Oral white lesions1 mohamed assasdawy

Dr Mohamed Assadawy
DrMohamedAssadawy

INTRODUCTION
CLASSIFICATION OF WHITE LESIONS
ETIOLOGY
CLINICAL FEATURES
HISTOPATHOLOGY
D/D
MANAGEMENT
Outlines
12/13/2018 2DRMohamed assadawy

LESIONS ARE GROUPED INTO THE THREE
CLASSIC CLINICAL PRESENTATIONS THAT
HAVE BEEN DESCRIBED: COLOR CHANGE,
RAISED,AND DEPRESSED

INTRODUCTION White lesions is a non-specific term used to describe any abnormal area of the oral
mucosa that on clinical examination appears whiter than the surrounding tissue
 Why do they appear White ?
 Increased production of keratin(hyperkeratosis)
 Abnormal thickening of st.spinosum(acanthosis)
 Intra-cellular and extra-cellular accumulation of fluid
 Necrosis of the oral epithelium when exposed to toxic chemicals White
pseudomembranous produced by microbial remnants and epithelial sloughing

CLASSIFICATION
a) According to cause
-Physical and Chemical Injuries
- Allergies
- Infections
- Immunologically-mediated diseases
- Premalignant Lesions
- Genokeratoses
- Systemic Diseases
- Miscellaneous

Physical and Chemical Injuries
o Linea Alba
o Morsicatio
o Frictional Keratosis
o Sloughing traumatic lesions
o Thermal burn
o Chemical Burn
o Nicotine stomatitis

Allergies
o Reaction to systemic drugs
• lichenoid and lupus-like
eruptions
o Contact stomatitis
• reaction to toothpaste,
mouthwash, cinnamon, amalgam

Infections
o Candidiasis
• Pseudomembranous
• Hyperplastic
o Syphilis
• Secondary (mucous patches)
• Tertiary (syphilitic glossitis)
o Hairy leukoplakia
o Diptheria
o Koplik spots of Measles
o Scarlet feve

Immunologically-mediated diseases
o Lichen planus
o Lupus erythematosus

Premalignant Lesions
o Idiopathic leukoplakia
o Actinic cheilitis
o Tobacco pouch keratosis
o Submucous fibrosis

Genokeratoses
o Leukoedema
o White sponge nevus
o Hereditary benign intraepithelial
dyskeratosis
o Pachyonychia congenita
o Dyskeratosis congenita
o Follicular keratosis (Darier’s
disease)
o Incontinentia pigmenti

Systemic Diseases
o Uremic Stomatitis

Miscellaneous
o White coated tongue
o White hairy tongue
o Skin graft
o Fordyce’s granules
o Palatal and gingival
cysts of the newborn
o Erythema migrans
o Verruciform xanthoma 12/13/2018 14DRMohamed assadawy

Genetic disorders characterized by white oral lesions

White Oral Lesions
1.Non-Keratotic
1.Can scrape off with Tongue blade or gauze
2.Causes
1.Surface debris (food accretion)
2.Necrosis
3.Thrush
2.Keratotic (cannot be rubbed off)
1.Leukoplakia (18% of Oral Lesions)
2.Reactive hyperkeratosis (most common)
1.Benign epithelial response
1.Fractured tooth,
2.Dental restoration 12/13/2018 17DRMohamed assadawy

White lesions that can be scraped off

White lesions that can't be scraped off

Diagnostic and Management Algorithm

Morsicatio (chewing injury)
• Etiology: Frictional irritation from chewing
habit
Similar lesions in glassblowers and
some musicians
• Risk: Stress; psychological illnesses; edge-edge
bite
• Gender: F > M
• Age: Any age
After age of 35 yo – stress 12/13/2018 22DRMohamed assadawy

Morsicatio (chewing injury)
• Site: Buccal mucosa
Can be seen on buccal mucosa mucosa, lateral
tongue
• Clinical features:
White, diffuse + erythema
Shredded/ragged, macerated appearance
DrMohamedAssadawy 12/13/2018 23DRMohamed assadawy

