2.  Red and white lesions

Q. 2. Classify white lesions of the oral cavity. Describe the aetiology, clinical features and management of leukoplakia.


Name some of the white lesions of oral mucosa. Describe the clinical features, differential diagnosis and treatment of leukoplakia of hard palate.


What are the keratinizing lesions of the oral cavity? Write about oral leukoplakia.


Define leukoplakia. Discuss the aetiopathogenesis, clinical features and treatment of oral leukoplakia.


Enumerate the ‘white lesions’ of the oral cavity. Describe leukoplakia in detail, giving differential diagnosis.


Classification of white lesions

I. Variations in structure and appearance of the normal oral mucosa

i. Leukoedema

ii. Fordyce granules

iii. Linea alba and other areas of frictional cornification.

II. Nonkeratotic white lesions

i. Habitual cheek biting

ii. Burns (thermal, aspirin, dental medicaments, radiation mucositis and uraemic stomatitis)

iii. Caused by specific infectious agents (Koplik spots, syphilitic patches)

III. Candidiasis

i. Acute pseudomembranous candidiasis (oral thrush)

ii. Acute atrophic candidiasis (antibiotic sore mouth)

iii. Chronic atrophic candidiasis (denture sore mouth and angular cheilitis)

iv. Median rhomboid glossitis

v. Chronic hyperplastic candidiasis

IV. Keratotic white lesions with no increased potential for the development of oral cancer

i. Stomatitis nicotina

ii. Traumatic keratosis

iii. Intraoral skin grafts

iv. Focal epithelial hyperplasia

v. Psoriasiform lesions (psoriasis, Reiter syndrome, geographic tongue ‘ectopic geographic tongue’)

V. Red and white lesions with defined or uncertain precancerous potential

i. Leukoplakia (homogenous, nodular or speckled and verrucous)

ii. Erythroplakia

iii. Oral lesions are with use of tobacco and alcohol (cigarette, cigar, and pipe smoking, snuff clipping tobacco and betel nut chewing, reverse smoking)

iv. Carcinoma in situ

v. Bowen disease

vi. OSMF

vii. Actinic keratosis

viii. Discoid lupus erythematosus

ix. Dyskeratosis congenita

x. Lichen planus

xi. Oral lichenoid reactions (erythema multiforme, lupus erythematosus, dermatomyositis, drug-induced lichenoid reactions, secondary syphilis and graft vs. host reactions).

This grouping provides a practical scheme for the clinician faced with for making decisions about particular lesions.


Leukoplakia is defined as ‘a white patch or plaque that cannot be characterized clinically or pathologically as any other disease’.

Leukoplakia is a keratotic plaque occurring on mucous membranes and is considered as a premalignant lesion.

Aetiologic factors

i. Tobacco products

ii. Ethanol

iii. Hot, cold, spicy and acidic foods and beverages

iv. Alcoholic mouth rinse

v. Occlusal trauma

vi. Sharp edges of prostheses or teeth

vii. Actinic radiation

viii. Syphilis

ix. Presence of Candida albicans

x. Presence of viruses.


Clinical types of leukoplakia are as follows:

a. Homogenous type

b. Speckled type

c. White and red patches

d. Verrucous type.

a. Homogenous leukoplakia

Homogenous white plaques have no red component but have a fine, white, grainy texture or a more mottled, rough appearance.

b. Speckled leukoplakia

Composed of fine or coarse variety of white and red flecks.

c. Combination of white and red patches

Basically erythroleukoplakic lesions demonstrating segregation of red and white components.

d. Verrucous leukoplakia

Has red and white components of which the white components are much thicker and protrude above the surface mucosa.

Histological types

Leukoplakia is mainly categorized into two types:

i. Those that show no atypia (dysplasia).

ii. Those that show different degrees of atypia.

A leukoplakia lesion may show severe atypia with malignant change throughout the depth of epithelial layer, but its basement membrane may still be intact, such lesion is referred to as carcinoma in situ or intraepithelial carcinoma. When intraepithelial carcinoma breaks through the basement membrane, it becomes an invasive SCC.

