Reactive Keratotic Lesions (Nonleukoplakias)

White keratotic mucosa lesions are some of the more commonly biopsied lesions and both benign and dysplastic lesions often pose a diagnostic challenge. Table 10.1 provides a list of mucosal conditions that are clinically white; these are discussed in this and other chapters. The term “leukoplakia” is not any white lesion, but rather a clinical term to denote a keratotic lesion that does not represent reactive keratosis or other known keratotic lesion, and has a high risk of developing dysplasia and carcinoma (see Chapter 11 ).

TABLE 10.1
Histologic Diagnoses for Maculopapular White Lesions
Developmental/Hereditary (see Chapter 2 )
  • Cannon white sponge nevus

  • Hereditary benign intraepithelial dyskeratosis

  • Oral pachyonychia congenita

  • Darier disease

Reactive/Inflammatory
Chemical or Heat
  • Leukoedema

  • Dentifrice-associated desquamation

  • Smokeless tobacco lesion

  • Nicotinic stomatitis

  • Irritant contact stomatitis (see Chapter 7 )

Frictional/Factitial
  • Morsicatio mucosae oris

  • Benign alveolar ridge keratosis (oral lichen simplex chronicus)

  • Frictional parakeratosis at the edge of traumatic ulcers

  • Other frictional/factitial keratoses

Retention Keratosis
Hairy tongue
Immune-Mediated or Autoimmune (see Chapter 8 )
  • Lichenoid stomatitis, lichenoid hypersensitivity reaction, or lichen planus

  • Lupus erythematosus

  • Chronic graft-versus-host disease

Infectious (see Chapter 4 )
  • Candidiasis

  • Hairy leukoplakia

  • Others (eg, geotrichosis)

Premalignant and Malignant (see Chapter 11 )
  • Epithelial dysplasia

  • Carcinoma-in-situ

  • Atypical endophytic squamous proliferation

  • Verrucous hyperplasia

  • Squamous cell carcinoma

  • Verrucous carcinoma

Others
  • Warty dyskeratoma

  • Epidermolytic hyperkeratosis

  • Palifermin-induced keratosis

Fibrosis (Not Involving the Epithelium)
  • Submucous fibrosis (see Chapter 11 )

  • Mucosal fibrosis in progressive systemic sclerosis

The oral mucosa appears white for several reasons:

  • Presence of keratin in a normally nonkeratinized site (namely buccal and lip mucosa, ventral tongue, floor of mouth, and soft palate).

  • Parakeratosis or hyper(ortho)keratosis in a normally keratinized site (hard palatal mucosa and attached gingiva); the tongue being normally parakeratinized is the only site that can show hyperparakeratosis.

  • Degeneration and/or coagulation of superficial keratinocytes.

  • Edema of keratinocytes.

  • Alteration of the epithelial cells because of benign but abnormal keratin formation or aggregation (benign dyskeratotic disorders, see Chapter 2 ).

  • Epithelial dysplasia (see Chapter 11 ).

  • Nonepithelial changes such as underlying scarring and fibrosis.

Mild irritation of the oral mucosa leads to acanthosis, and keratinocyte damage that initially takes the form of keratinocyte edema, then degeneration of superficial keratinocytes, and in some cases spongiosis; there may be parakeratosis or in more chronic lesions, hyperkeratosis. In general, reactive keratotic lesions have poorly demarcated margins with keratosis tapering at the edges, whereas true leukoplakias, which are either dysplastic or represent keratoses of unknown significance, are white plaques with abrupt keratinization. Correlating the histopathologic and clinical findings is essential in arriving at an accurate diagnosis.

Leukoedema

This term should be reserved for the clinical presentation; the histopathologic feature is keratinocyte edema.

Clinical Findings

  • This is present in up to 90% of the population and is more readily discerned in dark-skinned individuals.

  • Delicate lacy, gray-white lines are present on the buccal mucosa or tongue (nonkeratinized site) that disappear with stretching ( Fig. 10.1 ).

    FIG 10.1
    Leukoedema. (A) Grayish reticulations of the right buccal mucosa. (B) Stretching the mucosa of the patient in A causes the lesion to disappear.

Etiopathogenesis and Histopathologic Features

Leukoedema usually results from mildly irritating substances (such as smoke from tobacco products or marijuana, caustic oral rinses, or toothpaste) in episodic contact with the mucosa. It is also associated with a minimally traumatic, parafunctional habit such as mucosal sucking.