Linea alba in an adolescent boy

. POTENTIALLY MALIGNANT DISORDERS:
Leukoplakia: Leukoplakia is defined as “white patch or plaque that cannot be characterized clinically or
pathologically as any other disease”.The term is strictly clinical.The habit of tobacco is closely
associated with leukoplakia development. Leukoplakia is divided into two clinical types,
homogeneous and non-homogeneous types.
Homogeneous lesions are slightly elevated grayish white non-scrapable plaques, which may appear
fissured or wrinkled. Non-homogeneous varieties include
a) Speckled: mixed white and red lesions, but retaining predominantly
white color
b) Nodular: small polypoid outgrowths
c) Verrucous: corrugated surface appearance
d) Proliferative verrucous leukoplakia (PVL): multiple keratotic plaques with roughened surface
projections.

Leukoplakia is a potentially malignant disorder with a malignant
transformation rate ranging from 4% to 47%. Habit cessation is recommended
along with clinical evaluation for every 6 months.
Actinic Cheilitis: Actinic cheilitis is a potentially malignant disorder
found on the vermillion border of the lower lip and is directly related to long-
term sun exposure. It appears as a white plaque, oval or linear in shape,
usually measuring less than 1 cm in size.

ETIOLOGY OF LEUKOPLAKIA:
 The habit of tobacco smoking appears most closely associated with leukoplakia
development.
 80 % of patients with leukoplakia are smokers.
 Smokers are much more likely to have leukoplakia than non-smokers.
 Heavier smokers have greater numbers of and larger lesions than light smokers.
 A large proportion of leukoplakias in persons who stop smoking either disappear
or become smaller soon after discontinuing the habit.

Alcohol, which seems to have a strong synergistic effect with
tobacco in oral cancer development, has not been associated
with leukoplakia.
Sanguinaria (blood root) is a herbal extract that has been
used in toothpaste and mouthwash.
Over 80 % of the patients with vestibular/maxillary alveolar
leukoplakias have a history of using a sanguinaria containing
product as compared to 3 % of the “normal” population; some
lesions have persisted after the patient stopped using the
product

Ultraviolet radiation has been associated with
leukoplakia of the vermilion of the lower lip.
This leukoplakia is usually associated with
actinic cheilosis

Treponema pallidum has been implicated
in leukoplakia of the dorsal surface of the
tongue in patients with syphilis.
Candida albicans has been demonstrated
histologically in the hyperplastic/dysplastic
epithelium of lesions termed candidal
leukoplakia and candidal hyperplasia

Human papillomavirus (HPV), particularly
subtypes 16 and 18, have been identified in
some oral leukoplakias.
However, HPV has also been demonstrated in
normal oral epithelial cells.

Several keratotic lesions, which until recently
have been viewed as variants of leukoplakia, are now
considered not to be premalignant.
Included in this group are lesions termed nicotine
stomatitis and frictional keratosis.
These keratoses are readily reversible after the
elimination of the trauma or chronic irritation.

Proliferative Verrucous Leukoplakia (PVL)
 PVL is a special high risk form of leukoplakia.
 It is characterized by multiple keratotic plaques with rough
surface projections although initially beginning as a simple
flat hyperkeratosis.
 PVL plaques tend to spread slowly, yet progressively.
 PVL usually transforms into a squamous cell carcinoma
within about 8 years.
 PVL has a strong female predilection (1:4 male to female)
and minimal association with tobacco usage.

LEUKOPLAKIA: HISTOPATHOLOGIC FEATURES
 Leukoplakia is characterized by a thickened keratin layer (hyperkeratosis) with or
without a thickened spinous layer (acanthosis).
 Some leukoplakias show surface hyperkeratosis but with atrophy or thinning of the
underlying epithelium.
 Variable numbers of chronic inflammatory cells are typically noted within the
underlying connective tissue

 While most leukoplakias show no dysplasia on
biopsy, some 5 to 25 % of the cases do show
evidence of epithelial dysplasia (or squamous
cell carcinoma).
 The histopathologic alterations of dysplastic
epithelial cells are outlined in the next slide.