Leukoplakia is also divided into two types according to its spontaneous disappearance following removal of chronic irritant as follows:

i. Reversible leukoplakia: Lesions of leukoplakia are reversible after removal of chronic irritants.

ii. Irreversible leukoplakia: Persistent lesions, even after removal of irritants.

Clinical features

i. Asymptomatic, discovered during routine oral examination.

ii. More common in older age group >35 years (40–70 years) of age range, more common in men.

iii. Frequent sites are lips, vermilion border, buccal mucosa, mandibular gingiva, tongue, oral floor, hard palate, maxillary gingiva, lip mucosa and soft palate. The floor of the mouth and lateral border of tongue are high rick sites for malignant transformation.

iv. Lesions may greatly vary in size, shape and distribution, the borders may be distinct or indistinct smoothly contoured or ragged.

v. The typical homogenous leukoplakia is characterized as white, well-demarcated plaque with an identical reaction pattern throughout the lesion.

vi. The surface texture can vary from smooth thin surface to leathery appearance with surface fissures referred to as ‘cracked mud’.

vii. The nonhomogeneous type of oral leukoplakia also known as erythroleukoplakia or speckled leukoplakia may have white patches or plaque intermixed red tissue elements.

viii. Verrucous or verruciform leukoplakias are the lesions in which white component is dominated by papillary projections similar to oral papillomas.

This variety of leukoplakia with more aggressive proliferation pattern and recurrent rate are designated as proliferative verrucous leukoplakia (PVL). This is more common in older women and lower gingiva is the predilection site.

ix. Malignant potential: Those lesions situated in the high-risk areas, such as floor of the mouth, ventral surface of tongue, margins of the tongue and retro molar regions have high risk for malignant transformation.

Differential diagnosis

i. Lichen planus

ii. Leukoedema

iii. Cheek-biting lesions

iv. Smokeless tobacco lesion

v. Lupus erythematosis

vi. Hyperplastic or hypertrophic candidiasis

vii. Verrucous or squamous cell carcinoma

viii. Verruca vulgaris

ix. White sponge nevus.


I. Elimination of aetiological factors

No appropriate treatment has been established for Sanguinaria-induced leukoplakia. So, complete discontinuation of Sanguinaria containing products is mandatory and cessation of any other harmful habits like alcohol and smoking by the Patients which are well established risk factors.

II. Conservative treatment

Vitamin therapy especially vitamin A and vitamin E, B complex, 13- cis-retinoic acid, antioxidant therapy.

Nystatin therapy (in candidal leukoplakia).

III. Surgical therapy

Cold knife surgical excision.

Laser surgery.

Cryosurgery (liquid nitrogen or CO2 snow is used).

Fulguration (electro-cautery or electro-surgery).

Laser (light amplification by especially CO2 lasers Stimulated fusion of radiation).

However, in the absence of evidence-based treatment, strategies for oral leukoplakias, surgery will remain the treatment of choice for leukoplakia and erythroplakia.

A general recommendation may be to re-examine the site every 3 months for first 1 year irrespective of surgical excision.

Follow up every 6 months to see whether there is any change in reaction pattern and relapse.

Self-examination is reasonable approach if there is no relapse for 5 years.

However, an initial biopsy is mandatory. If a histopathologic diagnosis of dysplasia is rendered, the condition should be treated in a fashion similar to the treatment of other potentially premalignant processes.

All patients should be given careful clinical follow-up, with a biopsy of any recurrent or worsening lesion(s).

Q. 3. Enumerate oral precancerous lesions and conditions. Describe clinical features and management of oral submucous fibrosis.


What conditions may produce trismus? Describe in detail the predisposing factors, clinical features, treatment of oral submucous fibrosis.


Write the clinical features, differential diagnosis and management of oral submucous fibrosis.


Describe in detail aetiology, clinical features and management of oral submucous fibrosis.


Describe in detail the aetiology, clinical features, treatment plan and prognosis of submucous fibrosis.


The premalignant lesions are defined as morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart.

