3. Introduction
Oral leukoplakia is a condition characterized
by the formation of thick, white patches on the
mucous membranes inside the mouth.
4. Oral leukoplakia
• The patches cannot be scraped off and often develop on the tongue,
gums, inner cheek lining, or the floor of the mouth.
• While oral leukoplakia is usually harmless and benign, it can sometimes
indicate an underlying issue or even be a precancerous condition.
5. Pathophysiology
1. Initiation:
• Exposure to risk factors, such as tobacco use, alcohol consumption, chronic
irritation, or viral infections (e.g., human papillomavirus).
• Epithelial cells in the oral mucosa are exposed to these risk factors.
2. Cellular Changes:
• Continuous exposure to risk factors leads to genetic and molecular alterations in
the oral epithelial cells.
• DNA damage occurs, leading to mutations in oncogenes or tumor suppressor
genes.
• The accumulation of genetic abnormalities disrupts normal cell cycle regulation and
apoptosis.
3. Hyperkeratosis:
• As a response to chronic irritation, the oral epithelium undergoes hyperkeratosis,
resulting in thickening of the mucosal surface.
• Increased production and accumulation of keratinocytes occur.
6. Pathophysiology
4. Dysplasia:
4. In some cases, the genetically altered cells progress to dysplasia, characterized by
abnormal cellular differentiation and architecture.
5. Dysplasia may range from mild to severe, depending on the degree of cellular
atypia and disorganized growth.
5. Leukoplakia Formation:
• The accumulation of keratinocytes and dysplastic cells forms a white or grayish
patch on the oral mucosa, known as leukoplakia.
• Leukoplakic lesions are predominantly found on the tongue, floor of the mouth, and
buccal mucosa.
6. Potential Progression:
• Leukoplakia may remain stable without further changes.
• However, in some cases, leukoplakic lesions can progress to oral squamous cell
carcinoma (OSCC), a malignant form of oral cancer.
• Further genetic alterations and acquisition of additional mutations contribute to the
transformation of dysplastic cells into invasive cancer cells.
8. 19th century, with reports of white patches or
plaques on the oral mucosa.
1970s, the World Health Organization
(WHO) established standardized
diagnostic criteria and classification
systems for oral leukoplakia
classification system aimed,
framework for diagnosing and
managing oral leukoplakia.
20th century,
link between oral leukoplakia and the
development of oral cancer.
History
10. Global
Prevalenc
e:
oral leukoplakia ranges
from around 1% to 5%
of the general
population globally.
Regional
and
Country-
specific
high rates of tobacco
use, alcohol
consumption, or
betel quid chewing
tend to have higher
prevalence rates
Southeast Asia (such as India, Sri
Lanka, and Bangladesh) and
certain countries in South
America.
High-
Prevalenc
e Areas:
high rates of tobacco
and betel quid
use, have
reported higher
prevalence rates
of oral
leukoplakia.
11. Age and Gender Differences:
Oral leukoplakia can occur at any age
but is more commonly seen in older
individuals.
The risk of developing leukoplakia
increases with advancing age.
Men tend to be more commonly
affected by oral leukoplakia than
women
12. • Not a
transmissible
condition and
does not have a
specific
transmission
route.
Not caused by
an infectious
agent
Mode of Transmission:
Development of oral
leukoplakia is
primarily associated
with long-term
exposure to risk
factors such as:
(tobacco use,
alcohol
consumption,
betel quid
chewing, HPV
infection, chronic
irritation, and poor
oral hygiene)
primarily related to personal behaviors
and lifestyle choices rather than
transmission from one individual to
another.
13. • Not a
transmissible
condition and
does not have a
specific
transmission
route.
Not caused by
an infectious
agent
Mode of Transmission:
Development of oral
leukoplakia is
primarily associated
with long-term
exposure to risk
factors such as:
(tobacco use,
alcohol
consumption,
betel quid
chewing, HPV
infection, chronic
irritation, and poor
oral hygiene)
primarily related to personal behaviors
and lifestyle choices rather than
transmission from one individual to
another.
14. 3. Alcohol Consumption:
Heavy Alcohol Consumption:
Regular and heavy alcohol consumption, particularly when combined
with tobacco use, is a significant risk factor for oral leukoplakia.
4. Betel Quid Chewing:
containing areca nut, slaked lime, tobacco, and other ingredients,
wrapped in a betel leaf.
Chewing betel quid is a common practice in certain regions,
primarily in South Asia and parts of Southeast Asia.
15. Human
Papillomavirus
(HPV) Infection:
Certain strains of
HPV, primarily HPV-
16, have been
associated with an
increased risk of oral
leukoplakia.
Poor Oral
Hygiene:
Inadequate oral
hygiene and oral
health practices can
increase the risk of
oral leukoplakia.
