Pigmented Lesions Flashcards
Lesions with sunburst appearance?
- chondrosarcoma
- osteosarcoma
- melanotic neuroectodermal tumor
Melanophores
Melanophores are macrophages engulfing the extruded extra-cellular melanin (DOPA
negative).
Types of nevi
1- Keratotic nevi → white spongy nevus.
2- Vascular nevi → hemangioma and lymphangloma.
3- Pigmented nevi or melanotic nevi.
How are nevus cells different from melanocytes
Nevus cells differ from melanocytes in that they are usually smaller size, without dendrites, arranged in groups and are less metabolically active. Indistinct cell border Small uniform nucleus Moderate cytoplasm Melanin may be found
Site of aquired melanotic nevus
- Site:
- Extraoral:
Skin above waist.
ii. Intraoral:
Head & neck are common sites..
Uncommon in oral cavity.
Mainly in palate & buccal mucosa & gingiva.
Nodular melanoma
Dark pigmented elevations
Skin & mucous membrane.
Vertical growth pattern.
Superficial spreading melanoma
The most common type (70%). o Well defined, slightly elevated, pigmented patch.
In interscapular area in males & back of legs in females.
Radial growth phase for several years then vertical growth phase.
Lentigomaligna
Slowly expanding macule with irregular borders.
o Variety of colors as tan, brown, black or white.
Sun exposed skin of midface of old
age.
Radial growth phase 25 years, so prognosis is excellent until it enters the vertical growth phase leading to metastases and so poor
prognosis.
Acral lentigous
Most common type of oral melanoma.
• Orally in blacks in hard palate, gingiva, alveolar mucosa.
o Skin (palms of hands & soles of feet).
Radial then vertical growth pattern.
Melanoma Prognosis depends on
Prognosis depends on: o Histopathologic picture.
Depth of tumor invasion (Breslow depth & Clarck’s level).
Oral Lesions are usually of great thickness and so more advanced at the time of biopsy. o Poor prognosis of oral lesion is related to late recognition and difficulty of treatment in the oral
cavity. Clinical stage (metastasis):
Stage 1 → no metastasis (5 years survival rate 89% ).
- Stage II →→nodal metastasis (5 years survival rate 61%). “Stage III → disseminated tumor (5 years survival rate 0% ).
Overall 10 years survival rate 79%. Site → some sites have worse prognosis as:
Interscapular area of back. Posterior upper arm.
Posterior and lateral neck.
Scalp.
Oral lesions.
o Age → better prognosis for patients < 50 years. o Sex→ better prognosis in females.
Melanoma spread
Local → limited.
Lymphatic→→ to the regional lymph nodes.
Blood spread to the lung and then every other organ in the body. Melanin pigment may reach the blood (melanaemia) and excreted in urine
Ttt of melanoma
Treatment:
D Surgical removal with:
1 cm safety margin for early lesions.
3-5 cm safety margin for large invasive lesions.
o Removal of regional lymph nodes for lesions with histopathologic depth of invasion more than 1.24mm
o Radiotherapy & chemotherapy are ineffective.
Origin of melanotic neuroectodermal tumor
Origin:
o It arises from primitive pigment producing cells from neural crest. o The neural crest origin was confirmed by that almost all patients show an
elevated level of vannillymandelic acid (VMA) in urine. o Vanillylmandelic acid is the major urinary metabolite of nor epinephrine and epinephrine
Other names explained in melanotic neuroectodermal tumor
At one time the tumor was thought to arise from remnants of odontogenic tissues and named (melanoamelobastoma).
The term progonoma means a nodule or mass resulting from displacement of tissue which occurs in embryonic development.
Clinical of melanotic neuroectodermal tumor
- Age first year of life. 2. Sitemaxilla > mandible.
- Painless, darkly expanding pigmented mass
- Slow or rapid growth.
Histology of melanotic neuroectodermal tumor
Biphasic cell tumor i.e. consists of large pigmented and small non-pigmented cells in a connective CT
tissue stroma.
o Large pigmented cells (flat or cuboidal with
large pale nuclei with prominent nucleoli and filled with melanin granules).
O Arranged in solid masses or lining cleft like
spaces.
o Small non-pigmented cells are rounded (with. large hyperchromatic nuclei with scanty
cytoplasm).
o Forming small groups either in the stroma or
in the spaces lined by the pigmented cells.
Xray of melanotic neuroectodermal tumor
oil or well defined radiolucency which may contain developing teeth.
o May have sunburst appearance (as osteosarcoma and
chondrosarcoma).
Ttt of melanotic neuroectodermal tumor
Although, the tumor is non encapsulated, conservative excision is
usually curative.
o Irradiation is contraindicated.
o 6% show malignant transformation resulting in metastasis and death.
Physiological pigmentation
Any age and in any location but the gingiva is the most common site. - Lesions are symmetric and persistent.
- It is due to increased melanocytes activity.
Vitiligo
Melanocytesdisappear from affected tissue → depigmentation process.
- The cause is unknown, although stress, trauma, chemicals, hormonal changes, and ultraviolet light are all possible precipitating factors.
- It appears as white areas with hyperpigmented margin.
- It arises in oral and perioral tissues, face, neck, knees and elbows are the most common areas.
Oral melanotic macule
- It is a term used clinically to describe a focal pigmentation that may be one of
several conditions (idiopathic pigmentation, intraoral lentigo, Addison’s
syndrome, Peutz -Jegher syndrome).
-They usually occur on the vermilion border of lips or gingival or on any mucosal surface.
Drug related discolorations of the oral mucosa
- Tetracycline & clotrimazole.
- Anti-malarial drugs (chloroquine & hydroxychloroquine).
- Tranquilizer.
- Drugs for AIDS.
Heavy metal pigmentation
Site → on gingiva gray or blue or black lines of pigmentation which follow the gingival contour (around the neck of teeth) due to reaction of heavy metal and hydrogen sulphide in the inflamed gingiva.
• Metals as:
Bismuth, Arsenic & gold were used for treatment of
several diseases in the past.
Lead, paint industry.
Mercury & silver are used in dental offices.
Heavy metal pigmentation Due to environmental, occupational exposure or therapeutic
administration.
- Site → on gingiva gray or blue or black lines of pigmentation which follow the gingival contour (around the neck of teeth) due to reaction of heavy metal and hydrogen sulphide in the inflamed gingiva.
- Metals as:
Bismuth, Arsenic & gold were used for treatment of
several diseases in the past.
Lead, paint industry.
Mercury & silver are used in dental offices.
Histology site and fate of amalgam tattoo
Site most common site is mandibular gingiva.
H/P:
o Brownish black granule, solid fragments of variable sizes.
o Usually found near collagen fibers, fibroblasts and around blood vessels.
Mild inflammatory reaction showing macrophages, Lymphocytes & giant cells.
• Fate:
o Amalgam is slowly eroded.
o Mercury and tin are lost leaving silver residues.
Smoking associated melanosis
Increase mucosal pigmentation is related to a tobacco component which stimulates melanocytes
-Anterior labial gingiva is the most common site while the palate and buccal
mucosa are more commonly affected in pipe smokers.
-Female sex hormones are also related since females taking contraceptive
pills are more affected than males.
Cafe au lait
Related to diseases like
Neurofibromatosis
Albright syndrome
Occurring alone
Ephelis
- Small brown macules which appear in childhood on sun exposed skin (face, hands legs lip and cheek
Lentigo
(Age spots) these are brown maculae of skin associated with aging and sun
exposure.
Rare in oral mucosa