For example,



Nicotiana palati


Dyskeratosis congenitis.

The premalignant condition is defined as generalized state of body, which is associated with significantly increased risk of cancer.

For example, oral submucous fibrosis, syphilis, lichen planus, white sponge nevus, etc.

The following are the conditions that produce trismus:

i. Odontogenic infections

ii. Traumatic fractures

iii. Neoplastic conditions

iv. Neurotoxic agents

v. Psychogenic factors

vi. Pharmacological substances.

Oral submucous fibrosis

It is a chronic disease that affects the oral mucosa as well as the pharynx and upper two third of the oesophagus.

It is a high-risk precancerous condition.

Aetiology and pathogenesis

i. Chronic irritation

a. Betel nut, i.e., areca nuts (alkaloids)

b. Chillies capsaicin (active ingredient causing irritation)

c. Tobacco

d. Lime Image

Areca nut, quid chewing habit and development of OSMF is dose dependant and the mechanism is described below:


ii. Genetic predisposition

Genetic predisposition is an important aetiologic factor behind OSMF.

Familial occurrence of OSMF has been reported.

iii. Nutritional deficiency

Vitamin B complex deficiency.

Deficiency is precipitated by the defective nutrition due to impaired food intake.

iv. Bacterial infections

For example, streptococcal toxicity.

Klebsiella rhinoscleromatis may be causative factors in OSMF.

v. Collagen disorders

OSMF is thought to be localized collagen disease of oral cavity.

It is linked to scleroderma and rheumatoid arthritis.

Scleroderma and OSMF have similar histological features.

vi. Immunological disorders

↑ESR and globulin levels indicate immunodeficiency disorder. Serum immunoglobulin levels of IgA, IgG and IgM are ↑ significantly in OSMF, which suggest an antigenic stimulus in the absence of any infection.

Circulating auto antibodies are present in some cases of OSMF.

Clinical features

i. Age and sex: Equally affects both the sexes and patients are between second and fourth decade.

ii. Site: Most frequent locations are buccal mucosa (98%) and retromolar areas. Commonly involved sites are: soft palate, (49%) palatal fauces, uvula, tongue and labial mucosa.

iii. Prodromal symptoms: Onset of OSMF is insidious and is often 2- to 5-year duration. Most common initial symptom is burning sensation of oral mucosa, aggravated by spicy food followed by either hypersalivation or dryness of mouth.

iv. The first sign is erythematous lesions, sometimes in association with petechiae, pigmentations and vesicles.

v. Initial lesions are followed by paler mucosa, which comprise white marbling.

vi. In the later course of the disease, the most prominent clinical features appear, i.e. fibrotic bands located beneath an atrophic epithelium.

vii. ↑fibrosis leads to loss of resilience, which causes interference with speech, tongue mobility and a decreased ability to open the mouth.

viii. The atrophic epithelium may cause a smarting sensation and inability to eat hot and spicy food.

ix. Diagnosis of OSMF is based on clinical features and patients report of a habit of betel quid chewing.

An international consensus has been reached where at least one of the following characteristics should be present to diagnose OSMF, they are as follows:

i. Palpable fibrous bands.

ii. Mucosal texture feels tough and leathery.

iii. Blanching of mucosa together with histopathologic features consistent with OSMF (i.e., atrophic epithelium with loss of rete ridges and Juxta epithelial hyalinization of lamina propria).


Early histopathological characteristics of OSMF are:

Fine fibrils of collagen, oedema, hypertrophic fibroblasts, dilated and congested blood vessels and infiltration of neutrophilic and eosinophilic granulocytes.

↓followed by

Down regulation of fibroblasts, epithelial atrophy and loss of rete pegs and early signs of hyalinization in concert with an infiltration of inflammatory cells.

Epithelial dysplasia (7–26%) of cases.

Malignant transformation of OSMF has been estimated in the range of 7–13% and incidence over 10-year period is 8%.


i. Stopping of chewing habits, especially areca nut as it is carcinogenic. If this is successfully implemented. Early lesions have a good prognosis as they may regress.

ii. Supportive treatment

Vitamin rich diet.

