Red White And Mixed Red And White Lesions Question And Answers

Red White And Mixed Red And White Lesions Essay Questions

Question 1. Define submucous fibrosis. Write about etiopathogenesis, clinical features, investigation, and medical management of oral submucous fibrosis.
Answer:

Submucous fibrosis Definition (Pindborg in 1966):

• Oral submucous fibrosis is an insidious, chronic disease affecting any part of the oral cavity and pharynx. Occasionally it is preceded by vesicle formation but is always associated with a juxtaepithelial inflammatory reaction.
• Inflammation is progressed to fibroelastic changes of the lamina propria, and submucosal myofibrils causing stiffness of the oral mucosa. The resultant symptoms include decreased mouth opening and tongue protrusion.

Read And Learn More: Oral Medicine and Radiology Question And Answers

Submucous fibrosis Etiopathogenesis:

• The etiologic factors are divided into initiators and promoters of oral submucous fibrosis.
• The initiators include—Habitual chewing of areca nut and tobacco and chilies.
• The promoters include—Iron deficiency anemia, deficiencies of B complex and folate vitamins, protein malnutrition, and immunologic disorders.
• Defect in collagen metabolism due to the imbalance in collagen production and breakdown is considered as a significant pathogenic part.
• The various components of areca nut play a different role in the pathogenesis. (Flow¬chart 1)
• Autoimmune condition: The increased frequency of HLA, A10/DR3, B8/DR3, and A10/B8 suggests the immunological cause for this condition.

Submucous fibrosis Clinical Features:

• Stage 1: Stomatitis: Mucosa appears erythematous. Oral ulcers, pigmentation, and petechia are frequent findings. Vesicles are rare.
• Stage 2: Fibrosis: The hallmark of oral sub-mucous fibrosis. Thick, fibrous bands are formed in the posterior buccal mucosa, running in a vertical direction, and palpable fibrous bands encircle the lips. Fibrosis results in a pale, marble-like mucosa and a restricted mouth opening.

The progressive changes include:

• Blanched mucosa.
• Decreased mouth opening (trismus)
• Difficulty in tongue protrusion
• Pale gingiva
• Decreased pliability of the soft palate
• Blanched and atrophied uvula (or) bud-shaped (or) hockey stick appearance of uvula: The thickness of the fibrous band differs between a whitish coat on the soft palate causing no symptoms and a dense fibrosis that shortens and deviation the uvula.
• Sinking of the cheeks, disproportionate to age or nutritional status.

Oral Submucous Fibrosis Of Pathogenesis:

Classification of Oral Submucous Fibrosis based on Clinical Findings:

• Lai Dr (1995) grouped oral submucous fibrosis into four categories based on inter-incisal distance:
  1. Group A: >35 mm
  2. Group B: Between 35-30 mm
  3. Group C: Between 20-30 mm
  4. Group D: <20 mm
• Rajendran R (2003) classified OSMF into two stages:

1. 1. Early oral submucous fibrosis: Burning sensation, recurrent oral inflammation or ulceration, excessive salivation, reduced taste perception, and dry mouth.
   2. Advanced oral submucous fibrosis: Blanched, pale, and firm mucosa, fibrous bands in the palate, faucial pillars, and buccal mucosa. Tongue movement is gradually restricted, and mouth opening becomes difficult.

Submucous fibrosis Differential Diagnosis:

• Oral manifestations in scleroderma
• Oral manifestations in Plummer-Vinson syndrome.

Submucous fibrosis Investigations:

• Complete hemogram
• Toluidine blue test
• Incisional biopsy.

Submucous fibrosis General Management:

1. Supportive Care:

• Elimination of the habit is the first step to be considered to prevent further progress, especially in the early stage, and improve the response to treatment.
• Minimizing chilies and spicy foods.
• Proper oral hygiene.

2. Nutritional support: Supplementation of iron, vitamins, and minerals with antioxidant potential (vitamins A, C, E, zinc, selenium) for 6-8 weeks, and a high protein diet.

• The topical vitamin A application is 50,000 IU/ day.
• The ferrous fumarate tablets 200 mg once daily.
• Lycopene therapy: Lycopene is a carotene, carotenoid pigment, and photochemical present in tomatoes, carrots, watermelons, and papayas. Lycopene has both anticancer and antioxidant properties. It has thera¬peutic benefits in potentially malignant disorders at the dose of 16 g/day.

Submucous fibrosis Medical Management:

Steroids:

• Steroids are immunosuppressive drugs and inhibit the release of inflammatory cytokines and thereby reduce the proliferation of fibroblasts and collagen deposition.
• Relapse is common following treatment. Steroids also prevent or suppress inflammatory reactions and hence reduce the symptoms.

Topical Steroids:

• The topical application of steroids reduces the symptoms.
• Triamcinolone acetonide 0.1% 2-3 times/ day. It heals inflammatory mucosal lesions.

Intralesional Injections:

• Triamcinolone acetonide (10 mg/mL) and hyaluronidase (1,500 IU) combination for 22 weeks at 15 days intervals.
  • Hyaluronidase facilitates the action of triamcinolone acetonide by dissolving the rigid connective tissue matrix hya¬luronic acid.
  • Triamcinolone acetonide increases vascularity due to its fibrinolytic, anti-allergic, and anti-inflammatory action.
• Placental extracts: Around 2 mL twice weekly for 4-6 weeks increases physiologi¬cal function. The actions include anti-inflammatory and analgesic effects, improves blood circulation and tissue vascularity, and lowers immune response factors.
• Hyaluronidase and chymotrypsin are the two enzymes used in the treatment of OSMF. Hyaluronidase (1,500 IU submucosal injections) exhibit rapid and effective action in reducing the burning sensation and painful ulceration.
• It improves mouth opening by decreasing collagen formation. But recurrence is common.
• Methylxanthine derivative (pentoxifylline) is a vasodilator. The use of pentoxifylline increases mucosal vascularity. It also suppresses the leukocyte function and stimulates fibrinolysis.
• This drug also stimulates the neutrophil degranulation and release of peroxides, promoting natural killer cell activity and inhibiting the production of tumor necrosis factors.

Oral Physiotherapy to Improve Mouth Opening: Muscle stretching exercises using a wooden spatula and Hister’s jaw exercises will improve the mouth opening and prevent relapse when complemented with medical management.

Submucous fibrosis Complication: Submucous fibrosis is a potentially malignant condition with 7-13% of patients developing oral cancer.

Question 2. Define leukoplakia. Write in detail about the various clinical types, etiology, malignant risk, and management.
Answer:

Leukoplakia Definition: Oral leukoplakia is a nontradable white patch or plaque that cannot be categorized as any other disease by clinical and histological examinations. The habit of tobacco consumption is the only causative factor.

World Health Organization Definitions For Leukoplakia:

• A white plaque not related to physical or chemical agents excluding tobacco products.
• A white patch or plaque that cannot be defined clinically or histopathologically as any other disease and has the potential for malignant transformation.

