1. Seborrheic Keratosis
    • • Extremely common skin lesion of older people and represents an acquired, benign proliferation of epidermal basal cells.
    • • Unknown cause, but + correlation w/ chronic sun exposure
    • o Sometimes hereditary (auto dom) tendency
    • • Somatic mutations in FGFR3 are important in the development of these lesions.
    • • Lesions do NOT occur in the mouth.
    • • Clinical Features
    • o Begin to develop on the skin of the face, trunk, and extremities during 4th decade of life.
    • • Become more prevalent with age
    • o Lesions are usually multiple, beginning as small tan to brown macules that are indistinguishable clinically from actinic lentigines, and which gradually enlarge and elevate.
    • o Individual lesions are sharply demarcated plaques and have surfaces that are finely fissured, pitted, or verrucous, but may be smooth.
    • o Tend to appear stuck onto the skin and are usually less than 2 cm in diameter.
    • o Dermatoses papulosa nigra – form of seborrheic keratosis that occurs in black people.
    • • Has autosomal dominant inheritance pattern
    • • Appears as multiple small black papules scattered about the zygomatic and periorbital region.
    • • Histo
    • o Acanthotic form – considerable acanthosis, surface hyperkeratosis, numerous pseudocysts.
    • o Epidermal proliferation extends upward, above the normal epidermal surface.
    • o Pseudocysts are actually keratin filled invaginations.
    • • Tx and Prognosis
    • o Seldom removed except for aesthetic purposes.
    • o Methods of removal:
    • • Cryotherapy w/ liquid nitrogen
    • • Curettage
    • o Other more significant skin lesions may develop in areas contiguous to it.
    • o In rare cases, melanomas may resemble seborrheic keratoses clinically.
    • o Leser-Trelat sign – sudden appearance of numerous seborrheic keratoses with pruritus associated w/ internal malignancy.
  2. Ephelis (plural: ephelides; lay term: freckle)
    • • Common small hyperpigmented macule of the skin that represents a region of increased melanin production.
    • • Seen most often on the face, arms, and back.
    • • Usually occurs in fair-skinned, blue-eyed, red or light-blond haired persons.
    • • May be associated w/ a strong genetic predilection (autosom dom).
    • o Variants of MC1R gene
    • • Skin discoloration produced by a relative excess of melanin deposition in the epidermis, not by a local increase in the number of melanocytes.
    • • Clinical Features
    • o Become noticeable during the first decade of life. New macules seldom arise after teenage years.
    • o Macules become less prominent during adult life. No sex predilection.
    • o Lesions become more pronounced after sun exposure and are associated closely w/ a history of painful sunburns in childhood.
    • o Macules are round or oval, and remain less than 3 mm in diameter.
    • o Have uniform light-brown coloration and are sharply demarcated from the surrounding skin.
    • o Brown color is not as dark as lentigo, and there is never elevation above the surface of the skin.
    • • Histo
    • o Stratified squamous epithelium w/ abundant melanin deposition in the basal cell layer.
    • o Number of melanocytes is normal, or may be somewhat reduced.
    • o No elongation of rete ridges.
    • • Tx and Prognosis
    • o None necessary. Use sunscreens to prevent new freckles and darkening of old ones.
  3. Actinic Lentigo
    • • Benign brown macule that results from chronic UV light damage to the skin. Rarely seen before 40 yo.
    • • Does not occur w/in the mouth, but is frequently seen on the facial skin.
    • • Pts who have ephelides are more likely to develop actinic lentigines.
    • • Clinical Features
    • o Common on the dorsa of the hands, on the face, and on the arms of older white people.
    • o Typically multiple, but individual lesions appear as uniformly pigmented brown to tan macules w/ well-demarcated but irregular borders.
    • o Adjacent lesions may coalesce, and new ones continuously arise w/ age.
    • o No change in color intensity is seen after exposure to UV light.
    • • Tx and Prognosis
    • o None required, except for aesthetic reasons.
    • o Methods
    • • Cryotherapy – hypopigmentation is a side effect
    • • Laser therapy/intense pulsed light
    • • Topical therapy
    • o Sunscreens recommended as preventive tx and for maintenance of tx success.
