Exogenous Pigmentation

7/30/2019 Exogenous Pigmentation

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ENDOGENOUS

PIGMENTATION


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MELANIN

Pigment derivative of tyrosine

Synthesised by melanocytes-which typically reside inbasal cell layer of epithelium

Presence of melanocytes in skin-protects against the

damaging effects of actinic irradiations as well as act asscanegers in protecting against various cytotoxicintermediates

It is synthesised within specialized structures called

melanosomes Melanin is composed of eumelanin-brown-black

pigement and pheomelanin-red-yellow color

Melanin pigmentation may be physiologic or pathologicand focal or diffuse

Melanosis-diffuse hyperpigmentation


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FOCAL MELANOCYTIC

PIGMENTATION fRECKLE/EPHELIS

Asymptomatic,small(1-3mm), well circumscribed,tan orbrown-colored macule that is often seen on sun-exposed regions of facial and perioral skin

Ephelis is commonly seen in light skinned individuals Polymorphism in the MC1R gene are strongly associated

with the development of childhood freckels

Usually more abundantant in number and darker inintensity during childhood and adolescence

Freckels tend to become darker during peroids of longsun exposure and less intensity during autum and winter

With increasing age number and colour intensity tend todimnish


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ORAL/LABIAL MELANOTIC

MACULE

Focal areas of melanin deposition either as

response to local irritation condition (mechanical

trauma,tobacco smoking,chronic autoimmune

mucositis),racial background(darker person) orsystemic medications,especially chloroquine

Oral melanotic macule-focal melanin deposition

which are not associated with race or an

appropriate syndrome are innocuous surfacediscolouration


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Clinical features

2:1 female predilection with average age of 43yrs

One third of lesion occurs on the vermillion bordeer of lowerlip-buccal mucosa, gingiva and palate are other common sites

Macule-well demarcated, uniformly tan to dark brown,

asymtomatic,round or oval discolouration less than 7mm diamter Lesion is not thickened and has the same consistency as

surrounding mucosa

Tends to hav abrupt onset and seldom enlarges after diagnosis

It is innocuous

TREATMENT

No treatment required except for esthetic consideration


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IDIOPATHIC PIGMENTATION

Laugier-hunziker pigmentation

Etiology and Pathogenesis

Acquired idiopathich macular hyperpigmentation

of lips and buccal mucosae Esophagel, genital and conjunctival mucosae

and the acral surfaces

Nail longitudinal melanotic streaks and without

any evidence of Fingernails are more commonly affected than

toe nails


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Clinical features

Multiple discrete irregularly shaped brown ordark brown oral macules.

Macules not more than 5mm diameter

Lesion may coalesce to produce a diffuse areaof involvement

Management

Pigmentation maybe esthetically unpleasy but itis innocuous.

Treatment is not generally indicating, lasercryotherapy have been used successfully


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ORAL MELANOACANTHOMA

Innocuous lesion that may spontaneously resolve,with or withoutsurgically intervention

Lesion reactive in nature

Rapid onset

History of chronic irritation or acute trauma precedes the development

of lesion.Biopsy is always warranted

CLINICAL FEATURES

Rapidly enlarging, ill-defined,darkly pigmented macular or plaquelike lesion

Black females

Buccal mucosa Size variable,small and localised-large,diffuse areas of involovement

Borders are irregular in appearance

Pigments may or maynot be uniform


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MELANOCYTIC NEVUS

Also called as oral nevi,nevocellularnevus,mole,mucosal melanocytic nevi

Nevi classified as congenital or acquired(Buchner and Hansen)

On histologic basis it can be classified as Junctional nevi-when nevus cells are limited to

the basal cell layer of epithelium

Compound nevi-nevus cells are in epidermis

and dermis intramucosal nevi-(common mole)-nest of

nevus cells are entirely in the dermis


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Junctional navy- first noted in infants, children

and young adults

During later adulthood the lesions mature into

itramucosal nevi. As the nevus cells penetrate into the dermis,

their pigmentation dimnnishes approximately

15% intramucosal nevi are non pigmented

Most common-intramucosal

Second most common- blue nevus


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CLINICAL FEATURES

Small and garment

Small nevi greater than 1 cm diameter and

usually 3-5 cms Garment nevi greater than 10 cm diameter and

covers large areas of skin

Congentive nevi occur in 1-2.5% of neonate,

with passage of time may change from flat, pale,tan macule to elevated verrucous hairy lesions

Acquired nevi are extremely common


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Intra dermal nevus- smooth flat vision or maybe elevatedabove the surface, it may or may not exhibit brownpigmentation and it often shows strands of hair growingfrom its surface

Junctional nevus- clinicaly similar to intra derma nevus

Distinction being chiefly historigical

Compound nevus- lesion composed of two elements-intra dermal nevus and overlying junctional nevus

Single cell and or epithelioid cell nevus (spitz nevus)occurs in children only 15% in adults, histologicallysimilar to malignant melanoma.


