The "part 1" discusses only the hereditary white lesions (as given in 10ed…and remember 9th ed has entirely different approach to this topic..)
In the 10 ed in complete contrast to 9 th ed the lesions are discussed under the following headings..
• Hereditary
• Inflammatory/traumatic
• Infectious white lesions
• Idiopathic “true”leuplakia.
• Bowen,s disease
• Lichenoid reaction
• Lupus erythematosis(discoid and systemic)
• Developmental white lesions like fordyce’s granules and gingival and palatal cyst of the born.
Any lesion that increases in thickness of epithielium and causes to appear white by increased distance to the vascular bed is a white lesion.
Most common reason-hyperkeratosis
Other reasons-acanthosis, oedema fluid in epithelium, decreased vascularity in the lamina propria, surface ulceration covered by a keratin cap and collapsed bullae.
HEREDITARY WHITE LESIONS:
LEUKOEDEMA:
common mucosal alteration and it is a variation of the normal mucosa.
90% seen in blacks(Afro-Americans). Variation in the mucosal is visible mote clearly in the darker coloured mucosa of these people.
Frequent site: bilateral buccal mucosa. Rarely in labial, soft palate and floor of the mouth.
Description: faint, diffuse, filmy appearance with mild wrinkling of the mucosa.
CANNOT BE SCRAPED.Disappear and fades on stretching of the mucosa.
Microscopy: thickening of the epithelium, Intracellular oedema in stratum spinosum.Surface may show thickened parakeratinization.
Tx:
NO Tx and NO malignant change.
[Stratum spinosum contains glycogen.
Due to the underlying melanin pigment the opalescence is clear.Highest inm Blacks of US and lowest in India, South Africa and New Guinea.
Sucking pad or callus is clinically and histologically similar to leukoedema and is seen on the inner aspect of the vermillion border of the lips of the suckling neonates. The vacuoles stain for keratin than for glycogen.]
WHITE SPONGE NEVUS(WSN)
Rare autosomal dominant disorder, high penetrance and variable expressivity. Predominantly affects the non cornified stratified squamous epithelium. Frequent site is the oral mucosa and less common sites are nose , oesophagus, genitalia and rectum.
May be present at birth or appear and more intense at puberty.
Pathophysiology: Missense mutation in one allele of keratin 13 that leads to proline substitution for leucine within keratin gene cluster.
Recent sequence analysis shows glutamine insertion localised in helix initiation motif of 1A and alpha domain of keratin 4 gene.
Features:
Bilaterally symmetrical. White, soft spongy or velvety thick plaques of buccal mucosa.Also seen in ventral tongue, floor of mouth, labial mucosa soft palate, and alveolar mucosa.
Asymptomatic and NO malignant change
Histopathology:
Epithelial thickening, parakeratosis, perinuclear condensation of cytoplasm, vacuolisation of the supra basal keratinocytes.
Eletron microscopy of exfoliated cells show numerous cellular granules composed of disordered aggregates of tonofilaments.
Tx and prognosis:
NO Tx. Palliative Tx for symptoms when needed. There is report of relief with tetracycline rinse.
Differential diagnosis:
HBID
Pachynonychia congenital
Candida
Cheek chewing
Chemical burns
Preneoplastic/neoplastic process.
[Conjunctival mucosa is usually spared. (Regezi 4th Ed)]
Also called as Cannon’s disease, White folded gingivostomatitis, Leukoedema exfoliate)
Histological appeareance of surface epithelium shows the large irregular cells with centally placed pyknotic nuclei and poorly stained “washed out” or “empty” cytoplasm.]
HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID, WITCOP’S DISEASE)
Rare autosomal dominant disorder in which is seen oral lesions and bilateral limbal conjunctival plaques. Seen in triracial of white, Native Americans and afro- American people.
High penetrance
Features:
Similar to WSN seen in buccal and labial mucosa and also in floor, lateral tongue, gingival and palate. Detected in first year and increasing intensity until teens. Significant aspect is the thick gelatinous foamy opaque plaques formed adjacent to cornea which manifest very early in life (within first year)
Seasonal prominence in spring and regression in summer. And in some relapsing ocular inflammation and photophobia is reported. Reports of blindness having been caused by the vascularisation of the cornea is also reported.
