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Oral Pigmentation - Clinical Jude

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Oral Pigmentation - Clinical Jude Powered By Docstoc
					 Melanocytes are pigment-producing cells that
  are derived from neural crest cells
 Melanin is formed from tyrosine by the action
  of tyrosinase
 Oral melanin pigmentation ranges from brown
  to black to blue according to the amount of
  melanin production and the depth of the
  pigment.
Etiology
 Congenital or acquired
 Benign or malignant
 Endogenous or exogenous
  Causes of Oral Pigmentation
 Congenital
 Racial (Melanoplakia)
 Naevi
 Peutz-Jegher’s syndrome
 Acquired
 Endocrinopathies
 Metabolic (Hemochromatosis)
 Neoplastic
 Metals
 Food/drugs (oral contraceptives, antimalarials ,
  minocycline tranquilizers)
 AIDS
Benign causes of oral pigmentation
Physiologic pigmentation
Ephelides
Lentigo
Oral melanotic macule
Smoking melanosis
Intraoral nevi
Malignant causes of oral
pigmentation
Melanoma
Neuroectodermal tumor of infancy
Endogenous causes
Postinflammatoty
 hyperpigmentation
Melanoacanthoma
Addison’s syndrome
Peutz- Jegher’s syndrome
Laugier-Hunziker syndrome
Exogenous
Drugs
Amalgam tattoos
Cultural or medical tattooing
Jailhouse tattoo
Heavy metals
  Racial pigmentation
 Results from increased amount of melanin
  pigmentation
 Usually in Blacks and Asians, but also
  Mediterranean littoral
 May be present in white descendents
 Usually involves the gingivae (attached), but can
  affect other oral sites
 Variable colour and extent
 Asymptomatic
Racial pigmentation
Differential diagnosis:
Addison’s disease
Albright’s Syndrome
Heavy metal pigmentation
Use of antimalarial drugs
Ephelides
 Ephelides are sun-induced freckles
  that are most commonly seen in very
  fair-skinned individuals, especially
  those with red or auburn hair.
 They occur most frequently in
  childhood, and tend to reduce in
  number with age.
  Lentigo
 Solar lentigos, in contrast to ephelides are more
  common in older individuals and persist indefinitely.
 They are common on the face and may be seen in the
  perioral region.
 They range in size from 2 mm to 2 cm and are usually
  tan to dark brown in colour.
 Variation in colour or irregularity of outline should raise
  the suspicion of lentigo maligna and is an indication
  for histological evaluation.
Naevi
They are seen in mostly young
 people between the ages of 20 and
 39 years.
Sixty per cent are intradermal
 naevi and approximately 25% are
 blue naevi.
Naevi
Usually elevated
Palate is commonly affected
 site
Less than 1cm diameter
Not premalignant
Naevus of Ota

an acquired oculodermal
 melanocytosis involving the skin of
 the face, the eyes and mucous
 membranes.
It is most common in Japan,
 appearing usually in female
 patients in early adult life.
  Melanoacanthoma
 Rare
 Usually a feature of blacks
 Aetiology unclear but probably secondary to
  physical trauma
 Areas of melanotic hyperpigmentation, typically
  beneath a denture
 They present as slightly elevated circumscribed
  solitary asymptomatic pigmented plaques.
 Melanoacanthomas have been reported to occur
  on buccal, palatal and gingival mucosa.
 Requires to be differentiated from Addison’s
  disease
 No premalignant potential
Endocrinopathies causing oral
pigmentation
Addison’s disease
Nelson’s syndrome
Ectopic ACTH production
Pregnancy
Addisonian pigmentation
 May arise with any cause of adrenocortical
  hypofunction (autoimmune, infection,
  tumour)
 Typically involves the buccal mucosa
 May be the only clinical features of
  adrenocortical hypofunction
 The pigmentation is secondary to increased
  ACTH production by the anterior pituitary
 Addisonian pigmentation
Pigmentation is not specific to
 Addison’s however if associated with
 candidal infection, endocrine studies
 should be performed
Brown or black color is seen in more
 than 75% of Addison’s patients
Nelson’s syndrome
 Rare
 Excess ACTH production and pituitary
  expansion secondary to bilateral
  adrenalectomy for Cushing’s disease.
 10% develop oral pigmentation
 Oral pigmentation like Addison’s
  disease
Ectopic ACTH production
 Rare
 Excess ACTH production by bronchial
  adenocarcinoma
 Oral hypermelanotic pigmentation
  similar to Addison’s disease, but
  possible additional involvement of the
  soft palatal mucosa
 Chloasma
Feature of late pregnancy
Manifests as melanotic
 hyperpigmentation of the midface
Involvement of the oral mucosa is
 extremely rare
Albright’s (McCune-Albright)
syndrome
 Rare
 Polyostotic fibrous dysplasia, sexual
  precosity, cutaneous
  hyperpigmentation, occasional other
  endocrinopathies
 Possible melanotic hyperpigmentation
  of the oral mucosa (in addition to
  unilateral or bilateral fibrous
Haemochromatosis
 Autosomal recessive
 Mechanism of iron overload not clear
 Iron deposition in hepatocytes
 More commom in males (female
  menstruation will lessen the iron load)
 Usually does not present clinically
  until the 5th decade
Haemochromatosis
Investigations:
Elevated serum iron,
 reduced TIBC, elevated
 ferritin
Iron in hepatocytes of biopsy
Thalassemia
Patients may have a dusky-brown
 complexion - reflects iron
 accumulation post-transfusion
Rarely there may be melanotic
 pigmentation of the oral mucosa
 and gingivae
 Melanoacanthoma
 Pigmentary incontinence
 Uncommon
 Usually arises in late age in association
  with oral lichen planus
 Patients are often tobacco smokers
 Areas of melanotic pigmentation in site of
  present or past lichen planus
 Asymptomatic
 Exclude Addison’s disease
 Smoker’s Melanosis
Drug-induced oral mucosal
pigmentation
Colours can be blue, brown, black,
 grey, green
Drug-induced oral mucosal
pigmentation
   Blue
   Amiodarone
   Antimalarials
   Bismuth (overdose)
   Mepacrine
   Minocycline
   Quinidine
   Silver
   Sulphasalazine
Drug-induced oral mucosal
pigmentation
                 Brown               HRT
               Betal nut     Ketoconazole
              Busulphan           Menthol
            Clofazimine       Minocycline
     Oral contraceptives    Pholphthalein
     Cyclophosphamide          Propanolol
            Doxorubicin        Zidovudine
            Doxycycline
            Fluorouracil
                   HRT
                 Heroin
Drug-induced oral mucosal
pigmentation
Black
Amiodaquine
Betal nut
Methyldopa
Drug-induced oral mucosal
pigmentation
 Green
 Copper