    • o Does not undergo malignant transformation. Rarely recurs if removed.
    • o New lesions can arise in adjacent or distant skin at any time.
  4. Lentigo Simplex (singular: lentigo. Plural: lentigines)
    • • Benign Cutaneous melanocytic hyperplasia of unknown cause.
    • • Usually occurs on the skin that is not exposed to sunlight, but it may occur on any skin surface and at any age.
    • • Color intensity does not change with variations in sun exposure.
    • • Darker in color than ephelis. May represent earliest stage of melanocytic nevus.
    • • They are generally darker and larger (3-5mm in diameter) than freckles. Usually, they are single rather than in groups like freckles
    • • Clinical Features
    • o Usually occurs in children, but may occur at any age.
    • o Lesion is sharply demarcated macule w/ uniformly tan to dark-brown color.
    • o Usually solitary, although some patients may have several lesions scattered on the skin of the trunk and extremities.
    • o Can be associated w/ Peutz-Jeghers Syndrome
    • • Characterized by freckle-like lesions of the hands, perioral skin, and oral mucosa, in conjunction w/ intestinal polyposis and predisposition for affected pts to develop cancer.
    • • Syndrome is inherited as an autosomal dominant trait.
    • • Circumoral lentigines
    • • Benign bowel polyps
    • • Pts have slight increase in malignancy of breast and other organs.
    • • Clinical Features
    • • Skin lesions usually develop early in childhood, and involve the periorifacial areas. Skin of extremities is also usually affected.
    • • Lesions resemble freckles, but they do not wax and wane w/ sun exposure.
    • • Intestinal polyps are scattered throughout the mucus-producing areas of the GI Tract [jejunum and ileum are most commonly affected].
    • • GI adenocarcinoma develops in a large percentage of affected patients.
    • • Oral lesions represent an extension of the perioral freckling. Primarily affect the vermilion zone, the labial and buccal mucosa, and the tongue.
    • • Some degree of fading of the pigmented lesions may be noted during adolescence.
    • • Histo
    • • Polyps do not show atypia
    • • Tx and Prognosis
    • • Should be monitored for development of intussesception [telescoping of a proximal segment of the bowel into a distal portion] or tumor formation.
    • • Histo
    • o Increased # of benign melanocytes w/in the basal layer of the epidermis, and these often are clustered at the tips of the rete ridges.
    • o Abundant melanin is distributed among the melanocytes and basal keratinocytes, as well as w/in the papillary dermis in association w/ melanophages [melanin incontinence].
    • • Tx and Prognosis
    • o May fade spontaneously after many years, but most lesions remain constant over time.
    • o Tx not required, except for aesthetics.
    • o Conservative surgical excision is curative, and no malignant transformation potential has been documented for lesions not removed.
  5. Café-au-lait Macule (“Spot”)
    • • Background
    • o Flat brown macules generally >1.5cm in diameter. Present in about 10% of normal individuals. Six or more constitute a presumptive diagnosis of neurofibromatosis
    • • Additional notes - Similar lesions are seen in Albright Syndrome. Rarely described in oral cavity
  6. Melasma
    • • Acquired, symmetrical hyperpigmentation of the sunexposed skin of the face and neck. Unknown cause.
    • • Associated w/ pregnancy. Exposure to exogenous estrogen and progesterone in the form of either oral contraceptives or hormone replacement therapy may cause it.
    • • Dark complexioned persons are more likely to develop this condition.
    • • Causes include: 1) genetic predisposition; more than 30% of patients have a family history of melasma. 2) Exposure to sunlight; sunscreens that primarily block UV-B radiation (290-320 nm) are unsatisfactory because longer wavelengths (UV-A and visible radiation, 320-700 nm) also stimulate melanocytes to produce melanin. 3) Hormonal influences, “mask of pregnancy”: the exact mechanism of this is unknown; estrogen, progesterone, and MSH are elevated in late pregnancy and estrogen & progesterone are included in birth-control pills. However this also occurs in patients who are nulliparous and have normal hormone levels
    • • Melasma is the most common cause of uncircumscribed, flat, facial pigmentation.
    • • The excess melanin can be visually localized to the epidermis or the dermis by use of a Wood lamp (wavelength, 340-400 nm).
