Pigmentation today

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Pigmentation today

  1. 1. By By Fat’heya Zahran Fat’heya Zahran Professor, Cairo University Professor, Cairo University
  2. 2.  Melanotic  Melanotic Localized Diffuse  Non Melanotic  Non Melanotic
  3. 3. Localized: Localized: Ectodermal alteration Ectodermal alteration Acanthosis Nigericans Acanthosis Nigericans Increased melanin production: Increased melanin production: Café au lait spots e.g. polyostotic fibrous dysplasia Café au lait spots e.g. polyostotic fibrous dysplasia and multiple neurofibromatosis.. and multiple neurofibromatosis Smoker’s melanosis Smoker’s melanosis Lichen planus Lichen planus Local irritation. Local irritation. Melanocyte proliferation: Melanocyte proliferation: Naevi Naevi Melanoma/malignant melanoma Melanoma/malignant melanoma Lentigo e.g. peutz Jegher’s syndrome Lentigo e.g. peutz Jegher’s syndrome Drug-Induced. Drug-Induced.
  4. 4. Diffuse: Diffuse: Racial pigmentation (basilar melanosis) Racial pigmentation (basilar melanosis) Metabolic pigmentation Metabolic pigmentation Hemochromatosis Hemochromatosis Porphyria Porphyria Pellagra Pellagra Endocrine Endocrine Addison’s disease Addison’s disease Hyperpituitrism Hyperpituitrism Autoimmune Autoimmune HIV melanosis HIV melanosis Lung/pancreas malignancy Lung/pancreas malignancy Drug-induced Drug-induced Drugs causing melanin formation e.g. ACTH, busulfan Drugs causing melanin formation e.g. ACTH, busulfan Drugs forming complex with melanin e.g. minocyclin Drugs forming complex with melanin e.g. minocyclin Drug deposited in skin and mucous membrane e.g. silver & gold Drug deposited in skin and mucous membrane e.g. silver & gold
  5. 5. Non Melanotic Vascular lesions: Vascular lesions: Lipopigments: Lipopigments: Hemangiomas Hemangiomas Kaposi’s sarcoma Kaposi’s sarcoma Varices Varices Hereditary hemorrhagic Hereditary hemorrhagic telangiectasia telangiectasia Lipochrome Lipochrome (carotene) (carotene) Lipofuscin Lipofuscin Fordyce’s Fordyce’s granules granules RBCS: RBCS: Extravasation Extravasation Qualitative changes in Hb Qualitative changes in Hb Pigments resulting from Pigments resulting from RBC destruction RBC destruction Chromogenic Chromogenic bacteria bacteria Black hairy Black hairy tongue tongue Heavy metals Heavy metals intoxication intoxication
  6. 6. Acanthosis Nigericans Unusual dermatosis characterized by skin Unusual dermatosis characterized by skin hyperkeratosis and melanin pigmentation and hyperkeratosis and melanin pigmentation and white oral lesion. white oral lesion. Types: Types: Benign form Benign form Associated with insulin resistant diabetes (defect in Associated with insulin resistant diabetes (defect in insulin receptors). insulin receptors). Insulin will bind to receptor for ILGF → growth of the Insulin will bind to receptor for ILGF → growth of the cells instead of glucose utilization → hyperkeratosis, cells instead of glucose utilization → hyperkeratosis, acanthosis and papillomatosis. acanthosis and papillomatosis. Malignant form Malignant form Internal malignancy releases certain peptides→ stimulate Internal malignancy releases certain peptides→ stimulate melanin production. melanin production.
