Pigmentation of Oral Mucosa Question And Answers

Pigmented Lesions Of Oral Mucosa Essay Questions

Question 1. Define pigment. Classify the pigmented lesions of oral mucosa and briefly describe the pathophysiology of Addison’s disease pigmentation.
Answer:

• The pigment is a substance that gives a particular color when it is present in something or is added to it.
• Pigmentation is abnormal skin or mucosal coloration due to excess deposition of normal pigments or ectopic pigment deposition.
• Oral pigmentation may be exogenous or endogenous in origin. Exogenous pigmen¬tation is commonly acquired from foodstuffs, tobacco products, and foreign-body implantation in the oral mucosa.
• Endogenous pigments include melanin, hemoglobin, hemosiderin, and carotene.

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Pigmented Lesions Classification:

1. Oral pigmentation is broadly classified into diffuse and focal.

• Diffuse pigmentation:
  • Developmental
    • Racial and physiologic pigmentation
    • Peutz-Jeghers syndrome
  • Predominantly adult onset
    • With systemic signs and symptoms:
    • Addison’s disease
    • Heavy metal pigmentation
    • Kaposi’s sarcoma
  • No systemic signs and symptoms:
    • Drug-induced pigmentation
    • Postinflammatory pigmentation
    • Smoker’s melanosis.
• Focal pigmentation:
  • Red-blue-purple discoloration
    • Hemangioma
    • Varix
    • Thrombus
    • Hematoma
  • Blue-gray discoloration
    • Amalgam tattoo
    • Blue nevus
  • Brown discoloration
    • Melanotic macule
    • Pigmented nevus
    • Melanoacanthoma
    • Melanoma.

2. Classification based on exogenous and endogenous pigmentation.

• Exogenous pigmentation:
  • Silver amalgam
  • Graphite
  • Lead, mercury, and bismuth
  • Chromogenic bacteria.
• Endogenous pigmentation:
  • Hemoglobin
    • Varix
    • Hemangioma
    • Kaposi’s sarcoma
    • Angiosarcoma
    • Hereditary hemorrhagic telangiectasia (HHT)
  • Hemosiderin
    • Ecchymosis
    • Petechia
    • Thrombosed varix
  • Melanin
    • Melanotic macule
    • Nevus
    • Melanoma
  • Carotene
    • Carotenemia.

Pigmentation in Addison’s Disease (Hypo- adrenals):

• Addison’s disease or hypoadrenocorticism is an endocrinopathy disease due to progressive bilateral destruction of the adrenal cortex by autoimmune disease, infection, certain medications or malignancy.
• The destruction results in a decreased level of corticosteroid hormone.

Pigmented Lesions Pathophysiology:

• When there is a decrease in corticosteroid secretion, the anterior pituitary gland is stimulated to increase the production and secretion of adrenocorticotropic hormone (ACTH) which acts on the adrenal cortex to stimulate corticosteroid production.
• This feedback mechanism causes the pituitary to slow ACTH secretion. But when the low corticosteroid levels persist, there is a continual ACTH secretion.
• The alpha-melanocyte-stimulating hormone (a-MSH) gene is also originating from the same host gene that produces ACTH.
• Hence, when serum ACTH levels rise, there is a concomitant rise in a-MSH secretion which directly stimulates melanocytes, increases melanin production and causes diffuse mucocutaneous pigmentation.
• Oral involvement presents as diffuse brown patches on the gingiva, buccal mucosa, palate, and tongue which may resemble physiologic pigmentation.
• Oral mucosal pigmentation is the first sign of Addison’s disease and is usually accompanied by systemic manifestations including weakness, nausea and vomiting, abdominal pain, constipation or diarrhea, weight loss, and hypotension.

Pigmented Lesions Diagnosis: Laboratory tests to assess the level of ACTH, plasma cortisol, and serum electrolytes.

Pigmented Lesions Treatment:

• Addison’s disease can be fatal if left untrea¬ted.
• Management involves treatment of the underlying cause and corticosteroid replacement therapy.

Question 2. Write about the pathogenesis and clinical manifestations of hereditary hemorrhagic telangiectasia.
Answer:

• Hereditary hemorrhagic telangiectasia also known as Rendu-Osler-Weber syndrome is a autosomal dominant disorder.
• Gene mutations lead to multisystem vascular dysplasia and the development of abnormal vascular structures, which may vary from dilated microvessels to arteriovenous malformations (AVMs) of skin, mucosa, and viscera.
• It affects individuals over a wide geographic distribution with an overall occurrence rate of 1/5,000-10,000 persons.

Hereditary hemorrhagic telangiectasia Pathogenesis:

• The clinical presentation of HHT results from abnormalities of vascular structure. Fragile walls and turbulent blood flow make these vessels more prone for hemorrhage than normal vessels.
• The individual lesion is known as telangiectasis. The telangiectasis appears as a 1-2 mm red spot in the skin and disappears upon slight pressure due to a shunt involving both dilated arterioles and venules.
• As the lesion increases in size, the capillary segments disappear and a direct arteriovenous communication is formed.

