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White Lesions of the Oral Mucosa, Lecture notes of Dentistry

Cairo UniversityDentistry

A comprehensive overview of various types of white lesions that can occur in the oral cavity. It discusses the pathogenesis, clinical features, and histopathological characteristics of conditions such as hyperkeratosis, frictional keratosis, oral hairy leukoplakia, lichen planus, and other non-epithelial white-yellow lesions. The document delves into the underlying mechanisms, associated factors, and diagnostic considerations for these diverse oral mucosal conditions. It serves as a valuable resource for healthcare professionals, particularly dentists and oral pathologists, in understanding the etiology, clinical presentation, and management of these common and sometimes challenging oral lesions.

Typology: Lecture notes

2023/2024

Available from 08/26/2024

DR.dent
DR.dent 🇪🇬

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White lesions
• The normal pink color of the oral mucosa principally, results from interplay between four factors. These
factors are vascularity, melanin pigment, epithelial thickness and keratinization.
• The normal pink color of the oral mucosa results from light passing through the translucent superficial
layers of the soft tissue, striking the capillary bed and then being reflected again through the superficial
translucent layer of the mucosa.
• Changes on and in the tissue that interfere with light reflection from the capillary bed leading to → white
appearing lesion. Such lesions may be associated with:
A thickened or an increased surface keratin layer (hyperkeratosis) which appears white when wet.
Increased thickness of the epithelium as the thickened spinous layers (acanthosis) masks the
normal vascularity (redness) of the underlying connective tissue.
Reduced vascularity of subjacent connective tissue.
Caustic agent or thermal burns produce coagulation and opacity of the superficial tissue.
Fungal colonies which provide pseudomembranes.
Abnormal changes in the connective tissue as those associated with tumour growth, submucosal
deposits or hyperkeratinization. These changes act as a mechanical barrier between the
transmitted light and the capillary bed → white appearance.
Fibrin exudates and surface debris covering an ulcer.
Classification of white lesions
1- Hereditary conditions
• Leukodema
• White spongy nevus
• Hereditary benign intraepithelial dyskeratosis
• Follicular keratosis
2-Reactive lesions
• Focal (frictional) hyperkeratosis
• Nicotine stomatitis
• White lesions associated with smokeless tobacco.
• Actinic cheilitis (discussed in premalignant lesions)
3- Other white lesions
• Leukoplakia (discussed in premalignant lesions)
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White lesions

  • The normal pink color of the oral mucosa principally, results from interplay between four factors. These factors are vascularity, melanin pigment, epithelial thickness and keratinization.
  • The normal pink color of the oral mucosa results from light passing through the translucent superficial layers of the soft tissue, striking the capillary bed and then being reflected again through the superficial translucent layer of the mucosa.
  • Changes on and in the tissue that interfere with light reflection from the capillary bed leading to → white appearing lesion. Such lesions may be associated with: A thickened or an increased surface keratin layer (hyperkeratosis) which appears white when wet. Increased thickness of the epithelium as the thickened spinous layers (acanthosis) masks the normal vascularity (redness) of the underlying connective tissue. Reduced vascularity of subjacent connective tissue. Caustic agent or thermal burns produce coagulation and opacity of the superficial tissue. Fungal colonies which provide pseudomembranes. Abnormal changes in the connective tissue as those associated with tumour growth, submucosal deposits or hyperkeratinization. These changes act as a mechanical barrier between the transmitted light and the capillary bed → white appearance. Fibrin exudates and surface debris covering an ulcer. Classification of white lesions 1 - Hereditary conditions
    • Leukodema
    • White spongy nevus
    • Hereditary benign intraepithelial dyskeratosis
    • Follicular keratosis 2 - Reactive lesions
    • Focal (frictional) hyperkeratosis
    • Nicotine stomatitis
    • White lesions associated with smokeless tobacco.
  • Actinic cheilitis (discussed in premalignant lesions) 3 - Other white lesions
    • Leukoplakia (discussed in premalignant lesions)
  • Squamous cell carcinoma (discussed in malignant epithelial non odontogenic)
  • Verrucous carcinoma (discussed in malignant epithelial non odontogenic)
  • Geographic tongue (discussed in developmental anomalies of soft tissue)
  • Hairy tongue (discussed in soft tissue anomalies).
  • Hairy leukoplakia
  • Lichen planus
  • Lupus erythematosus 5 - Non epithelial white yellow lesion
  • Candidiasis (discussed in infectious diseases)
  • Mucosal burn
  • Oral submucous fibrosis (discussed in premalignant lesions)
  • Fordyce’s granules
  • Ectopic lymphoid tissue
  • Gingival cyst (discussed in cyst)
  • Lipoma (discussed in benign non.odontogenic tumors) 1 - Hereditary conditions Leukodema Etiology and pathogenesis: To date, the cause of leukodema hasn’t been established. Ethnic and racial clustering suggests hereditary factors. It is considered as normal variation. Clinical features Age: Adults and children. Site: Leukodema typically occurs bilaterally on the buccal mucosa and may extend forward onto the labial mucosa. Race: It occurs more commonly in blacks (persons of racial pigmentation of the oral mucosa). Signs and symptoms
  • It’s asymptomatic and usually discovered as an incidental finding.
  • It presents as a gray white or translucent milky white mucosal lesion.
  • Its surface frequently appears filmy or slightly wrinkled.
  • Leukodema can be easily diagnosed clinically because the white appearance greatly diminishes or disappears when the cheek is everted and stretched.

