red & white lesions OMED 1

Macules
Well-circumscribed, flat lesions that noticeable because
of their change from normal skin color. They may be
red due to the presence of vascular lesions or
inflammation, or pigmented due to the presence
melanin, hemosiderin and any foreign material .

Papules &Plaques
 Papules: Solid lesions raised above the skin surface
that are smaller than 1 cm in diameter.
 Plaques: Solid raised lesions that are over 1 cm in
diameter; they are large papules.

Nodules
These lesions are present deep in the dermis, and the
epidermis can be easily moved over them.

Vesicles & Bullae
 Vesicles: Elevated blisters containing clear fluid that
are under 1 cm in diameter.
 Bullae: Elevated blister like lesions containing clear
fluid that are over 1 cm in diameter

Pustules
Pustules : Raised lesions containing purulent material.

Erosions & Ulcers
Erosions: Moist red lesions often caused by the rupture
of vesicles or bullae as well as trauma.
Ulcers: A defect in the epithelium; it is a well-
circumscribed depressed lesion over which the
epidermal layer has been lost.

The normal colour of the oral
mucosa
The color of the oral mucosa is pink
due to the passage of light through the
translucent superficial layer of soft
tissue. The light strikes the capillary
bed and reflects back resulting in the
pink color of the oral mucosa.

Four factors contribute to the
color of the oral mucosa:
1- Quantity and quality of blood
2- Thickness of oral mucosa
3- Presence of melanin
4- Degree of keratinization

White colour of the oral mucosa is due to:
1.Keratin or parakeratin (hyperkeratosis or
hyperparakeratosis).
2.  Prickle cell layer (acanthosis).
3. Intracellular edema (spongiosis).
4. Intercellular edema.
5.  Collagen fibers (fibrosis).
6. Pseudomembrane over the oral mucosa.
1- Keratin layer
2- Granular cell layer
3- Prickle cell layer
4- Basal cell layers

Red colour of the oral mucosa is due to:
1. Thinning of the epithelium (atrophy).
2.  Vascularity: as in inflammation due to
vasodilatation

Complete:
 White color of the oral mucosa is due to:
1- ……………………………….
2- …………………………
3-………………………………
4- ……………………………..
 Red color of the oral mucosa is due to:
1- ……………………………….
2- …………………………
 Four factors contribute to the color of the oral mucosa:
1. ………………………………..
2. ………………………………
3. …………………………
4. ……………………….

Classification of red and white lesions
Hereditary
Reactive/Inflammatory
Infectious Leukoplakia
Erythroplakia
Autoimmune
1. Oral Lichen Planus
2. Lichenoid Reactions
3. Lupus Erythematosus
1- Leukoedema
2- White Sponge Nevus
3- Hereditary Benign
Intraepithelial Dyskeratosis
4- Dyskeratosis Congenita
1- Linea Alba (White Line)
2- Frictional (Traumatic) Keratosis
3- Cheek Chewing
4- Chemical Injuries of the Oral Mucosa
5- uremic stomatitis
6-Actinic Keratosis (Cheilitis)
7- Smokeless Tobacco–Induced Keratosis
8- Nicotine Stomatitis
1- Oral Hairy Leukoplakia
2- Koplik’s spots
3- Candidiasis
4- Mucous Patches
5- Parulis
Miscellaneous Lesions
Fordyce’s Granules
Geographic Tongue
Hairy Tongue (Black Hairy Tongue)
Oral Submucous Fibrosis

Hereditary White Lesions
1- Leukoedema
3- Hereditary Benign Intraepithelial
Dyskeratosis

Hereditary White Lesions
1-Leukoedema
Leukoedema is a common mucosal alteration that represents a
variation of the normal condition rather than a true
pathologic change
Clinical features:
 The buccal mucosa bilaterally, and it may be seen rarely on
the labial mucosa, soft palate, and floor of the mouth.

Leukoedema
It usually has a faint, whitish-grey, diffuse, and filmy
appearance, with numerous surface folds resulting in wrinkling
of the mucosa.
It cannot be scraped off, and it disappears or fades upon
stretching the mucosa. It increases in black races.

Leukoedema
 Microscopic examination:
Thickening of the epithelium,
with significant intracellular
edema of the stratum
spinosum. The surface of the
epithelium may demonstrate a
thickened layer of parakeratin.
 Treatment
No treatment is indicated for
leukoedema since it is a
variation of the normal
condition. No malignant
change has been reported.

 White sponge nevus (WSN) is a rare autosomal
dominant disorder .
 The disease usually involves the oral mucosa and (less
frequently) the mucous membranes of the nose,
esophagus, genitalia, and rectum.
 The lesions of WSN may be present at birth or may
first manifest or become more intense at puberty.
 Genetic analyses of families with WSN have identified
a mutation in one allele of keratin 13 that leads to
proline substitution for leucine within the keratin gene
cluster on chromosome.

Clinical features:
White sponge nevus presents as bilateral symmetric white, soft,
“spongy,” or velvety thick plaques of the buccal mucosa.
Other sites in the oral cavity may be involved as the ventral
tongue, floor of the mouth, labial mucosa, soft palate, and
alveolar mucosa. The condition is usually asymptomatic
and does not exhibit tendencies toward malignant
change.

The Eye
 Conjunctiva
Mucous membrane lining the inner surface of the eyelids and covering the
front part of the sclera (white part of eye), responsible for keeping the eye
moist.

Hereditary Benign Intraepithelial Dyskeratosis
Witkop’s disease
 Rare autosomal dominant disorder characterized by oral
lesions and bilateral limbal conjunctival plaques.
Clinical features:
 The oral lesions are similar to those of WSN, with thick,
corrugated, asymptomatic, white “spongy” plaques
involving the buccal and labial mucosa. Other intraoral
sites include the floor of the mouth, the lateral tongue, the
gingiva, and the palate.

 The most significant aspect of HBID involves the
bulbar conjunctiva, where thick, gelatinous, foamy,
and opaque plaques form adjacent to the cornea. The
ocular lesions manifest very early in life (usually within
the first year). Some patients exhibit chronic relapsing
ocular irritation and photophobia. A few cases of
blindness due to corneal vascularization. The disease
is called red eye disease.

Treatment:
No treatment is required for the oral lesions.
For evaluation and treatment of the ocular
lesions, the patient should be referred to an
ophthalmologist.

Dyskeratosis Congenita
 It is a recessively inherited genodermatosis, high
incidence of oral cancer in young affected adults.
 It is characterized by a series of oral changes that lead
to an atrophic leukoplakic oral mucosa, with the
tongue and cheek most severely affected.

Dyskeratosis Congenita Dystrophic nails
 A prominent reticulated hyperpigmentation of the skin of the face, neck, and chest.
 The oral lesions commence before the age of 10 years as crops of vesicles with associated
patches of white ulcerated necrotic mucosa often infected with Candida.
 Some cases exhibit hematologic changes; pancytopenia, hypersplenism, and anaplastic
anemia.