  7. 7. Acanthosis Nigericans
  8. 8. Acanthosis Nigericans
  9. 9. Café au lait pigmentation These lesions have the colour of coffee and cream that varies from small to large diffuse macule. They are found in two rare conditions; neurofibromatosis and polyostotic fibrous dysplasia. (A) Multiple neurofibromatosis (Von Recklinghausen’s disease of skin) It is an inherited autosomal dominant condition which is characterized by proliferation of fibrous element of nerve sheath and cafe au lait
  10. 10. Clinical Features (1) Multiple nodules: Sessile or pedunculated, superficial or deep nodules that mainly affect the trunk. Malignant transformation to neurogenic sarcoma is common in 5 % of cases. The lesion may involve the whole body causing cosmetic problem. Tongue involvement results in multiple nodules due to proliferation of fibrous element of lingual nerve. In addition, macroglossia, scrotal tongue and enlarged fungiform papillae had been reported
  11. 11. Multiple Neurofibromatosis
  12. 12. Sessile Nodules with Café au Lait Pigmentation
  13. 13. (2) Neurologic manifestation: Centrally located lesions within bone cavities are associated with neurological manifestations such as pain, deafness, seizures, mental retardation and headache. Mandibular nerve involvement can be detected radiographically as radiolucent area and is associated with lip numbness and pain. (3) Café au lait pigmentation.
  14. 14. (3) Café au lait pigmentation.
  15. 15. B) Polyostotic Fibrous Dysplasia( Jaffe type Jaffe type Unilateral bone involvement Unilateral bone involvement Most bones are intact Most bones are intact Skin café au lait spots Skin café au lait spots No endocrinal disturbance No endocrinal disturbance Albright syndrome Albright syndrome Unilateral Unilateral Most bones are affected Most bones are affected Café au lait spots Café au lait spots Endocrinal disturbance is present: Endocrinal disturbance is present: present Parathyroid Parathyroid Thyroid Thyroid Pituitary Pituitary Gonads (precocious puberty) Gonads (precocious puberty)
  16. 16. Albright Syndrome
  17. 17. Oral Findings: Slowly progressive expansion of jaw bone: Jaw bone is replaced by fibrous tissue and the cortex becomes thin leading to pathologic fracture Radiographically the lesion may show one of these patterns: Ground glass radio-opaque pattern Mottled radiolucent & radio-opaque pattern Unilocular or multilocular radiolucencv
  18. 18. Smoker’s Melanosis It is basilar melanosis that occurs in some It is basilar melanosis that occurs in some smokers where tobacco smoke products smokers where tobacco smoke products stimulate synthesis of melanin. stimulate synthesis of melanin. It appears as diffuse brown flat macules, It appears as diffuse brown flat macules, mainly on anterior labial gingiva in mainly on anterior labial gingiva in cigarette smokers and on palate in pipe cigarette smokers and on palate in pipe smokers but may also appear on cheek and smokers but may also appear on cheek and lip mucosa. lip mucosa.
  19. 19. Smoker’s Melanosis
  20. 20. Pigmented Lichen Planus Lichen planus is dermatologic disease Lichen planus is dermatologic disease which is characterized by white papules, which is characterized by white papules, erosive and atrophic areas. Rarely erosive and atrophic areas. Rarely erosive or papular form may be erosive or papular form may be associated with diffuse melanosis. associated with diffuse melanosis. This increase in melanogenesis may be This increase in melanogenesis may be stimulated by infiltrate of T-lymphocytes stimulated by infiltrate of T-lymphocytes
  21. 21. Pigmented Lichen Planus
  22. 22. Definition: Definition: It is benign proliferation of melanocytes It is benign proliferation of melanocytes that appears after birth and during that appears after birth and during childhood, reaching certain size then childhood, reaching certain size then remains static. remains static.
  23. 23. Clinical Features: (i) Nevocellular nevi: Junctional nevi: Nevus cells maintain their location at the junction of the epithelium and connective tissue. They are flat, brown round and oval lesions. Compound nevi: Nevus cells proliferate down into the connective tissue. They are dome-shaped, brown lesions. Intradermal/intramucosal nevi: Nevus cells are localized in connective tissue. They appear as elevated brown nodules. (ii) Blue nevi: The nevus cells reside deeply in connective tissue. On skin they appear blue in colour because the overlying vessels dampen the brown colour of melanin.