Leukoplakia Etiology:

• Tobacco consumption is a well-recognized causative agent. Smokers are affec¬ted more than nonsmokers.
• Alcohol plays an additive effect along with tobacco.
• Human papillomavirus (HPV) also plays a recognized role in etiology.

Types of Leukoplakia:

1. Homogeneous lesions are uniformly flat and thin and usually asymptomatic. Clinical appearance may be focal and smooth or homogeneous with an associated low risk of malignant transformation.
2. Other lesions may be heterogeneous or nonhomogeneous (speckled, erosive, ulcerative) which may be interspersed with red or atrophic areas but retain the predominant white color, and has the probability for dysplastic and malignant changes.
3. Exophytic type (verrucous leukoplakia and proliferative verrucous leukoplakia). Proliferative verrucous leukoplakia is an aggressive type of leukoplakia that carries a high risk for cancerous changes. This type occurs as a diffused lesion and is resistant to treatment. Gingiva, buccal mucosa, and alveolar ridge are the commonly involved sites.
4. Leukoplakia has the tendency for transitions from one clinical form to another. The location of the leukoplakia is recognized in eight sites: The tongue, the floor of the mouth, buccal and lower labial mucosa, hard palate, upper and lower alveolar ridges, and gingiva.

Leukoplakia Malignant Transformation:

• Around 1-2% of leukoplakia tends to become malignant in 5 years. Leukoplakia occurring at the floor of the oral cavity, tongue, and ventral surface has a high risk for malignant transformation.
• Risk factors that initiate malignant trans-formation in leukoplakia:
  • Female gender
  • Long-standing leukoplakia
  • Leukoplakia in nontobacco users (idio-pathic leukoplakia)
  • Leukoplakia involving the tongue and floor of the mouth
  • Size >200 mm2
  • Nonhomogeneous variety
  • Presence of invasive C. albicans
  • Epithelial dysplasia
  • History of head-and-neck carcinoma.

Leukoplakia Investigations:

• Biopsy and histopathological diagnosis is the confirmatory method to differentiate between dysplastic and nondysplastic lesions.
• A brush biopsy is a noninvasive method to collect the basal layer of cells for patho¬logical examination.
• Toluidine blue vital staining is used to identify the presence of dysplastic changes in the lesion and select the appropriate site for biopsy.
• Chemiluminescence (ViziLite system) is based on the fluorescence property of the healthy and leukoplakia tissue to a specific light wavelength.

Leukoplakia Treatment:

• The treatment goal for leukoplakia is to prevent the malignant transformation.
• In the absence of histologically demonstrated dysplastic changes, routine follow-up observation is appropriate in conjunction with the elimination of any tobacco habit and medical management.

Chemoprevention: It is aimed for scavenging the free radicals, destroying the carcinogenic byproducts of tobacco, and inhibiting mutation.

• Retinoids
• Vitamins (A, C, E)
• Carotenoids
• Topical retinoic acid (vitamin A) — prevents keratin production, inflammatory response and carcinogenesis.
• Candida-associated leukoplakias respond to topical antifungal therapy (clotrimazole 1% cream 4 times/day for 2 weeks).

If dysplastic changes are present:

• Topical bleomycin 1% (cytotoxic antibiotic) can be used for 2 weeks.
• Surgical treatment is also recommended (conventional surgery, electrocauterization, laser ablation, or cryosurgery).

Question 3. Classify oral candidiasis. Explain the clinical features, investigations, and management of acute candidal infections.
Answer:

Oral candidiasis Classification:

1. Primary oral candidiasis (group 1)

• Acute types:
  • Primary pseudomembranous candi¬diasis (thrush)
  • Erythematous.
• Chronic types:
  • Pseudomembranous (occurs in HIV infected individuals and in patients using steroid inhalers for long periods)
  • Erythematous
  • Hyperplastic
  • Nodular
  • Plaque-like.
• Candida associated:
  • Angular cheilitis
  • Denture stomatitis
  • Median rhomboid glossitis.
• Keratinized primary lesions superimposed with candida:
  • Leukoplakia
  • Lichen planus
  • Lupus erythematosus.

2. Secondary oral candidiasis (group 2)

• Candidiasis endocrinopathy syndrome
• Mucocutaneous candidiasis.

Candidal Causative Agent:

• Candida albicans is the frequently associated organism in 70-95% of reported patients.
• Candida tropicalis, Candida krusei, and Candida glabrata are also associated in oral infection.

Candidal Predisposing Factors:

• Chronic local irritants like removable dentures.
• Altered oral biology or changes in the oral flora caused by long-time medications (antibiotics and corticosteroids).
• Dry mouth
• Deficiencies of iron and vitamins.
• Immunological and endocrine disorders
• Malignant and chronic diseases
• Radiotherapy and chemotherapy
• Extremities of age
• Hospitalization
• Epithelial alterations
• Heavy smoking.

Acute Oral Candidiasis:

1. Acute pseudomembranous candidiasis (oral thrush)

• It manifests as pseudomembranous white patches on the oral mucosa, palate, and tongue composed of desquamated cells, fibrin, and fungal hyphae.
• The surface appears white or whitish-yellow confluent plaque resembling curd or cheese. When swiping with a swab, the membrane is scraped off and leaves a red base.
• Commonly affects newborn babies (due to immature immune system), older individuals (immune decline), individuals using steroid inhalers (inhibits local immunity) or an underlying disease.
• The patient may present with the mild symptom of altered taste or slight tingling sensation in acute disease, whereas the chronic form may cause dysphagia.

2. Erythematous (or) acute atrophic candidiasis:

• It is a rare form. The occurrence is associated with prolonged use of corticosteroids and broad-spectrum antibiotics administration or HIV infection.
• It may also a squeal of persistent acute pseudomembranous candidiasis, when the pseudomembranes shed, the acute form changes to the atrophic form.
• It appears as red, depopulated surfaces on the dorsum of the tongue, erythematous patches on the palate, or buccal mucosa. Pain and discomfort are frequently associated symptoms.

3. Angular stomatitis (perleche, angular cheilitis):

• Fissuring and cracking at the commissural areas of the mouth. It is commonly associated with denture stomatitis, iron deficiency anemia, vitamin deficiencies, and HIV infection.
• It is either asymptomatic or associated with pain and irritation at one or both commissars.

Acute Oral Candidiasis Investigations:

1. Smears detection:

• The smear should be collected from the active lesion site using a wooden spatula and fixed immediately on two slides, one for Gram staining and the other for the periodic-acid Schiff (PAS) technique.
• Direct microscopic examination of smears reveals yeast cells appearing dark blue in Gram staining and red or purple in PAS preparations.

2. Swabs: The lesion site is swabbed and seeded on Sabouraud agar growth medium. Incubation at 25°C will encourage growth.