Enumerate:
Hereditary white lesions are:
1-……………………………………………..
2- ……………………………………………….
3- ……………………………………………….
4- ………………………………………………..

Case:
14 year old female
patient reporting
history of thick,
corrugated,
asymptomatic,
white “spongy”
plaques with bulbar
conjunctiva.
1- What is the
clinical diagnosis?

Case:
This patient presented to clinic on examination white
patches on the buccal mucosa were observed . Lesion
could not be rubbed off and showed normal physical
properties without loss of flexibility and patient reports
its presence since birth.
What is the clinical diagnosis?

Case:14 year old female patient
reporting history of white
lesions on the tongue,
dystrophic nails and a
prominent reticulated
hyperpigmentation of the
skin of the face, neck, and
chest.
1- What is the clinical
diagnosis?
2- Is this lesions
precancerous lesions?

Case:
This patient is complaining of white patches on the
buccal mucosa that can not be rubbed off and
disappear upon stretching the mucosa. White
patches exhibit normal physical properties.
a) What is the clinical diagnosis?

Reactive/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
 Uremic stomatitis

Reactive and inflammatory white lesions
1- linea Alba (White Line)
It is a horizontal streak on the buccal mucosa
bilaterally at the level of the occlusal plane extending
from the commissure to the posterior teeth.
Treatment: No treatment is indicated for patients
with linea Alba.

2- Frictional (Traumatic) Keratosis
Clinical features:
 Frictional (traumatic) keratosis is defined as a white
plaque with a rough surface that is clearly related to an
identifiable source of mechanical irritation.
 Frictional keratosis is frequently associated with rough
or maladjusted dentures and with sharp cusps and
edges of broken teeth.

Frictional (Traumatic) Keratosis
Treatment:
 Traumatic keratosis has never been shown to undergo
malignant transformation.
 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.

3- Cheek Chewing
Cheek chewing is most commonly
seen in people who are under stress
or in psychological situations in
which cheek and lip biting become
habitual.
The occurrence is twice as prevalent in
females and three times more
common after the age of 35 years.

Cheek Chewing
 The lesions are most frequently found bilaterally on the posterior buccal
mucosa along the plane of occlusion.
 Patients often complain of roughness or small tags of tissue that they actually
tear free from the surface. The lesions are poorly outlined whitish patches that
may be intermixed with areas of erythema or ulceration.
Treatment and prognosis:
 Since the lesions result from an unconscious
and/or nervous habit, no treatment is indicated.
 A plastic occlusal night guard may be fabricated.

4- Chemical Injuries of the Oral Mucosa
Transient non-keratotic white lesions of the oral mucosa are
often a result of 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,
 Dental Cavity Varnishes,
 Acid Etching Materials,
 Hydrogen Peroxide
 Dentifrices & Mouthwashes (Cinnamon-flavored
Dentifrice).

Chemical Injuries of the Oral Mucosa
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 pseudo membrane, and very painful.

Chemical Injuries of the Oral Mucosa
 The best treatment of chemical burns of the oral
cavity is prevention.
 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. Deep-tissue
burns and necrosis may require careful débridement
of the surface, followed by antibiotic coverage.

Uremic Stomatitis
Uremic stomatitis is considered as chemical burn. It is a rare
disorder that may occur in patients with acute or chronic renal
failure due to increased concentration of urea and its products in
the blood and saliva. The pathogenesis of oral lesions is not clear. It
usually appears when blood concentration of urea exceeds 30
mmol/1.
Treatment:
 The oral lesions usually improve after hemodialysis.
 A high level of oral hygiene, mouthwashes.

6- Actinic Keratosis (Cheilitis)
 Actinic (or solar) keratosis is a premalignant epithelial
lesion that is directly related to long-term sun exposure.
 These lesions are classically found on the vermilion border
of the lower lip as well as on other sun-exposed areas of the
skin (forehead, cheeks, forearms). The surface may be
crusted and rough to the touch.

Actinic Keratosis (Cheilitis)
 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.
 Avoid exposure to solar radiation.
 Use sun screen lotion or cream (Para aminobenzoic acid),
absorbs sunlight.
 Use of sun blockers (zinc oxide), scatters the sunlight .
 Periodic recall is mandatory.
 Biopsy should be performed on lip lesions that do not show
regression after stop the sun light exposure. If biopsy reveals
epithelial dysplasia, laser surgery, cryotherapy may be
performed.
 Chemotherapeutic agents such as topical 5% fluorouracil
(antimetabolite) have been used with some success.

7-Smokeless Tobacco–Induced Keratosis
snuff dipper’s keratosis
tobacco pouch keratosis
Typical features:
Smokeless tobacco are seen in the area contacting the tobacco.
The most common area of involvement is the anterior mandibular
vestibule, followed by the posterior vestibule.
The surface of the mucosa appears white and is granular or
wrinkled.
These lesions are accepted as precancerous

Smokeless Tobacco–Induced Keratosis
Commonly noted is a characteristic area of gingival recession
with periodontal-tissue destruction in the immediate area of
contact. This recession involves the facial aspect of the tooth or
teeth and is related to the amount and duration of tobacco use.
The lesion is usually asymptomatic and is discovered on routine
examination.

Smokeless Tobacco–Induced Keratosis
Cessation of use almost always leads to a
normal mucosal appearance within 1 to
2 weeks. Biopsy specimens should be
obtained from lesions that remain after
1 month.

8- Nicotine Stomatitis
stomatitis nicotina palati
smoker’s palate
 White lesion that develops on the hard and soft palate
in heavy cigarette, pipe, and cigar smokers.
 The lesion is not considered to be premalignant.
 Reverse smoking” produces significantly more
pronounced palatal alterations that may be
erythroleukoplakic and that are definitely considered
premalignant.

Nicotine Stomatitis
Typical features:
 This condition is most often found in older males with a
history of heavy long-term cigar, pipe, or cigarette
smoking.
 Due to the chronic insult, the palatal mucosa becomes
diffusely gray or white. Numerous slightly elevated papules
with punctate red centers that represent inflamed altered
minor salivary gland ducts are noted.

Nicotine Stomatitis
Nicotine stomatitis is completely reversible once the habit is
discontinued. The lesions usually resolve within 2 weeks of
cessation of smoking. The severity of inflammation is
proportional to the duration and amount of smoking. A
biopsy should be performed on any white lesion of the palatal
mucosa that persists after 1 month of discontinuation of
smoking habit.

Enumerate:
Reactive and inflammatory white lesions
1- ……………………………………
2-………………………………………
3- …………………………………….
4- ……………………………………..
5- ……………………………………..
6-…………………………………….
7-……………………………………
8-………………………………………

Case
Ventral surface of the tongue and floor of the mouth
after 2 weeks of peroxide mouthwash.