  24. 24. Raised painless sessile or pedunculated. Raised painless sessile or pedunculated. If melanomas become painful, with increased If melanomas become painful, with increased pigmentation, bleeding or ulceration this may pigmentation, bleeding or ulceration this may be a sign of malignancy. be a sign of malignancy. Malignant melanoma is a rare neoplasma of Malignant melanoma is a rare neoplasma of the oral cavity. the oral cavity. Most commonly found on the palate and Most commonly found on the palate and anterior labial gingiva. anterior labial gingiva.
  25. 25. Peutz-Jegher’s Syndrome Definition: It is an autosomal dominant syndrome that is characterized by multiple intestinal polyposis and melanotic macules mainly on the face and oral cavity
  26. 26. Clinical Features: Clinical Features: Brown Pigmentation: Brown Pigmentation: Multiple melanotic macules appearing as freckles, Multiple melanotic macules appearing as freckles, mainly perioral, perinasal and perioccular. mainly perioral, perinasal and perioccular. Melanotic macules are present intraoral, mainly on Melanotic macules are present intraoral, mainly on palate and lip. palate and lip. Intestinal polyposis: Intestinal polyposis: Polyposis of small intestine may result in abdominal Polyposis of small intestine may result in abdominal pain, hemorrhage or intestinal obstruction .. pain, hemorrhage or intestinal obstruction Malignant transformation can occur. Malignant transformation can occur. Intestinal polyps are better to be diagnosed by Intestinal polyps are better to be diagnosed by barium enema. barium enema.
  27. 27. Peutz-Jegher’s Syndrome
  28. 28. Physiologic Pigmentation )(Racial Pigmentation It is basilar melanosis that evolves in childhood, commonly in dark-skinned individuals. It appears as multiple, diffuse flat brown macules, mainly on gingiva, labial and cheek mucosa.
  29. 29. Racial Pigmentation
  30. 30. )Hemochromatosis (Bronze Diabetes Primary :: Primary Disorder of inborn error of iron metabolism secondary to Disorder of inborn error of iron metabolism secondary to increased intestinal iron absorption. increased intestinal iron absorption. Secondary: Secondary: Due to increased iron intake or increased destruction of Due to increased iron intake or increased destruction of RBCs. RBCs. Excess iron is deposited in various tissue and Excess iron is deposited in various tissue and organs: organs: In the liver producing liver cirrhosis. In the liver producing liver cirrhosis. In the pancreas producing diabetes mellitus. In the pancreas producing diabetes mellitus. In the adrenal gland inducing Addison’s disease. In the adrenal gland inducing Addison’s disease. In the heart inducing heart failure. In the heart inducing heart failure.
  31. 31. Porphyrias Hereditary diseases caused by abnormalities in the pathway Hereditary diseases caused by abnormalities in the pathway of heme biosynthesis, resulting in over production of of heme biosynthesis, resulting in over production of porphyrins and porphyrin precursors. porphyrins and porphyrin precursors. Two types are characterized by skin pigmentation: Two types are characterized by skin pigmentation: Cutaneous hepatic porphyria “Porphyria cutenea tarda” Cutaneous hepatic porphyria “Porphyria cutenea tarda” Starts as erythema and progresses to vesicles that become confluent Starts as erythema and progresses to vesicles that become confluent to form bullae, that heal by scar with skin hyperpigmentation. to form bullae, that heal by scar with skin hyperpigmentation. Congenital erythropoietic porphyria: Congenital erythropoietic porphyria: Excessive formation of porphyrin in bone marrow leads to its Excessive formation of porphyrin in bone marrow leads to its deposition on the skin producing photosensitivity → vesicular and deposition on the skin producing photosensitivity → vesicular and bullous reaction on the light exposed skin. bullous reaction on the light exposed skin. Vesicles contain serous fluid with red fluorescence. Vesicles contain serous fluid with red fluorescence. Healing is by scars and red brown hyperpigmentation. Healing is by scars and red brown hyperpigmentation. Urine is red in colour. Urine is red in colour. Lavender teeth: due to incorporation of porphyrins in decidous and Lavender teeth: due to incorporation of porphyrins in decidous and permanent teeth permanent teeth
  32. 32. Pellagra It is niacin (Nicotinic acid) deficiency. It is niacin (Nicotinic acid) deficiency. It progresses through: It progresses through: Dermatitis with melanin pigmentation of the Dermatitis with melanin pigmentation of the exposed skin surfaces (hands, feet and face). exposed skin surfaces (hands, feet and face). Dementia (impaired memory) Dementia (impaired memory) Diarrhea, Diarrhea, Death (if untreated) Death (if untreated) Oral manifestations: Oral manifestations: Stomatitis, Glossitis, Acute necrotizing ulcerative Stomatitis, Glossitis, Acute necrotizing ulcerative gingivitis, Sialorrhea, Angular cheilosis, Herpes gingivitis, Sialorrhea, Angular cheilosis, Herpes labialis, Deminution of taste sensation. labialis, Deminution of taste sensation.
