Physiological and Pathological Oral Pigmentations Endogenous Pigments and Exogenous Pigments

1. ORAL PIGMENTATION
Dr. Hadi Munib
Oral and Maxillofacial
Surgery Resident

5. COMMON SITES
Gingiva
BM
Hard Palate
Tongue
Soft Palate
Floor of the Mouth

6. PHYSIOLOGICAL PIGMENTATION
Physiologic pigmentation is the most common source of multifocal or diffuse oral
mucosal pigmentation.
Dark-complexioned individuals, including blacks, Asians, and south- Americans.
Mostly restricted to the gingiva, melanosis of other mucosal surfaces is not
uncommon.
The pigment is often observed in childhood and usually does not develop de novo
in the adult.
Differential Diagnosis; idiopathic, drug-induced, or smoking-induced melanosis.
If esthetics are disturbed, Gingivectomy and Laser therapy can be used to remove
the pigment

8. EPHELIS AND ORAL
MELANOTIC MACULE
Melanin Overproduction
Skin vs. Oral Mucosa
Skin: Asymptomatic, small (1–3 mm), well-circumscribed, brown-colored macule
that is often seen on the sun-exposed regions of the facial and perioral skin.
Oral: Small (<1 cm), well-circumscribed, oval or irregular in outline and often
uniformly pigmented.
Light-skinned individuals and in red- or light blond–haired individuals.
No therapeutic intervention is required.
Biopsy after 2 weeks if persistent
DDx: Nevus, Amalgam Tattoo, Focal Ecchymosis and Melanoma

11. MELANOCYTIC
NEVUS
Melanocytic Proliferation
More in Females, over 30 years old
Hard Palate, the buccal and labial mucosae and gingiva
Asymptomatic, small (<1 cm), solitary, brown or blue, well-circumscribed nodule
or macule.
Up to 15% of oral nevi may not exhibit any evidence of clinical pigmentation.
Biopsy is necessary for diagnostic confirmation.
Treatment: complete but conservative surgical excision

14. MELANOMA
Highly malignant oral tumors.
Amelanotic melanomas can manifest as red lesions.
Isolated dark brown or black lesions that tend to occur on the palate, initially may
be symptomatic, nodular or macular lesion that is firm to palpate.
Male predilection, but it’s one of the most commonly occurring cancers in women of
childbearing age.
The prognosis for oral melanoma is poor.
De Novo or from existing Nevus
15 – 40% 5 –year survival rate, if distant lymph nodes are involved then it drops to
less than 10%

18. DRUG-INDUCED MELANOSIS
10 – 20% of all cases
May remain after withdrawal of the medication
Antimalarials, Hydroxyquinolones, Quinolones, Gold, Oral Contraceptives
and Minocycline.
Large Diffuse pigmentation on the hard palate or diffuse multifocal
pigmentation.

20. SMOKER’S MELANOSIS
Anterior maxillary and mandibular gingivae, buccal mucosa, lateral
tongue, palate, and floor of the mouth.
Most smokers (including heavy smokers) usually fail to show such
changes.
Brown, flat, and irregular; some are even geographic or map-like in
configuration.
If there is a reduction in smoking, the pigmentation may eventually
resolve

21. ENDOCRINOPATHIES
Addison’s Disease
Adrenocortical Insufficiency
Weakness, poorly defined fatigue, depression and mucocutaneous
hyperpigmentation.
Serum cortisol and electrolyte levels
Cushing’s Disease
Prolonged exposure to Corticosteroids
Diffuse Mucocutaneous pigmentation.

23. PEUTZ-JEGHERS
SYNDROME
Autosomal dominant disease.
Intestinal polyposis, cancer susceptibility, and multiple, small, pigmented
macules of the lips, perioral skin, hands, and feet measuring <0.5 cm in
diameter.
Lips and perioral skin but may also develop on the anterior tongue and
buccal and labial mucosae.

