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Red and white lesions of the oral cavity: Part 2

Author: akil, Posted on Thursday, September 23 @ 14:08:18 IST by RxPG  

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Dental

REACTIVE AND INFLAMMATORY WHITE LESIONS

Linea Alba (White Line)
Frictional (Traumatic) Keratosis
Cheek Chewing
Chemical Injuries of the Oral Mucosa
Actinic Keratosis (Cheilitis)
Smokeless Tobacco–Induced Keratosis
Nicotine Stomatitis
Sanguinaria-Induced Leukoplakia

REACTIVE AND INFLAMMATORY WHITE LESIONS

Linea Alba (White Line)
linea alba is a horizontal streak on the buccal mucosa at the level of the occlusal plane extending from the commissure to the posterior teeth.
a very common finding and is most likely associated with pressure, frictional irritation, or sucking trauma from the facial surfaces of the teeth.

CLINICAL FEATURES
usually present bilaterally and
more prominent in individuals with reduced overjet of the posterior teeth.
It is often scalloped and restricted to dentulous areas.

TREATMENT
No treatment . The white streak may disappear spontaneously in some people.

Frictional (Traumatic) Keratosis
white plaque with a rough and frayed surface that is clearly related to an identifiable source of mechanical irritation and that will usually resolve on elimination of the irritant. These lesions may occasionally mimic dysplastic leukoplakia; therefore, careful examination and sometimes a biopsy are required to rule out any atypical changes.
varying degrees of hyperkeratosis and acanthosis.
Such lesions are similar to calluses on the skin.
never been shown to undergo malignant transformation. Lesions belonging to this category of keratosis include linea alba and cheek, lip, and tongue chewing. Frictional keratosis is frequently associated with rough or maladjusted dentures

TREATMENT
Upon removal of the offending agent, the lesion should resolve within 2 weeks.
Biopsies should be performed on lesions that do not heal to rule out a dysplastic lesion.

Cheek Chewing
White lesions of the oral tissues may result from chronic irritation due to repeated sucking, nibbling, or chewing. These insults result in the traumatized area becoming thickened, scarred, and paler than the surrounding tissues.
most commonly seen in people who are under stress or in psychological situations in which cheek and lip biting become habitual.
The white lesions of cheek chewing may sometimes be confused with other dermatologic disorders involving the oral mucosa, which can lead to misdiagnosis.

Chronic chewing of the labial mucosa (morsicatio labiorum) and the lateral border of the tongue (morsicatio linguarum) may be seen with cheek chewing or may cause isolated lesions.
a high prevalence rate of children in mental health treatment facilities; these rates support the role of stress and anxiety in the etiology of this condition.

TYPICAL FEATURES
most frequently found bilaterally on the posterior buccal mucosa along the plane of occlusion.
seen in combination with traumatic lesions on the lips or tongue. Patients often complain of roughness or small tags of tissue that they actually tear free from the surface. This produces a distinctive frayed clinical presentation poorly outlined whitish patches that may be intermixed with areas of erythema or ulceration. The occurrence is twice as prevalent in females and three times more common after the age of 35 years.
hyperparakeratosis and acanthosis. The keratin surface is usually shaggy and ragged with numerous projections of keratin that demonstrate adherent bacterial colonies.When the lesion is seen on the lateral tongue, the clinical and histomorphologic features mimic those of oral hairy leukoplakia.

TREATMENT AND PROGNOSIS
no treatment is indicated. those desiring treatment and unable to stop the chewing habit, a plastic occlusal night guard may be fabricated. Isolated tongue involvement requires further investigation to rule out oral hairy leukoplakia especially when appropriate risk factors for infection with human immunodeficiency virus (HIV) are present.

Differential diagnosis also includes WSN, chemical burns, and candidiasis.

Chemical Injuries of the Oral Mucosa
Transient nonkeratotic white lesions are caused by a variety of agents that are caustic when retained in the mouth for long periods of time, such as aspirin, silver nitrate, formocresol, sodium hypochlorite, paraformaldehyde, dental cavity varnishes, acidetching materials, and hydrogen peroxide. The white lesions are attributable to the formation of a superficial pseudomembrane composed of a necrotic surface tissue and an inflammatory exudate.

