and skin aging.

The eyes are protected by tintedcontact lenses or sunglasses.

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Melanocytes are reduced or lost,hypopigmented patches (leukoderma)

Autoimmunity against melanocytes or

melanin is thought to cause vitiligovulgaris; however, the pathogenesis isunknown.

Topical steroids and PUVA are usefultreatments.

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Vitiligo vulgaris is classified into focal,segmental, generalized and universaltypes

Vitiligo vulgaris in which leukodermadistribution is not associated withcutaneous innervation is calledgeneralized vitiligo vulgaris.

When unilateral leukoderma runs parallelto cutaneous nerves, it is calledsegmental vitiligo vulgaris.

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Vitiligo vulgaris often occurs in men andwomen about age 20.

The incidence has been calculated as between1% and 2% of the population.

Familial cases account for 1% to 2% of allcases.

Sharply circumscribed complete leukoderma

occurs. There is a slight increase in pigmentation at

the periphery of the eruptions

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The lesions are irregular in shape and size,and they often coalesce

Gray hair is seen around the leukoderma.

It is asymptomatic

Generalized vitiligo vulgaris occurs mostfrequently on areas prone to mechanicalstimulation, such as the seborrheic areas and

the extremities, lumbar region, abdomen,intertriginous areas,face and neck

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Segmental vitiligo vulgaris occursunilaterally on certain innervatedareas.

Young people are most commonlyaffected.

Pernicious anemia, hyperthyroidism,

and autoimmune diseases such asAddisons disease may develop ascomplications

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The cause has not been identified. \ Autoimmunity against melanocytesand melanins and abnormal peripheral

nerve function are thought to beinvolved

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In the early stages, there ismelanocyte degeneration with reducedor lost dopa response and lymphocytic

and histiocytic infiltration into in thedermal upper layer.

In the final stages, melanocytes are

lost and melanin granules are absentin the basal layer.

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The disease should be differentiatedfrom piebaldism, nevusdepigmentosus, senile leukoderma,

Vogt-Koyanagi-Harada disease,melanoleukoderma, pityriasisversicolor and Hansens disease.

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Topical and oral PUVA therapies and topicalsteroids are the first-line treatments.

Leukoderma on the face and fingers can beconcealed by special cosmetics to alleviatepsychological distress.

Steroids and sedatives are given in smalldoses, and surgical intervention and

narrowband UVB exposure are also conducted

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Synonym: Partial albinism

DEFINITION : Piebaldism is characterized by localized

leukoderma with leukotrichia on the foreheadand frontal region of the head.

Few melanocytes are found around the areasof leukoderma and white hair; albinism

develops locally. A congenital, autosomal dominant disease, it

occurs with a frequency of 1 in 200,000

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Triangular or diamond-shaped leukotrichiaand leukoderma are seen on the forehead andfrontal region of the head (white forelock) atthe time of birth.

These do not enlarge or shrink with age

Contralateral geographic vitiligo occurs onthe extremities and trunk.

Small pigmented patches often occur withinthe leukoderma.

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Piebaldism is caused by abnormality in the c-kit gene.

In fetal development, melanoblasts migratefrom the neural crest to the epidermis toanchor and differentiate into melanocytes.

The c-kit gene on chromosome 4 encodes areceptor that is associated with the migration

and anchoring of melanoblasts

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Because piebaldism is autosomaldominant, abnormality occurs in halfof each receptor, leaving an area on

which melanoblasts do not anchor,and resulting in leukoderma.

Histopathologically, melanocytes are

lacking at the sites with leukotrichiaand leukoderma.

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Diagnosis is made by history-taking ofautosomal dominant expression, and whiteforelock and small pigmented patches onleukoderma.

Skin graft and cultured pigmented celltransplantation have been reported to beeffective

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Synonym: Halo nevus Definition, Pathogenesis, Clinical

features

Sutton nevus has nevocellular nevus(lentigo) in the center, surrounded byoval leukoderma

It tends to occur in children and youngmen and women, on the trunk, faceand neck

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Autoimmunization occurs against melanin atthe center of the lentigo, and immunoreaction occurs against melanin at theperiphery of the lentigo; this is thought to be

the mechanism of Sutton nevus. Leukoderma may also be produced at the

periphery of a malignant melanoma,angioma, blue nevus, soft fibroma, andseborrheic keratosis; it is called Suttonsphenomenon

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Degenerated or destroyed nevus cellsand melanocytes, with denselymphocytic and macrophagicinfiltration, are found at the periphery.Treatment:

The treatments for vitiligo vulgaris areapplied.