3. Imprint culture technique:

• A sterile, square, plastic foam pad (2.5 x 2.5 cm) dipped in peptone water is placed over the mucosal lesion for 30-60 seconds. Then the plastic foam is incubated on Sabouraud’s agar at 37°C for 48 hours.
• Candida density is expressed as colony-forming units per mm². More than 30 colony-forming units (CFU) per cm² of mucosa in dentulous patients and 49 CFU per cm² in denture wearers suggest candidal infection.

4. Salivary culture technique:

• This is done by collecting 2 mL of mixed, unstimulated saliva in a sterile, container and incubated in Sabouraud’s agar medium.
• The number of candida in the salivary sample is expressed as CFU.

5. Oral rinse technique:

• The patient should rinse the mouth for 60 seconds with 10 mL of sterile saline or sterile water and then returns the oral rinse to the sterile container.
• The collected oral rinse is centrifuged and inoculated on appropriate media to assess CFU per mL of the sample.
• Serological tests for invasive candidiasis: Useful to detect candida antibodies by-
  • Slide agglutination
  • Latex agglutination
  • Immunodiffusion
  • Phytohemagglutination.

Acute Oral Candidiasis Management: Oral candidiasis in immunocompetent individuals are treated with topical antifungals, and in immunocompromised individuals, both topical and systemic antifungals are used.

• Eliminating the predisposing factors
• Proper oral hygiene home practices
• Using anticandidal mouthwashes like:
  • Triclosan
  • Chlorhexidine gluconate (0.12%) 15 mL mouth rinse 3 times per day.
  • Essential oil formulations: Plant derivatives like thymol, eucalyptol, and bio-flavonoids have an anticandidal property by fungal cell membrane disruption and enzyme inhibition.
• Antifungal agents:
  • Topical azoles
    • Clotrimazole 1% cream 4 times/day for 2 weeks.
    • Clotrimazole 10 mg/mL suspension, swab 1-2 mL over the lesion 3 times/ day for 2 weeks.
  • Transmucosal drugs: It should be used until 2 days after symptoms subside
    • Miconazole buccal tablet 50 mg-1 tab/day for 2 weeks; applied in gum region.
    • Nystatin suspension 4,00,000-6,00,000 units, 4-6 mL/day, swish and swallow.
  • Systemic medication:
    • Fluconazole (400 mg as starting dose followed by 200 mg/day for 15 days).
    • Ketoconazole 200 mg tab/day for 7-10 days.
  • For angular cheilitis:
    • A mixture of topical antifungal and antibacterial ointment (for example nystatin and mupirocin) is preferred 3 times/ day for 2 weeks.
    • Miconazole is an antifungal drug with an effective antistaphylococcal effect. Hence, miconazole oral gel can be used for angular cheilitis.

Question 4. Define lichen planus. Describe its clinical features, diagnosis, and management briefly.
Answer:

• Lichen planus is a chronic inflammatory disease of the skin and mucosa.
• The occurrence of oral lichen planus (OLP) is more common than the cutaneous form. Oral lesions are long-lasting and resistant to treatment.

Lichen Etiology:

• Lichen planus is an autoimmune disorder characterized by abnormal T-cell-mediated immune response. The basal epithelial cells are recognized as antigens due to their cell surface changes.
• Activation of mast cells (associated with the vascular and neuronal supply of oral mucosa) directs inflammatory cells in the bloodstream towards mucosa and facilitates OLP.

Lichen Predisposing Factors:

• Cell-mediated hypersensitivity reactions.
• Stress induces a significant change in the immune response.

Lichen Clinical Features:

• Lichen planus has a preference for middle-aged women.
• Men and children are occasionally affected.

Lichen Clinical Types:

1. Reticular Oral Lichen Planus:

• It is the most prevalent type. Lesions manifests as multiple radiating keratotic striae with an elevated white dot at the point of intersection of these line known as Wickham’s striae.
• The white striae are present bilaterally on the buccal mucosa, vestibule, gingiva, tongue, palate, and rarely lips.
• Usually asymptomatic but may associate with a burning sensation on taking spicy foods.

2. Erosive Oral Lichen Planus (Atrophic form):

• The erosive form is the second common type of OLP. It presents as a combination of red and ulcerated surfaces surrounded by faint radiating white striae at the periphery.
• It is commonly present in the gingiva and erosive lichen planus involvement of the gingiva is called as desquamative gingivitis. Involvement of buccal mucosa, vestibule, and floor of the mouth also occurs.
• The lesions may become widespread and the patient’s complaints range from intermittent pain to severe discomfort that interferes with chewing.

3. Plaque-like Oral Lichen Planus:

• Plaque-like form clinically resembles homogeneous leukoplakia. These plaque-like lesions are smooth and flat or irregular and
  elevated in appearance.
• This type involves the dorsum of the tongue and buccal mucosa. This is a variant form of the reticular lesion, usually asymptomatic but may associate with a burning sensation on taking spicy foods.

4. Bullous Lichen Planus:

• The bullous form is a rare variety and affects the buccal mucosa and the lateral borders of the tongue.
• The bullae rupture immediately and lead to an ulcerative form of lichen planus. Nikolsky’s sign is positive in bullous form.

5. Lichen Papular: The papular form is sporadic and is the transient form of other types of OLP. Multiple white spots are present with faint radiating white lines at the periphery.

Lichen Differential Diagnosis:

• Reticular type: Lichenoid reaction, candidiasis, discoid lupus erythematosus, frictional keratosis.
• Plaque type: Leukoplakia.
• Erythematous and bullous type: Pemphigus, pemphigoid.

Lichen Investigations:

• Incisional biopsy and histopathological examination.
• Immunohistochemical reactions.

Lichen Management:

• Primary care should involve good oral hygiene with the elimination of all local irritants and superadded candidal infection using 0.12% chlorhexidine gluconate rinse.
• Corticosteroid: The drug of choice to revise the immune reaction.
  • Topical corticosteroid is used in mild to moderately symptomatic lesions.
  • The following preparations are used in terms of increasing potency:
  • 0.1% triamcinolone acetonide ointment 3 times/day
  • 0.05% clobetasol propionate gel
  • 0.1% or 0.05% betamethasone valerate gel
  • 0.05% fluocinonide gel
  • 0.05% clobetasone butyrate ointment or cream.
  • For widespread lesions, 1.0 mg/mL aqueous triamcinolone acetonide or 0. 1 mg/mL dexamethasone elixir is effective. Patients should use 5 mL of this solution for 2 minutes after every meal and at night time.

Advantages of topical steroid application:

• Side effects are more minimal than systemic preparations.
• Direct release of the drug at the lesion site.