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Blue nevus true misodermal structure composed

of dermal melanocytes which only rarely

undergo malignant transformation.

Present at birth or appear in early childhood andpersist unchanged throughout life

Lesion is smooth exhibits hair growing from its

surface. Varies in color from brown to blue or

bluish black


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ORAL MANIFESTATION

Most common hard palate, second most buccalmucosa.

Other common sites-vermilion border of the lipand the labial mucosa. 10 % on gingiva

Mostly asymptomatic

Pigmentation vary from brown to black or blue

Nevi are well circumscribed round or oval andare raised or slightly raised.

Treatment- surgical excision.


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MALIGNANT MELANOMA

Neoplasm of epidermal melanocytes.

ETIOLOGY

Environmental factors

Sun exposure : Long hours of sunlight exposure. Artificial UV sources : PUVA (combination of

psoralen (P) and long way ultraviloet raditaion(UVA) therapy.

Socioeconomic status: More prevalent in highsocioeconomic status

Fair skin, freckles and red hair

Number of Melnocytic nevi


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Genetic factors

Familial melanoma: Patients with

abnormality on chromosome 9p21.

Xeroderma pigmentosum : Defective DNA

repair mechanism relate to excessive

chronice UV damage and development of

sun related skin tumors.


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CLINICAL FEATURES

Superficial spreading melanoma

Most common in caucasian

Exist in radial growth phase called premaligantmelanosis or pagetoid melanoma insitu

Tan, brown, black or admixed lesion on sun exposedskin especially the back. It also occurs on skin of thehead and neck, chest, abdomen, extremities.

Phase last for several months to several years.

Vertical growth phase characterized by an increase insize, change in color, nodularity and at times ulceration


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HEMOGLOBIN AND IRON

ASSOCIATED PIGMENTATION


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ECCHYMOSIS

Traumatic ecchymosis common on lips and face

Immediately following the traumatic event erythrocyteextravasation into the submucosa will appear as a brightred macule or as a swelling if a hematoma forms

Brown coloration within few days after the hemoglobindegraded to hemosiderin

Patients taking anti coagulant drugs may be present oralecchymosis particularly on buccal mucosa or tongue

Maybe encountered in patients with liver cirrhosis,leukemia and end stage renal disease undergoingdialysis treatment.


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PURPURA OR PETECHIEIAE

Causes:-

Amyloidosis

Aplastic anemia

Chronic renal failure

Forceful coughing Hemophilia

HIV or AIDS

Infectious mononucleosis

Leukemia

Liver cirrhosis OSMF

Thrombocytopenia

SLE


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Capillary hemorrhage will appear red initially and turn brown in fewdays once the extravasated blood cells have lysed and have beendegraded to hemosiderin.

Petechiae- pinpoint or slightly larger than pinpoint.

Purpura-multiple,small 2-4 mm collection of extra vasated bloods

Identified on soft palate in most cases When trauma is suspected the patient would be instructed to cease

whatever activity maybe contributing to the presence of the lesion.

Within two weeks lesion should be resolved.

Failure to do so should arouse suspicion of a hemorrhagic diathsis,a persistent infectious disease, or other systemic disease.


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HEMOCHROMATOSIS

Chronic, progressive disease that is characterized byexcessive iron deposition in liver and other organs andtissues.

Idiopathic, neonatal, blood transfusion and heritable form Complications include liver cirrhosis, diabetes, anemia,

heart failure, hypertension and bronzing of the skin.

Oral pigmentation is often diffused and brown to gray in

appearance Palate and gingiva most commonly affected.


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DEPIGMENTATION

VITILIGO

Etiology and Pathogenesis

Acquired auto immune disease that isassociated with hypomelanosis

Etiology and mechanism remain unknown-

end result is a destruction of melanocytes

Multifactorial with both genetic and

environmental factors play role


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Clinical Features

Focal areas of depigmentation

An entire segment on one side of the body may be effected

In occasional cases the skin and hair of most of the body may looseits pigmentation (vitiligo universalis)

Characterized by bilateral symmetric areas of relatively generalizedhypo melanosis

Present as well circumscribed round oval or elongated, pale or whitecoloured macules that may coalesce into large areas of diffusedepigmentation.

Onset at any age-signs developed before the third decade.