The central nevus may be removed.

It may heal spontaneously

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Leukoderma enlarges centrifugally. Atthe same time, the central nevusdiscolors, flattens and eventuallydisappears.

As the nevus disappears, theleukoderma heals spontaneously.

Excision of the central nevus induces

spontaneous healing and preventsvitiligo vulgaris, a complication.

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Sharply circumscribed, round or irregular-shapedleukoderma of 4 mm to 10 mm in diameterappear diffusely on the trunk and extremities ofmen and women in their 30s, increasing in

number with age. Senile leukoderma is essentially identified with

idiopathic guttate hypomelanosis.

Pathological findings show a reduction in the

number of activated melanocytes andmelanosomes and dysfunction in melanocytesand melanosomes from melanocytic senescence.

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Nevus depigmentosus is a common nevoidabnormality present in about 1 in 125 neonates.

Because of the congenital melanocyticdysfunction in skin, incomplete hypopigmented

patches are seen at birth or shortly thereafter The patches vary in shape and distribution from

solitary and irregular to multiple and band-like.

Size, distribution and number of nevus

depigmentosus patches remain the same overthe course of a lifetime.

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Clinical Feature : Multiple round smooth-surfaced brown

patches about 3 mm in diameter occur on

the sun-exposed areas of the face, neck andforearms

Ephelides darkens with sun exposure(especially exposure to UVR) in summer and

tends to fade in winter. It worsens with age and is most remarkable at

puberty; it lightens thereafter.

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Ephelides tends to run in families; it isthought to be autosomal dominant.

However, it can be autosomal recessive insevere cases.

Melanocytes are activated by hereditaryfactors, and melanosomes markedly increasein the basal keratinocytes.

Melanocytes in patients with ephelides have

well-developed dendritic spines andenhanced functions; however, the number ofmelanocytes does not change.

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Differentiation from lentigo, Peutz-Jeghers syndrome, xerodermapigmentosum, and progeria is

necessary. Sunscreen is useful for blocking UVR

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Synonym: ChloasmaClinical Feature : Melasma tends to occur in women in

their 30s or older. It is rare in men. Sharply demarcated light brownpatches occur on the face (forehead,cheeks, and around the mouth, inparticular), usually symmetrically.

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Melasma patches are irregular in size andshape.

The disorder is aggravated by UVR insummer, and it subsides in winter

Pregnancy may trigger the onset (chloasmagravidarum)

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Abnormalities in sex hormones andadrenocortical hormones that activatemelanocytes are known to cause

melasma

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Riehls melanosis should be distinguished frommelasma.

Unlike Riehls melanosis, melasma isasymptomatic and is not preceded by dermatitis-like symptoms.

Histologically, there is an increase in the contentof melanin throughout the epidermis and anincrease in the number of epidermalmelanocytes.

Differentiation from nevus of Ota is alsoimportant; the periphery of the eyes is affectedby nevus of Ota but not by melasma.

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The causal factors, such as artificial sexhormones, are discontinued.

Chloasma gravidarum occurs duringpregnancy and subsides several months after

delivery. Protection from UVR is useful.

Today topical hydroquinone and tretinoin are

used for bleaching treatment.

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A diffuse, vaguely circumscribed grayish-purplish-brown network of pigmentdeposition appears, most commonly on theface of middle-aged women.

Riehls melanosis may be accompanied byfollicular keratotic papules.

In most cases, inflammatory symptoms suchas flush and itching precede pigmentation

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The cause is recurrent contact dermatitis onthe face.

The antigens in most cases are cosmeticproducts containing tar pigment.

Most of such products are no longerproduced, because of restrictions oncomponents used in cosmetics.

Histopathologically, macrophages that havephagocytosed melanosomes are observed inthe dermal upper layer.

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Synonym: Towel melanosisDefinition , Clinical Feature : Prolonged and vigorous use of nylon

towels or brushes may stimulate theskin mechanically, resulting inpigmentation.