Case :
40 years-old nervous female came to the clinic
complaining of roughness and small tags of
tissue in the buccal mucosa.
1- What is the clinical diagnosis?
2- What is the treatment?

This abnormal buccal mucosa was detected
by routine examination. The patient
claimed that the lesion is present since
birth.
a)what is the clinical diagnosis?
b)What is the treatment?
Case:

Case
Describe what is observed ?

After severe pain from an exposed tooth, this
white lesion was appeared.
What is this lesion?
Can this lesion be scrubbed off?
Case

This smoker patient's palatal appearance was
noticed on routine examination.
1. What is the clinical diagnosis?
2. Is this lesion a premalignant?
CASE:

Case:
This patient is complaining from
hypersensitivity and root caries.

Case:
This patient is complaining from this crusted lip.
The patient exposed to sun light all the day.

14 year old female patient reporting history of thick,
corrugated, asymptomatic, white “spongy” plaques with
bulbar conjunctiva.

Case:
This patient is complaining from painful, white
plaque patches on the retromolar area,
related to a source of mechanical irritation
What is the treatment?

This patient is complaining from painful, white plaque
patches on the tongue, blood concentration of urea 40
mmol/1.
What is the treatment?

Case
14 year old female patient reporting history of white lesions
on the tongue, dystrophic nails and a prominent reticulated
hyperpigmentation of the skin of the face, neck, and chest.
2- Is this lesions precancerous lesions?

Case:
This patient is complaining from painful, white
plaque patches on the retromolar area, related
to a source of mechanical irritation

Infectious white lesions and white
and red lesions
 Oral Hairy Leukoplakia
 Koplik’s spots
 Candidiasis
 Mucous Patches
 Parulis

Oral Hairy Leukoplakia
 Oral hairy leukoplakia is a corrugated white lesion that usually occurs
on the lateral or ventral surfaces of the tongue in patients with severe
immunodeficiency.
 The most common disease associated with oral hairy leukoplakia is
HIV infection.
 Epstein-Barr virus (EBV) is implicated as the causative agent in oral
hairy leukoplakia.
 Oral hairy leukoplakia may present as a plaque-like lesion and is often
bilateral.

Diagnosis
 The definitive diagnosis can be established by
demonstrating the presence of EBV through in situ
hybridization, electron microscopy, or polymerase
chain reaction (PCR).

Treatment and prognosis
 No treatment is indicated. The condition usually
disappears when antiviral medications such as zidovudine,
acyclovir, or gancyclovir are used in the treatment of the
HIV infection and its complicating viral infections.

Koplik’s spots
 Measles is a virus infection caused by Paramyxovirus.
 Measles is predominantly the disease of children, which appear in
winter and spring following incubation period of 7-10 days.
 Koplik’s spots have been reported in 97% of children. After 1-2 days
follow prodromal symptoms and 2-3 days before the developments
of skin lesion (cutaneous rash of measles) Koplik’s spots begin to
exist.

Koplik’s spots
 As soon as the skin rash develops Koplik’s spots disappear.
 Koplik’s spots do not appear in German measles.
 Koplik’s spots are commonly seen on mucosa of the cheeks and
lips as a small bluish white specks surrounded by a bright red
margin or a grain of rice on an erythematous base.
 Complications of measles are encephalitis and thrombocytopenia
purpura.

Candidiasis
 Candidiasis” refers to a multiplicity of diseases caused
by a yeast like fungus, Candida albicans, and is the
most common oral fungal infection in humans.
 Candida species are normal inhabitants of oral flora in
40% -60% of the population at low concentration.
 Candida is predominantly an opportunistic infectious
agent that is poorly equipped to invade and destroy
tissue.
 The disease may be either acute or chronic in nature
according to the course of the disease.

Predisposing factors
Antibiotics
 Marked changes in oral microbial flora occur following
administration of antibiotics
 Topical or systemic antibiotics reduce the count of oral bacteria
so give a chance for Candida to grow causing infection.
Smoking localized epithelial alterations allowing candidal colonization .
Cigarette smoke may also provide nutrition for candida albicans .
Xerostomia
 Xerostomia may be secondary to smoking, salivary gland
disease, certain drugs, radiation, .....
 Reduced salivary secretion that reduced salivary IgA which
allows for candidal invasion into the tissue.
Corticosteroid
therapy
 Corticosteroids are immunosuppressive drugs which inhibit
lymphocytes. .
 Topical or systemic corticosteroids results in candidal
infection so, use of antifungal drug for one week out of four
weeks of corticosteroid therapy.

Predisposing factrors
Age
 Infants acquire the infection from: their mothers during labor or
defective hygiene of bottles.
-The immune system is not well developed in infants, thus they are liable
for infection.
 Old age due to: Malnutrition and malabsorption, defective immune
response or low vertical dimension.
Pregnancy
 During pregnancy the following changes may be responsible for
candidal infection:
-Increased estrogen and progesterone which may act as substrate for
pathogens.
- Defective cell mediated immunity.
Diabetes  Diabetic individuals are liable to develop oral candidiasis due to the
defect in immunity (especially neutrophils).

Classification of Oral Candidiasis
Acute Chronic
Pseudomembranous
Thrush
Atrophic
Candida antibiotic
Antibiotic sore
mouth
Iron deficiency
anemia
Atrophic
1-Denture sore mouth
2-Angular cheilitis
3-Median rhomboid
glossitis
Hyperplastic
1-Candidal leukoplakia
2-Papillary hyperplasia
of the palate
3-Median rhomboid
glossitis (nodular)

Acute Candidiasis
1- Acute Pseudomembranous
Candidiasis (Thrush)
Clinical Features:
 It is a superficial infection of the outer layers of the epithelium, and it
results in the formation of patchy white plaques or flecks on the
mucosal surface.
 Removal of the plaques by gentle rubbing or scraping usually reveals
an area of erythema or even shallow ulceration.

Diagnosis and DD
 A smear demonstrating a yeast or myelin is helpful
when the diagnosis is uncertain.
 The differential diagnosis of thrush includes food
debris, habitual cheek biting, and rarely, a genetically
determined epithelial abnormality such as white
sponge nevus.

Acute Atrophic Candidiasis
 Acute atrophic candidiasis presents as a red patch of
atrophic or erythematous raw and painful mucosa,
with minimal evidence of the white
pseudomembranous lesions observed in thrush.

Acute Atrophic Candidiasis
 Forms:
- Antibiotic sore mouth, develops symptoms of oral burning,
bad taste, or sore throat during or after therapy with broad-
spectrum antibiotics.
- Patients with chronic iron deficiency anemia may also
develop atrophic candidiasis.
 Removal of the cause such as withdrawal of the offending
antibiotic and institution of appropriate oral hygiene leads
to improvement.