  • Acanthosis is always present and there is keratinocyte edema of superficial cells causing cells to be enlarged, pale, and ballooned; anucleation may be caused by plane of section and/or nuclear degeneration; cell membranes have a compact “jigsaw puzzle” appearance and keratinocytes often exhibit perinuclear halos (but they do not represent koilocytes because the nuclei are not shrunken or hyperchromatic) ( Fig. 10.2 ).

    FIG 10.2
    Leukoedema. (A) Oral mucosa with acanthosis. (B) Acanthosis and pale cells. (C) Superficial anucleate cells with “jigsaw puzzle” cell membranes and cells with perinuclear halos (bottom).
  • Minimal to no keratin is noted, although parakeratin chevrons may be present, similar to smokeless tobacco lesions ( Fig. 10.3 ). There is minimal to no inflammation in the lamina propria.

    FIG 10.3
    Leukoedema. (A) Parakeratosis, acanthosis, and pale ballooned cells. (B) Parakeratin chevrons and keratinocyte edema. (C) Keratinocyte edema with “jigsaw puzzle” outlines.

Differential Diagnosis

  • Keratinocyte edema is seen in contact lesions and in association with frictional/factitial keratoses, although the latter will also show marked parakeratosis or hyperkeratosis.

  • Hairy leukoplakia shows chromatin condensation against the nuclear membrane and Cowdry inclusion bodies, and are positive for Epstein-Barr virus (EBV).

Management and Prognosis

  • No treatment is necessary for leukoedema, although patients should be educated about the causes and avoidance of the causative agent if appropriate.

References

  • Axell T: Leukoedema—an epidemiologic study with special reference to the influence of tobacco habits. Community Dent Oral Epidemiol 1981; 9: pp. 142-146.
  • Canaan TJ, Meehan SC: Variations of structure and appearance of the oral mucosa. Dent Clin North Am 2005; 49: pp. 1-14.
  • Heyl T, Raubenheimer EJ: Sucking pads (sucking calluses) of the lips in neonates: a manifestation of transient leukoedema. Pediatr Dermatol 1987; 4: pp. 123-128.
  • Martin JL: Leukoedema: an epidemiological study in white and African Americans. J Tenn Dent Assoc 1997; 77: pp. 18-21.
  • Van Wyk CW, Ambrosio SC: Leukoedema: ultrastructural and histochemical observations. J Oral Pathol 1983; 12: pp. 319-329.
  • Versteeg PA, Slot DE, van der Velden U, van der Weijden GA: Effect of cannabis usage on the oral environment: a review. Int J Dent Hyg 2008; 6: pp. 315-320.
  • Clinical Findings

    • This is present in up to 90% of the population and is more readily discerned in dark-skinned individuals.

    • Delicate lacy, gray-white lines are present on the buccal mucosa or tongue (nonkeratinized site) that disappear with stretching ( Fig. 10.1 ).

      FIG 10.1
      Leukoedema. (A) Grayish reticulations of the right buccal mucosa. (B) Stretching the mucosa of the patient in A causes the lesion to disappear.

    Etiopathogenesis and Histopathologic Features

    Leukoedema usually results from mildly irritating substances (such as smoke from tobacco products or marijuana, caustic oral rinses, or toothpaste) in episodic contact with the mucosa. It is also associated with a minimally traumatic, parafunctional habit such as mucosal sucking.

    • Acanthosis is always present and there is keratinocyte edema of superficial cells causing cells to be enlarged, pale, and ballooned; anucleation may be caused by plane of section and/or nuclear degeneration; cell membranes have a compact “jigsaw puzzle” appearance and keratinocytes often exhibit perinuclear halos (but they do not represent koilocytes because the nuclei are not shrunken or hyperchromatic) ( Fig. 10.2 ).

      FIG 10.2
      Leukoedema. (A) Oral mucosa with acanthosis. (B) Acanthosis and pale cells. (C) Superficial anucleate cells with “jigsaw puzzle” cell membranes and cells with perinuclear halos (bottom).
    • Minimal to no keratin is noted, although parakeratin chevrons may be present, similar to smokeless tobacco lesions ( Fig. 10.3 ). There is minimal to no inflammation in the lamina propria.

      FIG 10.3
      Leukoedema. (A) Parakeratosis, acanthosis, and pale ballooned cells. (B) Parakeratin chevrons and keratinocyte edema. (C) Keratinocyte edema with “jigsaw puzzle” outlines.

    Differential Diagnosis

    • Keratinocyte edema is seen in contact lesions and in association with frictional/factitial keratoses, although the latter will also show marked parakeratosis or hyperkeratosis.

    • Hairy leukoplakia shows chromatin condensation against the nuclear membrane and Cowdry inclusion bodies, and are positive for Epstein-Barr virus (EBV).