Nutritional deficiencies
Genetic Disorders
16. Clinical Manifestation
small and discreet or cover
a larger area, asymmetrical
to more defined outlines.
White patches
flat, slightly raised, or
wrinkled
Non-Removability
firm attachment to
the underlying
tissue.
Size and shape Texture
texture of leukoplakic
lesions can vary.
Site of occurrence
inside the mouth, floor of
the mouth, or the roof of
the mouth (palate)
Sensitivity
sensitive to touch,
heat, spicy foods, or
other irritants.
19. Diagnosis
The gold standard for diagnosis of leukoplakia is always a biopsy from
the site of the lesion.
Most often, doctors diagnose leukoplakia by examining the patches in the
mouth, attempting to wipe off the white patches, discussing the patient's
medical history and risk factors, and ruling out other possible causes
Before a diagnosis of leukoplakia is made, other possible causes of the
white patches are investigated
The clinical diagnosis is primarily based on visual inspection and manual
palpation
20. Here are some ways that leukoplakia can be diagnosed and evaluated:
Visual examination
A doctor can diagnose leukoplakia by examining the patches in the mouth
and attempting to wipe off the white patches
Medical history and risk factors
A doctor may discuss the patient's medical history and risk factors to help
diagnose leukoplakia
21. Biopsy
A definitive diagnosis of leukoplakia is made when any etiologic cause other than
tobacco/areca nut use has been excluded and histopathology has not confirmed
any other specific disorder.
Biopsy obtainment, repeated as necessary, is essential. A biopsy involves removing
a small sample of tissue from the lesion and examining it under a microscope to
determine if it is cancerous or precancerous.
Oral brush biopsy
This involves removing cells from the surface of the lesion with a small, spinning
brush. This is a non-invasive procedure, but does not always result in a
definitive diagnosis
22. Excisional biopsy
This involves surgically removing tissue from the leukoplakia patch or removing
the entire patch if it's small. An excision biopsy is more comprehensive and
usually results in a definitive diagnosis.
Toluidine blue dye
This is a diagnostic aid that can help detect areas of abnormal tissue in the
mouth. The dye is applied to the mouth and areas of abnormal tissue will absorb
the dye and turn blue.
23. Salivary tests
Salivary tests can help detect certain biomarkers that may be associated with
oral cancer. These tests are not used to diagnose leukoplakia but may be used
to monitor patients who are at high risk for developing oral cancer.
It is important to diagnose and evaluate leukoplakia early, as treatment is
most successful when a lesion is found and treated early, when it's small.
Regular checkups and routine inspections of the mouth for areas that don't
look normal are important
24. Within 15 years, about 3% to 17.5% of people with leukoplakia will develop
squamous cell carcinoma, a common type of skin cancer.
The statistical analysis from several studies piloted on the Indian subcontinent in
general and in India concluded the prevalence of leukoplakia ranging from 0.2%
to 5.2% and the malignant transformation of 0.13% to 10%.
Leukoplakia is usually diagnosed late in the development of proliferative verrucous
leukoplakia (PVL), as it takes time to spread to multiple sites. Treatment is a
challenge and results are often mixed, but leukoplakia treatment is most successful
when a lesion is found and treated early, when it's small.
Evolution
25. Management and
treatment
Professional Evaluation:
In any suspected case of oral leukoplakia, it is
essential to seek professional evaluation from a
dentist or oral surgeon. They will examine the
lesion and determine the extent of the
condition.
26. .
1.Biopsy:
A biopsy may be recommended to confirm the
diagnosis and rule out the presence of any
cancerous changes. During a biopsy, a small
piece of affected tissue is removed and
examined under a microscope
27. .
1.Biopsy:
A biopsy may be recommended to confirm the
diagnosis and rule out the presence of any
cancerous changes. During a biopsy, a small
piece of affected tissue is removed and
examined under a microscope
28. .
TREATMENT:
Topical Medications:
Topical medications like retinoids (e.g., tretinoin) or corticosteroids
(e.g., fluocinonide) may be prescribed to treat or manage oral
leukoplakia. These medications are typically applied directly to the
affected area.
29. .
Surgical Treatment:
Depending on the size, location, and severity of the
leukoplakic lesion, surgical intervention may be necessary.
Options include:
1. Surgical Excision: The removal of the leukoplakic patch
and a small margin of surrounding healthy tissue.
2. Laser Surgery: The use of laser technology to vaporize
or remove the affected tissue.
3. Cryosurgery: Freezing the lesion with liquid nitrogen to
destroy the abnormal cells.
4. Electrosurgery: The use of electrical current to remove
the leukoplakia.
30. .
Follow-up Care:
After treatment, regular follow-up appointments will be
necessary to monitor for any recurrence or the
development of new lesions. These appointments may
include visual examinations and biopsies if required.
31. Recursos de la investigación
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