Chronic Candidiasis
Atrophic:
 Denture sore mouth
 Angular cheilitis
 Median rhomboid glossitis
Hypertrophic/hyperplastic:
 Candidal leukoplakia
 Papillary hyperplasia of the palate
 Median rhomboid glossitis (nodular)

Denture Stomatitis
(Denture Sore Mouth)
 Denture stomatitis is a common form of oral candidiasis
that manifests as a diffuse inflammation of the maxillary
denture-bearing areas and that is often (15 to 65% of cases)
associated with angular cheilitis.
 Candida act as an endogenous infecting agent on tissue
predisposed by chronic trauma to microbial invasion.

Denture Stomatitis
 Soft liners in dentures provide a porous surface and an opportunity for
additional mechanical locking of plaque and yeast to the appliance. In
general, soft liners are considered to be an additional hazard for
patients who are susceptible to oral candidiasis.
 Denture sore mouth is rarely found under a mandibular denture due to
the negative pressure that forms under the maxillary denture excludes
salivary antibody (IgA) from this region, and yeast may reproduce,
undisturbed, in the space between the denture and mucosa.
 Lesions of chronic atrophic candidiasis have also been frequently
reported in HIV-positive and AIDS patients.

Clinical Stages
 The first stage
consists of numerous
palatal petechiae
 The second stage
displays a more
diffuse erythema
involving most of the
denture- covered
mucosa
 The third stage
includes the
development of
tissue granulation or
nodularity (papillary
hyperplasia).

Denture sore mouth has to be differentiate from
contact stomatitis in denture wearer
Denture sore mouth Contact stomatitis
Onset After long time of wearing
denture
24-48 hrs after wearing
denture
Site Denture bearing areas mainly
upper denture
Denture bearing and
contacting areas, both arches
Patch test Negative Positive
Treatment Antifungal drugs Antihistaminic

A comparison between allergic
stomatitis and contact stomatitis
Allergic stomatitis Contact stomatitis
Route of
administration
Systemic (injection, ingestion or
absorption across skin or oral
mucosa)
Topical
Type of
hypersensitivity
Humoral
type III
Cellular
Type IV
Site of lesion
produced
Anywhere on the body Only at site of contact
Skin test for
allergen
Patch test weak positive Positive patch test
Onset Early onset within few hours Appear later (48 hrs)
Severity More severe Less severe

Denture sore mouth Allergic stomatitis Contact stomatitis
Superficial local
infection
Systemic (injection, ingestion or
absorption across skin or oral
mucosa)
Topical
Candida infection Humoral
type III
Cellular
Type IV
Denture bearing areas
mainly upper denture
Anywhere on the body Only at site of contact
both arches
Negative Patch test weak positive Positive patch test
After long time of
wearing denture
Early onset within few hours Appear later (48 hrs)
Less Severe More severe Less severe

Treatment
 Antifungal treatment will modify the bright red
appearance of denture sore mouth and papillary
hyperplasia specifically but will not resolve the basic
papillomatous lesion where surgical excision may be
required.
 Antifungal therapy and cessation of denture wearing
usually is advisable before surgical excision since
elimination of the mucosal inflammation often reduces the
amount of tissue that needs to be excised.
 Yeast attached to the denture plays an important etiologic
role in chronic atrophic candidiasis. Rinsing the appliance
with a dilute (10%) solution of household bleach, soaking it
in boric acid, or applying nystatin cream before inserting
the denture will eliminate the yeast.

Angular Cheilitis
 Angular cheilitis is the term used for an infection involving
the lip commissures. The majority of cases is Candida
associated and respond promptly to antifungal therapy.
 Lesions are moderately painful, fissured due to
accumulation of saliva in the skin folds at the commissural
angles.

Angular Cheilitis
Etiologic cofactors include:
 Reduced vertical dimension
 A nutritional deficiency (iron deficiency anemia and
vitamin B or folic acid deficiency)
 Diabetes
 AIDS
 Co-infection with staphylococcus and beta-hemolytic
streptococcus.

Median Rhomboid Glossitis
 Erythematous patches of atrophic papillae located in
the central area of the dorsum of the tongue are
considered a form of chronic atrophic candidiasis.
When these lesions become more nodular, the
condition is referred to as hyperplastic median
rhomboid glossitis.

Chronic Hyperplastic Candidiasis
 mycelial invasion of the deeper layers of the mucosa and
skin occurs, causing a proliferative response of host tissue
 Candidal leukoplakia is considered a chronic form of oral
candidiasis in which firm white leathery plaques are
detected on the cheeks, lips, palate, and tongue.
 The differentiation of candidal leukoplakia from other
forms of leukoplakia is based on finding periodic acid–
Schiff (PAS)–positive hyphae in leukoplakic lesions.

IV-Immunocompromised (HIV)-
associated candidiasis
 patients who are on immunosuppressive drug
regimens or who have HIV infection, cancer, or
hematologic malignancies have an increased
susceptibility to oral candidiasis.
 This supports an important role for T lymphocytes in
immunity to Candida, especially in regard to chronic
candidiasis.
 In HIV-infected patients who develop oral candidiasis,
the level of salivary anti-Candida IgG is increased
while serum and salivary IgA decrease.
 Candidiasis in AIDS patient caused by
…………………………. & ……………………………………………..

Treatment of oral candidiasis
 Removal of predisposing factor but in patients whom
cannot eliminate predisposing factors such as
xerostomia and immunodeficiency may need either
continuous or repeated treatment to prevent
recurrences.
 The consumption of yogurt (L. acidophilus ) two to
three times per week and improved oral hygiene can
also help, especially if underlying predisposing factors
cannot be eliminated. L. acidophilus is producing
lactic acid, which keeps the pH level low and
inhospitable to Candida

Treatment of oral candidiasis
 topical administered medications are now available as
nystatin and amphotericin B. The majority of acute oral
Candida infections respond rapidly to topical nystatin 4
times daily for three weeks and will not recur.
 Nystatin in cream form may also be applied directly to the
denture or to the corners of the mouth
 Systemic therapy includes the use of any one of these three:
ketoconazole, itraconazole, and fluconazole.
 A once-daily dose of 200 mg of ketoconazole, 100 mg of
fluconazole, or itraconazole oral suspension (100 to 200
mg/d) for 2 weeks. When these medications are used for
this short period, side effects such as increased liver
enzymes, abdominal pain, and pruritus are rare.

Mucous Patches
 Seen in secondary syphilis and usually develops within 6 weeks after
the primary lesion (Treponema pallidum)
 It is characterized by diffuse maculopapular eruptions of the skin and
mucous membranes. On the skin, these lesions may present as macules
or papules. In the oral cavity, the lesions are usually multiple painless
grayish white plaques overlying an ulcerated necrotic surface.
 The lesions occur on the tongue, gingiva, palate, and buccal mucosa.
Associated systemic signs and symptoms (including fever, sore throat,
general malaise, and headache) may also be present.
 The mucous patches of the secondary stage of syphilis resolve within a
few weeks but are highly infective because they contain large numbers
of spirochetes.