Iodine, B-complex preparations (e.g., injection ranodine) Injection of arrsenotyphoid and iodine (arrsenotyphoid is a fibrin dissolving agent).

iii. Steroids

Both Topical—e.g., hydrocortisone injection along with procaine HCl intralesionally every fortnight.
Systemic—e.g., cortisone, hydrocortisone 25 mg tab in doses of 100 mg/day. Triamcinolone or 90 mg dexamethasone.

Increased vascularity at the affected site attributed to fibrolytic, antiallergic and anti-inflammatory action of corticosteroid.

The fibrosis is prevented by decreasing fibroblastic production and deposition of collagen.

iv. Placental extract

It is an essential biogenic stimulator. Only the aqueous extract of placenta acts as biogenic stimulator. It accelerates cellular metabolism, stimulated regenerative process, aids in absorption of exudates, increases physiologic function of organs and significant enhancement of wound healing and it has notable anti-inflammatory effect. Dose—Intralesionally 2 mL of solution is deposited in five divided regions of the lesions at intervals of 3 days or about 15 days. If required the course is repeated after a month.

v. Hyaluronidase: It acts by breaking down the hyaluronic acid, i.e., the ground substance of connective tissues.

vi. Surgical procedures: When there is marked limitation of opening the surgery is the treatment method of choice.

a. Excision of fibrous bands followed by use of tongue flap as a graft or bilateral full thickness nasolabial flap.

b. New technique of bilateral palatal flaps to cover exposed area in combination with the bilateral temporalis myotomy and coronoidectomy.

c. LASER—with CO2 laser under GA incise the buccal mucosa and vaporize the submucosal connective tissue to the level of buccinator muscle.

d. Cryosurgery—local destruction of tissue by freezing it in sites.

vii. Oral physiotherapy: oral exercises are advised in early and moderately advanced cases.

viii. Diathermy: Microwave diathermy is useful in early and moderate lesions like mouth opening and ballooning of mouth.

Q. 4. Write an essay on oral candidiasis.


Classify oral mucosal candidiasis. Write the aetiopathogenesis, clinical features, investigations and management of chronic atrophic candidiasis.


Enumerate the various white lesions that can be scrapped. Describe the clinical features, differential diagnosis and treatment of candidiasis.


Enumerate predisposing factors of candidiasis. Mention the various types and discuss in detail the treatment plan.


Classify candidiasis. Write in detail about the aetiology, clinical features and management of oral thrush.


Classify candidiasis and give clinical features, laboratory diagnosis tests and treatment of oral candidal infection.


Treatment of acute pseudomembranous moniliasis.

Ans. Oral candidiasis is the most prevalent opportunistic infection affecting oral mucosa.

Most candida infections only affect mucosal linings, but the rare systemic manifestations may have fatal course.

Aetiology and pathogenesis

C. albicans, C. tropicalis and C. glabrata

C. albicans constitute 80% of species isolated from human candidiasis.

Candida is a common, harmless, dimorphic yeast.

Predisposing factors to oral candidiasis

I. Drugs and medications

Broad-spectrum antibiotics (e.g., tetracycline)

Multiple antibiotic regimens


Cytotoxic agents

Immunosuppressive agents

Anticholinergics (xerostomia producing)

II. Endocrinopathies

Diabetes mellitus





III. Haematologic disorders

Aplastic anaemia




IV. Immune deficiency

HIV disease

Thymic alymphoplasia (Neselof syndrome)

Thymic hypoplasia (DiGeorge syndrome)

Severe combined immunodeficiency syndrome (Swiss type)

Chronic mucocutaneous candidiasis

V. Leukocyte disorders

Myeloperoxidase deficiency


VI. Malignancy



Advanced cancer

Nutritional deficiencies

Iron deficiency

Folic acid deficiency

Vitamin B deficiency

Vitamin C deficiency



VII. Others

Radiation therapy

Sjogren syndrome


Old age

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Apr 11, 2016 | Posted by in Orthodontics | Comments Off on 2.  Red and white lesions
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