    Management and Prognosis

    • No treatment is necessary for leukoedema, although patients should be educated about the causes and avoidance of the causative agent if appropriate.

    References

  • Axell T: Leukoedema—an epidemiologic study with special reference to the influence of tobacco habits.Community Dent Oral Epidemiol 1981; 9: pp. 142-146.
  • Canaan TJ, Meehan SC: Variations of structure and appearance of the oral mucosa.Dent Clin North Am 2005; 49: pp. 1-14.
  • Heyl T, Raubenheimer EJ: Sucking pads (sucking calluses) of the lips in neonates: a manifestation of transient leukoedema.Pediatr Dermatol 1987; 4: pp. 123-128.
  • Martin JL: Leukoedema: an epidemiological study in white and African Americans.J Tenn Dent Assoc 1997; 77: pp. 18-21.
  • Van Wyk CW, Ambrosio SC: Leukoedema: ultrastructural and histochemical observations.J Oral Pathol 1983; 12: pp. 319-329.
  • Versteeg PA, Slot DE, van der Velden U, van der Weijden GA: Effect of cannabis usage on the oral environment: a review.Int J Dent Hyg 2008; 6: pp. 315-320.
  • Contact Desquamation

    Clinical Findings

    • Painless, thready white tissue lies on the mucosa (usually nonkeratinized sites) which easily peels off, leaving normal mucosa ( Fig. 10.4 ); surrounding leukoedema may be seen and patients may also exhibit contact desquamative cheilitis.

      FIG 10.4
      Dentifrice-induced desquamation: superficial keratinocytes are degenerated and peel off, leaving normal-appearing mucosa. Note the subtle leukoedema.

    Etiopathogenesis and Histopathologic Features

    This condition results from caustic mouth washes high in alcohol content, strong toothpastes, or other contactants that are irritants but not strong enough to cause necrosis and ulceration (as aspirin would).

    • Strips of desquamated keratinocytes appear eosinophilic and degenerated or coagulated ( Figs. 10.5 and 10.6 ).

      FIG 10.5
      Dentifrice-induced desquamation: degenerated epithelium from patient shown in Fig. 10.4 .

      FIG 10.6
      Dentifrice-induced contact desquamation. (A) Strips of epithelium (arrows) lie detached from the mucosa. (B) Ribbons of coagulated keratinocytes.

    Management

    • Resolution occurs on discontinuation of use of dentifrice.

    References

  • Foti C, Romita P, Ficco D, et. al.: Allergic contact cheilitis to amine fluoride in a toothpaste.Dermatitis 2014; 25: pp. 209.
  • Francalanci S, Sertoli A, Giorgini S, et. al.: Multicentre study of allergic contact cheilitis from toothpastes.Contact Dermatitis 2000; 43: pp. 216-222.
  • Kowitz G, Jacobson J, Meng Z, Lucatorto F: The effects of tartar-control toothpaste on the oral soft tissues.Oral Surg Oral Med Oral Pathol 1990; 70: pp. 529-536.
  • Kuttan NA, Narayana N, Moghadam BK: Desquamative stomatitis associated with routine use of oral health care products.Gen Dent 2001; 49: pp. 596-602.
  • Clinical Findings

    • Painless, thready white tissue lies on the mucosa (usually nonkeratinized sites) which easily peels off, leaving normal mucosa ( Fig. 10.4 ); surrounding leukoedema may be seen and patients may also exhibit contact desquamative cheilitis.

      FIG 10.4
      Dentifrice-induced desquamation: superficial keratinocytes are degenerated and peel off, leaving normal-appearing mucosa. Note the subtle leukoedema.

    Etiopathogenesis and Histopathologic Features

    This condition results from caustic mouth washes high in alcohol content, strong toothpastes, or other contactants that are irritants but not strong enough to cause necrosis and ulceration (as aspirin would).

    • Strips of desquamated keratinocytes appear eosinophilic and degenerated or coagulated ( Figs. 10.5 and 10.6 ).

      FIG 10.5
      Dentifrice-induced desquamation: degenerated epithelium from patient shown in Fig. 10.4 .

      FIG 10.6
      Dentifrice-induced contact desquamation. (A) Strips of epithelium (arrows) lie detached from the mucosa. (B) Ribbons of coagulated keratinocytes.

    Management

    • Resolution occurs on discontinuation of use of dentifrice.