Enlarged nuclei and cells.
Large and prominent nucleoli.
Increased nuclear-cytoplasmic ratio.
Hyperchromatic (dark-staining) nuclei.
Pleomorphic (abnormally shaped) nuclei and
cells.
Dyskeratosis (premature keratinization)
Increased mitotic activity and abnormal mitotic
figures

Bulbous or teardrop-shaped rete ridges.
Loss of polarity (lack of progressive
maturation toward the surface).
Keratin or epithelial pearls.
Loss of typical epithelial cell
cohesiveness

LEUKOPLAKIA: TREATMENT AND PROGNOSIS
 Complete removal of oral leukoplakia can be accomplished with equal
effectiveness by surgical excision, electrocautery, cryosurgery or laser
ablation.
 Long-term follow-up after removal is mandatory because of recurrence
potential and because new leukoplakias may occur.
 Malignant transformation potential is related to clinical appearance and the
degree of dysplasia

LEUKOEDEMA: CLINICAL FEATURES
Occurs in 50%+ Whites and over 90% of
African-Americans; uniform opacification of
buccal mucosa bilaterally.
Need to recognize; remains indefinitely; no ill
effects
The cause of leukoedema is unknown
Treatment : None necessary.

Leukoedema is a normal anatomic variant 12/13/2018 47DRMohamed assadawy

Nicotine Stomatitis
 Asymptomatic generalized opacification of palate with
red dots representing inflamed salivary gland orifices
scattered throughout.
 Heat and smoke associated with combustion of tobacco;
typically seen in pipe smokers.
 Discontinue smoking; lesion typically regresses
 Rarely develops into palatal cancer; malignant
transformation risk no greater than for “normal” palatal
mucosa.

stomatitis palatini 12/13/2018 49DRMohamed assadawy

smoker's palate 12/13/2018 51DRMohamed assadawy

Smokeless Tobacco Users Lesion
 Asymptomatic white folds surrounding area where
tobacco is held; usually found in labial and buccal
vestibules; a common oral lesion.
 Chronic irritation from snuff or chewing tobacco.
 Increased risk for development of verrucous and
squamous cell carcinoma after many years.

Erythema Migrans
 The cause of erythema migrans is unknown.
 Generally, no treatment is required, however,
symptomatic treatment for pain may be necessary in
certain patients.
 The lesion is completely benign and the patient
should be reassured of this.
 Some lesions spontaneously regress after months to
years.
 Beware of ectopic lesions

Chewing Tobacco 12/13/2018 58DRMohamed assadawy

Lichen Planus
 Lichen planus is a relatively common, chronic
dermatologic disease, often affecting the oral
mucosa.
 Current evidence indicates it is an immunologically
mediated disorder.
 Its relationship to stress is controversial.
 A variety of drugs are known to induce similar
appearing lesions for which the term lichenoid
mucositis is used.

Clinical Features
 Affect 2 % of the population.
 The majority of patients are middle-aged or older and there
is a female gender predilection (3:2).
 Skin lesions appear as pruritic, purple, polygonal papules
with a fine, lace-like network of white lines known as
Wickham striae
 Oral and other mucous membranes may be involved as well
as the nails.

The cause of LP remains unknown. Although LP is a multi factorial
disease, the role of any one of them as a sole causative factor is
still to be established.Various factors known to play a role in LP
such as
 Genetic factors
 immunological factors,
 emotional stress
 metabolic abnormalities
 infective factors

Based on the site of involvement, there are
many types. Among them Oral involvement
is common, occur in 60-70% of patients with
LP. It may be the only manifestation of LP in
20-30% of the patients

Lichen Planus related disorders
Several disorders are associated with Lichen Planus
more often with ulcerative colitis, alopecia areata,
vitiligo, dermatomyositis, morphea, lichen sclerosus
et atrophicus, thymoma, myaesthenia gravis,
hypogammaglobulinemia, primary biliary cirrhosis
and hepatitis C virus infection.