   Grey
   Amiodiaquine
   Chloroquine
   Fluoxetine
   Hydroxycholoquine
   Lead
   Silver
   Tin/zinc
Local causes of oral pigmentation
 Ecchymoses
 Ephelis
 Melanoma and other malignancies
 Melanoacanthoma
 Naevus
 Melanotic macule
 Tattoos (amalgam, ink, graphite etc)
Local causes of oral pigmentation -
melanotic macules
Brown or black
Usually affect lips or gingivae
Arise at any age
Not premalignant
 Oral Melanotic Macule
 - tattoos
 Caused by intentional or accidental implantation of
  exogenous pigments into the mucosa
 Amalgam tattoo or focal argyrosis is the most common
  and appears as blue-black, non-elevated discoloration
  that is usually irregular in shape and variable in size.
 Deterioration of the silver compounds of the amalgam
  impart the characteristic color of the lesion
 Can affect any where but the favorable site is the
  gingiva.
 The clinical diagnosis can be confirmed by radiography
  otherwise failure of radiographic evidence necessitates
  biopsy to rule out more serious lesions
tattoos
Other tattoos include graphite
 pencil wounds and India ink
 tattoos
Can reflect ritual (eg gingivae, lips)
May reflect lifestyle
Harmless
 Amalgam Tattoo
Local causes of oral pigmentation -
bacillary angiomatosis
 Rare
 Usually a feature of HIV disease
 Caused by Bartonella quintana or
  Bartonella henselae
 Gives rise to pigmented nodules
 Can affect the skin, bone and liver
 Responds to erythromycin
  Local causes of oral pigmentation -
  malignant melanoma
 Oral disease is rare
 Male:female ratio=2:1
 Mostly in persons>50 years of age
 Often affects the palate, mainly maxillary alveolar ridge,
  anterior gingiva and labial mucosa, but can involve
  other oral sites
 Oral lesions may be primary or secondary tumours
 Localised brown or black macule, papule, or nodule,
  often with ulceration and destruction. Rarely lesions
  may spread superficially
  malignant melanoma
 Early recognizable signs: asymmetric lesion,
  border irregularity, color variation, and diameter
  enlarging
 Late signs: bleeding and ulceration, firmness on
  palpation and rock-hard regional lymph nodes
 Early diagnosis when tumors are less than 1.5
  mm in diameter and complete resection are
  critical to long term survival.
 Poor outcome likely
 Malignant Melanoma
 Ephelis (Freckle)
 Light to dark-brown macule on the lip due
  to exposure to light
 Remains unchanged in size but may darken
 Has predilection to light-skinned or red-
  headed persons
Investigation of oral pigmentation
 History of present complaint
 Medical history - hypoadrenocorticism, pulmonary
  disease, drug history etc
 Social history - tobacco or betel nut habit? ethnicity?
 Extra-oral examination - evidence of cutaneous disease etc
 Intra-oral examination - localised or generalised ?
 Blood pressure
 Serum electrolytes
 24 hour urinary cortisol
 Synacthen test
 Biopsy
Discoloration of teeth
 Extrinisic           Intrinsic
 Smoking              Tetracycline
 Beverages            Fluorosis
 Drugs(iron,          Amelogenesis
  chlorehexidine,       imperfecta
  minocycline)         Kernicterus
 Poor oral hygiene    Porphyria
 Betel chewing

				
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posted:8/5/2014
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