2. Introduction
• Definition: White and red lesions refer to
abnormal changes in the oral mucosa color and
texture.
• Importance: May indicate benign conditions,
infections, or potentially malignant disorders.
3. White appearance of oral
mucosa
1. Hyperkeratosis
2. Abnormal but benign thickening of stratum
spinosum (acanthosis).
3. Intra and extracellular fluid accumulation
(edema).
4. Whitish pseudomembranes by microbes
(plaque).
5. Fibrosis
4. Red appearance of oral
mucosa
1. Atrophy of epithelium.
2. Increased vascularization.
6. I.Infectous disease
I.ORAL CANDIDIASIS
■The most prevalent opportunistic infection affecting
the oral mucosa.
■majority of cases, the lesions are caused by Candida
albican.
■Divided into primary &secondary infections
7. ■number of predisposing factors have been
shown to convert C. albicans from the normal
commensal flora (saprophytic stage) to a
pathogenic organism:
Denture wearing
Smoking
Quality and quantity of saliva
Immunosuppressive diseases
Immunosuppressive medications
Endocrine disorders
8. Types of primary candidiasis
a.pseudomembranous :creamy white, removable plaques or
patches on the oral mucosa,may resemble cottage cheese
and
can be scraped off, often revealing a red, inflamed, or
bleeding
surface underneath.
●soreness, burning sensation, difficulty swallowing (if it
spreads
to the throat). asymptomatic in mild cases.
9. b.erthematous:doesn't present with white plaques
but
instead appears as red, inflamed patches on the oral
mucosa. It's often associated with a smooth, shiny
surface and can be painful.
10. C.Chronic Hyperplastic Candidiasis
■(Chronic Plaque Type)
•Also known as candidal leukoplakia. •thick, white,
adherent plaques that cannot be easily scraped off
•Usually asymptomatic but may cause mild discomfort
or a rough texture
■(Chronic Nodular Type)
rare, small, raised, nodular lesions
rather than flat plaques
or diffuse redness.
11. d.candida assossiated lesion
(Denture stomatitis )
Type I minor erthematous site duo to denture
trauma
Type II major denture covered mucosa
Type III granular mucosa
12. (Angular cheilitis)
■ infected fissures of the commissures of the
mouth
surrounded by erythema
■The lesions are frequently infected with both
Candida
albicans and Staphylococcus aureus.
■Causes :Vitamin B12 deficiency, iron deficiencies,
and loss of vertical dimension and Dry skin
13. (Median Rhomboid Glossitis)
■ asymptomatic erythematous lesion in the
center
of the posterior part of the dorsum of the
tongue
with an oval configuration.
■This area of erythema results
from atrophy of the filiform papillae
and the surface may be lobulated.
■ the lesion frequent shows a mixed
bacterial/fungal microflora
14. SECONDARY CANDIDIASIS
●group of disorders, which, in addition to
oral
candidiasis, also affect the skin, nail, genital
Mucosa.
● The face and scalp may be involved.
●Causes : endocrine disorder, severe
combined
immunodeficiency , thymoma and HIV .
15. MANAGEMENT
☆Reduction of predisposing factor like improving
denture hygiene , reduction denture porosity , smoke
cessation.
☆pseudomembranous ,erythematous__topical
antifungal
☆chronic hyperplastic __systemic antifungal
☆type III denture stomatitis __surgical removal
☆Angular cheilitis __topical antifungal like miconazole
and moisturizing cream.
☆secondary candidiasis __systemic antifungal
16. II.Oral hairy leukoplakia
It is caused by the Epstein-Barr virus (EBV).
▪︎
white, corrugated, or "hairy" patches that cannot be
▪︎
scraped off.
On the lateral borders of the tongue, though it can
▪︎
occasionally appear on other oral mucosal surfaces like
the buccal mucosa or palate.
The lesions are typically asymptomatic
▪︎
associated with immunocompromised individuals like
▪︎
HIV/AIDS, organ transplant recipients.
17. ■Treatment:
Focuses on improving immune function. For example,
in HIV patients, antiretroviral therapy can resolve
OHL by boosting immunity.
Antiviral medications (e.g., acyclovir) may be used
▪︎
to target EBV directly
18. 2.premalignant disease
I.LEUKOPLAKIA
white patches or plaques on the mucous
■
membranes of the mouth that cannot be wiped
off
it has the potential to develop into oral cancer,
■
particularly squamous cell carcinoma
risk factors (smoking , excessive alcohol
■
consumption, chronic irritation (e.g., from sharp
cusps or ill-fitting dentures).
19. main types include:
1. Homogeneous Leukoplakia
• Uniformly white, flat, and smooth plaques
with a consistent texture.
• lower risk of malignant transformation.
2. Non-Homogeneous Leukoplakia
• Irregular, mixed white and red patches
(sometimes called erythroleukoplakia), with a
nodular, verrucous (warty), or speckled
surface.
• higher risk of progressing to cancer 15-40%.
20. • Subtypes:
Nodular: Small, raised bumps on the surface.
■
Verrucous: Warty or corrugated appearance.
■
Speckled: Mixed red and white areas, often with
■
an uneven texture.
21. 3. Proliferative Verrucous Leukoplakia (PVL)
• A rare, aggressive subtype with multiple,
widespread warty lesions that tend to recur and
spread over time.
• Highly resistant to treatment and has a strong
tendency to transform into squamous cell
carcinoma (up to 70-100%).