Adverse Effects:

• Secondary candidal infection and mucosal atrophy.
• High-potent topical corticosteroids can cause adrenal suppression when for long periods.
  • Intralesional injection of corticosteroid: Administered for recalcitrant lesions. Around 0.2-0.4 mL of a 10 mg/mL solution of triamcinolone acetonide is used.
  • Systemic steroid therapy: It should be reserved for patients in whom topical steroids are ineffective. Prednisone tablet 10-20 mg/day for moderately severe conditions and up to 35 mg/per day for severe conditions.
  • Other preferred medications:
    • 0.1% tacrolimus ointment
    • Topical retinoids and vitamin A
    • Antioxidants.

Lichen Clinical Significance: Oral lichen planus is a potentially malignant disorder, especially erosive and atrophic forms. This necessitates appropriate management with regular follow-up care.

Question 5. Briefly mention the reason for oral white lesions and Classify white lesions of the oral mucosa.
Answer: The whitish appearance of the mucosa is due to:

• Increase in thickness of one or more epi¬thelial layers
• The abnormally thick keratin layer
• Reduced vascularity of underlying mucosa.
• Increase in the amount of edema in the epithelium (leukoderma).
• They are classified by keratotic or non-keratotic nature.

Classification Based on Keratinization:

• Keratotic white lesions: Nonscrapable white lesions.
  • Frictional keratosis
  • White sponge nevus
  • Reticular lichen planus
  • Leukoplakia
  • Hairy leukoplakia.
• Nonkeratotic white lesions: Scrapable white lesions.
  • Candidiasis
  • Chemical burns.

Classification Based on Origin and Pathogenesis:

• Hereditary or developmental white lesions
  • Leukoedema
  • White spongy nevus
  • Hereditary benign intraepithelial dyskeratosis
  • Pachyonychia congenita
  • Dyskeratosis congenita
• Reactive white lesions
  • Frictional keratosis
  • Morsicatio buccarum
  • Nicotine stomatitis
  • Tobacco pouch keratosis
  • Chemical burn
• Immunologic white lesions
  • Lichen planus
  • Lichenoid mucositis
  • Discoid lupus erythematosus
  • Graft-versus-host disease
• Bacterial or viral or fungal white lesions
  • Candidiasis
  • Mucous patches of secondary syphilis
  • Oral hairy leukoplakia
• Systemic disease-causing oral white lesions
  • Uremic stomatitis
• Potentially malignant disorders
  • Leukoplakia
  • Actinic cheilitis.

Red White And Mixed Red And White Lesions Short Notes

Question 1. Actinic keratosis (or) actinic cheilitis.
Answer:

• Chronic exposure to sunlight may cause keratotic changes in the lip. It has the tendency for malignant transformation.
• Usually, patients are asymptomatic. In atrophic form, ulceration, pain, and blee¬ding are common.

There are 4 types:

1. Hyperkeratotic form
2. Pigmented form
3. Lichenoid form
4. Atrophic form.

Actinic keratosis Treatment:

• Strict advice to be given to the patient to avoid sun exposure as much as possible.
  • Diclofenac sodium 3% gel, topical application for 60-90 days.
  • Cryosurgery with liquid nitrogen for freezing off the actinic keratosis.
  • 5-fluorouracil—a cytotoxic topical cream that causes the lesion to become red and inflamed before they fall off.
  • Photodynamic therapy.
  • CO₂ or Er: YAG laser therapy. The laser resurfacing technique is used to treat diffuse form.
  • Electrocautery.

Question 2. Denture stomatitis (or) denture sore mouth (or) chronic atrophic candidiasis.
Answer:

• The characteristic features of denture-induced stomatitis include the erythema¬tous and edematous changes of the mucosa that contacts the fitting maxillary denture base (palate and gingiva).
• The involvement of mucosa contacting the lower denture base is infrequent. The patients are asymptomatic but occasionally complain about soreness. The associated angular stomatitis may cause difficulty in mouth opening.

Etiology includes local and systemic factors.

• Local factors:
  • Poor oral and denture hygiene
  • Microbial colonization
  • Old dentures
  • Hypersensitivity for denture base materials and residual monomer
  • Dryness of mouth.
• Systemic factors include:
  • Diabetes mellitus
  • Immunodeficiency
  • Nutritional disorders.

Newton’s classification of denture stomatitis:

1. Type 1-A localized simple inflammation or pinpoint hyperemia.
2. Type 2-Erythematous type: more diffuse erythema involving a part of or the entire denture-covering mucosa.
3. Type 3-Granular type (inflammatory papillary hyperplasia) frequently affec¬ting the middle of the hard palate and the alveolar ridge.

• The causative factorcandida. The yeast form of candida colonizes the oral mucosa beneath the denture along with bacterial colonization.
• The attachment is facilitated by mucous and serum and decreased by the presence of salivary pellicle.
• The use of soft liners in dentures adds hazards by providing mechanical locking for plaque and yeasts to the denture base.

Actinic keratosis Management:

• Disinfection of the denture with:
  • 10% solution of household bleach.
  • Socking in boric acid.
  • Applying nystatin cream before inserting the denture.
  • Denture adhesives should be removed on a daily basis.
  • Overnight storage of dentures in water.
  • An antifungal treatment will resolve the bright red appearance of the mucosa.
  • The papillomatous appearance of mucosa requires surgical excision following anti-fungal therapy and discontinuing the denture wearing.

Question 3. Discuss hairy tongue (or) black hairy tongue.
Answer:

• Hairy tongue is a term for the abnormal acquired coating on the dorsal surface of the tongue. It is a temporary condition that gives the tongue a furry, carpet-like appearance.
• There is defective desquamation and shea¬ding of the papilla that leads to the accumulation of keratinized layers. The filiform papillae are approximately 1 mm in length, and become elongated and hypertrophic due to keratinization and can reach 12-18 mm in length, with a width of 2 mm, giving a hair-like appearance.
• The over-retention of papillae causes food and bacteria, to accumulate in the hair-like mesh and various colors like brown, white, green, and pink to the surface of the tongue.
• Secondary bacterial and fungal infections can even a black appearance, referred to as a black hairy tongue.

Hairy tongue Etiology:

• Multifactorial:
  • It can occur from poor oral hygiene, prolonged or excessive use of antibiotics, radiotherapy for the head and neck region, food habits like coffee or tea drinking, or tobacco usage.
  • It may also develop in edentulous persons because of their soft food diet that will not aid in the stimulation of normal shedding of the papillae.
  • Regular use of mouthwashes containing oxidizing agents, such as peroxide, or astringent agents, such as menthol also causes this condition.
  • Decreased consumption of coarse food and restricted tongue movement also leads to poor desquamation of the papilla.

Hairy Tongue Clinical Features:

• Asymptomatic but occasionally associated with a burning sensation.
• Gagging or a tickling sensation in the soft palate due to the contact of elongated structures.
• Halitosis and unusual taste due to the taste buds holding onto debris in the mouth.