    • • Epidermal pigment is enhanced during examination with a Wood light, whereas, dermal pigment is not.
    • • Clinically, a large amount of dermal melanin is suspected if the hyperpigmentation is bluish black.
    • • * In individuals with dark brown skin, examination with a Wood light does not localize pigment, and these patients are thus classified as indeterminate
    • • Clinical Features
    • o Bilateral light to dark brown Cutaneous macules that vary in size.
    • o Lesions develop slowly with sun exposure and occur primarily on the midface, forehead, upper lip, chin, and the arms.
    • o Common for the entire face to be involved.
    • o Pigmentation may remain faint or darken over time.
    • o Rarely seen in men.
    • • Histo
    • o Increased melanin deposition within an otherwise unremarkable epidermis.
    • o Pigment may be seen w/in numerous melanophages in the dermis.
    • • Tx and prognosis
    • o Difficult to treat.
    • o First line therapy: triple combination of topical therapy.
    • • Can also use dual combo therapy, or single topical agents.
    • o 2nd line therapy: glycolic acid chemical peel, laser therapy, dermabrasion.
    • o Lesions may resolve after parturition or after discontinuing oral contraceptives.
    • o There is no potential for malignant transformation.
  7. Oral Melanotic Macule
    • • Flat, brown, mucosal discoloration produced by a focal increase in melanin deposition and possibly a concomitant increase in the number of melanocytes. Cause is unclear.
    • • Not dependent on sun exposure. Commonly seen.
    • • Clinical Features
    • o Small, uniformly pigmented brown macule
    • o Well-demarcated
    • o Occurs on gingival mucosa or on lip vermilion.
    • • Histo
    • o Characterized by an increase in melanin (and melanocytes) in the basal and parabasal layers of an otherwise normal stratified squamous epithelium.
    • o Melanin may be seen free or within melanophages in the subepithelial CT [melanin incontinence].
    • • Tx and Prognosis
    • o Tx usually not required, except for aesthetic considerations.
    • o Excisional biopsy is preferred treatment.
    • o Other methods: electrocautery, laser ablation, cryosurgery. [no tissue remains for exam]
    • o The intraoral melanotic macule has no malignant transformation potential, but an early melanoma can have a similar clinical appearance.
    • o All oral pigmented macules of recent onset, large size, irregular pigmentation, unknown duration, or recent enlargement should be examined.
    • o Sometimes, flat pigmented lesions are encountered that are clinically and microscopically similar to the melanotic macule. These lesions represent a sign of systemic or genetic disease, or may be a consequence of the use of certain meds.
  8. Oral Melanoacanthoma
    • • Melanoacanthoma is uncommon, but represents an oft-times alarming situation when it is encountered. Small emphasis, not no emphasis
    • • Clinical features
    • o Seen exclusively in blacks, female predilection, and is most common during the 3rd and 4th decades of life.
    • o Smooth, darkly pigmented macule of the buccal mucosa that enlarges dramatically.
    • • Tx and Prognosis
    • o Alarming growth rate. Incisional biopsy is indicated to rule out the possibility of melanoma.
  9. Acquired Melanocytic Nevi
    • • Background: aka Mole. Generic term nevus refers to malformations of the skin that are congenital or developmental in nature. Nevi may arise from the surface epithelium or any of a variety of underlying CT. the most commonly recognized nevus is the AMN (mole) – so much so that the term nevus is often used synonymously for these pigmented lesions. However, many other development nevi also are recognized. AMN represents a benign, localized proliferation of cells from the neural crest, often called nevus cells. Although there is little debate as to their neural crest origin and their ability to produce melanin, various authorities are divided on the issue on whether these cells represent melanocytes or are merely ‘first cousins’ of melanocytes. These melanocytic cells migrate to the epidermis during development, and lesions appear shortly after birth. The acquired melanocytic nevus is probably the most common of all human ‘tumors’ and white adults have an avg of 10-40 cutaneous nevi/person. Intraoral lesions occur but are not common.