SPECIFIC CAUSATIVE AGENTS

Aspirin Burn. Acetylsalicylic acid (aspirin) is a common source of burns of the oral cavity. Usually, the tissue is damaged when aspirin is held in the mucobuccal fold area for prolonged periods of time for the relief of common dental pain

Silver Nitrate. Silver nitrate is commonly used by health care practitioners as a chemical cautery agent for the treatment of aphthous ulcers It brings about almost instantaneous relief of symptoms by burning the nerve endings at the site of the ulcer. However, silver nitrate often destroys tissue around the immediate area of application and may result in delayed healing or (rarely) severe necrosis at the application site

Hydrogen Peroxide. Hydrogen peroxide is often used as an intraoral rinse for the prevention of periodontal disease. At concentrations of = 3%, hydrogen peroxide is associated with epithelial necrosis.

Sodium Hypochlorite. Sodium hypochlorite, or dental bleach, is commonly used as a root canal irrigant and may cause serious ulcerations due to accidental contact with oral soft tissues.

Dentifrices and Mouthwashes. An unusual sensitivity reaction with severe ulcerations and sloughing of the mucosa has been reported to have been caused by a cinnamon-flavored dentifrice However, these lesions probably represent a sensitivity or allergic reaction to the cinnamon aldehyde in the toothpaste. This reaction can appear to be very similar to the reactions caused by other chemical agents such as aspirin and hydrogen peroxide.

Caustic burns of the lips, mouth, and tongue have been seen in patients who use mouthwashes containing alcohol and chlorhexidine.
A case of an unusual chemical burn, confined to the masticatory mucosa and produced by abusive ingestion of fresh fruit and by the concomitant excessive use of mouthwash, has also been reported.
TYPICAL FEATURES
The lesions are usually located on the mucobuccal fold area and gingiva. The injured area is irregular in shape, white, covered with a pseudomembrane, and very painful. The area of involvement may be extensive.
When contact with the tissue is brief, a superficial white and wrinkled appearance without
resultant necrosis is usually seen.
Long-term contact (usually with aspirin, sodium hypochlorite, phenol, paraformaldehyde, etc) can cause severer damage and sloughing of the necrotic mucosa. The unattached nonkeratinized tissue is more commonly affected than the attached mucosa.

TREATMENT AND PROGNOSIS
best treatment of chemical burns of the oral cavity is prevention. Children especially should be supervised The proper use of a rubber dam during endodontic procedures reduces the risk of iatrogenic chemical
burns.
Most superficial burns heal within 1 or 2 weeks. A protective emollient agent such as a film of methyl cellulose may provide relief. However, deep-tissue burns and necrosis may require careful débridement of the surface, followed by antibiotic coverage.
In case of ingestion of caustic chemicals or accidental exposure to severely corrosive agents, extensive scarring that may require surgery and/or prosthetic rehabilitation may occur.

Actinic Keratosis (Cheilitis)
Actinic (or solar) keratosis is a premalignant epithelial lesion that is directly related to long-term sun exposure.classically found on the vermilion border of the lower lip as well as on other sun-exposed areas of the skin. A small percentage of these lesions will transform into squamous cell carcinoma.
Biopsies should be performed on lesions that repeatedly ulcerate, crust over, or show a thickened white area.
commonly found in individuals with extensive sun exposure, such as those with outdoor occupations and/or fair complexions.

TYPICAL FEATURES
seen on the skin of the forehead, cheeks, ears, and forearms.
On the lip, it appears as a white plaque, oval to linear in shape, usually measuring or = 3%, hydrogen peroxide is associated with epithelial necrosis.
Sodium Hypochlorite -dental bleach -serious ulcerations

Dentifrices and Mouthwashes
An unusual sensitivity reaction caused by a cinnamon-flavored dentifrice However, these lesions probably represent a sensitivity or allergic reaction to the cinnamon aldehyde in the toothpaste.
similar to the reactions caused by
aspirin and hydrogen peroxide.
Caustic burns of the lips, mouth, and tongue
in patients who use mouthwashes containing alcohol and chlorhexidine.
A case of an unusual chemical burn, confined to the masticatory mucosa and produced by abusive ingestion of fresh fruit and by the concomitant excessive use of mouthwash, has also been reported
The lesions are usually located on the mucobuccal fold area and gingiva
irregular in shape, white, covered with a pseudomembrane, and very painful

