oral pathology lec# 2 - web viewterm used clinically to describe the appearance of lesions...

Sun 22\9\2014 Oral pathology Lec #2

White lesion

White lesion: term used clinically to describe the appearance of lesions presenting as white area on oral mucosa.

Etiological classification of white lesions:Hereditary

Traumatic

Infective

Idiopathic

Dermatological

Neoplastic

Leukoplakia:

Defined as:‘‘A white plaque of questionable risk having excluded

(other) known diseases or disorders that carry no increased risk for cancer” WHO 2005

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#a predominantly white lesion of the oral mucosa that can't be characterized as any other definable lesion.

#White lesion without known cause.

So diagnosis of these lesions by excluding the other cause of white lesions.

Prevalence: Less than 1% of people

Gender:Male > Femal

Usually in elderly pt. or in middle age pt.

Site:Affect any site on oral mucosa

*leukoplakias involving the ventral tongue and\or floor of the mouth have high risk of malignant transformation than lesion at other site.

Size:

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Vary from a quite small and circumscribed plaque to an extensive lesion involving a large area of oral mucosa.

Color: maybe: # white

# whitish-yellow

# gray

Characteristic of leukoplakia :Potentially malignant.

Clinical classification of leukoplakia: there are 2 types of leukoplakia:

Homogeneous 2\non-homogeneous 1\

Non-homogeneous Homogeneous

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If we see one of these things:

1-not flat surface, irregular nodular. (Thickening surface) some case may take a warty

appearance. 2-variation in color , show

areas of redness producing a speckled appearance.

3-ulcer.Non-homogeneous lesion have a worse prognosis

50% of cases have dysplasia.

1-plaque-like,flat,uniform2-predominantly white

plaque.3 -may show shallow

cracks\fissures on surface.

Only 10% of cases have dysplasia.

# Non-homogenous is more dangerous than homogenous .

Erythroplakia:

Is a bright-red patch on the oral mucosa which can't be categorized clinically or pathologically as being due to any other condition.

Erythroplakia lesion may be homogeneous with well-defined outline. Or . may be intermingled with patch of leukoplakia which called speckled leukoplakias or erythroleukoplakia.

Histologically Erythroplakia may represent carcinoma in situ or even invasive carcinoma.

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Etiology: is Unknown similar to leukoplakia

The Incriminated factors for leukoplakia are:

# Tobacco

#Alcohol

#candida

#viruses: HPV 16 + 18

#Epithelial atrophy

In atrophic area there are High chance to develop leukoplakia and oral cancer.

Causes of atrophy in oral mucosa:

1\Iron deficiency as : Sideropenic dysphagia, Patterson Kelly, plummer-vinson syndrome.

2\ Vit. deficiency (vit. A&B).

3\submucous fibrosis.. especially in chewing habit area.

4\tertiary syphilis.

Histopathological features of leukoplakia:

No specific histological feature..there is a wide range in histological appearances:

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*Ortho or parakeratosis or mixture in the same area. Hyperplasia of epithelium* .

In case of speckled there is an atrophy*.

*Chronic cell infiltrate in lamina properia.

But the most imp. Feature for pathologist is presence of Dysplasia or not. because leukoplakia has a potential change to cancer we should take a biopsy to decide if there is a dysplasia or not.

Leukoplakias should be followed-up and managed because these lesions may change into cancer.

Pathologist classification of dysplasia according to its severity :

1 -Basal cell hyperplasia.

2 -Milddysplasia in lowe1\3 of thickness of epith.

3 -Moderatedysplasia up to 1\2 of thickness epith.

4 -Severedysplasia more than 1\2

5 -Carcinoma in situfull thickness of epith.

An increased in severity of dysplasia increase the risk of oral cancer.

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Prognosis:

-unpredictable

( -0.3-18% )of cases could change to cancer.

Prognostic factors of leukoplakia:

* Family history: if the pt. has family history for oral cancer this will increase the susceptibility in changing the leukoplakia to cancer.