Friction melanosis occurs frequentlyin persons in their 20s and 30s.

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A network pattern or diffuse brownpigmentation is seen in thenskinabove the clavicular region, neck, ribs

and vertebral region Subjective symptoms such as itchingare not present.

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Melanosomes sink into the dermisfrom mechanical stimulation andinflammation.

As a result of histological pigmentaincontinence, increase ofmelanophages in the upper dermis

leads to friction melanosis.

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Histopathologically, multiple migrantmelanosomes and melanophages areseen.

Amyloid deposition is found in somecases

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The skin color gradually returns tonormal by discontinuation of themechanical irritation, such as

discontinuation of vigorous rubbingwith nylon towels.

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Definition, Pathogenesis, Clinicalfeatures Multiple brown patches and

hypopigmented patches of 3 mm to8 mm in diameter occur on theextremities, including the dorsa of

hands and feet, coalescing intoreticular forms

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The patches are flat and smooth. The onset is age 6 or younger in mostcases.

It is autosomal dominant, which runs infamilies, and is caused by mutation inthe RNA-specific adenosine deaminase

gene (DSRAD). It progresses with age, until adulthood.It most commonly occurs in Asians

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Can be diagnosed by the characteristiccutaneous features and familial incidence.

It should be differentiated from acropigmentatioreticularis (Kitamura), a similar autosomal

dominant disease with reticular pigmentation inthe distal extremities.

Acropigmentatio reticularis is distinguished bythe fact that the pigmented patches are concave

and there are no hypopigmented patches

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Special concealing cosmetics areuseful.

Dermabrasion may be conducted for

pigmented patches.

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Synonym: Solar lentigoDEFINITION, CLINICAL FEATURE Senile lentigo appears in almost all men and

women middleaged and older. Round brown patches of various sizes occur on

sun-exposed areas of the face, dorsa of hands,and extensor surfaces of the arms.

The patches are relatively clearly circumscribed. Mild scaling may be present

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Alexandrite lasers andcryotherapies are conducted.

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Secretion of ACTH and MSH from theanterior lobe of the hypophysis isenhanced by reduced secretion of

adrenocortical hormones, and thiscauses pigmentation by stimulatingmelanocytes.

Pigmentation is seen on the entirebody.

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The face, genitalia, axillary fossae andumbilical region are most severelyaffected.

The pigmentation is also found onareas that normally contain lesspigmentation than skin, such as the

tongue, gingiva and oral mucosa; thisis helpful for diagnosis.

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Multiple, sharply circumscribed,brown, petal-shaped or spiny patchesof several millimeters to 1 cm in

diameter occur on the shoulders andupper back

Multiple patches often occur in

persons with light complexion, 1 to 3months after intense sunburn such asfrom a beach outing.

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Synonym: Ashy dermatosis Multiple, small erythematous lesionsoccur on the trunk and extremities of

non-Caucasians, and these soon turninto grayishwhite to grayish-bluepatches of 1 cm to 3 cm in diameter.

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Erythematous elevation is seen at theperiphery in many cases

Itching may be present; however, it is

asymptomatic in most cases anddevelops slowly.

Drug eruption or lichen planus

resembling erythema dyschromicumperstans may appear.

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Synonym: Aurantiasis cutisDefinition, Pathogenesis, Clinical features

Carotene concentration increases inthe blood, resulting in carotenedeposition in the epidermal horny celllayer and subcutaneous fat tissues.

This yellows the skin

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The coloration is marked in the palmsand soles, whose horny cell layer isthick.

The color may appear in the face (e.g.,forehead, ala nasi, nasolabial groove);however, it does not occur in thesclera or other mucous membranes,

and it rarely becomes generalized. It is asymptomatic.

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Coloration tends to appear when the caroteneconcentration in the blood reaches 0.5 mg/dl. Caused by high intake of carotene-containing

foods (citrus fruits, pumpkins, carrots, spinach,

seaweeds, corn, egg yolks, butter), by liverdysfunction (carotene concentration in theblood increases when carotene fails to bemetabolized into vitamin A), or byhyperlipidemia (carotene concentration tendsto increase by hyperlipidemia because of itsliposolublility).

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Jaundice is differentiated fromaurantiasis cutis by yellowed sclera,itching and bilirubin level.

