PIGMENTATIONS OF ORAL MUCOSA-DR NIMISHA

1. ORAL PIGMENTATIONS
ORAL PIGMENTATIONS

2. Colour
variations
Vascularity of
mucosa
Distribution of
melanin
Degree of
keratinization
Degree of
epithelialization

3. ■ PIGMENT : Any organic/inorganic coloring substance
■ PIGMENTATION : process of deposition of pigments in
tissues
■ Pigments
• Melanin
• Hemosiderin
• Hemoglobin
■ Pigmented lesions of oral cavity are due to:
• Augmentation of melanin production
• Increased number of melanocytes ( melanocytosis )
• Deposition of accidentally introduced exogenous materials

4. EXOGENOUS PIGMENTATIONS

5. Patient with oral pigmentation comes to clinic,
1. HISTORY
 Occupation
- Industrial exposure to heavy metals
- Dust / vapours containing heavy metals

6. • Bluish – black pigmentation around the gingival margin
• Nausea, vomiting, Constipation
• Burtonian lines
LEAD POISONING
 Characteristic generalized cutaneous ‘lead hue’ (described as a combination
of pallor and lividity)
Due reaction between circulating lead with sulphur ions released by oral
bacteria

8. • Mostly in children
• Hand, feet, nose and cheeks becomes pink in colour
• CNS symptoms
• Tongue may be enlarged and painful
• Slate-grey gingival hyperpigmentation
• ACRODYNA – PINK DISEASE, SWIFT DISEASE
MERCURY POISONING

10. • First symptom - Slate-blue silver line along the gingival margins
• Oral mucosa often exhibits a diffuse blue-black discoloration
• Cyanotic look
• Acute intoxication causes - coma, pleural edema, hemolysis, bone marrow failure
• Known as Argyria
SILVER POISONING

12. • Diffuse blue gray discoloration of the skin
• Removable black discoloration of normal filiform papillae
• Resemble black hairy tongue but papillae are not elongated
Bismuth poisoning
• Blue -gray line along the gingival margin – Bismuth lines – Bismuth gingivitis

13. • Blue -gray line along the gingival margin

14. Patient with oral pigmentation comes to clinic,
1. HISTORY
 Occupation
- Industrial exposure to heavy metals
- Dust / vapours containing heavy metals
 Drug history

19. Patient with oral pigmentation comes to clinic,
1. HISTORY
 Occupation
- Industrial exposure to heavy metals
- Dust / vapours containing heavy metals
 Drug history
 Dental/ Medical history

20. • Painless, gray-blue macules that range in size from a few millimeters to
greater than 1 cm
• Caused by the presence of metallic material in the oral tissues
• Accidental implantation of dental filling material into the gingival or buccal
mucosa
AMALGAM TATOO

22. • H/O accidental injury with pencil
• Occurs most frequently in the anterior
palate of young children as an irregular
green to black macule
GRAPHITE TATOO

23. Patient with oral pigmentation comes to clinic,
1. HISTORY
 Occupation
- Industrial exposure to heavy metals
- Dust / vapours containing heavy metals
 Drug history
 Dental/ Medical history
 Habit history

26. • Discrete or coalescing multiple brown macules
• 25 to 31% of tobacco users
• Usually involve palate, buccal mucosa, gingiva
• Opening of minor salivary gland in palate
SMOKER’S MELANOSIS
(SMOKER’S PALATE)

27. • Painless, benign disorder caused by defective desquamation & reactive
hypertrophy of the filiform papillae of the tongue
• Show various colors from yellow-brown to black depending on extrinsic factors,
and intrinsic factors
• Exact pathogenesis unclear.
BLACK HAIRY TONGUE

28. • Precipitating factors
o Poor oral hygiene
o Antipsychotic drug olanzapine
o Broad spectrum of antibiotics such as erythromycin,
o Therapeutic head and neck radiation.
• Diagnosis : typical clinical presentation, no biopsy needed
• Scraping or brushing the tongue and smoking cessation enhance the
resolution of black hairy tongue.