Clinically:
oral lichen planus has specific and clearly identifiable
features, usually presenting in one of two main forms - the
reticular and the erosive forms - although other forms
were originally described: the papular, “plate-like”,
bullous and atrophic forms

Annular form of lichen planus on the right buccal mucosa. Note the
pigmentation and the ring-like pattern of Wickham striae (yellow
arrows).

Bullous or vesicular lichen planus. Note the fluid-filled vesicles, which project out from the surface
(arrow)

Lichen planus. : Note the small papules on the dorsum tongue (yellow arrow) intermingled with
areas of pigmentation. Cutaneous involvement of lichen planus. Note the well-defined macular
lesions on the legs of the same person with oral manifestations of lichen planus

Erosive Lichen Planus
This form is usually symptomatic due to ulceration.
The lesions appear atrophic, erythematous with central
areas of ulceration.
Usually the fine, white, radiating striae can be seen at the
edge of the lesion.
With gingival involvement, this form is part of a group of
specific disease entities, which produce a reaction pattern
called desquamative gingivitis

erosive lichen planus

erosive lichen planus 12/13/2018 78DRMohamed assadawy

Lichenoid Mucositis
Lichenoid Reaction
lichenoid reaction. Note the lichenoid reaction on the left buccal mucosa due to type IV hypersensitivity
reaction to amalgam filling in the buccal aspect of first and second molars on the left lower jaw. 12/13/2018 81DRMohamed assadawy

Histologic features include:
 hyperparakeratosis or
 hyperorthokeratosis;
 liquefaction degeneration of the basal cell layer;
 epithelial atrophy;
 a dense subepithelial band of predominantly T lymphocytes;
 elongated, widened, and flattened rete pegs;
 acanthosis;
 civatte bodies

Lichen Planus: Diagnosis
 The diagnosis of the reticular form can often be
made on clinical findings alone.
 Biopsy is often necessary to rule out other
vesiculoerosive disease in cases of the erosive type.

Management:
•Maintenance of good oral hygiene
•Elimination of precipitating factors
•Treatment of super added fungal infection
•Topical steroids
•Topical isotretinoin gel & tretinoin ointment
•Topical tacrolimus & cyclosporins
•Systemic isotretinoin
•Systemic steroids

 The reticular form typically produces no symptoms and
requires no treatment.
 The erosive form is usually treated by topical (or
systemic if necessary) corticosteroids.
 With steroid treatment, the patient should be monitored
for candidal infection.
 Potential malignant transformation, associated mainly
with the erosive form, is small.

Squamous Papilloma
 Painless, exophytic, granular to cauliflower-like lesion; predilection
for tongue, floor of mouth, palate, uvula, lips, faucial pillars; generally
solitary; soft in texture; color is white or same as surrounding tissue;
young adults and adults; is a common oral lesion.
 The squamous papilloma occurs in 1 in every 250 adults and makes
up about 3% of the lesions sent for biopsy.

Most due to HPV; viral subtypes 6 and 11 have been
detected in up to 50% of the oral papillomas.
Treatment: Excision
Lesion has no known malignant potential;
recurrences are rare if properly excised.

Verrucous Carcinoma
 Broad-based, exophytic, indurated lesion; usually found
on buccal mucosa or in vestibule; adult males are most
frequently affected
 May be associated with use of tobacco, especially
smokeless tobacco; HPV present in some lesions
 Slow-growing malignancy; well-differentiated with
better prognosis than usual squamous cell carcinoma;
growth pattern is more expansile than invasive;
metastases are uncommon

Verrucous Carcinoma: Treatment
Excision is treatment of choice
 radiation may have a role in therapy today

White Sponge Nevus
Asymptomatic, bilateral, dense, shaggy, white or gray,
generalized opacification; primarily buccal mucosa
affected, but other membranes may be involved; rare entity
Hereditary entity; autosomal dominant with high degree of
penetrance and variable expressivity; keratin 4 and/or 13
affected (genes are mutated).