Hairy tongue Treatment:

• Maintenance of improved oral hygiene and eliminating the contributing factors will resolve black hairy tongue.
• Use of a tongue scraper and rinsing with dilute hydrogen peroxide mouth rinse will promote desquamation. Increased consumption of raw fruits and vegetables is helpful.
• Topical use of 30% urea solution and trichloroacetic acid can be used. It may cause mild local irritation.

Question 4. Lichenoid reactions (or) oral lichenoid lesions.
Answer:

• Oral lichenoid reactions (or) lesions represent a similar clinical manifestation to a reticular pattern of oral lichen planus but are often unilateral.
• It is a response to external agents (drugs, dental restorative materials, allergens) or altered self¬antigens and can be cured if the inciting factor is identified and eliminated.
• Oral lichenoid reactions may also result from systemic drug exposure [oral lichenoid drug reaction; (OLDR)] or local allergic contact hypersensitivity (OLCR).
• Dental amalgam restoration is the most common etiological factor. The amalgam reacts with oral fluid and releases degra¬dation products which initiate the lichenoid reaction.

Lichenoid Drug Reactions:

• It may involve the skin, oral mucosa, or both. The duration between drug administration and development of OLDR is variable, with an average of 2-3 months.
• Based on the causative drug, the lesions appear either as white reticular papules or as erosions and are sometimes associated with pain. These lesions are associated with the use of nonsteroidal anti-inflammatory drugs (aspirin, ibuprofen, indomethacin), antihypertensives (atenolol, enalapril, hydrochlorothiazide, methyldopa, metoprolol), and HIV antiretrovirals (zidovudine).
• There are no universal criteria for the diagnosis. Proposed diagnostic criteria include a history of systemic medication intake, clinical and histological features of lichenoid mucositis, and resolution of lesions with drug discontinuation.

Lichenoid Drug Reactions Treatment:

• Discontinuation of the suspect medication and substitution with an alternate medication will resolve the lesion within a few weeks to months, but delayed responses may also occur.
• If the causative medication cannot be discontinued or if residual lesions persist after drug elimination, the topical corticosteroid can be used.

Question 5. Allergic contact stomatitis.
Answer:

• It is an immune-mediated (T-cell-media- ted) inflammatory reaction to an exogenous allergen that has direct contact with oral mucosa. Pain, burning sensation, and itching sensation are the associated symptoms.
• Lesions are located in apposition or near proximity (within 1 cm) to the offending allergen, and lesions are restricted to the sites of contact. Typical sites include the lateral borders of the tongue and buccal mucosa.
• Dental restorative materials, cinnamon and other spices, chewing gums, impression materials, and orthodontic appliances may induce hypersensitivity reactions. Erythema, vesicles, ulcers, and hyperkeratotic patches are the various clinical forms.

Allergic contact stomatitis Differential Diagnosis: Plasma cell gingivitis, anemic stomatitis, lichen planus.

Allergic contact stomatitis Diagnosis: It is confirmed based on examination findings and by the disappearance of the lesion following the elimination of the causative factor.

Allergic contact stomatitis Treatment: Elimination of causative agent.

Question 6. Oral hairy leukoplakia.
Answer:

• Oral hairy leukoplakia is a vertically radiating white lesion of the lateral border of the tongue with a slightly elevated, ill-defined, and corrugated hairy surface.
• Lesions cannot be rubbed off and are symptomless. It is caused by the Epstein-Barr virus (EBV) and is a sign of immunosuppression.
  • Present in patients with acquired immunodeficiency syndrome (AIDS) and less often seen in drug abusers, hemophilic, blood transfusion recipients and organ transplant patients.
• The lesions are bilateral and asymptomatic but rarely cause a burning sensation. Treatment is not essential as they would not cause any serious symptoms.
• People with widespread lesions and who is experiencing discomfort or altered taste are treated with topical application of podophyllin resin.

Question 7. Describe graft-versus-host disease.
Answer: Graft-versus-host disease (GVHD) is a complication of allogeneic hematopoietic stem cell transplantation (HSCT). GVHD occurs in two forms: Acute and chronic.

1. Acute graft-versus-host disease:

• It occurs within 100 days following transplantation, whereas the chronic form manifests at a later period is more than 100 days, and reveals some of the features of autoimmune diseases.
• The chronic form may develop either de novo or the following resolution of/or as an extension of acute GVHD.
• The acute form is precipitated by many conditions like radiotherapy, chemo¬therapy, neutropenia, herpes infection, and treatment with cytokines. Oral findings include mucosal erythema, ulcerations, and painful desquamative lesions.

2. Chronic graft-versus-host disease:

• Involves the skin, oral, vaginal, and conjunctival mucosa, salivary and lacrimal glands, and liver. Around 40-70% of engrafted patients develop cGVHD which can persist for months to years and require long-term management from multiple disciplines.
• The oral presentation is variable and includes lichen planus-like changes of the mucosa, hyperkeratotic plaques, mucosal atrophy and ulcers, and secondary Sj ogren’s syndrome.

Graft-versus-host disease Management: Topical corticosteroid or tacrolimus can be used to reduce pain and discomfort.

Question 8. Describe erythroplakia.
Answer:

• Erythroplakia Definition: Erythroplakia is a red patch that cannot be diagnosed as any other lesion by clinical or pathological findings.
• Erythroplakia Predisposing Factors: Tobacco and alcohol.
• Erythroplakia Clinical Features:
  • Erythroplakia appears as a fiery-red, flat, or depressed lesion with a smooth or granular surface.
  • In many cases, the lesion appears as a mixed form with predominantly red and some white spots and is called as erythroleukoplakia.
• Erythroplakia Differential Diagnosis: Erythematous lichen planus and atrophic candidiasis—these lesions have multifocal involvement.
• Erythroplakia Symptoms: Pain and burning sensation.
• Erythroplakia Histopathology: Erythroplakia shows some degree of dys- plastic features or features of carcinoma in situ or invasive carcinoma.
• Erythroplakia Treatment: Cold knife or laser surgery is the recommended treatment modality.

Question 9. What is frictional keratosis?
Answer:

• Frictional or traumatic keratosis appears as a white patch with a rough and ragged mucosal surface adjacent to a source of mechanical irritation.
• Sharp cusps, broken teeth, rough denture borders, clasps, and irregular edges of orthodontic appliances are the potential source and usually resolve.
• Asymptomatic.
• Keratotic patches disappear gradually within 2 weeks following the removal of irritants.
• Differential diagnosis: Leukoplakia, lichenoid reactions.
• Biopsy should be considered in nonhealing lesions that persist after the removal of irritation.

Question 10. Median rhomboid glossitis.
Answer:

• Median rhomboid glossitis is a central papillary atrophy of the tongue and is located around the midline of the dorsum of the tongue. It appears as a well-defined, symmetrical depopulation, anterior to the circumvallate papillae.
• The surface of the lesion is smooth or lobulated and demarcated from the surrounding sites. Usually asymptomatic, but occasionally associated with pain, irritation, or pruritus.

