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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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