  33. 33. Endocrinopathic Pigmentation Bronzing of skin and patchy melanosis of the oral mucous membrane are features of adrenal cortex insufficiency (Addison’s disease) or hyperfunction of pituitary gland (due to increased ACTH). The oversecretion of ACTH results in melanosis since it is a hormone that have stimulating properties on melanocytes.
  34. 34. HIV Oral Melanosis HIV positive patients show hyperpigmentation of the nails and mucous membrane. The etiology is unknown but may be due to the destruction of adrenal cortex (Addison’s disease). It appears as diffuse flat brown macules, mainly on buccal and labial mucosa.
  35. 35. HIV Oral Melanosis
  36. 36. Lipopigments Lipochrome: “Carotene” Lipochrome: “Carotene” Carotenes are yellow or red fat soluble pigments found in Carotenes are yellow or red fat soluble pigments found in carrots, tomatoes, sweet potatoes, green leafy plants, milk, carrots, tomatoes, sweet potatoes, green leafy plants, milk, body fat and egg yolk. body fat and egg yolk. Carotenes found in plants consist mainly of two molecules Carotenes found in plants consist mainly of two molecules of vitamin A, Joined by a double bond ..Orally ingested of vitamin A, Joined by a double bond Orally ingested carotenes are broken down by Carotenase enzyme into carotenes are broken down by Carotenase enzyme into vitamin A, the main storage of vitamin A is in the liver. vitamin A, the main storage of vitamin A is in the liver. Excessive intake of carotene results in carotenemia Excessive intake of carotene results in carotenemia The resultant yellow colour of skin is known as The resultant yellow colour of skin is known as ((carotenodermia). carotenodermia). Carotene is water insoluble so can not reach the eye.. Carotene is water insoluble so can not reach the eye
  37. 37. Lipochrome Pigments
  38. 38. Sebaceous glands: Yellowish white spots on skin or mucous membrane occur due to ectopic collection of sebaceous glands. It may occur in: Oral cavity → Fordyce’s granules Nipple → Montogomry tubercles Upper eye lid → Mebomian glands. The lipopigment is the colouring matter of the sebum and fatty tissues.
  39. 39. Fordyce’s Granules
  40. 40. Fordyce’s Granules
  41. 41. Pigmentation Related to RBCs Extravasation: Extravasation: May be due to trauma, bleeding May be due to trauma, bleeding tendency and B.V. abnormality. tendency and B.V. abnormality. Extravasated RBCs are red in colour Extravasated RBCs are red in colour then turn brown due to degradation of then turn brown due to degradation of Hb into hemosidrin ((localized iron Hb into hemosidrin localized iron overload). overload).
  42. 42. Petechiae
  43. 43. Qualitative Changes in Hb: Qualitative Changes in Hb: Reduced hemoglobin-reduced hemoglobin is Reduced hemoglobin-reduced hemoglobin is associated with cyanosis and bluish associated with cyanosis and bluish discoloration of the skin and oral mucosa, discoloration of the skin and oral mucosa, secondary to heart and lung disease due to secondary to heart and lung disease due to over extraction of oxygen from hemoglobin. over extraction of oxygen from hemoglobin. Carboxy hemoglobin- carboxy hemoglobin is Carboxy hemoglobin- carboxy hemoglobin is pink (cherry red) color, due to inhalation of pink (cherry red) color, due to inhalation of carbon monoxide. carbon monoxide.