Aurantiasis cutis heals spontaneouslywhen intake of the causative food isrestricted.

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Definition, Pathogenesis, ClinicalFeatures Argyria results from deposition of

silver in the skin. This occurs from the use of silvermedical supplies (silver needles,

sutures, dental fillings) or prolongedintake of silver-containing foods.

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Cases caused by silver-containing healthfood products in Europe and the UnitedStates have been reported.

Silver compounds deposit in collagen in

the sweat glands, seborrheic glands,connective tissues and basalkeratinocytes, giving the skin a bluish-gray hue.

The condition tends to occur in exposedareas such as the face, neck andforearms.

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Fine brown granular masses are foundhistopathologically.

Silver can be observed by X-ray microprobeanalysis.

There is no effective treatment for argyria,except to refrain from intake of silver.

Systemic complications of argyria include

pulmonary fibrosis, pneumonitishepatotoxicity and myopathy.

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Tattoos are images or text artificiallycreated in the skin by injection ofpigment or ink

Pigmented granules tend to remain inthe dermal upper layer; however,some are phagocytosed bymacrophages and carried in the lymphflow to deposit in the lymph nodes.

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Allergic reaction against the injectedpigment or photosensitivity may occuras complications.

Laser therapies are useful in removingtattoos of certain colors

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Dr. H.W Wong Dip.Derm.DermatoVenereology Dept.Medical Faculty of UKRIDA

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The hair apparatus plays a role subsidiary tothat of the sensory nerves in protecting the

scalp from external forces and light, and inmoderating heat in the head.

Eyelids protect the eyes from dirt, and armpithair and pubic hair absorb mechanical

friction.

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The number of hairs on a persons headaverages 100,000.

The hair apparatus is found throughout theskin except on the lips of the mouth.

It consists of hair and hair follicles thatenclose the hair.

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The layer of tissue that encloses a hair iscalled a hair follicle.

It is aligned obliquely to the skin surface. Partof the hair follicle is slightly enlarged to form

a hair bulge to which the base of the arrectorpili muscle is connected

Dermal stem cells reside in the hair bulge.

Sebaceous glands are seen above the bulgestem cells, and apocrine glands open furtherabove.

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The bottom of the hair root during thegrowth stage bulges out spherically; it iscalled a hair bulb and contains a hair groupof cells known as the hair papilla.

The hair follicle opens in a funnel shape (hairinfundibulum).

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The hair follicle is double-bounded with twolayers, with an epithelial interior andconnective tissue component on the exterior

The epithelial components are the inner and

outer root sheaths. The connective tissue component is called the

connective tissue sheath.

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The connective tissue sheath (CTS) covers theoutside of the hair follicle and is a layerconnected with the dermis.

Collagen fibers run circularly inside the

connective tissue sheath and longitudinallyoutside of it.

Several elastic fibers can be found amongthese collagen fibers.

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The outer root sheath (ORS) is the outermost partof the hair infundibulum (inner two layers).

It is keratinized and comprises keratinocytes thatcontrain a light cytoplasm without keratohyaline

granules. The outside of the outer root sheath meets the

connective tissue sheath at the basal membrane.

The inside of the outer root sheath is connected

by desmosomes with the Henles layer, theoutermost layer of the inner root sheath.

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The inner root sheath (IRS), found inside theouter root sheath, consists of capsular layers,Huxleys layer (a double layer ofcells), andHenles layer (a single layer of cells).

The capsular cuticles anchor and entangleeach other, with the differently directed apicaltips functioning as hooks to stabilize the hair.

The Henles layer is connected with the outer

root sheath by desmosomes.

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Keratinization occurs in the inner root sheathclose to the interfollicular epidermis.

IRS has the appearance of trichohyalingranules.

These granules, often found in Henles layerand Huxleys layer, stain eosinophilically.

Keratinization finishes at the height of thesebaceous gland opening, and it is followedby exfoliation.

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The hair bulb is the bulge of the hair follicle,with a dermal hair papilla at its center. The keratinocyte follicle enclosing and

covering the dermal hair papilla semi-

spherically is the hair matrix layer, where hairand inner root sheath cells grow and extendupward.

The outer root sheath forms the outermostlayer of the hair bulb.