25. CAFÉ AU- LAIT PIGMENTATIONS
Tan/ Brown – Coloured irregularly shaped macule
Neurofibromatosis type I; Neurofibromas with Multiple Café Au- Lait pigmentations
McCune-Albright syndrome; Polyostotic Fibrous Dysplasia, Café Au- Lait spots and
Precocious puberty

26. HIV/ AIDS ASSOCIATED MELANOSIS
Diffuse or multifocal mucocutaneous pigmentation has been frequently
described in HIV-seropositive patients
Could be due to antifungal and antiretroviral drugs or as a result of
adrenocortical destruction
CD4+ T-Lymphocytes count cells/µL less than or equals 200
May present with a history of progressive hyperpigmentation of the skin,
nails, and mucous membranes.
BM

27. HEME-ASSOCIATED
PIGMENTATION

28. ECCHYMOSIS – PURPURA –
PETECHIAE
Ecchymosis; Bright red macule due to trauma, resolves by 2 weeks.
Capillary hemorrhage; Red initially then turns blue
Purpura; Multiple, small 2 to 4 mm collections of extravasated blood.
Petechiae; pinpoint or slightly larger than pinpoint collections of extravasated
blood
Purpura and Petechiae on the soft palate can be due to viral infections or suction

30. HEMOCHROMATOSIS
Chronic, progressive disease, excessive iron deposition (usually in the form of
hemosiderin) in the liver and other organs and tissues.
Primary and Secondary (Excessive iron, anemia, liver cirrhosis)
The oral pigmentation is often diffuse and brown to gray in appearance.
Palate and Gingiva are most commonly affected.
Prussian blue stain will confirm the presence of iron

31. HEMOGLOBIN – ASSOCIATED
PIGMENTATION

32. HEMANGIOMA
Childhood
Skin, Scalp and Mucous Membranes
Color depends on depth
Tongue and Lip
Most resolve by the age of 10
Sturge- Webber Syndrome; Hemangioma, Seizures and Tram-line calcifications of
the skull
It treatment is needed: Conventional or Laser Surgery or Intralesional 3% Sodium
Tetradecyl Sulphate

34. VARIX
Sublingual area – Ventral tongue
Differences from Hemangioma
1. Old age
2. Doesn’t resolve spontaneously
3. Size
4. Etiology

35. KAPOSI’S SARCOMA
• Classic Kaposi’s sarcoma is seen on the oral mucosa and the skin of the
lower extremities in older men, or in the lymph nodes of children in
equatorial Africa.
• HIV associated Kaposi’s Sarcoma is a diagnostic sign for AIDS, seen on
the palate+ and facial gingiva.
• The early plaque or macular lesions are painless and
require no therapy.
– Electrocautery
– Intralesional injections of sclerosing agent; painful
– Intralesional multiple biweekly injections of 1% vinblastine sulfate is
beneficial ( no significant postoperative pain).

37. HEREDITARY HEMORRHAGIC
TELANGTESSIA
Autosomal Dominant
Multiple round oval papules < 0.5 cm in diameter may be more than 100 in number
Nasal mucosa (epistaxis is common, fatal epistaxis has been reported), lips, tongue,
buccal mucosa, facial skin and neck.
Platelet studies can be ordered to rule out blood dyscrasia.

38. EXOGENOUS
PIGMENTATIONS

39. AMALGAM TATTOO
1% of the general population
Iatrogenic in origin
Bluish- Gray to black in appearance

40. GRAPHITE TATTOOS
Most commonly on the palate
Traumatic implantation of graphite particles from a pencil.
Solitary gray or black macule.

41. HAIRY TONGUE
Discoloration of the dorsal tongue, particularly the middle and posterior one-
third.
The filiform papillae are elongated, sometimes markedly so, and have the
appearance of fine hairs.
Variant colours of chromogenic bacteria; white, green, brown, or black.
Treatments consist of having the patient brush the tongue, or use a tongue
scraper, and limit the ingestion of color-forming foods and drinks until the
discoloration resolves

43. HEAVY METAL INGESTION
• May be an occupational hazard
• Lead, mercury and bismuth.
• Seen along the free marginal gingiva (eyeliner- like)
• Associated with systemic symptoms: behavioral changes, neurologic
disorders, and intestinal pain.
• Rarely seen now

44. REFERENCES
Chapter 6: Pigmentations of the oral mucosa

45. THANK YOU