Parulis
 A parulis, or gumboil, is a localized accumulation of
pus located with the gingival tissues. It originates from
either an acute periapical abscess or an occluded
periodontal pocket.
 The cortical bone is destroyed by the inflammatory
process, and the gumboil often appears as a yellowish
white bump on the gingiva. The lesion is usually
painful, and pain relief occurs when the “boil” ruptures
or drains spontaneously.

Idiopathic “True” Leukoplakia
 Leukoplakia is a white keratotic patches that cannot be
rubbed off and a precancerous lesion with a
recognizable risk for malignant transformation.
 Precancerous lesion as a “morphologically altered
tissue in which cancer is more likely to occur than in
its apparently normal counterpart.”
 Leukoplakia is defined as “a white patch or plaque that
cannot be characterized clinically or pathologically as
any other disease”.

Etiology
Unknown
Tobacco usage
Alcohol consumption
Sunlight

Etiology
Candida albicans
 Human papilloma virus (HPV)
Electrogalvanic current
Chemical irritation
Systemic predisposing factors:
nutritional deficiency (Vit B 12, Iron deficiency) when
exposed to various local insults may predispose to
both leukoplakia and carcinoma.

Clinical Features
 Leukoplakia: adult men older than 50 years of age.
 Occur on any mucosal surface, buccal mucosa, vermilion
border of the lower lip, and gingiva. They are less common
on the palate, maxillary mucosa, retromolar area, floor of
the mouth, and tongue and infrequently causes discomfort
or pain.
 Lesions of the tongue and the floor of the mouth account
for more than 90% of cases that show dysplasia or
carcinoma.
 Early lesions are usually soft in consistency, while late
appears as a leathery white patch and may show evidence
of loss of elasticity and flexibility.
 Borders may be well or ill defined and surface may be
smooth or rough, flat or elevated or verrucous.

Subtypes
 “Homogeneous leukoplakia” (or “thick
leukoplakia”) well-defined white patch, localized or
extensive, that is slightly elevated and that has a
fissured, wrinkled, or corrugated surface. On palpation,
these lesions may feel leathery to “dry, or cracked mud-
like.”

Subtypes
 Nodular (speckled) leukoplakia (Candida
leukoplakia) is granular or non-homogeneous. It is a
mixed red-and-white lesion in which keratotic white
nodules or patches are distributed over an atrophic
erythematous background. This type of leukoplakia is
associated with a higher malignant transformation
rate.

Subtypes
 Verrucous leukoplakia” or “verruciform
leukoplakia” is a thick white lesion with papillary
surfaces in the oral cavity. These lesions are usually
heavily keratinized and are most often seen in older
adults in the sixth to eighth decades of life.

Histopathologic Features
Benign form: there may be various
combinations of hyperkeratosis,
hyperparakeratosis and acanthosis
and the basal cell layer is always
intact. There is diffused chronic
inflammatory cell infiltration into
the underlying connective tissue.

 Epithelial dysplasia: the diagnosis is made when less than
the complete thickness of the epithelium demonstrates the
characteristic features of dysplasia, this includes the
presence of:
 Mitosis is increased and abnormal
 Individual cell keratinization
 Alteration in the nuclear cytoplamic ratio
 Loss of polarity and disorientation of the cells
 Hyperchromatism
 Large prominent nucleoli
 Basiar hyperplasia
 Division of nucleus without division of cytoplasm

Carcinoma in situ & Carcinoma
 Carcinoma in situ: the epithelium demonstrates
dyplasia throughout its full thickness (from top to
bottom), but the basement membrane is intact,
 Carcinoma: a loss of basement membrane and
invasion of the underlying tissue.

Diagnosis and Management
elimination of an irritant
leukoplakic lesion disappears
No treatment and follow up
the persistent lesion, Topical antifungal drugs for
2 weeks. Re-evaluation after antifungal
the lesion regress the follow up
of the lesion would be enough.
Lesions that are not respond to therapy,
biopsy has to be performed. toluidine blue
and cytobrush techniques
No sign of dysplasia No time should be wasted and the lesion
should be removed and follow up.
Small lesion
removed by
excisional biopsy
Large lesion
Remove remainder of lesion surgical ,
follow up
Leave lesion and reevaluation
Repeated biopsy 6-12 months

Diagnosis and Management
1) A diagnosis of leukoplakia is made when adequate
clinical and histologic examination fails to reveal an
alternative diagnosis and when characteristic
histopathologic findings for leukoplakia are present.
2)The use of antioxidant nutrients and vitamins have not
been reproducibly effective in management. Programs
have included single and combination dosages of
vitamins A, C, and E.

toluidine blue and
cytobrush techniques

Case:
This patient presents with white patches on the buccal
mucosa with loss of flexibility in a heavy smoker
1. What is the clinical diagnosis?
2. How to manage this case?

Erythroplakia
 “bright red velvety plaque or patch which cannot be
characterized clinically or pathologically as being due
to any other condition.
 The majority of erythroplakias (particularly those
located under the tongue, on the floor of the mouth,
and on the soft palate and anterior tonsillar pillars)
exhibit a high frequency of premalignant and
malignant changes.
 The etiology of erythroplakia is uncertain, most cases
of erythroplakia are associated with heavy smoking,
(reverse smoking) with or without concomitant
alcohol abuse.

Clinical Features
 Older men, in the sixth and seventh decades of life.
 Almost all of the lesions are asymptomatic
 Erythroplakias are more commonly seen on the floor of the
mouth, the ventral tongue, the soft palate, and the tonsillar
fauces, all prime areas for the development of carcinoma.

Clinical Features
1. “Homogeneous erythroplakia,
2. Erythroplakia interspersed with
patches of leukoplakia,
3. Granular or speckled erythroplakia”.

Erythroplakia
Histopathologic Features:
Erythroplakia are histopathologically demonstrating
severe epithelial dysplasia, carcinoma in situ, or
invasive carcinoma.
Differential Diagnosis:
 Differentiation of erythroplakia from benign
inflammatory lesions of the oral mucosa can be
enhanced by the use of a 1% solution of toluidine blue,
applied topically with a swab or as an oral rinse.
 Clinically similar lesions may include erythematous
candidiasis, areas of mechanical irritation,
denture stomatitis, vascular lesions, and a variety
of nonspecific inflammatory lesions.

Treatment and Prognosis
 The treatment of erythroplakia should follow the same
principles outlined for that of leukoplakia.
 Observation for 1 to 2 weeks following the elimination
of suspected irritants is acceptable, but prompt biopsy
at that time is mandatory for lesions that persist
 Epithelial dysplasia or carcinoma in situ warrants
complete removal of the lesion. Actual invasive
carcinoma must be treated promptly according to
guidelines for the treatment of cancer.
 Since recurrence and multifocal involvement is
common, long term follow-up is mandatory.