White Sponge Nevus:
Treatment
 None required.
 Remains indefinitely; no ill effects.

LUPUS ERYTHEMATOSUS
a chronic autoimmune inflammatory disease
which involves the connective tissue with
multi organ involvement

LUPUS SYMPTOMS
The most common signs and symptoms include:
 Fatigue;
 Fever;
 Joint pain, stiffness and swelling;
 'Butterfly rash' - a skin rash on the face that is shaped like a butterfly and covers
the cheeks and nose (also known as malar rash);
 Skin lesions or a skin rash that appears with sun exposure (also known as
photosensitivity);
 Poor circulation in the fingers and toes (also known as Raynaud's
phenomenon): causes the fingers and toes to turn white or blue when exposed
to cold or during times of stress;
 Shortness of breath;

•Chest pain, especially with deep breathing;
•Nose, mouth or throat sores;
•Dry eyes;
•Headaches, confusion and memory loss;
•Weight loss;
•Bald patches or hair loss.

ORAL IMPLICATIONS
 Mucocutaneous lesions (desquamative gingivitis,
marginal gingivitis or erosive mucosal lesions)
 Indwelling odontogenic and other head and neck infections
with no obvious symptoms, because of a reduced immune response
 Temporomandibular joint disorders (arthralgia, arthritis)
 • Sjögren’s syndrome (keratoconjunctivitis sicca,
 xerostomia and generalized hypohidrosis)
 Suboptimal oral hygiene because of painful oral lesions
 Caries in patients with Sjögren’s-like syndrome

TESTS AND DIAGNOSIS
 Clinical
 oral …….
 Extra……….
 Lab investigations
 ANA antibodies. The presence of antinuclear antibodies (ANA). Antibodies are small proteins produced by the
immune system when it detects harmful substances. Most people with SLE have the antinuclear antibody in their blood.
However, it is possible to have ANA without SLE, so it is not used to diagnose the condition on its own.
 Anti-DNA antibodies. The presence of anti-DNA antibodies in their blood. Many people with SLE
also have this antibody in their blood.
 Complement.The level of a chemical known as complementc2,c3 c 4. This is part of the
immune system, and can show how active the SLE is.
 ESR. Erythrocyte sedimentation rate (ESR) is not a diagnostic test specifically for
lupus, but it can show if inflammation is present in the body.

COMPLICATIONS AND EFFECTS OF LUPUS
Kidney problems: SLE can cause long-term inflammation in the kidneys and
a serious kidney disease called lupus nephritis.
Infection: People with SLE have a weakened immune system and are therefore
more likely to develop infections, including respiratory infections, yeast infections,
urinary tract infections, herpes and shingles.
Cardiovascular disease: People with SLE are more likely to develop
problems in their heart and arteries (known as cardiovascular disease or CVD).
 Pregnancy complications. SLE does not usually affect a woman's ability to get
pregnant, but it can increase the risk of problems such as miscarriage, pre-
eclampsia (a condition that causes high blood pressure during pregnancy), and
premature birth.

TREATMENT
• Avoiding the sun: Exposure to sunlight can aggravate symptoms of SLE, so it is
important to avoid the sun whenever possible. People with SLE should use a
sunscreen with an SPF of 50+ and wear long-sleeved clothing and a wide-brimmed
hat on sunny days.
• Avoiding infections: People with SLE are more prone to infection, especially if they
use steroids or medicines that reduce immune system activity. It is therefore important
to try to avoid contact with people who have infections.
• Having regular check-ups: People with SLE should see their doctor regularly, not
just when symptoms get worse. The doctor can make sure the most appropriate
treatment is being used.
• Getting enough rest: Fatigue is a common symptom of SLE, so it is important to get
plenty of rest and not overdo things.
• Not smoking: Smoking can worsen the effects of SLE on the heart and blood
vessels.