• When median rhomboid glossitis is associated with a palatal inflammation, it is called a kissing lesion.
• It is frequently seen in HIV-infected individuals and hence when present, necessary investigations should be carried out to rule out AIDS.
• Predisposing factors associated are smoking, diabetes mellitus, a prolonged course of antibiotic treatment, and candidal infection. It is asymptomatic. Topical anticandidal medication is the treatment of choice.

Question 11. Candidal leukoplakia.
Answer:

• Candidal leukoplakia is a nontradable, chronic candid infection that resembles leukoplakia in appearance.
• The terms chronic hyperplastic candidiasis and candidal leukoplakia are used synonymously.

Candidal leukoplakia Clinical Presentation:

• White plaque that cannot be rubbed off and presenting at the following oral sites in decreasing order of frequency: Oral commissars, cheek mucosa, palate, and the tongue.
• Candidal hyphae invade the superficial layers of the epithelium and cause epithelial atrophy, hyperplasia, and dysplasia.
• Systemic conditions like diabetes, poor immunological conditions, and deficiencies of vitamins A, B1, B2, folic acid, and iron predispose this condition.

Candidal leukoplakia Clinical Features:

• It appears as a distinct, elevated lesion either small transparent or large opaque plaques which are nontradable and hence resemble leukoplakia.
• Some areas of the plaque may have nodular characteristics.

Candidal leukoplakia Management:

• Medical management: Antifungal therapy, topical application of retinoids, bleomycin, and P-carotene.
• Surgical excision.

Question 12. Proliferative verrucous leukoplakia.
Answer:

• Proliferative verrucous leukoplakia is a severe form of oral leukoplakia. It preferably occurs in women (female-to-male ratio of 4:1) not having the habit of tobacco.
• It presents as a multifocal white patch or plaque with rough surface projections. These lesions tend to spread slowly and involve other oral mucosal regions. More frequently occurs on the gingival but other sites may also be affected.
• It tends to recur after surgical excision and has the risk for transformation into squamous cell carcinoma usually within 8 years of initial diagnosis.
• Five major and four minor criteria were proposed to allow for a definitive diagnosis of PVL.

Candidal leukoplakia Major Criteria:

• Leukoplakia presents at more than two different oral sites preferably in the gingiva, alveolar processes, and palate.
• The existence of a verrucous surface.
• The lesions should be widespread.
• There has been a recurrence in a previously treated area.
• Histopathologically leukoplakia should present as simple epithelial hyperkeratosis or verrucous hyperplasia or verrucous carcinoma or oral squamous cell carcinoma or in situ or infiltrating.

Candidal leukoplakia Minor Criteria:

• Oral leukoplakia measuring a minimum of 3 cm in size.
• Female patient.
• The patient must be free of tobacco habit.
• More than 5-year duration.

To confirm the diagnosis of PVL, the following guideline if followed:

• Three major criteria (with histopathological criteria, as one in 3).
• Two major criteria (histopathological change as one criterion) + two minor criteria.

Candidal leukoplakia Management:

• There is no definitive treatment.
• Surgical excision, CO₂ laser evaporation, laser surgery, chemo, and radiotherapy are the different modalities preferred for management.

Question 13. Chemical burn (or) scrapable white lesions of the oral mucosa (or) nonketotic white lesions of the oral mucosa.
Answer:

Chemicals with caustic potential like aspirin, silver nitrate, formoterol, sodium hypochlorite, hydrogen peroxide, and cavity varnish and acid-etching materials, when retained in the mouth for a long period lead to the formation of whitish pseudomembrane with necrotic surface and exudates.

• Aspirin burn: When aspirin is held in the mesiobuccal fold adjacent to the painful tooth for relief, it causes focal superficial necrosis with white pseudomembrane that can be easily scraped off leaving an underlying erythematous mucosa.
• Silver nitrate: This chemical is sometimes used in the treatment of aphthous ulcers as a cautery agent. It gives immediate pain relief by burning the nerve ends at the ulcer site. At the same time, it causes severe necrosis at the application site with pseudomembrane formation.
• Hydrogen peroxide: A concentration of hydrogen peroxide is greater than 3% as an oral rinse for periodontal problems may lead to epithelial necrosis.
• Sodium hypochlorite: It is used as an intracanal irrigant in endodontic procedures and when accidental contact with the oral mucosa or gingiva causes severe ulceration with superficial necrosis.
• Dentifrices and mouth rinse: Cinnamon-flavored dentifrices often cause sensitivity or allergic reaction on the oral mucosa resulting in necrosis and sloug¬hing of the epithelium.
• Mouthrinses containing chlorhexidine and alcohol also occasionally cause caustic burns in some individuals.

Chemical Burn Clinical Features:

• It is commonly seen on the mucobuccal fold and gingiva as an irregularly shaped area with a white pseudomembrane.
• When the tissue involvement is extensive, severe damage with sloughing of necrotic mucosa will cause pain.
• In case of mild contact of the agent with mucosa, a superficial white and wrinkled appearance without necrosis is present.

Chemical Burn Management:

• A protective emollient agent like methyl-cellulose can be used for milder cases and heals within 1-2 weeks.
• For deep tissue necrosis, debridement of the surface followed by systemic antibiotic and anti-inflammatory coverage is essential.

Question 14. Snuff dipper’s lesion (or) Pouch keratosis (or) smokeless tobacco keratosis.
Answer:

• The habit of keeping tobacco quid in the buccal or labial vestibule causes white patches or plaque lesions on the vestibule. These lesions may involve adjoining tissues like the gingiva and buccal mucosa.
• Early lesions may show slight wrinkling that disappears when the tissues are stretched. Older lesions appear as hyperkeratotic, granular patches. Long-standing lesions, with persistent habit exhibit grayish-white mucosa with well-developed folds and fissures. There will be no associated pain or burning sensation.
• Smokeless tobacco keratosis takes about 5 years to develop but breaking the habit leads to a normal mucosa within 2-6 weeks. For lesions that remain for more than 6 weeks, a biopsy should be considered.

Question 15. Nicotina stomatitis (or) smokers palate.
Answer:

• Nicotine stomatitis develops as a response to cigar smoking or from cigarette smoking. The hot smoke released strikes the palate and causes hyperkeratotic alteration of the palatal mucosa.
• The palatal mucosa becomes thickened and whitish in appearance with a fissured surface. Papular elevations with red centers are also a common feature which represents the partial occlusion of the duct orifice with keratotic plugging and inflamed orifice of the minor salivary gland ducts.
• The changes are more localized to the glandular zone of the hard palate alone.
• Though nicotine stomatitis is a tobacco-related condition, it has no malignant transformation potential. Discontinuation of the smoking habit reverses the condition.

