59560825 White Lesions Part I Lecture by Dr Eman Metwally AmCoFam
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Transcript of 59560825 White Lesions Part I Lecture by Dr Eman Metwally AmCoFam
BY
DR. IMAN METWALY
White lesions
White lesions are a group of pathological conditions affecting the oral mucosa giving clinically grayish or white lesions The color of the oral epithelium is derived from:
1. Vascularity 2. Melanin pigmentation 3. Epithelial thickness 4. Keratinization
Any alteration in one of these factors causes discoloration of the oral mucosa. Example
1. Bluish in color indicating vascular lesion 2. Brownish in color indicating excess melanin 3. Yellowish in color indicating jaundice 4. White due to :
i. Thickening of the keratin , ii. Epithelial hyperplasia ,
iii. Intracellular edema iv. Reduced vascularity of sub adjacent connective
tissue v. Surface necrosis
All white lesions are microscopically similar showing 2 main features:
1. Abnormal keratinization 2. Increases in the thickness of epithelium through hyperplasia or
hypertrophy of epithelium
1. Thickening of the keratin
Keratosis: keratinization of epithelium that is not normally keratinized Hyperkeratosis: Excessive formation of keratin Hyperorthokeratosis: Excessive formation of keratin,
o Appearing as flattened cells with
no nuclei
o Below the keratin layer there is a granular layer
Hyperparakeratosis : Excessive formation of keratin,
• With flattened cells • Containing persistent degenerative nuclei in the
superficial cells • Below the keratin layer there is no granular cell
layer
2. Increases in the thickness of epithelium through : Hypertrophy : it is the increase in the size of the cells Hyperplasia : Is the increase in the number of cells
Acanthosis : Is the increase in the thickness of prickle cell layer due to increased number of prickle cells {i.e. due to hyperplasia}
Etiological classificationHereditary
Reactive
Dermatological
Idiopathic leukoplakia
Neoplastic
1-Lichen planus
2-Lupus Erythematosus
Infective
1-Candidiasis
2-Hairy leukoplakia1-Frictional keratosis
2-Chemical
3-Thermal
1-Leukodema
2-White spongy nevus
Squamous cell carcinoma
1. Hereditary conditions
A-Leukodema Definition It is a generalized opacification of the buccal mucosa that is
regarded as a variation of normal It is more apparent in non-whites , specially African –Americans
Clinical features
1. Grayish- white filmy, milky opalescent appearance 2. The surface appears folded resulting in wrinkles or white streaks 3. Occurs bilaterally on the buccal mucosa 4. Asymptomatic
Diagnosis : the white appearance greatly disappears or diminishes when the cheek is stretched Histopathologic features :
1. Epithelium is parakeratotic & acanthotic 2. Marked intracellular edema of the prickle cells 3. The enlarged cells have small piknotic {condensed }
nuclei in clear cytoplasm 4. The rete ridges are broad and elongated
Differential diagnosis
1. White spongy nevus 2. Habitual cheek biting 3. Lichen planus
These lesions may show clinical similarities to leukodema but they all persists on stretching
B- white spongy naevus Definition : It is an autosomal dominant hereditary disorder that may affect different mucosal sites Clinical features Age : appears early in life typically before puberty Appearance :
1. White , thickened , corrugated or velvety , diffuse plaques 2. Lesions have a spongy consistency 3. Almost always bilateral & symmetric 4. It starts small then increases in size to reach its maximum size at
the age of adolescence 5. Best observed on the buccal mucosa 6. Other intraoral sites : the ventral tongue, labial mucosa, soft
palate, alveolar mucosa& floor of the mouth , 7. Other extraoral sites : vagina & nasal cavity
Histopathologic features : The epithelium is greatly thickened with marked spongiosis,
acanthosis & Shaggy hyperparakeratosis Prickle cells show : 1. Hydropic or clear cell changes 2. Perinuclear eosinophilic condensation of cytoplasm 3. Prominent cell membrane producing a basket weave appearance
Treatment: No treatment since it is asymptomatic Differential diagnosis : The bilateral & symmetrical distribution of the lesion is similar to