    References

  • Foti C, Romita P, Ficco D, et. al.: Allergic contact cheilitis to amine fluoride in a toothpaste.Dermatitis 2014; 25: pp. 209.
  • Francalanci S, Sertoli A, Giorgini S, et. al.: Multicentre study of allergic contact cheilitis from toothpastes.Contact Dermatitis 2000; 43: pp. 216-222.
  • Kowitz G, Jacobson J, Meng Z, Lucatorto F: The effects of tartar-control toothpaste on the oral soft tissues.Oral Surg Oral Med Oral Pathol 1990; 70: pp. 529-536.
  • Kuttan NA, Narayana N, Moghadam BK: Desquamative stomatitis associated with routine use of oral health care products.Gen Dent 2001; 49: pp. 596-602.
  • Frictional/Factitial Keratoses

    The majority of parakeratotic and hyperkeratotic lesions in the oral cavity are reactive, frictional keratoses. Two histologically well-defined frictional keratoses in the oral cavity are morsicatio mucosae oris (generally on the nonkeratinized mucosa), and benign alveolar ridge keratosis (generally on the keratinized mucosa). The linea alba on the buccal mucosa is considered a variation of normal and represents either leukoedema or mild morsicatio mucosae oris ( Fig. 10.7A ).

    FIG 10.7
    (A) Linea alba: keratotic linear lesion with fading margins. (B) Morsicatio mucosae oris: poorly demarcated yellowish-white, macerated plaque that fades into normal mucosa. (C) Morsicatio mucosae oris: white papules of right lateral tongue that fade into normal mucosa. (D) Morsicatio mucosae oris of lower lip mucosa with irregular macerated papules and plaques.

    Morsicatio Mucosae Oris (Morsicatio Buccarum, Pathominia Mucosae Oris)

    Clinical Findings

    • These occur at any age; the most common locations lie close to the biting surfaces of the teeth, namely buccal mucosa, lateral/ventral tongue, and lower lip mucosa (rare on upper lip mucosa); more than 50% of patients are unaware of their habit (which may be nocturnal).

    • Poorly demarcated papules and plaques often display a shaggy, macerated, sometimes papillary surface, and may be associated with areas of erythema and ulceration depending on the severity of the parafunctional chewing habit ( Fig. 10.7B–D ).

    • Chronic irritation of the mucosa against an oral appliance or other hard foreign object results in similar findings.

    Etiopathogenesis and Histologic Features

    Parafunctional habits such as raking of the teeth, prosthesis, or other foreign object against the nonkeratinized mucosa result in these benign reactive keratotic lesions with distinctive histopathology. It is important that these lesions not be signed out as merely “parakeratosis or acanthosis” but as a frictional or reactive keratosis so that they do not get relegated to the category of leukoplakia (see Chapter 11 ).

    • Linea alba shows leukoedema ( Fig. 10.8 ).

      FIG 10.8
      Linea alba. (A) Acanthosis and keratinocyte edema. (B) Anucleate superficial cells and keratinocyte edema.
    • Classic lesions show mild to severe parakeratosis with fissures and clefts often rimmed by bacteria, but without inflammation; candidal hyphae are infrequently seen; parakeratosis diminishes toward the lateral edges, and there is acanthosis and keratinocyte edema ( Figs. 10.9–10.11 ); ulcers may be present and long-standing lesions show hyperkeratosis similar to benign alveolar ridge keratosis ( Fig. 10.12 ).

      FIG 10.9
      Morsicatio mucosae oris. (A) Marked parakeratosis with fissures and clefts rimmed by bacteria, and acanthosis. (B) Marked parakeratosis with bacterial colonization and no inflammation. (C) Prominent keratinocyte edema.

      FIG 10.10
      Morsicatio mucosae oris. (A) Tapering parakeratosis (right) and acanthosis. (B) Parakeratosis with bacterial colonies and keratinocyte edema.

      FIG 10.11
      Morsicatio mucosae oris. (A) Parakeratosis that tapers toward the edges and acanthosis. (B) Lateral areas showing only mild parakeratosis with slight surface undulations.

      FIG 10.12
      Morsicatio mucosae oris. (A) Parakeratosis and acanthosis. (B) Basal cell degeneration, subepithelial fibrin deposition, and mild chronic inflammation (edge of a traumatic ulcer).
    • Slight surface papillomatosis may be present and rete ridges are tapered; inflammation is usually absent unless an ulcer is present and there may be “plasma pooling” from trauma ( Fig. 10.13 ).

      FIG 10.13
      Morsicatio mucosae oris. (A) Acanthosis, plasma pooling, and mild chronic inflammation. (B) Plasma pooling between superficial keratinocytes.

    Differential Diagnosis

    • Hairy tongue is characterized by true hyperparakeratosis and hyperplastic filiform papillae composed of thick spires of parakeratin with many bacterial colonies ( Figs. 10.14 and 10.15 ). This is a retention keratosis caused by dehydration and poor diet leading to retention of keratin rather than normal shedding. Lesions resolve on improved hydration and diet.