Question 16. Viadent leukoplakia (or) sanguinaria- associated keratosis (or) sanguinaria leukoplakia.
Answer:

• Sanguinaria canadensis (a type of flower) has been found to be effective against plaque build-up and gingivitis. Sanguinaria-associated leukoplakia is a unique form of oral leukoplakia attributed to the chronic use of oral rinses and toothpaste containing the extract of the sanguinaria plant.
• It is usually located on the attached gingiva and the alveolar mucosa of the maxillary vestibule.
• The duration of usage of the product and development lesion may vary between 6 months to 12 years.
• The lesion appears as a white, velvety, wrinkled or corrugated patch in the maxillary vestibule involving both attached gingiva and vestibular mucosa. Involvement of mandibular anterior vestibule is also common.
• The site specificity is due to the prolonged retention of the product in the vestibule due to its greater distance from major salivary gland ducts. The lesion is well-demarcated from the surrounding mucosa.

Chemical Burn Management: Discontinue the use of sanguinaria-containing products and careful follow-up.

Question 17. Describe parulis (or) gumboil.
Answer:

• Parulis is an oral lesion characterized by a soft erythematous papule (or red spot) that develops on the alveolar process or attached gingiva of a tooth in association with periapical abscess or with a periodontal abscess.
• It represents the drainage tract of pus with an inflamed orifice and is made up of granulation tissue.
• The lesion appears as a red or normal mucosal-colored gingival swelling surrounded by erythema. It is fluctuant on palpation and is less than 5 mm in size.
• On examination with a periodontal probe, a small orifice adjacent to the fistulous tract can be identified. Pus discharge may present at the orifice.
• The parulis presents with variable symptoms. It may be painless or produces noticeable pain. The pain persists until pus drains out through the surface opening.

Chemical Burn Diagnosis:

• A sterile gutta-percha (GP) point can be inserted into the orifice of the fistulous tract and a periapical radiograph should be taken with the GP point.
• The proximity of the gutta¬percha point to the apex of the nonvital tooth can be evaluated on the radiograph.

Chemical Burn Treatment:

• Endodontic procedures or extraction is indicated if the affected tooth is nonvital. If the tooth is associated with a deep periodontal pocket, periodontal therapy is indicated.
• Once the underlying cause is treated, the parulis resolves and does not recur.

Question 18. Discoid lupus erythematosus.
Answer:

• Discoid lupus erythematosus (DLE) is an autoimmune, connective tissue disorder affecting the skin and oral mucosa. The oral discoid lesions present with a characteristic central erythematous zone and a periphery of white radiating lines or hyperkeratotic plaques and striae.
• The distribution of discoid lupus erythematosus is usually asymmetric. Peripheral striae are faint. The oral lesions occur along skin lesions or before the onset of skin lesions and rarely oral lesions alone may be present without skin involvement.
• The labial mucosa, the vermilion border of the lip, and the buccal mucosa are the commonly involved sites. Burning sensa¬tion, tenderness, dryness, and pain are the associated symptoms.
• The diagnosis is based on the coexistence of skin lesions, histopathology, and immuno- fluorescent studies.

Differential diagnosis of lichen planus:

• Topical steroid (triamcinolone acetonide 0. 1. is effective in treating the skin and oral lesions).
• Intralesional steroids are helpful for treating chronic conditions.
• In resistant cases, antimalarial drugs like chloroquine, hydroxychloroquine, and mepacrine are used.

Other topical agents:

• 0.1% tacrolimus ointment twice daily
• 0.05% clobetasol propionate ointment twice daily
  Failure of early treatment may lead to permanent scarring and pigmentation.

Question 19. Uremic stomatitis.
Answer:

• Uremic stomatitis is a complication of advanced renal failure. The onset is abrupt, with white plaques present predominantly on the buccal mucosa, tongue, and floor of the mouth.
• The odor of ammonia or urine may be smelled on the patient’s breath. The principal cause is the elevated levels of ammonia.
• Uremia-induced hemorrhagic disorders to cause a decrease in the resis¬tance of mucosal tissues to infection resulting in ulceration and pseudomembrane formation.

Four forms of uremic stomatitis are recognized:

1. Ulcerative form
2. Hemorrhagic form
3. Pseudomembranous form
4. Hyperkeratotic form.

Pseudomembranous form and hyperkera- totic form appear white.

Uremic stomatitis Management:

• In some conditions, uremic crystals may clear within 2-3 weeks following dialysis.
• In persistent conditions, acidic mouth rinses like hydrogen peroxide may clear the uremic deposits.
• Palliative therapy with ice cubes is also advisable.

Question 20. What is the classification and staging of leukoplakia?
Answer:

• LSCP classification and staging of leukoplakia:
  • L—Extent of the lesion
  • S—Site of the lesion
  • C—Clinical aspects
  • P—Histopathological features.

Leukoplakia Classification:

• The extent of the lesion:
  • L₀ = No evidence of lesion
  • L₁ = Lesion <2 cm
  • L₂ = Lesion 2-4 cm
  • L₃ = Lesion >4 cm
  • Lx= Not specified
• Site of the lesion:
  • S₁ = All oral sites except the floor of the mouth and tongue.
  • S₂ = Floor of mouth and/or tongue.
  • S_x = Not specified
• Clinical aspects:
  • C₁ = Homogeneous
  • C₂ = Nonhomogeneous
  • C_x = Not specified
• Histopathological features
  • P₁= No dysplasia
  • P₂ = Mild dysplasia
  • P₃ = Moderate dysplasia
  • P4= Severe dysplasia
  • P_x = Not specified

Leukoplakia Staging:

• Stage 1: Any L, S₁; C₁; P₁; or P₂
• Stage 2:
  • Any L, S₁ C₂, P₁, or P₂
  • Any L, S₂ C₁, P₁, or P₂
• Stage 3: Any L, S₂ C₂, P₁, or P₂
• Stage 4: Any L, any S, and C, P₃, or P₄

In the case of widespread lesions, the highest L and the highest S should be considered.

Red White And Mixed Red And White Lesions Multiple Choice Questions

Question 1. Gallenkamp colony counter is used to assess 

1. Candida density
2. Viral load
3. Lactobacillus count
4. Oral flora

Answer: 1. Candida density.

Question 2. One of the following genetic (hereditary) disorders cause white lesions on the mucosa is

1. Cowden’s syndrome
2. Digeorge’s syndrome
3. Dyskeratosis congenita
4. Peutz-Jeghers syndrome
   (Note: Genetic (hereditary) disorders that cause white lesions on mucosa are white sponge nevus, hereditary benign intraepithelial dyskeratosis, and dyskeratosis congenita).

