White Lesions - Part I (Lecture by DR - Eman Metwally @AmCoFam)
White Lesions - Part I (Lecture by DR - Eman Metwally @AmCoFam)
White Lesions - Part I (Lecture by DR - Eman Metwally @AmCoFam)
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. 2. 3. 4. Vascularity Melanin pigmentation Epithelial thickness Keratinization
Any alteration in one of these factors causes discoloration of the oral mucosa.
Example
1. 2. 3. 4.
Bluish in color indicating vascular lesion Brownish in color indicating excess melanin Yellowish in color indicating jaundice 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
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
Acanthosis : Is the increase in the thickness of prickle cell layer due to increased number of prickle cells {i.e. due to hyperplasia}
Etiological classification
Hereditary 1-Leukodema 2-White spongy nevus Infective Reactive 1-Frictional keratosis 2-Chemical 3-Thermal 1-Candidiasis 2-Hairy leukoplakia Dermatological 1-Lichen planus 2-Lupus Erythematosus Neoplastic Squamous cell carcinoma Idiopathic leukoplakia
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
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 1. 2. 3.
Prickle cells show : Hydropic or clear cell changes Perinuclear eosinophilic condensation of cytoplasm 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. 2. 3. 4. 5. 6. Habitual cheek biting {Linea Alba} Orthodontic appliance Prothodontic appliance {ill fitting denture } Broken tooth Rough edges of a carious tooth 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