•Non-steroidal anti-inflammatory drugs (NSAIDs):Used to help with
joint pain and swelling. Examples include ibuprofen, naproxen and diclofenac. They should not be used in
people with kidney problems.
•Hydroxychloroquine (brand name Plaquenil):Used to treat skin
problems, tiredness and joint pain that isn't relieved with NSAIDs. People using this medicine usually have
their vision checked before starting and then regularly each year.
•Steroid tablets (e.g. prednisone): Used to reduce inflammation and swelling in
people with severe symptoms. Steroids may cause side-effects if taken for long periods, so the lowest
possible dose is recommended.
•Immunosuppressant medicines: Used to reduce immune system activity.
Examples include azathioprine, cyclosporin, cyclophosphamide (e.g. brand names Cycloblastin,
Endoxan), methotrexate.
•Belimumab (brand name Benlysta): A monoclonal antibody used to reduce the activity of the immune
system in people with severe SLE. This medicine is given as an infusion into a vein by a doctor or nurse.

HEREDITARY BENIGN INTRAEPITHELIAL
DYSKERATOSIS (HBID)
●Synonym: Witkop-Von Sallmann Syndrome
● HBID is rare genodermatosis seen primarily in triracial isolate
(African-American, White and Native American) originally
discovered in NC.
● Autosomal dominant trait.

●Clinical Features: Usually appears during childhood.
● Oral and conjunctival lesions; oral lesions similar to white sponge
nevus in appearance and location; milder cases resemble
leukoedema.
● Ocular lesions appear as thick, opaque, gelatinous plaques
affecting conjunctiva and sometimes cornea.
●Eyes may tear, itch and patient may have photophobia.
●Plaques (eye) most prominent in spring and tend to regress in the fall.
●Blindness may occur from vascularity of cornea secondary to
shedding of the plaque.

HEREDITARY BENIGN INTRAEPITHELIAL
DYSKERATOSIS

HBID: Histologic Features
●Histologic Features: Hyperparakeratosis with acanthosis; upper
spinous layers show a dyskeratotic process with epithelial cells
appearing to be surrounded or engulfed by adjacent cells resulting
in “cell-within-a-cell” phenomenon.

HBID: Treatment and Prognosis
●No treatment is usually necessary for oral lesions.
● Patients with ocular lesions should see the ophthalmologist;
plaques obscuring vision require
●surgery but they ultimately recur.

DARIER’S DISEASE
●Synonyms: Keratosis Follicularis; Dyskeratosis Follicularis,
Darier-White Disease.
● Uncommon autosomal dominant trait with high penetrance and
variable expressivity.
● A lack of cohesion among surface epithelial cells characterizes
the disease.
● A mutant gene that encodes an intracellular calcium pump has
been identified as the cause for the abnormal desmosomal
organization.

●Numerous erythematous, pruritic papules on trunk and scalp develop during
second decade; lesions are rough and degradation of the accumulated
keratin gives a foul odor.
● Palms and soles may exhibit pits and keratosis.
● The nails may show lines, ridges or painful splits.
● Between 15% and 50% of patients have oral lesions, which are often
multiple, normal-colored to white, flat- topped papules.
● If clustered together, the papules present a cobblestone appearance.
● The hard palate and alveolar mucosa are most commonly involved.
● Parotid swelling occurs in some patients.

DARIER’S DISEASE: Histologic
Features
●This is a dyskeratotic process characterized by a central keratin
plug which overlies epithelium exhibiting a suprabasilar cleft
● The intraepithelial clefting is known as acantholysis and is not
unique to Darier’s disease.
● The rete pegs are long, narrow and “test-tube shaped”.
● Dyskeratotic cells (corps ronds or grains) are observed.

DARIER’S DISEASE: Treatment
and Prognosis
●Photosensitive patients should avoid heat and sun
exposure and use sunscreens.
● Systemic retinoids may be beneficial in severe
cases.
● The condition is not premalignant.