    • • Clinical Features: Acquired melanocytic nevi begin to develop on the skin during childhood, and most cutaneous lesions are present before 35yo. Racial differences are seen. Most lesions are distributed above the waist, and the head and neck region is a common site of involvement. AMN evolves thru several clinical stages, which tend to correlate with specific histopthological features. The earliest presentation (known microscopically as junctional nevus) is that of a sharply demarcated, brown or black macule, typically less than 6mm in diameter. Although this lesional appearance may persist into adulthood, more often the nevus cells proliferate over a period of years to produce a slightly elevated, soft papule with a relatively smooth surface (compound nevus). The degree of pigmentation becomes less; most lesions appear brown or tan. Throughout the adult years, many acquire MN will involute and disappear; therefore fewer of these lesions can be detected in older persons.
    • • Firuges:
    • • 10-48. Nests of melanocytic nevus cells along the basal layer of the epithelium.
    • • 10-49. High power view showing nests of pigmented nevus cells within the epithelium and the superficial lamina propria.
    • • 10-50. Collections of melanocytic nevus cells within the lamina propria.
  10. Congenital Melanocytic Nevus
    • • Affects 1% of newborns in the US.
    • • Clinical Features
    • o Similar in appearance to an acquired melanocytic nevus, but is frequently larger in diameter.
    • o Lesions show hypertrichosis [excess hair] – could turn into a giant hairy nevus.
    • o Larger lesion appears as brown to black plaque, usually with a rough surface or multiple nodular areas.
    • o Clinical appearance often changes with time: early lesions are flat and light tan, becoming elevated, rougher, and darker with age.
    • • Histo
    • o Similar to that of the acquired melanocytic nevus, and some small congenital nevi cannot be distinguished microscopically from the acquired nevus.
    • o Characterized by benign, unencapsulated proliferation of small, ovoid cells (nevus cells).
    • • Tx and Prognosis
    • o Many are excised for aesthetic purposes.
    • o 3-15% of large congenital nevi may undergo malignant transformation into melanoma.
  11. Halo Nevus
    • • Melanocytic nevus w/ a pale hypopigmented border/Halo of the surrounding epithelium.
    • o Could be a result of nevus cell destruction by the immune system.
    • o Halo develops b/c the immune cells also attack the melanocytes adjacent to the nevus.
    • o Cause of immune attack is unknown, but regression of the nevus usually results.
    • o Development of multiple halo nevi has been seen in pts w/ recent excision of melanoma.
    • • Clinical features
    • o Isolated, associated w/ preexisting acquired melanocytic nevus.
    • o Most common on the skin of the trunk during the 2nd decade of life.
    • o Typically appears as a central pigmented papule or macule, surrounded by a uniform zone of hypopigmentation.
    • • Tx and Prognosis
    • o Tx not required, because it eventually will regress entirely.
    • o If tx is called for, then conservative surgical removal is curative and recurrence is unlikely.
  12. Blue Nevus
    • • The blue color of this melanin-producing lesion can be explained by the Tyndall effect – relates to the interaction of light with particles in a colloidal suspension.
    • • Melanin particles are deep to the surface, so that the light reflected back has to pass through the overlying tissue.
    • • Colors w/ long wavelengths (red and yellows) tend to be more readily absorbed by the tissues; the short wavelength blue light is more likely to be reflected back to the observer’s eyes.
    • • Clinical features
    • o Well circumscribed, deep-blue macular lesion
    • • Histo
    • o Abundant melanin w/in spindle-shaped melanocytes located relatively deep w/in the lamina propria and parallel to the surface epithelium.
    • o Heavily pigmented spindle-shaped cells.
    • • Tx and Prognosis
    • o Conservative surgical excision is the tx of choice.
    • o Oral blue nevus can mimic an early melanoma, so it is usually advisable to perform a biopsy of intraoral pigmented lesions, esp b/c of the extremely poor prognosis for oral melanoma.
  13. • Nevus of Ota
    o A hamartoma of dermal melanocytes, which clinically presents as flat blue-black-grey macules in the facial area innervated by div I & II of the trigeminal nerve. Ocular & oral mucosa may be involved. These may represent melanocytes that have not migrated completely from the neural crest to the epidermis. Common in Japan (approx. 0.5%), Also occurs in just about everyone else, but much less common. Most cases have onset in infancy, but a second peak occurs in adolescence. May have association with neurofibromatosis, Nevus of Ito, or Sturge-Weber Syndrome. 90% are unilateral
  14. “Mongolian spot”
    • o congenital; The prevalence varies among different ethnic groups. Most common among Asians (more than 90% of East Asian, Indonesian, Polynesian, Micronesian, Amerindian, & Eskimo infants), reported in 80% of East African children, in 46% of Hispanic children, and in 1-9% of Caucasian children.