29. ENDOGENOUS
PIGMENTATIONS

30. ENDOGENEOUS
PIGMENTATION
ENDOCRINE
DISORDERS
Addisons
disease
Diabetes
Pregnancy
Hyperthyroidism
SYNDROME
ASSOCIATED
Peutz jegher
Mc cune
Albright
Neurofibrom
atosis
Hemochroma
tosis
Leopard
syndrome
INFECTION
HIV
CHRONIC
IRRITATION
Post
traumatic
Post
inflammatory
REACTIVE
Oral
melanotic
macule
Oral
melanoacant
homa
NEOPLASTIC
Benign:nevus
Malignant:
melanoma

31. 2. EXAMINATION
Colour
Blue, Red, Purple HEMOGLOBIN
Brown HEMOSIDERIN
Brown – black, Grey MELANIN
Yellow BILIRUBIN
Yellow - Orange CAROTENE

32. BLUE/ RED/ PURPLE/ BROWN PIGMENTATION
• Present from birth
• Diascopy positive
HEMANGIOMA

33. • Types – Mucosal, Intravenous, Central, Portwine stain
• Mucosal – lip, buccal mucosa – flat/ raised
- capillary – small, superficial – STRAWBERRY HEMANGIOMA
- cavernous hemangioma – large, dome shaped
• Intramuscular hemangioma – masseter – ERECTILE HEMANGIOMA
• Central hemangioma – within bone – slow growing, rebound mobility of teeth
painless swelling – soap bubble appearance on radiograph
• Portwine stain - flat hemangioma, but not hemangioma – malformed dilated
blood vessels
• Unilateral distribution, along trigeminal nerve distribution

34. Investigations
• Diascopy
• FNAC
• USG
• CT/MRI
Management
• Intralesional corticosteroid
• Laser therapy
• Surgical excision
• Cryotherapy
• Sclerosing injection

35. • Syndrome associated
1. Sturge Weber syndrome (Port wine stain, Tram line appearance on skull
radiograph, tumour like growth in brain, ocular involvement)
2. Maffuci syndrome – Multiple enchondroma + multiple hemangioma
3. Kasabach – Merritt syndrome – hemangioma+ thrombocytopenia

36. • Nodule / swelling
• Size increases with time
• May have h/o trauma
• Pulsatile
• Diascopy positive
ARTERIO – VENOUS
MALFORMATIONS (Avm)

37. • Purplish dome shaped / raised lesion
• Usually old age
• Diascopy positive
• In tongue -Caviar tongue
VARIX
• Purplish dome shaped / raised lesion
• Usually old age, Lower lip
• H/O trauma / bite , Saliva spillage
• Diascopy negative
SUPERFICIAL
MUCOCELE

38. • Due to permanently dilated capillaries under epithelium
• < 5 mm in size
• Diascopy positive
• Associated with CREST syndrome, Rendu – Osler Weber syndrome
TELANGIECTASIA

39. • Due to blood leakage from vessels to connective tissue
• Diascopy negative
• Three types
Size < 0.3 cm - pinpoint
Size 0.4 – 0.9 cm Size > 1 cm
PETECHIAE
PURPURA ECCHYMOSIS

40. • HIV associated, immunocompromised
• Systemic involvement
• Diascopy negative
• Involve mucosa & invade bone
• Hutchinson's sign positive - Pigmentation may spread from the proximal nail fold
into the surrounding skin
KAPOSI SARCOMA

41. • Due to excessive iron deposition
• Congenital
• Blue-gray to brown pigmentation affecting mainly the palate and
gingiva
HEMOCHROMATOSIS

42. • Chronic, progressive disease that is characterized by excessive iron
deposition - in the form of hemosiderin in the liver and other organs and
tissues.
• Types - Idiopathic, neonatal, blood transfusion, heritable
• Complications - liver cirrhosis, diabetes, anemia, heart failure,
hypertension, and bronzing of the skin.