22. MANAGEMENT
a.homogenous __eliminate the irritant +follow up
every (3_6)weeks.
b.non homogenous__eliminate the
irritant+surgical removal+follow up biopsy to role
out cancer.
C.PVL__wide surgical excision +biopsy follow up
every (1_3)months.if biopsy show malignant
transformation then chemotherapy or
radiotherapy needed.
23. II. ERYTHROPLAKIA
• red lesion or patch that has appearance of
Smooth, velvety, or granular red areas, often
sharply defined.
• Commonly found on the floor of the mouth,
tongue, or soft palate
• Rare, less frequent than leukoplakia.
• Risk Factors: smoking or , alcohol consumption,
and sometimes human papillomavirus (HPV)
infection.
•Malignant Potential: High risk-up to 90%
25. III.ORAL SUBMUCUS FIBROSIS
•A progressive, precancerous fibrosis of the
submucosal tissues leading to stiffness and
restricted mouth opening.
• Cause: chronic use of areca nut (betel quid),
nutritional deficiencies, genetic predisposition, and
autoimmune processes.
26. •Pale, marble-like mucosa with palpable fibrous
bands in the cheeks, lips, or palate. May develop ulcers
.
•Reduced mouth opening (trismus), stiff cheeks,
difficulty swallowing or speaking, and sometimes
hearing loss due to Eustachian tube involvement.
MANAGEMENT
EARLY __cessation habit +Intralesional steroids
+physiotherapy (excersice to adjust mouth opening).
ADVANCED __ surgical intervation.
27. 3.lmmunopathologic disease
I. LICHEN PLANUS (LP)
is a common chronic immunologic inflammatory
mucocutaneous disorder.
(Skin lesion )
characterized by Kobner's phenomena (development of
new
lesion on normal looking skin following trauma as
scratching).
28. (Oral lesion)
•Bilateral esions surrounded by a network of bluish
white lines called Wickham's striae radiating from
periphery of the lesion.
•pain or discomfort, which interferes with function.
FORMS OF THE LESION
RETICULAR
PAPULAR
PLAQUE
ATROPHIC
EROSIVE
BULLOUS
29. Causes
. Autoimmune reaction
. Stress
. Medications
. Hepatitis c
. Diabetes millitus
MANAGEMENT
Reticular, plaque, papules __No treatment and
follow up
Atrophic, erosive__ Corticosteroids + Retinoids
30. II.LICHENOID REACTION
associated with the administration of a drug,
contact with a metal, the use of a food flavoring, or
systemic disease.
resolution when the drug or other factor was
eliminated
31. III.LUPUS ERYTHEMATOUS
•Systemic lupus erythematosus (SLE)
multi-organ damage with disk shaped
skin scar .
• Discoid lupus erythematosus (DLE) is
affecting the oral cavity+skin lesion has
butterfly distribution on tip and bridge
of the nose.
• Subacute cutaneous lupus
erythematosus intermediate between SLE
32. Causes
1-Immunologic formation.
2- Genetic factors.
3-Infectious (EBV, CMV, VZV).
4. environmental (e.g.sun exposure).
5- Endocrine factors: (hormones).
(Oral lesion)
•central atrophy, scar formation, and occasional loss
of surface pigmentation.
• The primary locations for these lesions include the
buccal mucosa, palate, tongue
34. 4.Allergic reactions
Dentifrices and mouthwashes allergy
•The Lesions are usually located on the
Mucobuccal folds and Gingiva.
•irregular in shape, white, covered with a
pseudomembrane, and very painful.
35. 5.Toxic reactions
I.SMOKLESS TOBACCO INDUCED
KERATOSIS
•The surface of mucosa appears white and granular
or
wrinkled.
•These lesions are accepted as precancerous.
• area of gingival recession with periodontal-tissue
destruction in the area of contact
on facial aspect of the teeth .
•The lesion is asymptomatic .
36. II.NECOTINE STOMATITIS
Due to the chronic insult, the palatal mucosa
becomes diffusely gray or white. Numerous
slightly elevated papuleswith punctate red
centers that represent inflamed altered minor
salivary gland ducts are noted.
37. 6.Reaction to mechanical trauma
I.LINEA ALBA
It is a horizontal white streak on the buccal Mucosa
bilaterally at the level of the occlusal plane from the
commissure of mouth to the posterior teeth.
38. II. FRICTIONAL KERATOSIS
• Frictional (traumatic) keratosis is defined as
a white plaque with a rough surface that is
clearly related to a source of mechanical
irritation .
•Frictional keratosis is frequently associated
with rough or maladjusted dentures and with
sharp cusps .
40. II. BENIGN MIGRATORY GLOSSITIS
asymptomatic red, smooth patches on the tongue
with irregular white borders.
• Patches change in size, shape, and location over time
(hence "migratory").
•papillae are absent or flattened in certain areas,
creating smooth, red patches.
•The loss of papillae in these patches is temporary and
reversible.
41. III.WHITE SPONGY NEVUS
• rare autosomal dominant disorder. It present from
birth and appear during childhood.
• Presents as bilateral white, soft, "spongy," or velvety
thick plaques of the buccal mucosa.
• Other sites in the oral cavity may be involved,
including the ventral tongue, floor of the mouth, labial
mucosa, soft palate, and alveolar mucosa.
• asymptomatic
• require no treatment