    • Again, DO NOT memorize the percentages, the idea here is that many people are born with these
  15. Melanoma
    • • Malignant neoplasm of melanocytic origin that arises from a benign melanocytic lesion or from melanocytes within otherwise normal skin or mucosa.
    • • Most melanomas occur on the skin, but they may develop at any site where melanocytes are present.
    • • Damage from UV radiation is considered a major causative factor, as suggested by the fact that the incidence of melanoma increases for light-complexioned populations as they approach the equator.
    • • Chronic sun exposure does not seem to be as significant as it is for other cancers [BCC and SCC].
    • o Acute sun damage may be of greater causative importance than chronic exposure in melanoma.
    • • Risk of melanoma is higher if a relative has a history of it.
    • o Additional risk factors: fair complexion, light hair, sunburning easily, history of painful or blistering sunburns as a child, indoor occupation w/ outdoor recreational habits, personal history or melanoma, dysplasia, or congenital nevus.
    • • 3rd most common skin cancer, and causes most deaths due to skin cancer.
    • • High proportion of melanomas possess mutations in the gene encoding BRAF, a protein kinase involved in the Ras-Raf-ERK signaling pathway.
    • • Tumors less than 0.75mm in thickness are lethal in less than 5% of patients.
    • • 53,000 per year recently in the USA; 7,000 will die
    • • melanoma-in-situ is effectively treated (cured) with 0.5cm margins
    • • thin melanoma <1.0mm has potential for long-term survival in more than 90% of patients after excision with 1.0cm margins.
    • • “melanoma is now the most common cancer in people aged 25-29” LA Times May 20, 02.
    • • 4% of skin cancer cases and 79% of skin cancer deaths
    • • Clinical Features
    • o ABCDE
    • • Asymmetry – uncontrolled growth pattern
    • • Border irregularity – often w/ notching
    • • Color variegation – varies from shades of brown to black, white, red, and blue
    • • Diameter greater than 6 mm – diameter of a pencil eraser
    • • Evolving – lesions that have changed w/ respect to size, shape, color, surface, symptoms
    • o Superficial Spreading Melanoma
    • • Most common form – 70% of Cutaneous lesions
    • o Nodular Melanoma
    • • 15% of Cutaneous melanomas, and 1/3 of such lesions develop in the head and neck area.
    • • Begins almost immediately in the vertical growth phase, so it typically appears as a nodular elevation that rapidly invades into the connective tissue.
    • • Usually a deeply pigmented exophytic lesion, although sometimes the melanoma cells are so poorly differentiated that they no longer can produce melanin, resulting in a nonpigmented amelanotic melanoma.
  16. o Lentigo Maligna Melanoma
    • • Develops from a lentigo maligna precursor [hutchinson’s freckle]
    • • Occurs on the sun-exposed skin of fair-complexioned older adults.
    • • Lesion appears as a large, slowly expanding macule w/ irregular borders and a variety of colors [tan, brown, black, white].
    • • Lesion slowly expands laterally for years – avg duration of radial growth is 15 years.
    • o Acral Lentiginous Melanoma (Mucosal Lentiginous Melanoma)
    • • Most common form of melanoma in blacks, also the most common form of oral melanoma. Typically develops on the palms of the hands, soles of the feet, subungual area, and mucous membranes.
    • • Histo
    • o Radial growth phase is characterized by the spread of atypical melanocytes along the basilar portion of the epidermis. Individual melanocytes invade the higher levels of the epithelium.
    • o There are numerous atypical melanocytes in the basilar portion of the epithelium with invasion into the superficial lamina propria.
    • • Tx and Prognosis
    • o Measurement of the depth of invasion is important in evaluation of Cutaneous melanoma b/c of its correlation w/ prognosis.
    • • Most accurate prognosis is based on the actual measurement of the distance from the top of the granular cell layer to the deepest identifiable point of tumor invasion.
