​Kembara Xtra - Medicine - Oral leukoplakia

​Kembara Xtra - Medicine - Oral leukoplakia 
The World Health Organization (WHO) describes leukoplakia as "a white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer."
impacted system(s): gastrointestinal Overgrowth of the squamous epithelium 

Epidemiology 
Most prevalent among Asian communities, where tobacco use, areca nut chewing, and smoking are more prevalent. 250,000 instances worldwide each year.
Prevalence
 Peak age at onset is in the 60s and is greater than 40 years old.
Males are three times as likely as females to be impacted, and smokers are six times as likely as nonsmokers to be afflicted . Aspects of Geriatrics
In older patients, malignant transition to carcinoma is more frequent.

Pathophysiology and Etiology 

Oral squamous epithelium hyperkeratosis or dyskeratosis. When tissue cells are exposed to carcinogens, adaptive alterations such as hyperplasia are triggered. Continuous irritation can cause the epithelium's cells to degenerate and finally undergo apoptosis or malignant transformation.
Any use of tobacco, alcohol, or alcoholism, periodontitis, and Candida albicans infection all have the potential to cause dysplasia and boost malignant transformation.
Epstein-Barr virus (oral hairy leukoplakia) Areca nut/betel (Asian populations) Sunlight Vitamin deficiency Syphilis Dental restorations/prosthetic appliances Estrogen therapy Chronic trauma or irritation Human papillomavirus types 16 and 18 Areca nut/betel Mouthwash preparations and toothpaste containing the herbal root extract sanguinaria Genetics
Epidermolysis bullosa and congenital dyskeratosis enhance the risk of mouth cancer.
Leukoplakia and, in particular, squamous cell carcinoma are correlated with PTEN allelic loss, P53 overexpression, and changes in the expression of the p53, p16INK4a, and the 3p, 9p, and 17 (mainly TP53) genes.
 Biomarkers: IL-6, IL-8, and TNF- have all been found in leukoplakia, and recent study suggests that Hsp27 and PTHRP/PTHLH may also be used as biomarkers.


Risk Factors The use of tobacco, particularly smokeless tobacco or areca/betel nut consumption, is linked to 70–90% of cases of oral leukoplakia.
 Comparable to squamous cell carcinoma risk factors Alcohol 1.5 times increases risk.
Risk factors for the malignant development of leukoplakia in females include: Recurrent or chronic mechanical damage from dental appliances or cheek biting Chemical irritation to oral regions Diabetes Age Socioeconomic status 
Long-lasting leukoplakia, non-smoker status, location on the tongue or floor of the mouth, size of >200 mm2, nonhomogenous type, epithelial dysplasia Recent studies suggest that those who have undergone malignant transformation may have altered oral microbiomes.


Prevention 

Avoid consuming alcohol, betel nuts, habitual tongue chewing, any form of tobacco, or any alcohol at all.
Use dental equipment that fits you properly.
 Routine dental examinations to prevent faulty restorations A diet high in fresh produce and immunization against HPV may both assist to avoid cancer.

Accompanying Conditions 
Hairy leukoplakia and HIV infection are intimately related, and erythroplakia, also known as "speckled leukoplakia," or erythroleukoplakia, is a sign of underlying dysplasia.
DIAGNOSIS
An asymptomatic white area on the oral mucosa is called leukoplakia.

History: Usually asymptomatic; history of use of cigarettes, alcohol, or oral irritants; timing of onset, progression, and presence of pain; sources of friction or persistent irritation; presence of pain.

clinical assessment 
The floor of the mouth, ventrolateral tongue, and the soft palate complex are where dysplastic lesions are most likely to form.
The appearance can range from uniform, nonpalpable, barely translucent white spots to thick, fissured, papillomatous, indurated plaques; the texture may be rough or leathery. Verruciform or exophytic lesions are possible.
– White, gray, yellowish white, or brownish gray are all acceptable colors. not removable with a cloth or scraper
Homogeneous is a WHO classification that describes color.
Nonhomogeneous relates to color and texture; flat, corrugated, wrinkled, or pumice are more likely to be dysplastic or cancerous.
Erythroleukoplakia (a reddish-white tumor)
PVL (proliferative verrucous leukoplakia; multifocal, primarily female) 

Multiple Diagnoses 
Acute pseudomembranous candidiasis causes white, rub-offable sores on the mouth.White oral lesions that won't go away with rubbing (2): - Genetic/developmental (rare):
Cannon white sponge nevus (buccal mucosa, tongue): diffuse bilateral white plaques Pachyonychia congenita and hereditary benign intraepithelial dyskeratosis
Geopathic diseases
Darier-White illness
Geographic tongue that is reactive or frictional
Leukoedema (fine, gray-white lines that vanish when stretched) Contact destruction
Mouth-biting (morsicatio mucosae oris)
Uncomfortable dentures can cause benign alveolar ridge keratosis.
 A hairy tongue (elongated filiform papillae that may become pigmented as a result of food or germs)  Nicotinic stomatitis and smokeless tobacco keratosis (South Asian "paan" or "gutka"; American/Swedish snuff; Ethiopian "toombak")  Aspirin burn Glassblower's white patch Actinic cheilitis
Contact stomatitis brought on by cinnamon and epithelial peeling
Keratoses lesions
Albina Linea
- Contaminated:
 Candidiasis Hairy leukoplakia (linked to those with EBV and HIV infection) Syphilis with an immune component:
Lichen planus (bilateral, symmetrical, reticular white lesions are typical) Lichenoid tumors
Autoimmune benign migratory glossitis
Chronic graft versus host disease is known as SLE.