Hereditary benign intraepithelial dyskeratosis (HBID)

  • Dyskeratosis is the keratinization of cells within the stratum spinosum, where the cells are not normally keratinized
  • HBID is rare autosomal dominant hereditary condition occurring mainly in North Carolina (USA). Clinical features Age: It is a syndrome that includes the early onset (during childhood usually within the first year of life until midadolescence), with a gradual increase in intensity. Site: It affects the oral and conjunctival mucosa.
  • Oral mucosal lesions characteristically involve buccal, labial mucosa. Also, floor of the mouth, lateral surfaces of the tongue, gingiva and palate may be involved. S igns and symptoms
  • Oral lesions consist of asymptomatic white plaques similar to those of white spongy nevus. Mild cases may exhibit the opalescent appearance of leukodema.
  • The most interesting feature of HBID is the bilateral ocular lesions which appears as thick, opaque, foamy gelatinous plaques affecting the conjunctiva. Histopathologic features
  • Similarities between oral and conjunctival lesions are noted microscopically.
  • Histopathologic features of the HBID include: Hyperparakeratotic epithelium with marked acanthosis. Dyskeratotic cells (premature keratinization) scattered through the superficial half of the epithelium. They are called waxy eosinophilic cells as they are enlarged hyalinized cells. With this dyskeratotic process, an epithelial cell appears to be surrounded or engulfed by an adjacent epithelial cell, resulting in the cell within cell phenomenon. Non dyskeratotic cells which are enlarged and oedematous cells with significant hydropic degeneration. These cells are admixed with the dyskeratotic cells.
  • The underlying connective tissue shows no changes. Treatment: It is self limiting with no risk of malignant transformation i.e. no require treatment.

Follicular keratosis (Darier`s disease)

  • It is an uncommon inherited disorder with skin involvement and relatively oral mucosal lesion. Clinical features Age: Onset of this disease is usually noticed in children or adolescence. Site: Skin lesions are symmetrically distributed over the face, trunk, palms, soles and dorsa of the hands. The fore head, scalp and ears are common sites.
  • Favoured oral mucosal sites include keratinized regions such as attached gingival and hard palate S igns and symptoms
  • The characteristic skin lesion consists of: Symmetrically distributed small erythematous, often pruritic papular lesions which coalesce, ulcerate and crust. The coalesced areas subsequently form patches of verrucous growths due to excessive keratin formation. Accumulation of keratin may be associated with foul smelling (odour) due to bacterial degradation of keratin as a result of secondary infection. Thickening of the palms and soles due to excessive keratin. They often exhibit pits and keratoses.
  • Nail changes are often helpful in establishing a diagnosis. Finger nail changes may include: fragility, longitudinal lines and splintering.
  • Oral lesions: They are typically asymptomatic multiple white flat topped papules. Histopathologic features
  • Microscopic examination of skin and mucosal lesions shows: Hyperkeratosis and acanthosis. Formation of intraepithelial clefts which appear as :
  1. Suprabasal clefts (lacunae) containing acantholytic epithelial cells, with upward proliferation of papillae lined by single layer of basal cells (villi) into the cleft
  2. Vertical clefts lined by parakeratotic and dyskeratotic cells. Presence of dyskeratotic cells (corps ronds and corps grains) in the roof of the suprabasal cleft and overlying epithelium. Corps ronds: Large abnormally keratinized cells with basophilic nuclei and intensely eosinophilic cytoplasm with clear perinuclear halo. Corps grains: Small flattened parakeratotic cells with pyknotic hyperchromatic nuclei. Treatment: Treatment of this disease depends on the severity of the involvement.