    • o Sentinal node biopsy [biopsy of the first lymph node in the lymphatic basin to receive drainage from the tumor] is used as an alternative to elective lymph node dissection to identify patients w/ occult nodal metastases who would benefit from total lymphadenectomy.
    • o There is a bad prognosis for patients with disseminated disease.
    • • Areas w/ a worse prognosis: BANS
    • • Interscapular area of the Back
    • • Posterior upper Arm
    • • Posterior and lateral Neck
    • • And Scalp
    • o Prognosis for oral melanoma is extremely Poor.
    • • Immunotherapy
    • • Cytokines: passive administration of immune effectors ( also antibodies, killer cells)
    • • interferon, interleukin-2
    • • Active immunization
    • • stimulate patient’s own effector cells in response to an injected vaccine
    • • * Melanoma vaccines: activation of the immune system takes place in the context of therapy, not prevention, as is the case with infectious diseases
  17. Biology of melanin & melanocytes:
    • Melanin is the major determinant of skin color. Oxyhemoglobin (red), deoxygenated hemoglobin (blue), and carotene (yellow-orange) provide supplementary coloration.
    • Constitutive skin color is genetically determined and is represented by the color of non-sun-exposed skin. Facultative skin color is the exposed skin color observed.
    • Skin Photo Types (SPT) range from type I in which no tanning can occur to type VI where tanning is dramatic and unexposed skin is dark brown-black.
    • Melanin: eumelanin-brown-black; pheomelanin-yellow-red; most melanins are mixtures of eu- and pheo-monomers. Each melanocyte serves about 36 keratinocytes.
    • Tyrosine is synthesized by ribosomes on the rough ER in melanocytes and packaged by the golgi apparatus into membrane-bound vesicles called melanosomes. The tyrosine is later converted by tyrosinase to one of the group of molecules called melanins. The melanosomes then develop (stage II) an oval shape and become recognizable by electron microscopy by virtue of their transverse striations. Deposition of melanin on the melanosome substructure is visible by electron microscopy (Stage III). Finally a uniformly electron-dense granule packed with melanin is produced (stage IV).
    • (The stages I-IV above are provided for understanding only, not for specific testing)
    • Melanocytes: Melanocytes are derived from the neural crest. They migrate during embryologic development to selected ectodermal sites (primarily the skin and the CNS) but also to the eyes and the ears. Ectopic melanocytes have been identified in the gastrointestinal and genitourinary tracts. Melanocytes are found in the basal layer of the epidermis. Melanocytes typically exhibit contact inhibition to each other, and 2 pigment cells are never found as adjacent cells.
  18. Constituative (racial) (a.k.a. physiologic) Pigmentation
    • Individual differences in pigmentation are due to variations in melanosome size, activity, degree of melanization & aggregation in keratinocytes; not differences in number of melanocytes.
    • Tanning: Solar radiation is about 95%UVA and 5% UVB. UVA is the main type in “tanning booths.” The SPF rating on sunscreen often does not cover the longer UVA wavelengths and refers only to the shorter-wavelength “burning” rays (UVB: 290-320nm). UVA rays penetrate more deeply than UVB; they create sunburns as well. UVA rays penetrate further into the dermis, damaging the elastin and collagen.
    • Sunscreen products that block UVA (340-400nm) include zinc oxide (also “micronized zinc oxide” titanium dioxide, and mexoryl)
    • When you tan, you get: immediate darkening of granules already present; new melanin in 2-3 days; UV light causes increased turnover of keratinocytes, therefore increased migration of pigment through the thickness of the epidermis.