Melanocytes that provide hairs with melaninsare also found in the hair matrix.

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The hair shaft is composed of a three-layeredstructure.

From innermost to outermost, the layers are themedulla, cortex and cuticula.

Tonofilaments align in the direction of the axis inthe cortex, and a pattern similar to that observedfor keratin by electron microscopy is observed atthe tips of the tonofilaments.

That is, keratinization is seen in the cortex;

however, unlike in the epidermis and inner rootsheath, no formation of keratohyaline granules ortrichohyaline granules is seen

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Unlike the keratins found in other epithelialcells, the keratins that are produced in haircortex are rich in cystines, glycines andtyrosines.

Such specific keratins are called hardkeratins, a general term, and they are alsofound at other sites, including the nails.

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In the hair cuticle, the cortex is covered byflat cells in a scalelike pattern, and they areattached to the capsular cuticles of the innerroot sheath.

This connection becomes the outermost layerof the hair shaft, protecting the shaft. The cuticles may be injured and the natural

glow of hair lost if there is excessive physicaldamage to hair, such as over-brushing, orexcessive use of chemicals such as hair dyesor permanent solutions.

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Hair color differs according to the size andnumber of melanosomes: Large and/ormultiple melanosomes are seen in dark hair,and red hair contains large amount of

pheomelanins.

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The hair has a regular period of growth(anagen), transition (catagen), and rest phase(telogen)

Head hair grows for several years after it

sprouts (anagen: about 80% of all head hair),after which its growth rate slows for 2 to 3weeks (catagen: about 1% to 2%) and thenstops.

The hair remains for several months after itstops growing (telogen: about 15%).

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As a new hair is produced, hair within thesame follicle in the telogen phase falls out.Hair in the catagen period grows 0.3 mm to0.5 mm per day.

When hair follicles in the anagen phase repeatcell division and transition to the catagenphase, they begin to contract and cell divisionstops.

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The hair follicle cells lose their ability todivide in the telogen phase and ascend to theelevated part of the hair.

The hair root presents a stick-like shape

called club hair. In the telogen phase, macrophages

phagocytose melanin pigments and cellfragments in the hair papilla.

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As the anagen phase comes around again,cell division begins at the surface of the hairfollicle.

A hair papilla forms and a new hair grows in

the hair matrix. It pushes out the club hair, which exfoliates.

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Only the part of the hair with stem cells belowthe hair bulge expands and contracts in thehair cycle.

That area is called the fluctuation area, and

the upper area is called the fixation area. The human hair cycle differs for each hair;

however, the overall quantity of hair remainsroughly constant.

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1. Alopecia areata Round, sharply margined hair loss suddenly

occurs.

Hair regrows spontaneously in severalmonths in most cases.

Cases with multiple alopecia areata mayprogress to alopecia totalis or alopecia

universalis. Topical steroids and PUVA are applied

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Alopecia areata is quite common, affecting upto 1% of the population.

Sharply margined hair loss occurs suddenlywithout prodromes or subjective symptoms

Alopecia areata is usually a round or oval,single but sometimes multiple, alopecia of 2cm to 3 cm in diameter.

The alopecia patches may coalesce,progressing to complete scalp hair loss(alopecia totalis) in some cases

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Besides occurring in the scalp, alopecia areatamay occur in the eyebrows, beard areas andthe extremities; cases in which hair on thewhole body is affected are called alopecia

universalis, which is intractable. In nails,desquamation, coarseness, cloudiness andslight depression occur.

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Hair matrix cells are impaired temporarily forunknown reason.

Theories include nutritional failure, heredityand mental stress; however, the pathogenesis

is unknown. Some cases are accompanied by autoimmune

thyroid deficiency and atopic dermatitis.

Autoimmune involvement is suspected

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In the lesion, there is infiltration of CD4+Tcells and the appearance of Langerhans cellsin the hair follicles at the anagen stage.

Expression of MHC class II in hair bulbepitheliocytes, and deposition of C3, IgG andIgM in the hair follicular basementmembrane are observed.

There is possible involvement ofautoimmunity.

The affected hair follicles form abnormalatrophic hair that falls out.

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Alopecia areata is easily diagnosed by theclinical features.

The hairs around the lesion easily fall out atthe early stages of the lesion.