43. • Yellow discoloration
• May be confused with jaundice, but no icterus
• A vitamin A precursor is found in yellow vegetables ,papaya and fruits
CAROTENEMIA

44. ENDOGENOUS
PIGEMENTATION

45. FOCAL PIGMENTATION
• Asymptomatic small (1-3mm),well circumscribed
• Tan or brown color, darker on prolonged sun exposure
• Developmental in origin
• Increased melanin production, but no increase in number of melanocytes
EPHELIS/ FRECKLE

46. • Small, well-circumscribed, brown-to-black
• Lips and gingiva, followed by the palate and buccal mucosa
• Female predilection
MELANOTIC MACULE

47. • Benign neoplasms of cutaneous melanocytes
• Small, well circumscribed macules but commonly appear as slightly
raised papules
• Brown, bluish-gray, or almost black and occasionally non pigmented
• Less common on the oral mucosa than skin
NEVUS

49. • Rare, benign pigmented, brown to brown-black, well circumscribed lesion
• Most common intraoral sites - buccal mucosa, lip, palate, gingiva.
• Average age of presentation - 28 years
ORAL MELANOACANTHOMA

50. • Multiple brown–black pigmented areas adjacent to reticular, erosive or
vesicular lesions
• Oral lichen planus, pemphigus or pemphigoid
POST INFLAMMATORY MELANOSIS

51. • Asymptomatic, slow-growing brown or black patch with asymmetric & irregular
borders or as a rapidly enlarging mass associated with ulceration, bleeding, pain and
bone destruction
• Most common site - hard palate, gingiva
• Malignant
MALIGNANT MELANOMA
TUMOUR MASSES

52. • Less than 1% of all oral malignancies
• Characterized by proliferation of malignant melanocytes along the junction
between the epithelial and connective tissues, as well as within the connective
tissue
• Risk factors: H/O multiple episodes of acute sun exposure
Immunosuppression
Positive family history
Presence of multiple cutaneous nevi
Oral: unknown
• Between 4th and 7th decades of life
• Men than in women
• Prolonged radial growth phase followed by a vertical growth phase

53. Staging (Clark’s classification)
• Level I: Cells confined to epithelium
• Level II: Cells penetrating papillary
dermis
• Level III: filling papillary dermis
• Level IV: extending into reticular
dermis
• Level V: invading subcutaneous fat

54. Criteria for clinical diagnosis of melanoma
(ABCDE-rule)
■ Asymmetry - is when one-half of the lesion
does not match the other half of lesion
■ Border irregularity - is when the edges are,
notched, ragged or blurred
■ Color irregularity - various colored
• pigmentation is seen ranging from black,
black, brown, tan, red, blue and white
white
■ Diameter - more than 6 mm (pencil eraser)
■ Evolving/surface elevation - lesion that
changed with respect to colour, size, shape,
surface, symptoms

55. Types of melanoma
■ Superficial spreading
■ Nodular melanoma
■ Lentigo maligna melanoma
■ Acral lentiginous melanoma
■ Mucosal lentiginous melanoma
■ Acral lentiginous and mucosal lentiginous melanoma - commonly occur in
the oral cavity.

57. • Distinctive neoplasm of early infancy with rapid expansile growth
• Lesion affects the maxilla of infants during the first year of life
• Soft and rapidly growing pigmented swellings
• High urinary level of VMA (3-methoxy-4-hydroxymandelicacid)
MELANOTIC NEURO ECTODERMAL TUMOUR OF INFANCY

58. DIFFUSE
• Common - increase in the production of melanin pigment
• Darker skinned individuals
• Light brown to almost black
• Attached gingiva : most common location
PHYSIOLOGICAL PIGMENTATION

59. SYNDROME ASSOCIATED PIGMENTATION
Coffee with hot milk added
CAFÉ – AU – LAIT SPOTS

60. • Regular smooth borders
• Cross midline
• Like Coast of California
NEUROFIBROMATOSIS

61. • von Recklinghausen’s disease of skin
• Multiple neurofibroma
• Axillary freckling – Crowe’s sign
• Translucent brown pigmented spots on iris – Lisch nodules

62. • Irregular margin, ten macules
• Rough on palpation
• Till the midline
• Resembles Coast of Maine
McCUNE – ALBRIGHT SYNDROME

