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ORAL PIGMENTATIONS
ORAL PIGMENTATIONS
Colour
variations
Vascularity of
mucosa
Distribution of
melanin
Degree of
keratinization
Degree of
epithelialization
■ 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
EXOGENOUS PIGMENTATIONS
Patient with oral pigmentation comes to clinic,
1. HISTORY
 Occupation
- Industrial exposure to heavy metals
- Dust / vapours containing heavy metals
• 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
• 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
• 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
• 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
• Blue -gray line along the gingival margin
Patient with oral pigmentation comes to clinic,
1. HISTORY
 Occupation
- Industrial exposure to heavy metals
- Dust / vapours containing heavy metals
 Drug history
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
• 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
• 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
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
• 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)
• 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
• 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.
ENDOGENOUS
PIGMENTATIONS
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
2. EXAMINATION
Colour
Blue, Red, Purple HEMOGLOBIN
Brown HEMOSIDERIN
Brown – black, Grey MELANIN
Yellow BILIRUBIN
Yellow - Orange CAROTENE
BLUE/ RED/ PURPLE/ BROWN PIGMENTATION
• Present from birth
• Diascopy positive
HEMANGIOMA
• 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
Investigations
• Diascopy
• FNAC
• USG
• CT/MRI
Management
• Intralesional corticosteroid
• Laser therapy
• Surgical excision
• Cryotherapy
• Sclerosing injection
• 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
• Nodule / swelling
• Size increases with time
• May have h/o trauma
• Pulsatile
• Diascopy positive
ARTERIO – VENOUS
MALFORMATIONS (Avm)
• 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
• Due to permanently dilated capillaries under epithelium
• < 5 mm in size
• Diascopy positive
• Associated with CREST syndrome, Rendu – Osler Weber syndrome
TELANGIECTASIA
• 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
• 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
• Due to excessive iron deposition
• Congenital
• Blue-gray to brown pigmentation affecting mainly the palate and
gingiva
HEMOCHROMATOSIS
• 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.
• Yellow discoloration
• May be confused with jaundice, but no icterus
• A vitamin A precursor is found in yellow vegetables ,papaya and fruits
CAROTENEMIA
ENDOGENOUS
PIGEMENTATION
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
• Small, well-circumscribed, brown-to-black
• Lips and gingiva, followed by the palate and buccal mucosa
• Female predilection
MELANOTIC MACULE
• 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
• 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
• Multiple brown–black pigmented areas adjacent to reticular, erosive or
vesicular lesions
• Oral lichen planus, pemphigus or pemphigoid
POST INFLAMMATORY MELANOSIS
• 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
• 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
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
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
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.
• 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
DIFFUSE
• Common - increase in the production of melanin pigment
• Darker skinned individuals
• Light brown to almost black
• Attached gingiva : most common location
PHYSIOLOGICAL PIGMENTATION
SYNDROME ASSOCIATED PIGMENTATION
Coffee with hot milk added
CAFÉ – AU – LAIT SPOTS
• Regular smooth borders
• Cross midline
• Like Coast of California
NEUROFIBROMATOSIS
• von Recklinghausen’s disease of skin
• Multiple neurofibroma
• Axillary freckling – Crowe’s sign
• Translucent brown pigmented spots on iris – Lisch nodules
• Irregular margin, ten macules
• Rough on palpation
• Till the midline
• Resembles Coast of Maine
McCUNE – ALBRIGHT SYNDROME
• 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
• 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
• 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
Leopard syndrome is characterized by
■ Lentigines,
■ Electrocardiographic abnormalities
■ Ocular hypertelorism
■ Pulmonic stenosis
■ Abnormalities of genitalia
■ Retardation of growth
■ Deafness
LEOPARD SYNDROME
• 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
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
• Generalised hyperpigmentation – “Bronzing of
skin”
• Sudden onset of oral pigmentation followed by skin
hyperpigmentation
• Increased levels of ACTH
ADDISON’S DISEASE
INTRINSIC PIGMENTATION OF
TEETH
• 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)
• Due to pulpal hemorrhage products
• Non vital teeth
• Pink tooth of Mummery
INTERNAL RESORPTION/
TRAUMATISED TOOTH
ENAMEL HYPOPLASIA
• Enamel hypoplasia
• Due to environmental factors
• Endemic
• With family history
DENTAL FLUOROSIS
• Hereditary type of enamel hypoplasia
• Defective enamel formation
• Congenital
• Affect both primary & permanent dentition
• Radiographically, loss of enamel
AMELOGENESIS IMPERFECTA
• Hereditary
• Hypersensitivity
• Opalescent dentin
• Blue sclera when associated with bone deformities
• R/f – multiple pulpal exposure
DENTINOGENESIS IMPERFECTA
• Brown discolouration
• Normal primary & permanent dentition clinically
• R/F – thistle shaped tooth , tulip shaped teeth
DENTIN DYSPLASIA
PIGMENTATION
PHYSIOLOGICAL PATHOLOGICAL
EXOGENEOUS
ENDOGENEOUS
Exogenous
Drug
induced
Tobacco-
chewed/smoking
Heavy metals
induced
Amalgam
tattoo,graphite
tatoo
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
PIGMENTATIONS OF ORAL MUCOSA.pptx

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PIGMENTATIONS OF ORAL MUCOSA.pptx

  • 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
  • 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
  • 7.
  • 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
  • 9.
  • 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
  • 11.
  • 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
  • 15.
  • 16.
  • 17.
  • 18.
  • 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
  • 21.
  • 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
  • 24.
  • 25.
  • 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.
  • 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
  • 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
  • 48.
  • 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.
  • 56.
  • 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
  • 64.
  • 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
  • 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
  • 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

Editor's Notes

  1. Melanin is produced by the oxidation of the amino acid tyrosine, followed by polymerization