The hairs are characteristically thin andatrophic at the end of the hair root, givingthem the appearance of exclamation marks(exclamation-point hair).

The hairs stop falling out and newly grownhairs are seen during the healing period.

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Trichotillomania and traumatic alopecia aredistinguished from alopecia areata.

Trichotillomania, which produces short,breakable, hard hair in the lesion, occurs

most commonly in children; however, there isno diseased hair in trichotillomania, and thehair around the lesion does not come outeasily.

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In traumatic alopecia, the lesion is not round,and it is caused by extrinsic factors such asscarring.

Fibrosis and pigmentation are also found.

Alopecia areata also should be distinguishedfrom systemic lupus erythematosus (SLE) andalopecia caused by syphilis.

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Alopecia areata resolves spontaneously inseveral months, although in some cases itmay be intractable or recurrent.

It is important to address the patients

distress about hair loss. Sedatives may be used if necessary.

Steroids, immunosuppressants and hair-growth lotions are topically applied.

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In severe cases, PUVA therapy, steroidinjection, cryotherapy, and application ofsquaric acid dibutylester (SADBE) areperformed.

Steroids and immunosuppressants areadministered orally in alopecia totalis oruniversalis.

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Synonim : Male-pattern baldness, Alopeciaprematura

Clinical features Androgenetic alopecia also called male

pattern baldness, is hair loss in adolescentand adult men.

Androgenetic alopecia is a very commondisorder, affecting at least 50% of men by theage of 50.

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The hairline recedes to form an M shape (withvellus hair at the frontal region of the head)or an O shape (with vellus hair on the top ofthe head).

These patterns may appear separately orsimultaneously.

The diameter of the vellus hair is smaller thanthat of normal hair.

The density (hairs per unit area), alsodecreases.

It progresses to complete hair loss.

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Familial history of baldness. Elevated sensitivity of hair follicles to

androgen (dihydrotestosterone, in particular)begins at some point.

The anagen period is shortened, hairs at

telogen decrease in number, hair folliclescontract, and vellus transformation occurs

The thin, sparse vellus hair produced inandrogenetic alopecia becomes less densely

distributed, eventually progressing toalopecia.

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Topical minoxidil and anti-androgeneticdrugs such as 5areductaseinhibitorfenasteride are effective in some cases.

Stimulating the affected site, stimulating the

local circulation of the scalp by massaging,and using hair growth lotions containingfemale hormones are helpful

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Atrichia congenita It is autosomal recessive. Hair may be present

at birth; however, it falls out between severalmonths after birth and puberty, until no hair

remains on the body. Involvement of the hairless (hr) gene has

been identified as a cause in some cases ofcertain subtypes.

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Hypotrichosis congenitaNormal hair is present at birth; however, alopecia

gradually leads to thin, sparse hair

Arrichia and alopecia associated withhereditary syndrome Arrichia and congenital alopecia are associated

with congenital ectodermal defect (aplasia cutiscongenita ,Werners syndrome, poikiloderma

congenital and Netherton syndrome.

Odontogenesis imperfecta, abnormal nail plates,palmoplantar keratosis and anhidrosis oftenoccur as complications.

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Pityriasis capitis (dandruff) occurs incombination with alopecia most frequently inmen after puberty.

Fine, dispersed, grayish-white scaling occurs

constantly on the scalp. The hair is thin and the natural gloss is not

present.

Itching and reddening of the scalp often occur

The treatments are the same as for seborrheicdermatitis.

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Both short and broken remaining hairs andnewly produced hairs are observed in thesame alopecia, which is within reach of thehand, often on the frontal and temporal

region of the head on the right side. The patients psychological background,

personality and domestic environment maytrigger trichotillomania; cooperation with a

psychiatrist is necessary for treatment.

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Patients with trichotillomania, who tend to bein their late childhood, have an uncontrollablecompulsion to pull out their own hair.

The patients may deny this hair-pulling

behavior. Vaguely circumscribed, irregular-shaped,

incomplete alopecia is present.

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As a result of scarring caused by injury, burn,or discoid lupus erythematosus.

The hair follicles are irreversibly destroyed,leading to alopecia.

Surgical treatment is necessary.

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skin pigmentation + hari disorder

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