ORAL CANDIDIASIS
white cottage cheese-like plaques on any surface inside the
mouth. Less commonly, it may appear as red irritated areas
inside the mouth.This red form is often present on the tissues
of the mouth that are covered by a denture or other prosthetic
appliance caused by Candida albicans
Candida species, which are seen in the oral cavity
Species of oral Candida are: C. albicans, C.glabrata, C.
guillermondii, C.krusei, C. parapsilosis, C.pseudotropicalis, C.
stellatoidea, C.tropicalis
These lesions are caused by the yeast Candida albicans 12/13/2018 125DRMohamed assadawy

Multiple white “cottage cheese‐like”
plaques surrounded by areas of
redness.
Red irritated areas affecting tissues
normally covered by a removable partial
denture.

Patients at an increased risk of developing an oral yeast
infection include
 newborn babies
 patients receiving chemotherapy or radiation treatment for cancer
 patients with HIV infection
 patients receiving tissue or organ transplantation
 patients with dry mouth secondary to disease, aging, or as a side
effect of drug therapy
 patients wearing upper dentures
 patients taking steroids and / or antibiotics

CLASSIFICATION OF ORAL CANDIDOSIS

PRIMARY ORAL CANDIDOSIS (GROUP I)
Acute
 Pseudomembranous
 Erythematous
Chronic
 Erythematous
 Pseudomembranous
 Hyperplastic
 Nodular
 Plaque-like
Candida-associated lesions
 Angular cheilitis
 Denture stomatitis
 Median rhomboid glossitis
Keratinized primary lesions
superinfected with Candida
 Leukoplakia
 Lichen planus
 Lupus erythematosus.

SECONDARY ORAL CANDIDOSES (GROUP II)
Candidosis (due to diseases such as
thymic aplasia and candidosis
endocrinopathy syndrome).

DIAGNOSIS OF CANDIDIASIS
 smears are taken from the infected oral mucosa, rhagades and the fitting side of the
denture, preferably with wooden spatulas. Smears were fixed immediately in
ether/alcohol 1:1 or with spray fix. Dry preparations may be examined by Gram
stain method and periodic acid Schiff (PAS) method
 Swabs are seeded on Sabouraud's agar (25ºC or room temperature), on blood agar
(35ºC), on Pagano-Levin medium (35ºC) or on Littmann's substrate (25ºC).
 Biopsy specimen should in addition be sent for histopathological examination
when chronic hyperplastic candidosis is suspected

imprint culture technique
 Sterile, square (2.2 × 2.5 cm), plastic foam pads are dipped in peptone water and
placed on the restricted area under study for 30-60 seconds. Thereafter the pad is
placed directly on Pagano-Levin or Sabouraud's agar, left in situ for the first 8 hours of
48 hours incubation at 37ºC. Then, the candidal density at each site is determined by
a Gallenkamp colony counter and expressed as colony forming units per mm2 (CFU
mm-2).
impression culture technique
Taking maxillary and mandibular alginate impressions, transporting them to the
laboratory and casting in 6% fortified agar with incorporated Sabouraud's dextrose
broth.The agar models are then incubated in a wide necked, sterile, screw-topped
jar for 48-72 hours at 37ºC and the CFU of yeasts estimated.

Oral rinse technique
Commercial identification kits
The Microstix-candida (MC) system consists of a plastic strip to
which is affixed a dry culture area (10 mm × 10 mm) of modified Nickerson
medium (Nickerson, 1953) and a plastic pouch for incubation.
 The OYeast-I dent system is based on the use of chromogenic substances to
measure enzyme activities. Ricult-N dip slide technique is similar to, but of higher
sensitivity than MC system.

SEROLOGICAL TESTS FOR INVASIVE CANDIDIASIS
 Detection of antibodies
 Slide agglutination
 Immunodiffusion
 Phytohemagglutination
 Coelectosynersis
 Immunoprecipitation
 A and B immunofluorescence
 Nonspecific Candida Antigens
 Latex agglutination
 Immunoblotting
 Cell Wall Components
 Cell Wall Mannoprotein (CWMP)
 b-(1,3)-D-glucan
 Candida Enolase Antigen testing.

MANAGEMENT

Oral white lesions1 mohamed assasdawy

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