Erythroplakic lesion
disappears
Lesions that are not respond to therapy,
biopsy has to be performed. toluidine blue
and cytobrush techniques
No sign of dysplasia No time should be wasted and the lesion
should be removed and follow up.
Small lesion
removed by
excisional biopsy
Large lesion
Leave lesion and reevaluation
Repeated biopsy 6-12 months

Oral Lichen Planus
 Oral lichen planus (OLP) is a common chronic
immunologic inflammatory mucocutaneous disorder
that varies in appearance from keratotic (reticular or
plaquelike) to erythematous and ulcerative.
 About 28% of patients who have OLP have skin
lesions. The skin lesions are flat violaceous papules
with a fine scaling on the surface. Unlike oral lesions,
skin lesions are usually self-limiting, lasting only 1 year
or less.

Etiology and Diagnosis
The etiology of lichen planus is not fully
understood and can be divided into:
Idiopathic lichen planus:
psychological stress and cell mediated
immune response.
Lichnoid reaction: drug induced or
graft versus host disease.
Virus C

Idiopathic Lichen Planus
 Emotional stress has been implicated in the development
of lichen planus as death of close relative or new
environment, job.
 Also, Diabetes, Hypertension and Lichen planus are
disorder sharing emotional stress factor were found to be
associated together ‟ Grinspan Syndrome.”
 Cell mediated immune response: due to lymphocyte-
epidermal interaction resulting in degeneration of basal
cell layer. Langerhans cell recognize, process and present
appropriate antigen altered kerationcytes to lymphocytes
which has been attracted to the area by interleukin-1
secreated by Langerhans macrophages. Interleukin-1 can
also stimulate T-cells to produce interleukin-2 which
causes T-cells proliferation

Cytotoxic T-cells can damage basal cells by two
mechanisms
 Cytotoxic T-cells release cytotoxic proteins called perforin
which form pores in the cell membrane of basal cells so
basal cells absorb extracellular fluid and swell. Cell death
occur by dilution of cytoplasmic components(liquefaction
degeneration of basal cell layer).
 Cytotoxic T-cells stimulate basal cells to undergo apoptosis
or programmed cell death. The basal cells become
shrunken with little eosinophilic cytoplasm and pyknotic
nuclear fragments.
- Those dead basal cells are called Civatte bodies which
will be phagocytosed by adjacent basal cells or by
macrophages.
- Dead cells which are not phagocytosed are extruded into
connective tissue and become coated with IgM and are
called Colloid bodies.

Clinical Features
 Age of onset: 50 years female
 The skin lesions of lichen planus have been classically
described as purple, pruritic, and polygonal papules
and most common in the flexor surface of extremities.
 The skin lesion resolves within 1-2 years, most
commonly leaving hyper-pigmentation.

Kobner’s phenomena
 Skin lesion characterized by Kobner’s phenomena
(development of new lesion on normal looking skin
following trauma as scratching).
Heinrich Köbner

Clinical Features
 OLP may occur at any oral mucosal site but the buccal
mucosa is the most common site followed by tongue
and gingiva.
 OLP may be associated with pain or discomfort, which
interferes with function and with quality of life.
 Lesions are bilateral and characterized by remission
and exacerbation.

Clinical Features
Lesions do not disappear on stretching,
cannot be rubbed off, do not cause loss
of flexibility of the oral mucosa.

Clinical Features
 Lesions are surrounded by a network of bluish white
lines called Wickham’s striae radiating from the
periphery of the lesion.
louis frédéric wickham

Reticular from
 It consists of slightly elevated fine white lines
(Wickham's striae) that produce lace-like pattern, fine
radiating lines or annular lesion.
 The patients may feel roughness while rubbing the
tongue against the buccal mucosa or may notice
change in the lip colour.

Papular form
 It appears as discrete papules 0.5-1mm in diameter on
the well keratinized areas of the oral mucosa.

Plaque form
 It appears as homogenous white patches which may
resemble leukoplakia but there is no loss of pliability
and flexibility.

Atrophic form
 It appears as diffused, erythematous patches. Wickham's
striae may radiate from the lesion.
 Atrophic lichen planus involving the gingiva results in
desquamative gingivitis (bright red edematous).
 Atrophic lichen planus may be seen on the dorsum of the
tongue resulting in atrophy of filiform and fungiform
papillae.
 Symptoms ranged from mild burning to severe pain.

Erosive from
 It appears as an ulcerated area with irregular borders and
covered by pseudomembrane. Erosive lesions probably
develop as a complication of the atrophic process when the
thin epithelium is abraded or ulcerated.
 The periphery of the lesion is usually surrounded by
wickham's striae.
 The malignant transformation is more commonly noted in
the erosive and the atrophic form.

Bullous form
 It is a rare form of lichen planus that appears as vesicle or
bullae that rupture resulting in chronic irregular ulcer.
 Bullous and erosive form of lichen planus occur in the
severe form of the disease when extensive degeneration of
the basal layer of epithelium causes a separation of the
epithelium from the underlying connective tissue.

(1) Areas of hyperparakeratosis or hyperorthokeratosis, often with a
thickening of the granular cell layer and a saw-toothed appearance to
the rete pegs.
(2) “Liquefaction degeneration,” or necrosis of the basal cell layer, which
is often replaced by an eosinophilic band.
(3) A dense subepithelial band of lymphocytes. Isolated epithelial cells,
shrunken with eosinophilic cytoplasm and one or more pyknotic
nuclear fragments (Civatte bodies), are often scattered within the
epithelium and superficial lamina propria. These represent cells that
have undergone apoptosis. The linear sub-basilar lymphocytic
infiltration is composed largely of T cells.

Immunofluorescent Studies
 Direct immunofluorescence demonstrates a shaggy
band of fibrinogen in the basement membrane zone
in 90 to 100% of cases. Patients also may have multiple
mainly IgM-staining cytoid bodies, usually located in
the dermal papilla or in the peribasalar area.

Differential Diagnosis
 Lichenoid lesions (eg, drug-induced lesions, contact
mercury hypersensitivity)
 Erythema multiforme,
 Lupus erythematosus,
 Graft-versus-host reaction
 Leukoplakia,
 Squamous cell carcinoma,
 Mucous membrane pemphigoid,
 Candidiasis.

Management of lichen planus
Reticular, plaque, papules
Atrophic, bullous , erosive
Corticosteroids + Retinoids
Topical Systemic Intra lesional injection
kenalog in orabase prednisone 5 mg-10 mg kenacort A
diabetes and hypertension.
Low dose systemic steroids and non steroidal anti-inflammatory drugs
Candida overgrowth with clinical thrush may develop, requiring
concomitant topical or systemic antifungal therapy.
Other topical and systemic therapies
reported to be useful, such as dapsone,
doxycycline, and antimalarials.
retinoid.
Topical application of cyclosporine or
tacrolimus appears to be helpful in
managing cases of OLP not response
to steroid.