      FIG 10.14
      Hairy tongue. (A) Hairy dorsum of tongue (B) Brown-black hairy dorsum of tongue.

      FIG 10.15
      Hairy tongue. (A) Hyperplastic filiform papillae. (B) Spires of parakeratin with many bacterial colonies.
    • Hairy leukoplakia usually shows sharp demarcation of the parakeratin from an underlying pale band of edematous keratinocytes, chromatin beading against the nuclear membrane, Cowdry inclusions, and presence of EBV in superficial keratinocytes.

    • Any other papular/nodular lesion, such as a dysplasia or even a fibroma, may show overlying secondary frictional/factitial keratosis.

    Management and Prognosis

    • Use of barrier devices to prevent patients from habitually chewing the mucosa may or may not be helpful because patients may continue to rake the mucosa against the appliance.

    • Lesions have no malignant potential and do not require further management.

    References

  • Glass LF, Maize JC: Morsicatio buccarum et labiorum (excessive cheek and lip biting).Am J Dermatopathol 1991; 13: pp. 271-274.
  • Hjorting-Hansen E, Holst E: Morsicatio mucosae oris and suctio mucosae oris.Scand J Dent Res 1970; 78: pp. 492-499.
  • Reichart PA, Philipsen HP: Betel chewer’s mucosa—a review.J Oral Pathol Med 1998; 27: pp. 239-242.
  • Woo SB, Lin D: Morsicatio mucosae oris—a chronic oral frictional keratosis, not a leukoplakia.J Oral Maxillofac Surg 2009; 67: pp. 140-146.
  • Morsicatio Mucosae Oris (Morsicatio Buccarum, Pathominia Mucosae Oris)

    Clinical Findings

    • These occur at any age; the most common locations lie close to the biting surfaces of the teeth, namely buccal mucosa, lateral/ventral tongue, and lower lip mucosa (rare on upper lip mucosa); more than 50% of patients are unaware of their habit (which may be nocturnal).

    • Poorly demarcated papules and plaques often display a shaggy, macerated, sometimes papillary surface, and may be associated with areas of erythema and ulceration depending on the severity of the parafunctional chewing habit ( Fig. 10.7B–D ).

    • Chronic irritation of the mucosa against an oral appliance or other hard foreign object results in similar findings.

    Etiopathogenesis and Histologic Features

    Parafunctional habits such as raking of the teeth, prosthesis, or other foreign object against the nonkeratinized mucosa result in these benign reactive keratotic lesions with distinctive histopathology. It is important that these lesions not be signed out as merely “parakeratosis or acanthosis” but as a frictional or reactive keratosis so that they do not get relegated to the category of leukoplakia (see Chapter 11 ).

    • Linea alba shows leukoedema ( Fig. 10.8 ).

      FIG 10.8
      Linea alba. (A) Acanthosis and keratinocyte edema. (B) Anucleate superficial cells and keratinocyte edema.
    • Classic lesions show mild to severe parakeratosis with fissures and clefts often rimmed by bacteria, but without inflammation; candidal hyphae are infrequently seen; parakeratosis diminishes toward the lateral edges, and there is acanthosis and keratinocyte edema ( Figs. 10.9–10.11 ); ulcers may be present and long-standing lesions show hyperkeratosis similar to benign alveolar ridge keratosis ( Fig. 10.12 ).

      FIG 10.9
      Morsicatio mucosae oris. (A) Marked parakeratosis with fissures and clefts rimmed by bacteria, and acanthosis. (B) Marked parakeratosis with bacterial colonization and no inflammation. (C) Prominent keratinocyte edema.

      FIG 10.10
      Morsicatio mucosae oris. (A) Tapering parakeratosis (right) and acanthosis. (B) Parakeratosis with bacterial colonies and keratinocyte edema.

      FIG 10.11
      Morsicatio mucosae oris. (A) Parakeratosis that tapers toward the edges and acanthosis. (B) Lateral areas showing only mild parakeratosis with slight surface undulations.

      FIG 10.12
      Morsicatio mucosae oris. (A) Parakeratosis and acanthosis. (B) Basal cell degeneration, subepithelial fibrin deposition, and mild chronic inflammation (edge of a traumatic ulcer).
    • Slight surface papillomatosis may be present and rete ridges are tapered; inflammation is usually absent unless an ulcer is present and there may be “plasma pooling” from trauma ( Fig. 10.13 ).

    Oct 3, 2019 | Posted by in Oral and Maxillofacial Pathology | Comments Off on Reactive Keratotic Lesions (Nonleukoplakias)
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