* Non-homogenous leukoplakia has higher chance to change to cancer.

If the pt. have homogenous lesion that changes with time to non-homogenous (speckle or modularity or ulcer or redness) he will have higher tendency to change into cancer.

* Size: increasing in size more than 2cm more susceptible to cancer.

* Duration: increase the durationincrease the chance to change to cancer

* Site: leukoplakia in the floor of the mouth has more susceptibility to change to cancer.

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**The Risk of developing malignancy at lesion site is 5 times greater in pt. with leukoplakia than with normal person.

Dysplasia:- In * Homogenous leukoplakia 10%

Non-homogenous 50%

Erythroplakia 80-90% either sever or carcinoma in situ or cancer (mild invasive)

But the diagnosis of dysplasia and estimating its degree is subjective with significant intra- and inter-observer variability

so

Is there any consistently reliable biomarker used to further identify those dysplasias that are more likely

to progress to invasive cancer?

Classification and Staging:

This staging is used to predict the transformation risk.

1-Size: L1 (less than 2cm)

L2 ( 2-4 cm)

L3 ( more than 4 cm)

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We use the size to predict the prognosis.

2-presence of dysplasia (P):

P0: no dysplasia

P1: mild to moderate dysplasia

P2: severe dysplasia

Stages:

Stage1: L1P0

Stage2: L2P0

Stage3: L3P0 or L1L2P1

Stage4: L3P1, any L P2

When stage increases in #, the risk to progress to cancer increases.

Dermatological white lesion:

Its skin disease & this disease has oral manifestation as white lesion.

Lichen planus: (easier in Dx.)

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-a common disease that we can see in pt. who visit our clinic.

-chronic inflammatory disorder affecting skin and mucous membranes

-affecting 1% of population.

-Mostly females (60%), 30-60 y

-Affect middle age 30-50 years.

-40% of pt. have skin + oral lesion both areas are affected.

-35% of pt. have just skin lesion without oral manifestation.

-25% of pt. have just oral manifestation without skin lesion. In this case we may have problem in diagnosis coz presence of skin lesion helps in diagnosis.

Feature of skin lesion :

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*Purplish, pruritic (itchy), papules (2-3mm) in diameter, has white striation on its surface called Wickham's striae. These striae help in Dx.

*Almost any area in skin can be affected but mostly in flexor surfaces of the wrist.

* Nail are involved in up to 10% of pt. they have atrophy and vertical ridges.

Skin lesion is not permanent they can disappear after one or two years and come back again in another place of the body… this is v. imp. When take history.

-we have to distinguish between lichen planus and

Psoriasis which is red or white lesion on skin and it

doesn't has Wickham's striae.

Oral lichen planus:

-most frequent site is Buccal mucosa.

-can affect other site as tongue, gingiva, lip, and vestibule.

-Least frequent (rarely seen) on the floor of the mouth & palate.

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Distribution of L.P is bilaterally and symmetrical this will help in diagnosis.

Types of lichen planus:

1-Reticular type:

-the most common type.

-Asymptomatic

-Site : appears on buccal mucosa bilaterallook like white spongy naevus.

-has wickham's striae has lace-like striae

-it seems like leukoedema, so we have to do stretch test for diagnosis.

2-Plaque-like:

-less frequent.

-Asymptomatic.

-white plaques resembling leukoplakia.

-Site: appear on buccal mucosa and on tongue or other sites.

3-Papular type:

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-rare not common

-Asymptomatic.

-small white papules that may coalesce give plaque-lesion.

4-Atrophic type:

-more frequent than popular and plaque-like and the 2nd most common type after reticular.

-atrophyred in color look like Erythroplakia.. So to differentiate between them we look for Wickham’s striae.

-Symptomatic… it causes pain because atrophy means loss of epi. That protects nerves, without epi. The

tissue becomes so sensitive .

-most common Site is Gingiva.. It looks like gingivitis.

**How to differentiate btn atrophic type & gingivitis??

Gingivitis: is the inflammation of marginal gingiva.