Greater prevalence in females


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PATHOLOGY

Microscopically there is a complete loss ofmelanocytes and melanin pigmentation in the

basal cell layer. MANAGEMENT

Objective-stimulate repigmentation

Topical corticosteroids and topical or systemic

photo chemotherapies. Autologous epithelial grafts

Punch grafting and micro pigmentation


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Early stages

The pigmentation maybe commonly a result of basilarmelanosis rather than iron associated pigment. Irondeposition within the adrenal cortex may lead to

hypoadrenocorticism and ACTH hypersecretion, with theassociated addisonial type changes

Later stages- pigmentation is the result of hemosiderosisand melanosis

Increased melainin pigment maybe seen in basal celllayer whereas golden or brown colour hemosiderin canbe seen diffusely scattered throughout the submucosaland salivary gland tissues.


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EXOGENOUS

PIGMENTATION


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AMALGAM TATTOO

ETOLOGY AND PATHOGENESIS

Single most commons source of solitary or

focal pigmentation

Iatrogenic in origin and typically a

consequence of the inadvertent deposition

of amalgam restorative material into the

submucosal tissue


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CLINICAL FEATURES

Small asymptomatic, macular, and blusih grey or even

black in appearances

Gingiva, alveolar mucosa, buccal mucosa, and floor of

the mouth.

Found in the vicinity of teeth with large amalgam

restorations or crowned teeth that probably had

amalgams, around apical region of endodontically

treated teeth with retrograde restorations or oburated

with silver points, and in areas in and around healed

extractions sites.


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PATHOLOGY

Microscopically-fine brown granular stippling of reticulum fibers with

a particular affinity for vessel walls and nerve fibers.

Large aggregates of black material

Foreign body type giant cell reaction- uncommon

MANAGEMENT

Surgical removal

Biopsy-if no radiographic evidence, lesion not in proximity to any

restored tooth.


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GRAPHITE TATTOOS Represent traumatic implantation of graphite particles

from pencil - childhood

Palate Solitary gray or black macule

Treatment- Cosmetic reasons


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Ornamental Tattoos Mucosal tattoos in the form of lettering or intricate.

Amateur tattoo inks consist of simple carbon particles originating

from- burnt wood plastic or paper

India ink, pen ink and plant derived matter.

Laser therapy

Pigment is plant derived


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MEDICINAL METAL INDUCED PIGMENTATION

Metallic compounds are used for treatment of varioussystemic diseases

Gold Therapy- rheumatoid arthritis. Gold and colloidal silver- diffuse cutaneois pigmentation

Silver may cause a generalized blue-gray discoloration(argyria)

Gold-blue gray or purple (chrysiasis) Pigmentation persistent if not permanent, even following

discontinuation of substance


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Metal salts remain a component of some topical

medications.

Eg:- Silver nitrate and zync oxide

Silver nitrate cautery to treat recurrent aphthous

stomatitis

Zinc oxide- common component sunblock creams

Both associated with focal mucocutaneous pigmentation

Gray Black in appearance Both appear as brown or black particulate matter that is

often dispersed through out submucosal tissue


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Generalized black pigmentation of tongue- chewing of

bismuth subsalicylate tablets- common antacid

Associated with elongation of filiform

papillae,hyperkertosis and superficial cobonization of

tongue by bacteria

Discontinuation of antacid and cleansing of tongue are

curative


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HEAVY METAL PIGMENTATION

Diffuse oral pigmentation- associated with ingestion ofheavy metals

Lead mercury bismuth arsenic.

Ingested metal salts tends to extravasate from vesseksin areas of chronic inflammation

Found along free marginal gingiva

Metallic line has gray to black appearance

Additional systemic signs and symptoms- behavioralchanges, neurologic disorder, intestinal pain, andsialorrhea. Diffuse mucocutaneous melanosis


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DRUG INDUCED PIGMENTATION

Minocycline- tetracycline derivative-treatment of acne

Pigmentation of developing teeth

Prescribed in early adult hood

Minocycline metabolites may be incorporated into the normal bone Whereas the teeth may appear normal but the surrounding may

appear green, blue or even black as a result the palatal and

alveolar mucosae may appear similarly and diffusely discolored

It can also induce actual pigmentation of the oral soft tissues as well

as skin and nails. May appear gray, brown or black

Pigmentation patchy or diffuse.


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Biopsy may reveal basilar melanosis morecommon, aggregates a fine brown or goldenparticles.

These are often intra cellular and containedwithin macrophages

Superficially submucosal pigment may resemblemelanin

No treatment necessary. The discoloration oftensubsides within months after discontinuation ofthe medication


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Exogenous Pigmentation