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Oral White and Red Lesions

The document discusses several common white and red oral lesions including Fordyce's granules, leukoedema, white sponge naevus, linea alba buccalis, lip and cheek biting, leukoplakia, erythroplakia, nicotine stomatitis, and oral submucous fibrosis. It describes the clinical presentation, causes, diagnosis, and treatment of each condition. Many of these oral lesions are benign but some like leukoplakia and erythroplakia can potentially become cancerous if not properly treated.

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Hanin Abukhiara
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0% found this document useful (0 votes)
151 views71 pages

Oral White and Red Lesions

The document discusses several common white and red oral lesions including Fordyce's granules, leukoedema, white sponge naevus, linea alba buccalis, lip and cheek biting, leukoplakia, erythroplakia, nicotine stomatitis, and oral submucous fibrosis. It describes the clinical presentation, causes, diagnosis, and treatment of each condition. Many of these oral lesions are benign but some like leukoplakia and erythroplakia can potentially become cancerous if not properly treated.

Uploaded by

Hanin Abukhiara
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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Oral white and red lesions

Fordyce’s granules
ectopic sebaceous glands
 Sebaceous glands without hair follicles
 Presents as painless, raised, yellowish white spots, 1-3 mm in diameter
 Buccal mucosa and vermilion border of upper lip are most common sites
 Occasionally seen on retromolar area and anterior tonsillar pillars
 Granules become prominent during puberty and increase in no with age
 Some patients have hundreds of granules while most have 1 or 2
 80% of the population are affected
Aetiology
 
 Developmental anomaly
Fordyce’s granules
Fordyce’s granules
Diagnosis

 Clinical examination
Treatment

 Eventually they go away


 Tretinoin gel or cream alone, or with alpha hydroxyacid agent
 Trichloroacetic acid (TCA) chemical peel
 Vaporising laser such as CO2 laser or electro desiccation
 Surgical diathermy or cryotherapy
 Pulse dye laser (expensive)

 
Leukoedema
 Normal anatomic variation
 Characterised by a filmy, opalescent to whitish gray tinge of buccal mucosa
 Always bilateral and surface tissue exhibit a corrugated folded configuration
 May begin as early as 3-5 yrs, but is not noticeable until adolescence
 More prevalent in people with dark skin and is more intense in smokers
 Patients are usually unaware of its presence since it is asymptomatic
 
Aetiology

 Developmental anomaly of buccal mucosa


Leukoedema
Leukoedema
Diagnosis

 When the cheeks are stretched the leukoedema disappears


 Histologically, intracellular oedema and thickened epithelium
Treatment

 No treatment is necessary
 Doesn’t change with age
 Has no malignant potential
 If stop smoking, lesion becomes less pronounced
White sponge naevus
Cannon's disease
 Rare asymptomatic lesion and several family members may be affected
 Always presents during childhood with no gender predilection
 Presents as thick bilateral white plaque with a spongy texture
 Affects buccal mucosa, but may labial mucosa, alveolar ridge, or floor of mouth
 Severe cases exhibit corrugated vertical folds that cover most of buccal mucosa
 Well demarcated as opposed to poor demarcation of leukoedema
 This condition is perfectly benign and often mistaken for leukoplakia
Aetiology

 Developmental anomaly inherited as autosomal dominant trait


White sponge naevus
Diagnosis
 
 Clinical appearance and a positive family history
 Incisional biopsy to differentiate it from leukoplakia
Treatment

 Reassurance
 If extends to lip vermilion then surgical removal
Linea alba buccalis
 A common finding on buccal mucosa
 Presents as asymptomatic, bilateral, linear white line
 Begins at mouth corner and extends posterior at the level of
occlusal plane of teeth
Aetiology

 Frictional keratosis due to sucking trauma from teeth


Linea alba buccalis
Diagnosis
 Usually present bilaterally
 Restricted to dentulous areas

Treatment
 No treatment is required
Lip and cheek biting
 Mild chronic biting of lip or cheek is common
 Occurs as an unconscious habit
 Most often begins in late childhood or early teens
 Lesion produced by repeated rubbing, sucking, or chewing
movements that abrade surface without ulceration
 Presents as diffuse irregular small furrows with ragged borders
 Asymptomatic, in severe cases may tenderness, swelling, burning
sensation  
Aetiology

 Self-inflected injury caused by stress and anxiety


 May genetic component
Lip and cheek biting
Lip and cheek biting
Lip and cheek biting
Diagnosis
 Clinically- rough lesion

Treatment
 Patient should be encouraged to stop the habit
 Chlorhexidine or hexitidine MW
 Severe cases - splint or dental guard, psychological evaluation
Leukoplakia
 Clinical term that describes adherent white patches of keratosis
 Term should never be used once histological information is available
 Potentially malignant oral lesion with a prevalence of 3-33% over 10 yrs
 Found in 3% of world's population, develops slowly over weeks to months
 Defined by WHO as a ‘white patch or plaque that cannot be rubbed off and
cannot be characterised clinically or pathologically as any other disease’
 Affects more tongue, mandibular alveolar ridge, and buccal mucosa in 50%
of cases
Clinical types