lichen planus & habitual cheek biting But the condition is readily recognized by the wide spread of the
lesions & family history is a confirmation
2. Reactive lesions A- Mechanical trauma {frictional keratosis } Definition Frictional keratosis is a white lesion caused by prolonged mild irritation of the mucous membrane N.B. acute trauma causes ulcers while long standing chronic trauma causes hyperkeratosis Etiology :
1. Habitual cheek biting {Linea Alba} 2. Orthodontic appliance 3. Prothodontic appliance {ill fitting denture } 4. Broken tooth 5. Rough edges of a carious tooth 6. Mal-aligned teeth
Clinical features
1. At first the patch is pale translucent, later it becomes dense & white
2. Occur in areas that are commonly traumatized e.g., buccal mucosa along the occlusal line{Linea Alba}, lips, the lateral margin of tongue
Histopathologic features :
1. Hyperkeratosis with a prominent granular cell layer 2. Moderate epithelial hyperplasia & acanthosis 3. Some chronic inflammatory cells may be seen
in the subjacent connective tissue 4. No dysplasia
Diagnosis of frictional keratosis By removal of the irritant, the lesion should resolve or at least be reduced in intensity
B-chemical Chemical insult to the oral mucosa may produce a variety of
reactions depending on the severity & the duration of the insult Low grade chronic insult results in hyperkeratosis
1 . Aspirin burn Aspirin tablets are used as local analgesic for the relief of
toothache The tablet is used mistakenly against the offending tooth This causes a burn , as aspirin contains acetyl salicylic acid It produces epithelial necrosis , sloughing & ulceration
2. Acid etch Causes sometimes chemical burn
3. Dentifrice-Associated Slough Is associated with the use of several different brands of tooth paste A superficial chemical burn or reaction to the detergent or
flavoring compounds It appears as a superficial whitish slough of the buccal mucosa
which resolves with a switch to another tooth paste 4. Smokeless tobacco The habit of chewing the tobacco leaves or holding finely ground
tobacco leaves in the mandibular vestibule is considered as chronic chemical insult to the mucosa
Close contact of tobacco to oral mucosa causes white lesions
{epithelial thickening & hyperkeratosis } Mild absorption of this irritant material through the oral mucosa
may lead to verrucous carcinoma or squamous carcinoma
C- Thermal
Most thermal burns of the oral cavity arise from hot food , hot tobacco fumes or iatrogenic heat burns Acute thermal trauma results in the formation of acute ulcers The ulcers are covered by a yellow-white fibrinous exudate &
surrounded by erythematous halo 1.Pizza burn caused by hot cheese , seen on the palate 2.Iatrogenic heat burns seen after injudicious {unwise } use of impression material such as wax or dental compound 3.Smoking induced keratosis : smokers who constantly dangle a cigarette or cigare from their lips may develop a localized keratosis Regular smokers of cigarettes, cigars & pipes often develop white lesion on their oral mucosa < the anterior parts of buccal mucosa tongue & palate}
Two factors causes the lesion :
1. Fumes generated causes hyperkeratosis 2. Chemicals in fumes {nicotine & tar} are carcinogenic
Nicotinic Stomatitis A specific white lesion of the palate in pipe & cigar smokers Clinical features
1. Initially the palatal mucosa shows erythematous changes followed
by keratinzation 2. Subsequently red dots surrounded by white keratotic rings
appear 3. The dots represent inflammation of the salivary gland excretory
ducts Histopathology
1. Epithelial hyperplasia & hyperkeratosis 2. Chronic inflammation of the minor salivary glands {palatal mucous
glands} 3. Excretory ducts may show squamous metaplasia
Treatment &prognosis
1. This type of keratosis regresses completely if smoking is stopped 2. The smoker may use an acrylic palatal plate during smoking but
soft palate may be affected then 3. Although there is no risk of malignant transformation ,nicotinic
stomatitis is a marker of heavy tobacco use & hence may indicate increased risk of epithelial dysplasia & neoplasia