    • o Racial pigmentation
    • o Addison’s
    • o Smoker’s melanosis
    • o Drugs
  20. Addison’s disease
    • o Background
    • • Insufficient production of adrenal corticosteroid hormones caused by the destruction of adrenal cortex
    • • Causes
    • • Autoimmune destruction
    • • Infection (TB, fungal, aids)
    • • Rare – metastatic tumors, sarcoidosis, hemochromatosis, amyloidosis
    • • Dysfunction of pituitary resulting in dec level of ACTH
    • o Clinical features
    • • Appear after 90% destruction
    • • Fatigue, irritability, depression, weakness, hypotension
    • • Bronzing – hyperpigmentation, due to ACTH stimulating melanocytes
    • • On sun-exposed skin and pressure points
    • • Oral – diffuse or patchy brown macular pigmentation of mucosa
    • o Tx and prognosis
    • • Management with corticosteroids – before this prognosis was poor
    • • Normal life span
    • • Death if not recognized
    • • Take steroids to account for stressful situations – dental procedures
    • o Melasma – see above
    • o Post-inflammatory hyperpigmentations
  21. Smokers melanosis
    • o Clinical – any mucosal surface but most common on anterior facial gingiva
    • o Tx – quite smoking, disappear over 3 years
    • o Biopsy if on hard palate (unexpected) or if increased melanin density or elevation
  22. Drug related discolorations of oral mucosa
    • o Most = diffuse melanosis, females more
    • • Linear band above the facial attached ginigva
    • • Broad zone of discolor on hard palate common
    • o Interferon alpha and ribovirn for hep c - tounge yellow and blue
    • o Phenolphthalein, minocycline, tranquilizers, antimalarial meds, estrogen, chemo agents, aids tx
    • o Minocycline - for acne - black spots on check caused
    • • Also blue grey teeth
    • o Cutright lesion
    • o Tx – stop drug, no long term effects
  23. Circumscribed hyperpigmentation
    • o Ephelides
    • o blue nevus
    • o Lentigines (lentigo simplex)
    • o Solar (Actinic) Lentigo
    • o Café-au-lait macule
    • o Junctional Nevus
    • o Oral Melanotic Macule
  24. Hypopigmented lesions Vitilgo
    • • Incidence is about 1%; no sex predilection. Onset at any age, most from 10-30 years of age. It has a familial tendency,(“segmental” vitiligo is not familial.) Patients often describe onset after stress, sun exposure, injury, etc. The most prominent current hypothesis is that it is an autoimmune condition.
    • • Thyroid disease is common in these patients (except thyroid carcinoma). Also, diabetes mellitus, Addison’s disease and others have slight increases.
    • • There are no melanocytes present in involved skin
  25. Hypopigmented lesions list:
    • o Vitiligo
    • o Albinism
    • o Chemical leukoderma
    • o Postinflam hypomelanosis – inc pityriasis alba
    • o Pityriasis Tinea vesicolor
  26.  Pityriasis (Tinea) versicolor
    • Hypopigmented lesions
    • o Background
    • • From a fungus, Malassezia furfur which can be found on normal skin as well as clinically affected areas. In patients with clinical disease, the organism is found in both the yeast (spore) stage and the filamentous (hyphal) form. Factors that lead to the conversion of the saprophytic yeast morphologic form to the parasitic, mycelia form include genetic predisposition; warm, humid environments; immunosuppression; malnutrition; and Cushing disease. Not considered contagious because it is a normal inhabitant
    • • Prevalence in the USA is roughly 5%, but may reach 50% in Western Samoa and other hot humid areas. Conversely, the incidence is about 1% in Sweden. Most common in young people aged 15-25. It becomes most obvious in the summer when exposed areas fail to tan
    • o Clinical
    • • Causes scaly skin macules. Affected areas may be hypopigmented or hyperpigmented.
    • • Hypopigmentation can be from tyrosinase or inhibition of an enzyme in the melanin synthesis pathway by dicarboxylic acids formed by oxidation of skin surface lipids
    • o Diagnosis
    • • The diagnosis is usually confirmed by potassium hydroxide (KOH) examination, which involves scraping stratum corneum onto a glass slide and adding the KOH and possibly a stain such as methelyne blue or fluorescent stain which highlights the organisms. This demonstrates the characteristic short, cigar-butt hyphae that are present in the diseased state. The KOH finding of spores with short mycelium has been referred to as the spaghetti and meatballs sign of tinea versicolor
    • o Treatment and prognosis
    • • Oral therapy is often preferred by patients because of convenience. Oral itraconazole and fluconazole have been used as well as ketoconazole. Oral therapy does not prevent the high rate of recurrence. Because tinea versicolor is a benign condition and oral therapy carries known risks, fully informed consent should be obtained. A topical spray form of terbinafine is now available
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