Homogenous leukoplakia
of low risk
affects BM, mucobuccal fold, oral floor
presents as uniformly raised white patch

Sublingual keratosis
of high risk
affects oral floor and ventrum tongue
presents as bilateral, homogenous, well defined lesion with irregular
border
Proliferative verrucous leukoplaki
affects elderly females
appears as diffuse warty or papillary white lesion
arises on mandibular ridge and vestibular region
spreads laterally
many progress to verrucous carcinoma or speckled leukoplakia
Candidal leukoplakia
hyperkeratotic lesion
infected by candida albicans
high risk for malignant transformation
Smokeless tobacco leukoplakia
due to tobacco chewing
presents as white lesion of mucobuccal fold
rough lesion with undulating or wrinkled surface
progression to invasive carcinoma is rare
Aetiology

 Tobacco use (smoked or chewed)


 Chronic irritants (sharp edges of teeth, HPV, Candida albicans, alcohol)
 Bloodroot (sanguinaria)
Homogenous leukoplakia
Homogenous leukoplakia
Homogenous leukoplakia
Sublingual keratosis
Sublingual keratosis
Proliferative verrucous leukoplakia

Verrucous carcinoma
Speckled leukoplakia
Candidal leukoplakia
Candidal leukoplakia
Smokeless tobacco leukoplakia
Diagnosis

 Serum vitamin A, B12, C, and folic acid


 Staining with toluidine blue for incisional biopsy
 Oral brush biopsy
 VELscope
Treatment

 Stop tobacco use


 Oral beta-carotene (vitamin A)
 Oral antifungal therapy in candidal leukoplakia
 Excise lesion if precancerous changes or cancer
 Cryotherapy and laser ablation
 Follow up at intervals of 3-6 months
Erythroplakia
erythroplasia
 Rare, asymptomatic, isolated flat red lesion in mouth that cannot be
attributed to any other pathology
 Found more at floor of mouth, tongue, and soft palate
 Appears as a soft, velvety red plaque with well-demarcated borders
 Leukoplakia may be found along with erythroplakia (speckled leukoplakia)
 75-90% exhibit severe dysplasia, carcinoma-in-situ or invasive squamous
cell carcinoma (SCC)
 Malignant change is 17 times higher in erythroplakia than in leukoplakia
Aetiology 

 Unknown cause
 Associated with smoking and alcohol consumption  
Erythroplakia
Erythroplakia
Erythroplakia
Diagnosis
 Biopsy

Treatment
 Complete excision
 Recurrence is common
 Long-term follow up
Nicotine stomatitis
smoker's palate
 Affects hard palate as asymptomatic white lesion
 Found more in men over 45 yrs of age
 First becomes red then white, thickened, and fissured appearance
 Minor salivary glands in palate become swollen and orifices become
prominent, giving tissue a speckled appearance
 Although caused by smoking but has no dysplastic or malignant potential
 Reverse smoking that causes severe palatal keratosis is an exception as the
concentrated heat and chemicals increase malignant potential
Aetiology

 Pipe and reverse cigarette smoking


 Heat and chemical irritation from tobacco use
 Dentures protect the palate
Early nicotine stomatitis
Advanced nicotine stomatitis
Reverse smoking and malignancy
Diagnosis
 Clinical appearance
 May punch biopsy (5mm)
 Stained teeth

Treatment:
 Lesion resolves after 1-2 weeks of smoking cessation
Oral submucous fibrosis
 A chronic debilitating disease of the oral cavity
 Buccal mucosa is the most commonly involved site
 Characterised by inflammation and progressive fibrosis of submucosa
 Symptoms include burning sensation followed by oral ulceration
 Lesion starts from posterior oral cavity and spreads anteriorly
 Initially palpation of oral mucosa causes a wet leathery feeling
 Later oral mucosa loses its resilience and becomes blanched and stiff
 Eventually inability to open mouth causes difficulty eating and deficiencies
 Can transform into malignancy, particularly to squamous cell carcinoma
(SCC)
 Occurs more in Southeast Asia and India
Aetiology

 Areca nut chewing (betel quid)


 Red chillies, genetic and immunologic factors, iron and vitamin
deficiency
Oral submucous fibrosis
Diagnosis

 Early stage- reversible


 Moderate to severe- irreversible
 Incisional biopsy
Treatment

 Avoid chewing areca nut, tobacco, alcohol, and spicy foods


 Vitamin A, B-complex, C, and iron supplements
 Antioxidant lycopene (16 mg/day)
 Moderate- topical steroid or steroid and hyaluronidase
 Advanced- pentoxifylline (400 mg 1x3/day) improves blood flow
 Intralesional injection of autologous stem cells
 Surgical treatment if severe trismus or dysplastic changes

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