Pigmented lesions Flashcards
Sources of pigment (4)
Melanin (majority)
Haemosiderin
Amalgam or heavy metals
Chromogenic bacteria
Haemosiderin (3)
Breakdown product from RBCs
Iron stored
Brown
Melanin (3)
Produced by melanocytes (or nevus cells)
Found in basal third of epithelium
Black/brown
How is melanin transferred to adjacent keratinocytes? (2)
Via membrane-bound organelles called melanosomes
Amalgam and heavy metals (4)
Heavy metals include lead, bismuth, mercury, silver, arsenic and gold
May directly leach into mucosa from dental restoration and crowns
Deposited due to drugs containing heavy metals e.g. Pepto-bismol
Work or home environment
Sources of occupational exposure (2)
Manufacture of: Ammunition, dental x-ray films, plumbing, ceramic glazes.
Jobs: Lead miners, plumbers, mechanics, glass manufacturers, construction workers, welding, processing of ore, production of paints and pigments.
Chromogenic bacteria (4)
Bacteria that produce pigment
Aspergillus and Actinomyces
Often seen in hairy tongue
Bacterial enzymes act on iron in saliva
Exogenous oral pigmented lesions (4)
Amalgam tattoo
Foreign body tattoo
Heavy metal (occupation or drugs)
Black hairy tongue (bacteria)
Developmental endogenous oral pigmented lesions (4)
Physiological (melanin)
Peutz Jehger’s syndrome (melanin)
Haemochromatosis (haemosiderin)
Pigmented naevus (melanin)
Acquired endogenous oral pigmented lesions (5)
Addison’s disease (melanin) Drug induced (melanin) Post inflammatory (melanin) Smoker’s melanosis (melanin) Melanotic macule (melanin)
Neoplastic oral pigmented lesions (1)
Melanoma (melanin)
Types of endogenous oral pigmented lesions (3)
Developmental
Acquired
Neoplastic
Black hairy tongue (4)
Affects posterior dorsal tongue
Decrease in normal desquamation process – associated with soft diet, smoking, antibiotic use
Elongated filiform papillae – can be black, brown, white
Discolouration caused by chromogenic bacteria, chlorhexidine, foods, smoking
Peutz-Jeghers (4)
Genetic disorder - autosomal dominant
Pigmented mucocutaneous macules, GI polyps, usually small intestine with normal increased risk of malignant change associated with polyps
Melanotic spots characteristically small and multiple
Very obvious around the lips
Histological features of endogenous pigmentation (1)
Increase in amount of melanin
Haemochromatosis (6)
Genetic disorder – autosomal recessive
Accelerated rate of intestinal iron absorption
Raised serum ferritin and transferrin saturation
Accumulation of iron (as haemosiderin)
Leads to ‘bronze’ skin pigmentation, liver cirrhosis, diabetes mellitus
Treated with regular venesection
What is melanin synthesised by? (3)
Nevus cells which are derived from the neural crest
Found in the skin and mucosa
Histological types of nevus (3)
Many
Junctional (epithelium)
Intradermal/ mucosal (CT)
Compound (both)
Addison’s disease (5)
Destruction of entire adrenal cortex
Approx. 90% of cases in UK caused by autoimmune disease
Lack of adrenocortical hormone:
= production of adrenocorticotropic hormone (ACTH) by the anterior pituitary gland.
ACTH induces melanocyte-stimulating hormone:
= pigmentation of the skin and oral mucosa
Diffuse brown patches on the buccal mucosa, palate and tongue and gingivae. Extraoral sites – palmar creases, new scars
Drugs associated with pigmentation (many)
Antimalarials: quinacrine, chloroquine, hydroxychloroquine Quinidine Zidovudine (AZT) Tetracycline Minocycline Chlorpromazine Oral contraceptives Clofazimine Ketoconazole Amiodarone Busulfan Doxorubicin Bleomycin Cyclophosphamide
Reasons for pigmentation (1)
Melanin can drop into lamina propria
Malignant melanoma (10)
<1% of all oral malignancies
Proliferation of malignant melanocytes along the junction between the epithelial and connective tissues, as well as within the connective tissue
Palate
4th - 7th decade
Men > women
Asymptomatic, slow-growing brown or black patch with asymmetric and irregular borders VS rapidly enlarging mass associated with ulceration, bleeding, pain and bone destruction
Some are non-pigmented (amelanotic)
Aggressive and often fatal disease (worse prognosis than skin lesions)
Treatment: radical surgical excision with clear margins. Radiation and chemotherapy are ineffective, which adds to the difficulties associated with management of this malignancy
Overall 5-year survival rate:15%