Hereditary hemorrhagic telangiectasia Clinical Features:

• Telangiectases are most evident on the lips, tongue, buccal mucosa, nasal mucosa, face, and fingers. They appear as pink to red, pinpoint lesions, or occasionally as larger purple lesions.
• It blanch with pressure and then immediately refills and are distinguished from petechiae and angiomata by this blanching property.
• It can rupture and bleed at proximity to the skin surface or to a mucous membrane.
• As the vessel walls are lacking capillaries (contractile elements), bleeding from telangiectases is vigorous and difficult to stop.

Hereditary hemorrhagic telangiectasia Dental Complications:

• Vascular lesions in the brain predispose patients to cerebral abscesses. This condition requires special care during invasive dental procedures.
• Antibiotic prophylaxis is mandatory, especially in treating periodontal infections, and dental abscesses.
• Patients with severe anemia (hemoglobin level <10 mg/dL) have the risk of exacerbation of anemia due to invasive dental treatment and should avoid invasive procedures.

Curacao’s Diagnostic: Criteria for Hereditary Hemorrhagic Telangiectasis

Hereditary hemorrhagic telangiectasia Criteria:

• Spontaneous, recurrent epistaxis. Nocturnal nose bleeds increase the risk for HHT.
• Mucocutaneous telangiectases
• Internal AVM (pulmonary, cerebral, hepatic, gastrointestinal, spinal).
• First-degree relative with HHT according to these criteria.

Hereditary hemorrhagic telangiectasia Diagnosis:

• Definite: Three or more features of Cura-cao.
• Possible: Two features of Curacao’s.
• Unlikely: Less than two features of Curacao’s.

Hereditary hemorrhagic telangiectasia Laboratory Tests:

• Significant changes in red blood cell count— hypochromic anemia with anisocytosis.
• High level of liver enzymes.
• No changes in coagulation.

Hereditary hemorrhagic telangiectasia Management:

• Systemic therapy: Tranexamic acid and antifibrinolytics
• Local ablation:
  • Laser: Argon, neodymium-doped yttrium aluminum garnet (Nd:YAG)
• Cauterization
  • Embolization.

Pigmented Lesions Of Oral Mucosa Viva Voce

Question 1. What is pigmented lichen planus?
Answer:

• An erosive form of lichen planus is occasionally associated with overlying diffuse brown macular foci.
• This pigmentation is due to the direct stimulation of melanocytes by inflammatory mediators (T lymphocytes) and is also caused by an excess of melanin production and deposition within the basal layer of the epithelium and connective tissue of areas affected by the chronic inflammatory nature of lichen planus.

Question 2. What is a smoker’s melanosis?
Answer:

• A diffuse, irregular, flat brown macule seen on the buccal mucosa, palate, floor of the mouth, and lateral tongue of cigarette smokers is known as smoker’s melanosis.
• It has no pre-malignant potential and is due to increased melanogenesis stimulation by tobacco smoke products.

Question 3. What is hemangioma?
Answer: Hemangioma is a hamartomatous proliferation of vascular channels. It is a developmental condition and usually regresses after puberty.

Question 4. What are lingual varicosities?
Answer:

• Torturous, serpentine, blue, red, and purple elevations seen on the ventral surface of the tongue of elderly individuals are known as lingual varicosities.
• They are painless and not subjected to rupture and hemorrhage.

Question 5. What are nevi?
Answer: Nevi are due to the benign proliferation of melano¬cytes and an increase in melanin production.

Question 6. What is drug-induced pigmentation?
Answer:

• Long-term use of phenothiazine may lead to skin deposition of metabolite and cause slate-gray color.
• Phenytoin use in females may cause chloasma-like pigmentation.
• Clofazimine may cause red color discoloration of the skin.
• A large dose of nicotinic acid causes brown pigmentation.
• Amiodarone causes violaceous hyperpigmentation in sun-exposed skin.
• Oral contraceptives produce chloasma.

Question 7. What is Laugier-Hunziker pigmentation?
Answer: Laugier-Hunziker pigmentation is characterized by multifocal pigmentation of the labial and buccal mucosa with melanotic streaks of the fingernails.

Pigmented Lesions Of Oral Mucosa Highlights

• Normal mucosal color depends on melanoma- genesis and distribution of melanin pigment, keratinization, the thickness of epithelium, and vascularity, Pigmented lesions are commonly found in the mouth.
• Such lesions represent a variety of clinical entities, ranging from physiologic changes to manifestations of systemic illnesses and malignant neoplasms.
• Although biopsy is a helpful and necessary aid in the diagnosis of focally pigmented lesions, with diffuse presentations lesions require a thorough history and laboratory studies to establish a definitive diagnosis.