63. • Polyostotic fibrous dysplasia + café au lait spots + multiple endocrinopathies
(pituitary adenoma, sexual precocity, hyperthyroidism)
• Multiple bones affected
• Hockey stick deformity of long bones
• Polyostotic fibrous dysplasia + café au lait spot = Jaffe – Lichenstein
syndrome

65. • Autosomal dominant genetic condition
• Perioral pigmentation – 1-4mm brown to blue gray macules primarily on vermilion
border
• Freckles in the extremities
• Multiple intestinal polyps
PEUTZ – JEGHERS SYNDROME

66. • Intraoral, intranasal, conjunctival, and rectal pigmented lesions as well as spots
localized on the acral surfaces may also be present
• The oral lesions are benign and histologically characterized by an increase in
melanin in the basal layer, without an obviously increased number of
melanocytes.
• A fading or a disappearance of the spots in older age

67. Leopard syndrome is characterized by
■ Lentigines,
■ Electrocardiographic abnormalities
■ Ocular hypertelorism
■ Pulmonic stenosis
■ Abnormalities of genitalia
■ Retardation of growth
■ Deafness
LEOPARD SYNDROME

68. • Diffuse hyperpigmentation of the oral mucosa and longitudinal melanonychia
• Asymptomatic, lenticular (lens-shaped), or linear, brown to black mucocutaneous
macules, <5 mm in diameter.
• Single or confluent, well-defined or indistinct margins, occurs spontaneously,
permanent
• Idiopathic
LAUGIER – HUNZIKER
SYNDROME

69. ENDOCRINE / SYSTEMIC DISEASE ASSOCIATED PIGMENTATION
• Occur due to liver disorders
• Causes improper metabolism of
bile pigments
• Excess bilirubin in blood stream
• Deposition of bile pigments in
skin and oral mucous membrane
JAUNDICE

70. • Generalised hyperpigmentation – “Bronzing of
skin”
• Sudden onset of oral pigmentation followed by skin
hyperpigmentation
• Increased levels of ACTH
ADDISON’S DISEASE

71. INTRINSIC PIGMENTATION OF
TEETH

72. • Reddish brown colour
• Erythrodontia
• Porphyrin deposition
GUNTHER’S DISEASE
(CONGENITAL
PORPHYRIA)
• Blackish brown discolouration
• Inborn error of metabolism in
tyrosine
• Homogentisic acid deposition
ALKAPTONURIA
(PHENYLKETONURIA)

73. • Due to pulpal hemorrhage products
• Non vital teeth
• Pink tooth of Mummery
INTERNAL RESORPTION/
TRAUMATISED TOOTH

74. ENAMEL HYPOPLASIA

75. • Enamel hypoplasia
• Due to environmental factors
• Endemic
• With family history
DENTAL FLUOROSIS

76. • Hereditary type of enamel hypoplasia
• Defective enamel formation
• Congenital
• Affect both primary & permanent dentition
• Radiographically, loss of enamel
AMELOGENESIS IMPERFECTA

77. • Hereditary
• Hypersensitivity
• Opalescent dentin
• Blue sclera when associated with bone deformities
• R/f – multiple pulpal exposure
DENTINOGENESIS IMPERFECTA

78. • Brown discolouration
• Normal primary & permanent dentition clinically
• R/F – thistle shaped tooth , tulip shaped teeth
DENTIN DYSPLASIA

79. PIGMENTATION
PHYSIOLOGICAL PATHOLOGICAL
EXOGENEOUS
ENDOGENEOUS

80. Exogenous
Drug
induced
Tobacco-
chewed/smoking
Heavy metals
induced
Amalgam
tattoo,graphite
tatoo

81. ENDOGENEOUS
PIGMENTATION
ENDOCRINE
DISORDERS
Addisons
disease
Diabetes
Pregnancy
Hyperthyroidism
SYNDROME
ASSOCIATED
Peutz jegher
Mc cune
Albright
Neurofibrom
atosis
Hemochroma
tosis
Leopard
syndrome
INFECTION
HIV
CHRONIC
IRRITATION
Post
traumatic
Post
inflammatory
REACTIVE
Oral
melanotic
macule
Oral
melanoacant
homa
NEOPLASTIC
Benign:nevus
Malignant:
melanoma