Long-term contact (usually with aspirin, sodium hypochlorite, phenol, paraformaldehyde, etc) can cause severer damage and sloughing of the necrotic mucosa

When contact with the tissue is brief, a superficial white and wrinkled appearance without resultant necrosis is usually seen.
best treatment of chemical burns of the oral cavity is prevention

Actinic Keratosis (Cheilitis
Actinic (or solar) keratosis is a premalignant epithelial lesion
A small percentage of these lesions will transform into squamous cell carcinoma.
seen on the skin of the forehead, cheeks, ears, and forearms
On the lip usually measuring < 1 cm
Histopathologically, the surface epithelium appears atrophic, with a basophilic homogenous amorphous alteration of the collagen (solar elastosis) in the lamina propria.
atypical features such as nucleocytoplasmic ratios, loss of cellular polarity and orientation, and nuclear and cellular atypia are found within the epithelium. A mild lymphocytic infiltrate may also be noted in the lamina propria
treatment of actinic keratosis is surgery Chemotherapeutic agents like 5-fluorouracil have been used showed that the dysplastic changes persist in clinically healthy-appearing epithelium

Smokeless Tobacco–Induced Keratosis
well-recognized white mucosal lesion in the area of tobacco contact, called smokeless tobacco keratosis, snuff dipper’s keratosis, or tobacco pouch keratosis.
are accepted as precancerous
a much lower risk of malignant transformation
Smokeless tobacco contains N-nitrosonornicotine (NNN), most common area of involvement is the anterior mandibular vestibule, followed by the posterior vestibule.
tobacco pouch keratosis
gingival recession involves the facial aspect of the tooth or teeth and is related to the amount and duration of tobacco use
Frank dysplasia is uncommon in tobacco pouch keratosis.
Cessation of use almost always leads to a normal mucosal appearance within 1 to 2 weeks.

Nicotine Stomatitis
Nicotine stomatitis (stomatitis nicotina palati, smoker’s palate) refers to a specific white lesion that develops on the hard and soft palate in heavy cigarette, pipe, and cigar smokers.
NOT considered to be premalignant
also develops in individuals with a long history of drinking extremely hot beverages. This suggests that heat, rather than toxic chemicals in tobacco smoke, is the primary cause.
“Reverse smoking
more pronounced palatal alterations that may be erythroleukoplakic and that are definitely considered premalignant.
. The lesions usually resolve within 2 weeks of cessation of smoking.
Nicotine stomatitis is completely reversible once the habit is discontinued
Sanguinaria-Induced Leukoplakia
Sanguinaria extract, a mixture of benzophenanthridine alkaloids derived from the common bloodroot plant (Sanguinaria canadensis), has been used in oral rinses and toothpaste products since 1982
, to be effective against plaque buildup and gingivitis
sanguinaria extract has also been shown to
be carcinogenic
A significantly higher (fourfold) DNA content and higher numbers of cells with hyperploid nuclei were found in the group with sanguinaria-associated keratoses
preparations containing sanguinaria should be avoided until the risk for malignant transformation is determined
lack of regression in some Viadent-induced leukoplakias months after the cessation of Viadent use.
Most patients are adults in the fourth to ninth decades of life.
the range of Viadent use before the development of lesions was 6 months to 12 years, with a mean of 4.4 years
the maxillary vestibule
both the attached gingiva and vestibular mucosa
lesions may also be seen in the anterior mandibular vestibule
Minimal atypical changes (including basilar hyperplasia, nuclear hyperchromatism,
and increased nucleocytoplasmic ratios) limited to the lower one-third of the epithelium are noted in most specimens.
No appropriate treatment has been established
the condition should be treated similar to the other potentially premalignant processes.
The less severe changes should be managed according to clinical judgment, depending on the extent and duration of the lesion.
In all cases, complete discontinuation of Sanguinaria-containing products and cessation of any other harmful habits such as tobacco or alcohol use is mandatory.
All patients should be given careful clinical followup, with a biopsy of any recurrent or worsening lesion(s).

[Important Note:
Candidiasis will have to wait folks.....the next chapter will be the "TRANSPLANTATION MEDICINE", AN ENTIRELY NEW CHAPTER IN BURKET'S 10ED!
the red and white lesions will be continued after the "Transplantation medicine"]



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