Laboratory Results 
The gold standard is a biopsy with a histopathologic evaluation.
Initial Examinations (lab, imaging) Laboratory tests are typically not recommended.
- If a C. albicans infection is suspected, take a salivary sample.
No imaging is recommended.

Tests in the Future & Special Considerations

If the lesion is persistent, changing, or inexplicable, a biopsy is required to rule out cancer.
Think about CBC and RPR (rapid plasma reaction).

Other/Diagnostic Procedures
In comparison to a routine oral examination, oral cytology is superior.
Oral cytology is not superior to computer-assisted cytology or liquid-based cytology.
A sensitive and targeted screening method includes DNA-image cytometry cell analysis and noninvasive brush biopsy.
Patients who had brush biopsy results that showed dysplastic or cancerous cells should get an official excisional biopsy.
A decisive procedure is an excisional biopsy.
Interpretation of Tests
Invasive cancer, dysplasia, hyperkeratosis, and keratosis of uncertain significance (KUS) are all examples of biopsy specimens.
Invasive carcinomas account for 6% of the initial biopsy sample, and malignant transformation occurs in 0.13–6% of cases. 60% of lesions on the floor of the mouth or the lateral edge of the tongue are carcinogenic; buccal mucosal lesions are often benign but necessitate biopsy if they do not go away.

Management Because oral leukoplakias have a high risk of developing into cancer, they should all be treated. - Surgical excision is the preferred treatment for lesions that are 2 to 3 cm in diameter.
- Cryosurgery or laser surgery should be considered for many or big lesions where surgery would result in an undesirable deformity.
Complete excision is the conventional treatment for dysplasia or malignancy. - Abstinence from predisposing behaviors (alcohol and smoke).
 Up to 30% of leukoplakia recurs after therapy, and some leukoplakia still develops into squamous cell carcinoma.
Treatment options for oral hairy leukoplakia include podophyllin and acyclovir cream.


General Actions 

 Stop repetitive lip-biting.
 Fix poorly fitting dental equipment, subpar restorations, or pointed teeth.
 Give up drinking and smoking.
Cryosurgery may be effective in treating some tiny lesions.
Retinoids, lycopene, -carotene, and COX-2 inhibitors may all result in partial regression.
Brush your tongue if it is hairy. 

Bleomycin, photodynamic treatment, carotenoids, vitamins A, C, and K, and other medications are ineffective at preventing malignant transformation and recurrence. There is currently no widely accepted conventional systemic medication regimen, however chemoprevention research is advancing.


Referral 
Referrals to oral surgeons or otolaryngologists may be appropriate for extensive disease.


Furthermore Treated 

Retinoids, cyclooxygenase-2 inhibitors, epidermal growth factor inhibitors, and peroxisome proliferator-activated receptor agonists are examples of systemic therapy that may slow development.


Scalpel excision, laser ablation, electrocautery, or cryoablation are surgical procedures that are available. Cryotherapy is somewhat less effective than photodynamic therapy in terms of response (73% vs. 90%) and recurrence (27% vs. 24%). (6)[A]
 Algorithm for biopsies and excisions (2)[C]: - KUS that is ill-defined and probably frictional: follow-up and rebiopsy.
- Follow-up every three months and rebiopsy every 12 months for KUS that are well defined and >3 cm.
- KUS that is less than 3 cm: Ablate/excise with narrow margins; monitor every three months; if recurs, ablate/excise with wider margins.
- PVL: Follow up every three months and remove any nodules or verrucae.
- Excise Dysplastic/SCC.

Alternative Therapies 

Systemic -carotene, herbal extracts, freeze-dried black raspberry gel, and Bowman-Birk inhibitor have low or extremely low evidence supporting them. 

Admission 

Eliminate the etiologic causes.
 After 7 to 14 days, reevaluate.
If a lesion is persistent, have a biopsy 

Patient Follow-Up Monitoring
3-6 months follow-up visits are typical, depending on the patient's preferences and predicted risk.

Patient Education If the biopsy results are negative, emphasize the value of routine follow-up checks.
To get rid of dental factors, start a dental referral.
 Emphasize the necessity of quitting drinking and using smoke.
 Promote involvement in programs to stop smoking.

The majority of leukoplakia are benign.
Leukoplakia can advance, stabilize, or regress.
0.13-6% of initially benign tumors go on to become cancerous.
Malignant development typically occurs at a rate of 2% to 3% per year in the absence of treatment.
Size >200 mm2 increases the chance of malignant transformation; mouth cancer has a 50% 5-year survival rate.


Complications Larger lesions and nonhomogeneous leukoplakia are associated with greater odds of malignant transformation. New lesions may arise following therapy.

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