Histopathology:
Marked parakeratin production with thickening of stratum spinosum (acanthosis) and numerous dyskeratotic cells.
[The dyskeratotic cells are demonstated well in Papanicolaou or Giemsa stained section or cell scraping. The cells are seen as “tobacco cells” or the “cell within cell” appearance. The lesion is similar to that seen in keratosis follicularis. (Darrie’s disease)
DYSKERATOSIS CONGENITAL [ZINNSNER-ENGMAN-COLE SYNDROME]
Recessively inherited genodermatoses X – linked disorder in which a series of oral changes that lead to atrophic leuplakia oral mucosa. Tongue and cheek ate most severely affected.
Severely dystrophic nails and prominent hyperpigmentation of the face, neck and chest.
Haematological changes: pancytopenia, hypersplenism and alpastic or Fancon’s anemia.
Oral lesions commence before 10 yrs and crops of vesicles with Patches of white necrotic mucosa infected with candida.erythroplakia and then nail dystrophy follows. Leukoplakia and carcinoma supervening an oral lesion early in childhood. (Premalignant)
High yield points:
LEUKOEDEMA
• bilateral buccal mucosa
• CANNOT BE SCRAPED.
• disappears
• on stretching the mucosa
• Epithelial thickening, Intracellular oedema in stratum spinosum (glycogen).
• Thickened parakeratinization.
• NO Tx and NO malignant change.
WHITE SPONGE NEVUS (WSN) Cannon’s disease, White folded gingivostomatitis, Leukoedema exfoliata
• Rare autosomal dominant disorder
• High penetrance and variable expressivity.
• affects the non cornified stratified squamous epithelium
• Missense mutation in one allele of keratin 13 that leads to proline substitution for leucine within keratin gene cluster.
• Recent sequence analysis shows glutamine insertion localised in helix initiation motif of 1A and alpha domain of keratin 4 gene.
• Bilaterally symmetrical. White, soft spongy or velvety thick plaques of buccal mucosa.
• NO malignant change
• Conjunctival mucosa is usually spared
• “Washed out” or “empty” cytoplasm.
HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID, WITCOP’S DISEASE
• Rare autosomal dominant disorder in which is seen oral lesions and bilateral limbal conjunctival plaques
• High penetrance
• Similar to WSN
• Detected in first year thick gelatinous foamy opaque plaques formed adjacent to cornea which manifest within first year
• Significant aspect is the thick gelatinous foamy opaque plaques formed adjacent to cornea which manifest very early in life (within first year)
• Seasonal prominence in spring and regression in summer.
• Marked parakeratin production
• acanthosis
• dyskeratotic cells are demonstated
• in Papanicolaou or Giemsa stained section
• “tobacco cells” or the “cell within cell” appearance
• is similar to that seen in keratosis follicularis
DYSKERATOSIS CONGENITAL [ZINNSNER-ENGMAN-COLE SYNDROME]
• Recessively inherited X – linked disorder
• Series of oral changes that lead to atrophic leuplakia oral mucosa. Tongue and cheek ate most severely affected.
• Severely dystrophic nails
• prominent hyperpigmentation of the face, neck and chest
• pancytopenia, hypersplenism and alpastic or Fancon’s anemia
• Premalignant
Note:
this chapter on red and white lesions has been written by new authors and has lots of variation from the previous edition in organisation of the topics Only 4 hereditary white lesions are included in 10 ed.. for the rest you are asked to follow the 9th edition itself. As for as those topics from new edition is considered I have included the points from 9th edition also. Those text within the brackets, for e.g. [ZINNSNER-ENGMAN-COLE SYNDROME] unless and other wise mentioned are taken from Burket’s oral medicine 9th ed. Hope I am clear….all the best..the next topic will be on inflammatory and traumatic white lesions OR on candidiasis, whichever i complete earlier..
oral candidiasis will include references from many books including Burket’s Oral Medicine(9th and 10 ed), Regezi Oral Pathology With Clinical Correlations 4th ed & Sap Contemporary Oral And Maxillofacial pathology(2004), shafer’s oral pathology(1993).
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Copyright 2004 Onwards by Akilesh Ramasamy |
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