Answer: 3. Dyskeratosis congenita

Question 3. Morsicatio buccarum denotes 

1. An ulcer caused by natal teeth
2. Chronic chewing of buccal mucosa
3. Traumatic ulcer of buccal mucosa
4. Dryness of buccal mucosa
   (Note: Buccal mucosa—morsicatio buccarum; Labial mucosa—morsicatio labiorum Lateral border of tongue—morsicatio lingua- rum)

Answer:  2. Chronic chewing of buccal mucosa

Question 4. Mucous patches are associated with 

1. NOMA
2. Canker sores
3. Secondary syphilis
4. HIV infection
   (Note: Mucous patches are mucosal necrosis appearing as grayish-white patches and seen in secondary syphilis).

Answer: 3. Secondary syphilis

Question 5. Bowens’s disease is the result of 

1. Lead ingestion
2. Mercury ingestion
3. Bismuth ingestion
4. Arsenic ingestion
   (Note: Bowens’s disease is the result of arsenic ingestion and is characterized by localized intraepidermal squamous carcinoma of the skin that may progress to invasive carcinoma).

Answer: 4. Arsenic ingestion

Question 6. Kobner’s phenomenon is associated with the appearance of new lesions 

1. After a relapse
2. Along the line of trauma
3. After complete healing
4. Along the midline

Answer: 2. Along the line of trauma

Question 7. Witkop’s disease manifestation in the oral cavity is white plaques.

1. White plaques
2. Erythematous patches
3. Bullous lesions
4. Mucosal nodules
   (Note: Witkop’s disease is hereditary benign intraepithelial dyskeratosis and associated with oral white plaques and bilateral limbal conjunctival plaques).

Answer: 1. White plaques

Red White And Mixed Red And White Lesions Viva Voce

Question 1. What is quid?
Answer: Quid is a mixture of substances containing tobacco and areca nut in either raw or manufactured form placed in the mouth, chewed, and kept in contact with oral mucosa.

Question 2. What are potentially malignant disorders?
Answer:

World Health Organization defines potentially malignant disorders (PMDs) of the oral cavity as an inherent cancerous nature of a lesion or condition in which the probability for malignant transformation at the lesion site or any part of the or digestive tract is higher in the succeeding phases.

• Precancerous lesion — A benign lesion with morphologically altered tissue which has a greater than normal risk of transforming into malignancy.
• Precancerous condition—A generalized disease state that may or may not alter the clinical appearance of tissues but is prone to develop a cancerous state than normal tissues.

Question 3. Give examples for premalignant lesions and disorders.
Answer:

• Premalignant lesions: Leukoplakia, erythroplakia, proliferative verrucous leukoplakia, palatal lesions in reverse smokers, submucous fibrosis, actinic cheilitis, and dyskeratosis congenital.
• Premalignant conditions: Lichen planus, discoid lupus erythematosus, xeroderma pigmentosum, Plummer-Vinson syndrome, immuno-suppressive diseases (AIDS).

Question 4. What is field mapping? (or) What is the field effect in cancer? What is field cancerization?
Answer:

• Morphologically normal epithelium present in close proximity to the tumor may have precancerous cells and genetic potential to develop into multiple primary tumors.
• Multiple biopsies in the clinically suspicious area is recommended to diagnose the multiple primary or recurrent tumor.

Question 5. What is orabase?
Answer:

• Orabase is an oral adhesive paste composed of gelatin, pectin, and sodium carboxymethyl-cellulose used to facilitate the adhesion of intraoral gel or ointment.
• The prescribed medication can be mixed with equal parts of orabase and applied to the mucosal tissues for better retention.

Question 6. Discuss leukoedema.
Answer:

• It is a normal variant of the oral mucosa. It manifests as a diffuse, faint, white, and filmy-wrinkling appearance of mucosa bilaterally.
• Common in buccal mucosa but involves labial mucosa, soft palate, and floor of mouth occasionally. No treatment is required.

Question 7. What is white sponge nevus?
Answer:

• It is an autosomal dominant disorder affecting oral mucosa and sometimes mucous membrane of the nose, esophagus, genitalia, and rectum.
• Bilateral symmetrical, white, soft, spongy, and velvety thick plaques appear on buccal and labial mucosa, ventral tongue, floor of the mouth, and soft palate. It is asympto¬matic and requires no treatment.

Question 8. What is linea alba?
Answer: Linea alb a is a bilateral horizontal white streak extending from the commissure to the posterior teeth. The causative factors include friction or irritation from the buccal cusps of teeth and reduced overjet of posterior teeth. No treatment is required.

Question 9. What is morsicatio buccarum or labiorum or linguarum?
Answer:

• Chronic irritation caused by self-chewing, nibbling or sucking results in a localized area of thickened, scared, and pale area of the oral mucosa.
• Patient experiences roughness or felling of delicate tissues. Sometimes erythema or ulceration is also present with the white patch.
• Stress or psychological disorder is considered as an underlying disorder.
• To stop the predisposing habits, an occlusal night guard or splint is advised. Antidepressants may be helpful for some patients.

Question 10. What is thrush?
Answer: Thrush is the superficial candidal infection of the outer layer of epithelium causing white plaques or flecks on the mucosal surface resembling the white belly of the singing bird thrush. The white plaques are easily scrapable.

Question 11. What are the predisposing factors for oral candidiasis?
Answer:

• Altered oral microflora due to routine use of antibacterial mouth rinse or prolonged use of antibiotics.
• Administration of steroid inhalants and topical steroids.
• Poor oral hygiene.
• Diabetes mellitus.
• Chronic local irritation due to dental appliances.
• Pregnancy
• Immunological deficiencies like HIV infec¬tion, cancer chemotherapy, head and neck radiation, leukemia and lymphomas, and bone marrow transplantation.
• Malabsorption and malnutrition.

Question 12. Why antioxidants are used in the management of submucous fibrosis?
Answer:

• The components of commercial betel nut products release free radicals that damage the cell structures, and biological molecules. Also, the associated nutritional deficient status delays the routine repair mechanism of the inflamed mucosa leading to an atrophic condition.
• Antioxidants stabilize and deacti¬vate the free radicals before they attack cells. Vitamins A, B complex, C, D, E, and minerals like iron, copper, and magnesium are used as standard or adjunct supplements in controlling the signs and symptoms of OSMF.

Question 13. What are Fordyce’s granules?
Answer:

• Fordyce’s granules are ectopic sebaceous glands within the oral mucosa. They are normal tissue in an abnormal location.
• They present as a group of multiple-yellowish orange papules on the buccal mucosa and vermilion borders of the lip. They are asymptomatic and require no treatment.

Question 14. Enumerate the six P’s of Lichen Planus.
Answer: Pruritic, purple, polygonal, planar, papules, and plaques—these are the six patterns of lichen planus manifestation.

Red White And Mixed Red And White Lesions Highlights

• Lesions that involve the epithelium and superficial connective tissue of oral mucosa are known as surface lesions. Surface lesions are divided into three categories based on their clinical appearance: White, red, and white and red.
• They may be due to a range of causes from hereditary to potentially malignant disorders.