Histopathologic features: Histological examination shows

  • Significant hyperkeratosis and moderate levels of acanthosis of the palatal mucosa.
  • Mild to severe inflammatory changes of the minor salivary glands.
  • Mild and patchy chronic inflammation of subepithelial connective tissue Treatment: The palate returns to normal usually within 1 to 2 weeks of smoking cessation. 3 - Other white lesions Oral hairy Leukoplakia (OHL)
  • Hairy Leukoplakia represents an opportunistic infection related to the presence of Epstein-Barr virus (EBV) found almost exclusively in human immunodeficiency virus (HIV) - infected individuals (AIDS patients). Clinical features
  • The vast majority of OHL have been located along the lateral margins of the tongue. It may be unilateral or bilateral.
  • In general, there are no associated symptoms.
  • Most cases of OHL present as white lesion that appears plaque like lesion or hair like projections. Histopathologic features
  • Hyperplastic epithelium with hyperparakeratotic surface, often with the formation of thin keratotic projections → surface irregularities and ridges.
  • Heavy Candidal infection of the parakeratin layer and the superficial epithelial cell layers is typical.
  • Ballooning degeneration and perinuclear clearing in the upper spinous layers. These cells have web like cytoplasm i.e. not clear. Nuclear alteration as pyknosis is created by extensive EBV replication.
  • No epithelial dysplasia i.e. not a premalignant lesion. Treatment: There is no specific treatment for OHL.
  • Responses to some antiviral drugs such as acyclovir have been reported, with a return of lesion often noted on discontinuation of therapy. Lichen planus
  • Lichen planus is a mucocutaneous disease which undergoes remissions and exacebations. Etiology:
  • The etiology of lichen planus is unknown but many factors have been implicated. These factors include genetic predisposition, infective agents, systemic diseases, vitamin deficiencies and psychiatric disorders or stresses.

Pathogenesis

  • The pathogenesis of lichen planus isn’t yet understood, but the earliest changes are damage to the basement membrane and some of the basal epithelial cells i.e. epithelial basal cells are the primary target in lichen planus. The mechanism of basal cell damage in lichen planus appears to be related to a cell mediated immune process involving langerhans cells, T-lymphocytes and macrophages. N.B: A variety of medications may induce lesions that appear clinically identical to lichen planus; however the term lichenoid reaction is a better name for these drug related alterations. Generally, it resolves rapidly after withdrawal of the offending drug. Signs & symptoms (1) Skin lesions
  • The characteristic skin lesions are violaceous, flat topped, itchy papules which may have distinctive white streaks on the surface (Wickham`s striae).
  • Almost any area of skin may be involved, but the flexor aspect of the wrist is the commonest site. (2) Oral lesions
  • In patients with oral lichen planus, the buccal mucosa is involved in the great majority of cases. Lesions are generally bilateral and a wide spectrum of clinical presentations may occur.
  • Clinical presentations (oral types) of lichen planus Reticular form (classic form). Plaque form (hyperplastic form). Atrophic form. Erosive or ulcerative form. Bullous form. The reticular (classic form)
  • It is the most common type.
  • Reticular lichen planus is thus named because of its characteristic pattern of interlacing white lines or striae (so called Wickham`s striae).
  • The buccal mucosa is the most common site and the striae are typically occurred in a symmetric pattern. The plaque form (hyperplastic form)
  • It tends to resemble leukoplakia clinically but has a multifocal distribution.
  • The primary sites for this variant are over the dorsum of the tongue and on the buccal mucosa. NB: The reticular and plaque patterns are usually symptom free.