Atrophy type: redness is on the whole thickness of gingiva (marginal gingiva & attached gingiva) and this called desquamative gingivitis.

5-Bollous type:13 | P a g e


-rare to see

- up to 2cm , mostly seen in skin not intraorally coz its easy to ruptures and produce an ulcers.

- Site: on posterior buccal mucosa.

6-Erosive type:

-Dangerous.

-most painful to the pt., difficulty in mastication, bleeding, suffering during swallowing.

-extensive areas of shallow irregular areas of epithelial loss (ulceration)

So it’s not red in color. It’s a yellowish membrane due to fibrin deposition.

-can occur in any area, its very persistent (chronic duration of ulceration)

-Diagnosis of erosive type by recognizing whitish areas around the lesion

Histological feature of lichen planus:

1.Focal acanthosis—the epi. Is ortho or parakeratinized.

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2 .saw-tooth rete pegs: this appearance results from acanthosis which make irregular elongation and widening of the rete processes.

3 .A dense, well-defined band of T-lymphocyte in superficial lamina propria.

4 .Inflammation extending to basal and parabasal cell layer.

5 .Liquefactive degeneration of the basal cells: which is the degeneration of the basal cells associated with oedema and lymphocytic infiltration.

6.Civatte bodies: the degenerating cells appear as hyaline condensed bodies and represent basal cells undergoing apoptosis.

The etiology of lichen planus: Unknown!!

But May be associated with some condition like:

1 \infective agents such as bacteria.

2 \systemic diseases: DM, hypertension, ulcerative colitis, liver disease such as hepatitis C, and graft-versus-host disease (GVHD).

3 \Psychiatric disorders: stress, depression.

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The pathogenesis:

1-Type IV hyper sensitivity reaction, change of antigens on keratinocytes will attract T-lymphocyte that will come and damage the basal epithelial cells.

A certain infective unknown agents come to the epithelium and its similar to the antigen of the keratinocytes, processed by Langerhans cells and presented to activate production of CD8.

So the treatment is by suppressing the immune reaction.

Lichenoid reaction: lesions resembling lichen planus and results from drugs: antimalarial, gold,

methyldopa, NSAID) or old amalgam restorations .

Are there any clinical or histological differences between Lichen planus and Lichenoid reactions?

Does Patch testing useful in identifying patients who will have Lichenoid reactions?

Lupus erythromatosus:Two main forms of this disease are recognized:

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1\Chronic discoid lupus erythematosus.

2 \Systemic lupus erythematosus.

1\ Chronic discoid lupus erythematosus :

* which is (Localized) disease.

* its restricted to the skin of the face, scalp & ears

*present as Scaly red patches and butterfly pattern (lesion has symmetrical distribution over the nose & cheeks).

*Oral lesions are present in 50% of the cases.

*can affect any part of the oral mucosa (cheeks, vermillion zone), there will be a discoid area of erythema surrounded by a white keratotic border with radiating striae like sun.

The histological appearance :

1\ Ortho- or parakeratinized.

2\ Hyperplasia or atrophy.

3\ Keratin plugging.

4\ subepithelium and deep perivascular lymphocytes (this is the difference btw chronic discoid and lichen planus).

5\ liquefactive degeneration in the basal cell layer.

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6\ Direct immunofluorescence test will be +ve for IgG, C3 and fibrinogen (coz they will be deposit as a granular linear in the basement membrane).

Systemic lupus erythematosus:*which is disseminated disease involving almost

every organ of the body.

*the lesions in sys. LE. Include skin rashes that occur on cheeks.

*Oral lesion occurs in 20% of the cases described as superficial erosions & erythematous patches on the buccal mucosa.

*there is systemic symptoms: fatigue, malaise, fever psychosis and lymphadenopathy.

Good Luck

Any corrections are more than welcome

Done by.. Lama Jaber .

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oral pathology lec# 2 - web viewterm used clinically to describe the appearance of lesions...

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