  44. 44. Pigmentation due to RBCs destruction: Hb Globin Globin Heme Heme Fe++ Fe++ Iron overload: Localized Generalized 2α +2β 2α +2β chains chains Proto-porphyrin Proto-porphyrin Porphyria: Hepatic Erythropoietic Thalassemia Jaundice: Hemolytic Obstructive Hepatocellular Sickle cell anemia
  45. 45. Jaundice A common manifestation of liver disease due to an increase A common manifestation of liver disease due to an increase of the yellow pigment bilirubin in the blood & tissue fluid. of the yellow pigment bilirubin in the blood & tissue fluid. A yellow tint appears in the sclera and is followed by yellow A yellow tint appears in the sclera and is followed by yellow coloration of the skin and mucous membrane. coloration of the skin and mucous membrane. Etiology: Etiology: Hemolytic jaundice::Excessive production of bilirubin due Hemolytic jaundice Excessive production of bilirubin due to abnormally RBCs. to abnormally RBCs. Hepatocellular Jaundice::e.g. Infective hepatitis with wide Hepatocellular Jaundice e.g. Infective hepatitis with wide spread damage of the liver with consequent disorganization spread damage of the liver with consequent disorganization of its structure. of its structure. Extrahepatic (obstructive) Jaundice::Due to obstruction of Extrahepatic (obstructive) Jaundice Due to obstruction of the bile duct system by gall stones or by carcinoma of the the bile duct system by gall stones or by carcinoma of the head of pancreas. head of pancreas.
  46. 46. Jaundice
  47. 47. Hemangioma
  48. 48. Unilateral portwine stain of face  Sturge-Weber syndrome (heamangioma)
  49. 49. Varices (varicositis)
  50. 50. Kaposi Sarcoma
  51. 51. Kaposi Sarcoma Multifocal smooth, red raised neoplasm, characterized by proliferation of blood vessels. Site: head, neck, tip of nose & intra-orally the palate is commonly involved in AIDS patient.
  52. 52. Exogenous Pigmentations Exogenous pigmentations include: Black hairy tongue Tattoo: Amalgam, graphite tattoo. Metallic intoxication: lead, mercury, bismuth.
  53. 53. Black Hairy Tongue
  54. 54. Exogenous pigmentation (1) Amalgam tattoo Etiology Amalgam tattoo is due to iatrogenic factors. For example: Dentist’s bur loaded with small fragment of amalgam particles that accumulate during removal of amalgam may accidentally introduce the metal flecks into the oral mucosa. Metal particles may fall unnoticed into extraction socket. Clinical Features Grey or black macule on gingiva, palate or buccal mucosa. Amalgam tattoo is not harmful so its removal is not required. Biopsy is necessary if the lesion arises at areas distant from any restoration to exclude melanoma
  55. 55. Amalgam Tattoo
  56. 56. (2) Graphite tattoo It is due to traumatic implantation of graphite from lead pencil, commonly seen on palate. The patient may not recall the injury since the event usually occurs during grade school. (3) Metallic intoxication High levels of heavy metals or metal salts may result in metallic intoxication. The exposure of the body to heavy metals may be either: Occupational hazard: as workers in lead factories. Therapeutic hazard: as certain drugs, that contain salts of heavy metals (bismuth, gold, mercury.
  57. 57. Clinical Features Clinical Features Systemic symptoms of toxicity including: Systemic symptoms of toxicity including: Behavioral change. Behavioral change. Intestinal pain. Intestinal pain. Neurological disorder. Neurological disorder. Oral features Oral features Grey to black pigmentation that outlines the Grey to black pigmentation that outlines the gingiva like “eyeliner”. The heavy metal tends gingiva like “eyeliner”. The heavy metal tends to extravasate from vessels in foci of increased to extravasate from vessels in foci of increased ability such as inflamed tissue. Thus the free ability such as inflamed tissue. Thus the free marginal gingiva is the most commonly affected marginal gingiva is the most commonly affected site. site.
  58. 58. Mercurialism
  59. 59. Mercurialism
  60. 60. Lipochrome Pigments

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