Lupus erythematosus (LE)

  • It the most common connective tissue disease in the United States.
  • Two main forms of this disease are recognized; discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE). Etiology & pathogenesis: LE is thought to result from an autoimmune process. Clinical features Discoid lupus erythematosus
  • The lesions in DLE are often restricted to the skin and usually occur on the face and scalp.
  • Lesions appear as red patches or plaques with hyperpigmented margins. As the lesions expand peripherally, the centre heals, with the formation of scar and loss of pigment. N.B: Involvement of hair follicles results in permanent hair loss (alopecia).
  • Oral lesions have been reported in up to 25 % of cases of DLE and although any part of the mucosa may be involved, the cheeks are most frequently affected.
  • There is considerable variation in the type of oral lesion seen, it may appear as lesions of erosive lichen planus: an ulcerated or atrophic erythematous central zone, surrounded by white, fine, radiating striae. Sometimes, the erythematous, atrophic central region of a lesion may show a fine stippling of white keratotic papules. Systemic lupus erythematosus
  • SLE is a serious multisystem disease with a variety of cutaneous and oral manifestations.
  • In this form of LE, skin and mucosal lesions are are generally similar to those seen in DLE but relatively mild and patient’s complaints are dominated by multiple system involvement.
  • Women are affected nearly 8 to 10 times more frequently than men.
  • Involvement of skin results in maculo-papular erythematous rash (typically occur on the cheeks). These skin rashes are photosensitive (sun light often makes the lesion worse). In 40 % to 50 % of affected patients, a characteristic butterfly pattern with symmetrical distribution over the nose and molar area of the cheek develops.
  • Kidney lesions are the most important and significant aspect of this disease because this complication may lead to kidney failure.
  • Cardiac involvement is also common, with pericarditis being the most frequent complication. SLE patients may display warty vegetations affecting the heart valves → bacterial endocarditis.
  • Involvement of the joints results in arthritis.

Histopathologic features: The Histopathologic features of skin and oral lesions of the various forms of LE show some features in common. These features include: (1) Liquefaction degeneration of the basal cell layer. (2) Hyperkeratosis, alternating atrophy and thickening of the spinous cell layer. (3) Subepithelial patchy or dense lymphocytic infiltration. In the deeper connective tissue, perivascular foci of lymphocytes are present. (4) Subepithelial oedema sometimes → vesicle formation.

  • LE and lichen planus can be distinguished by the presence of (in LE): o Patchy deposits of a periodic acid-schiff (PAS) – positive material in the basement membrane. o Subepithelial oedema. o And a more diffuse, deep inflammatory infiltrate, often in a perivascular orientation. Treatment: Topical and systemic steroids are usually used for treatment of DLE and SLE, respectively. 4 - Non-epithelial white yellow lesions Mucosal burn Etiology: In cases of short-term exposure to agents capable of inducing tissue necrosis, a localized mild erythema may occur. As the severity of the offending agent increases and as the contact time increases, surface coagulative necrosis is more likely to occur, resulting in a white slough or membrane. With gentle traction, the surface slough peels from the denuded connective tissue (rubbed off) → painful surface that bleeds easily on manipulation. (1) Chemical burns
  • It is associated with topical applications of caustic chemical agents as: Aspirin burns: Mucosal necrosis produced by the topical use of aspirin ( i.e. aspirin being held in the mouth) is not rare. Caustic materials absorbed by cotton roll used for moisture control during dental procedures hold against the mucosa for an extended period. Dentifrices associated slough: This is a relatively common phenomenon that has been associated with the use of several different brands of tooth paste. It is believed to be a reaction to a component of the dentifrice, possibly the detergent or flavouring compounds. Clinical features: It appears as a superficial whitish slough of the buccal mucosa, typically detected as oral peeling. Treatment: The problem resolves with a switch to other toothpaste.