Lichenoid Reactions
Lichenoid reactions were differentiated from lichen
planus on the basis of:
(1) Their association with the administration of a drug,
contact with a metal, the use of a food flavoring, or
systemic disease.
(2) Their resolution when the drug or other factor was
eliminated or when the disease was treated.
Lichenoid reaction in buccal mucosa, reaction to amalgam contact

Drugs Induce Lichenoid Reaction
Gold therapy
Non-steroidal anti-inflammatory
drugs (NSAIDs)
 Diuretics other anti-hypertensives
Oral hypoglycemic agents of the
sulfonylurea type

Drugs Induce Lichenoid Reaction

Graft-versus-host Disease
 The interaction of immune-competent cells from one
individual (the donor) to a host (the recipient) who is
immune-deficient.
Clinical features:
 The epidermal lesions of acute GVHD range from a
mild rash to diffuse severe sloughing.

 Oral mucosal lesions occur in only about one-third of
cases and are only a minor component of this problem.
 Chronic GVHD is associated with lichenoid lesions.
 In some cases, the intraoral lichenoid lesions are
extensive and involve the cheeks, tongue, lips, and
gingivae.

 In most patients with oral GVHD, a fine reticular
network of white striae that resembles OLP is seen.
Patients may often complain of a burning sensation of
the oral mucosa. Xerostomia is a common complaint
due to the involvement of the salivary glands.

 The development of a pyogenic granuloma on the
tongue has been described as a component of chronic
GVHD. The mouth is an early indicator of a variety of
reactions and infections associated with
transplantation-related complications. The majority of
these infections are opportunistic Candida infections

Treatment and prognosis
 The principle basis for management of GVHD is
prevention by careful histocompatibility matching and
judicious use of immunosuppressive drugs.
 Topical corticosteroids and palliative medications
may facilitate the healing of the ulcerations.
Ultraviolet A irradiation therapy with oral psoralen
(increases skin’s sensitivity to high intensity long wave
ultraviolet light (UVA)has also been shown to be
effective in treating resistant lesions.
 Topical azathioprine suspension
(immunosuppressive drug) has been used as an oral
rinse and then swallowed, thereby maintaining the
previously prescribed systemic dose of azathioprine

A 50 year old female patient presented to the clinic with
severe pain , a white and red lesion was observed related
to buccal mucosa bilaterally . Patient complains of itching
skin lesions.
1) What is the diagnosis?
2) What is the treatment of such case?
CASE

A 50 year old female patient presented to the
clinic with severe pain , a white and red lesion
was observed related to buccal mucosa
bilaterally . Patient complains of itching skin
lesions.
1) What is the diagnosis?
2) What is the treatment of such case?
3) What is the name of gingiva?

Lupus Erythematosus
(Systemic and Discoid)
 Systemic lupus erythematosus (SLE) is an
immunologically mediated inflammatory condition that
causes multi-organ damage and considered as a collagen or
connective tissue disease.
 Discoid lupus erythematosus (DLE) is a relatively
common disease and has a great cosmetic significance
because of its predilection for the face. It is less aggressive
form affecting the skin and rarely progressing to the
systemic form.
 Subacute cutaneous lupus erythematosus described as
lying intermediate between SLE and DLE. It has a mild
systemic involvement and the appearance of some
abnormal autoantibodies.

Etiology of Lupus Erythromatosus
1-Immunologic factors: Auto-antibody
formation
2- Genetic factors
3-Infectious (EBV, CMV, VZV) and
environmental factor (sun exposure, drugs,
chemical substances).
Ex of drugs: hydralazine, methyldopa,
chlorpromazine, isoniazid, quinidine and
procainamide)
4- Endocrine factors: (hormones) high
incidence in women in their child bearing
years.

Drugs
Hydralazine lowers blood pressure
Methyldopa antihypertensive effect
Chlorpromazine antipsychotic medication
Isoniazid antibiotic used for the treatment of
tuberculosis
Quinidine antiarrhythmic agent in the heart
Procainamide treatment of cardiac arrhythmias

Discoid Lupus Erythematosus
 Females in the third or fourth decade of life.
 DLE is confined to the skin and oral mucous membranes and has a
better prognosis than SLE.
 DLE can present in both localized and generalized forms and
is called chronic cutaneous lupus (CCL).
 favor sun-exposed areas such as the face, chest, back, and
extremities

These lesions characteristically:
1- Expand by peripheral extension
2- Disk-shaped
3- Scar formation
4- Central atrophy
5- Loss of skin pigmentation

 Skin lesions occur on the face, it involves malar regions
and cross the bridge of the nose which gives butterfly
distribution

 The oral lesions can occur in the absence of skin lesions,
but there is a strong association between the two. As the
lesions expand peripherally, there is central atrophy, scar
formation, and occasional loss of surface pigmentation.
 The primary locations for these lesions include the buccal
mucosa, palate, tongue, and vermilion border of the lips.

Differential diagnosis:
1. Reticular or erosive lichen planus. Unlike lichen
planus, the distribution of DLE lesions is usually
asymmetric, and the peripheral striae are much more
subtle.
2. Leukoplakia: the diagnosis must be based not only
on the clinical appearance of the lesions but also on
the coexistence of skin lesions and on the results of
both histologic examination and direct
immunofluorescence testing.

Systemic lupus Erythematosus
 The lesions are frequently symptomatic,
 often consist of one or more of the following
components: erythema, surface ulceration,
keratotic plaques, and white striae or papules.
 They typically respond well to topical or systemic
steroids. Clobetasol (a potent topical steroid) placed
under an occlusive tray is very effective for temporary
relief of these lesions.

Raynaud's phenomenon is characterized by blood vessel spasms in the fingers, toes, ears
or nose, usually brought on by exposure to cold. Raynaud's phenomenon and Raynaud's
disease, a similar disorder, may be associated with autoimmune disorders such as
rheumatoid arthritis, systemic lupus erythematosus and scleroderma.

Laboratory findings
 Antinuclear antibodies are found in patients with SLE.
 Moderate to high titers of anti-DNA and anti-Smith,
antibodies are almost pathognomonic of SLE.

 hyperorthokeratosis with keratotic plugs, atrophy of
the rete ridges, and Liquefaction degeneration of the
basal cell layer. Edema of the superficial lamina
propria is also quite prominent.

 No band-like leukocytic inflammatory infiltrate seen in
patients with lichen planus. Immediately subjacent to the
surface epithelium is a band of PAS-positive material, and
frequently there is a pronounced vasculitis in both
superficial and deep connective tissue.
 Another important finding in lupus is that direct
immunofluorescence testing of lesional tissue shows the
deposition of various immunoglobulins and C3 in a
granular band involving the basement membrane zone.
This is called the positive lupus band test, and discoid
lesions will not show this result.

Malignant Potential of Oral Lesions
 The precancerous potential of intraoral discoid lupus
is controversial.
 Basal cell and squamous cell carcinomas have been
reported to develop in healing scars of discoid lupus.
However, this malignant change may have been caused
by the radiation and ultraviolet light used in the
treatment of lupus.
 The development of squamous cell carcinoma has
been described in lesions of discoid lupus involving
the vermilion border of the lip, and actinic radiation
may play an important adjunct role.

Case:
A female patient presented to the clinic with central
atrophic and ulcerated area with small white dots,
surrounded by keratotic zone skin lesion on sun exposed
areas
What is diagnosis of disease?
What is the skin lesion?

Case :
A female patient presented to the
clinic with central atrophic and
ulcerated area with small white dots,
surrounded by keratotic zone skin
lesion on sun exposed areas.
What is diagnosis of disease?
What is the skin lesion?

Developmental White Lesions
 Fordyce’s granules are ectopic sebaceous glands within
the oral mucosa. Fordyce’s granules do not exhibit any
association with hair structures in the oral cavity.
 Fordyce’s granules present as multiple yellowish white
or white papules. most commonly on the buccal
mucosa and vermilion border of the upper lip.
Occasionally, these may be seen on the retromolar pad
area and the anterior tonsillar pillars.

 Men ˃ femal
 The granules tend to appear during puberty and increase in
number with age.
 Fordyce’s granules are completely asymptomatic and are often
discovered on routine examination. They are bilateral and
become accentuated on stretching the oral mucosa.
 Histologically: normal sebaceous glands
Treatment
no treatment is indicated, no biopsy is usually
required. Fordyce’s granules on the vermilion
border of the upper lip may require surgical
removal for esthetic reasons.

Describe what is observed ?
What is the nature of this lesion?
Case :

Geographic Tongue
 Geographic tongue is a common benign condition
dorsal surface of the tongue. women more than men.
 This condition is characterized initially by the
presence of small, round to irregular areas of
dekeratinization and desquamation of filiform
papillae. The elevated margins around the red zones
are white to slighty yellowish white.

Etiology of Geographic Tongue
1. Association with psoriasis
2. Atopic patients who have intrinsic asthma and rhinitis.
3. Family history of asthma, eczema, and hay fever.
4. Juvenile diabetes
5. Patients with pernicious associated with folic acid deficiency
6. Pregnant patients: hormonal fluctuations.
7. Reiter’s syndrome. (arthritis, urethritis, conjunctivitis, lesions of the
skin and mucosal surfaces)

Mention the diagnosis of this asymptomatic
condition?
Case

What is the diagnosis of this lesion?
Case

Hairy Tongue (Black Hairy Tongue)
Hairy tongue” is a clinical term describing an abnormal
coating on the dorsal surface of the tongue. Hairy
tongue results from the defective desquamation of
cells that make up the secondary filiform papilla. This
buildup of keratin results in the formation of highly
elongated hairs, which is the hallmark of this entity.

The cause of black hairy tongue
Unknown may be:
 Tobacco (heavy smoking) and psychotropic agents.
 Broad-spectrum antibiotics such as penicillin.
 The use of systemic steroids.
 The use of oxidizing mouthwashes or antacids
 The overgrowth of fungal or bacterial organisms.
 Radiation therapy for head and neck malignancies
 Poor oral hygiene can exacerbate this condition.
The common etiologic factor for all of these influences
may be the alteration of the oral flora by the
overgrowth of yeast and chromogenic bacteria.

black hairy tongue
 Anterior two-thirds of the dorsum of the tongue, with a
predilection for the midline just anterior to the
circumvallate papillae. The patient presents with elongated
filiform papillae and lack of desquamation of the papillae.
 The tongue appears thickened and matted. Depending on
the diet and the type of organisms present, the lesions may
appear to range from yellow to brown to black or tan and
white.

Black Hairy Tongue
 Although the lesions are usually asymptomatic, the
papillae elongated and may cause a gag reflex or a
tickle in the. They may also result in halitosis or an
abnormal taste.
 A biopsy is usually unnecessary. Treatment consists of
eliminating the predisposing factors if any are present.
Cessation of smoking or discontinuation of
oxygenating mouthwashes or antibiotics will often
result in resolution.
 Improvement in oral hygiene is important, especially
brushing or scraping of tongue.

Case :
This patient's tongue appearance was noticed on
routine examination.
What is the diagnosis?

Oral Submucous Fibrosis
 Oral submucous fibrosis (OSF) is a slowly progressive
chronic fibrotic disease of the oral cavity and oropharynx,
characterized by fibroelastic change and inflammation of
the mucosa, leading to a progressive inability to open the
mouth, swallow, or speak.
 Causes: direct stimulation from exogenous antigens like
Areca alkaloids or changes in tissue antigenicity that may
lead to an autoimmune response. The inflammatory
response releases cytokines and growth factors that
promote fibrosis by inducing the proliferation of
fibroblasts, up-regulating collagen synthesis and down-
regulating collagenase production.
 OSF is regarded as a premalignant condition, and many
cases of oral cancer have been found coexisting with
submucous fibrosis.

Etiology
Several factors are believed to contribute to the
development of OSF, including:
 General nutritional and vitamin deficiencies.
 Hypersensitivity to certain dietary constituents such as
chili peppers, chewing tobacco.
 The habitual use of betel and its constituents.

Clinical features
 The disease first presents with a burning sensation of the
mouth, particularly during consumption of spicy foods.
 It is often accompanied by the formation of vesicles or
ulcerations and by excessive salivation or xerostomia and
altered taste sensations.
 Gradually, patients develop a stiffening of the mucosa, with
a dramatic reduction in mouth opening and with difficulty
in swallowing and speaking.

Clinical features
 The mucosa appears blanched and opaque with the
appearance of fibrotic bands that can easily be
palpated. The bands usually involve the buccal
mucosa, soft palate, posterior pharynx, lips, and
tongue.
 OSF usually affects young individuals in the second
and third decades of life but may occur at any age.

Classification of red and white lesions
white lesions associated with
Skin lesion
Premalignant white lesions
Variation in normal mucosa Immunological
white lesions
Oral Lichen Planus
Lichenoid Reactions
Lupus Erythematosus
Graft-versus-host
Disease
2- Actinic keratosis
3- Mucous patches
4- Lichen planus
5- Lupus erythrematousum
6- Graft versus host disease
2- Actinic keratosis
3- Smokless tobacco
4- Revese smoking
5- Leukoplakia
6- Erythroplakia
7- Lichen planus
8- Lupus erythrematousum
9- Oral submucous fibrosis
1- Linea alba
2- Leukodema
3- Fordyce’s granules

red & white lesions OMED 1

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