Oral Patho 3

7/29/2019 Oral Patho 3

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Lets start our lecture ,

Last time we defined leukoplakiaas a white patches that

cant be removed by scrubbing and it cant be diagnosed as

any clinical disease , it doesnt reflect a true

histopathological features and true picture . sometime the

appearance of leukoplakia -as homogenous or nonhomogenous- can tell us if leukoplakia is having a higher

tendency for epithelial dysplasia or not ( non is higher), but

we cant rely on this clinical appearance to determine if

theres high risk or low because some of homogenous

leaukoplakia ll have dysplasia .

Histopathological appearances of leaukoplakia are

epithelial dysplasia , keratosis alone , hyperplasia alone ,keratosis and hyperplasia together or karatosis hyperplasia

dysplasia , squamous cell carcinoma ( malignant change ) .

The factors that ll give us clinical pic of leaukoplakia are :

-keratosis,

-epithelial thickness,

-epithelial dysplasia,

-chronic inflammation

Now we mention keratosis and as we know it can be

parakeratosis (with nuclei ) or orthokeratosis ( without


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neuclei). We can see an prominent layer here (the arrow )

and its called granular layer ( its more obvious in

orthokeratosis than parakeratosis ) .

Para ortho

The thickness of epithelium is variable , Some

leaukoplakia can give you increased epithelial thickness

( acanthosis ) , or atrophy espesialy if the leakoplakia is

speckled . because of atrophy the lesion is red .

( *remember from histology : as we know the epithelium

is avascular and its supplied by the vascular connective

tissue that lied under it , so when the epithelium is thinner

the blood vessels of connective tissue will be more

prominent so the red color ll appear .


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Acanthosis atrophy

Epithelial dysplasia may show clear cut (abrupt) junctionbetween dysplastic epithelium and normal one , or may

show gradual transition between them. In dysplastic

epithelium we can see hyperchromatism like as in the pic .

Dysplastic side normal side

Features of dysplasia that indicate smoking :

1- chevron peaks(triangular curve) of keratin or epithelium

itself


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2- increased melanin production in basal keratinocytes

( melanin incontinence ) , its over production of melanin

that ll escape to the underlying tissue then itll be engulfed

by macrophages , so most of the time we see melanin in theunderlying connective tissue inside the cytoplasm of

macrophages .

So these two features are highly suggestive of smoking as

etiological factor that associated with leaukoplakia .

Now epithelial dysplasia isnt present in most

leaukoplakias , it depend on geographic location , habits ,

risk factors . the percents of finding dysplasia is usually18% ( less than 20%) .

The dysplasia is an architecture change in the epithelium

that include cellular atypia and the over all morphology of

the epithelium . as we know the cellular atypia is the

change in the individual cell , but the dysplasia is the

change in whole epithelium . we can classify dysplasia

according to cellular atypia extension into mild , moderate

and severe :

-Mild dysplasia when atypia isnt extending beyond the

lower(basal) third of the epithelium


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-moderate dysplasia when atypia involves the basal two

thirds

-severe one when atypia involves the superficial third

In the pic below we can say its severe because we can see

atypical cells ( large and have increased nuclear to

cytoplasmic ratio ) in the upper third .

We said that we cant predict the histopatholigical features

of leaukoplakia based on the clinical pic alone , however

theres indication by homogenous and non homogenous ,

non homogenous usually have dysplasia ( 50% according to

some studies ) more than homogenous(10%) .Speckled leaukoplakia have 100% of presence of

dysplasia .

Now in the figure below :


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First we can see the normal , then the homogenous we can

notice increase thickness of keratin in comparison to

normal , increase thickness of epithelium and theres some

lymphocytic infiltrate but the dysplasia isnt present .Now when we have thick fissured leaukoplakia it still

homogenous except some grooves and fissures and here we

can see some dysplastic ( mild in the lower third ) features .

but the surface of leakoplakia start to be nodular with more

fissuring then the dysplasia ll be more present and in

higher rate , so here its moderate severe and then there ll

be erythroplakia and now we can notice how the

epithelium start to be atrophic ( so the epithelium ll beatrophic when there is erythroplakia . if it is erythroplakia

and hyperplastic then itll be speckled leaukoplakia .

The dysplastic features ll reflect change in maturation ,

proliferation and differentiation of the epithelium . features

of dysplasia :


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1. Increased and abnormal mitoses , now the normal

location of mitoses is in the basal layer , while in

dysplasia it ll be higher suprabasal , and in the basal

layer there ll be increase in number and this ll giveabnormal shape .

As we see in the pics its not the normal mitoses that

we know ( not two parallel lines of chromosomes in

the midline ), here we have X shape or star shape

appearance . here we may find normal mitoses but it

can be suprabasal .

2. Basal cell hyperplasia, its cuboidal and

hyperchromatic ( dark color) cells , here we can see

these cells more than in the basal third of normal

epithelium . so here we can see thick layer of basaloid

cells , so this is basal cell hyperplasia and reflect

abnormal proliferation . mitotic figures also reflectabnormal proliferation .


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3. Drop-shaped rete ridges that the epithelium ll be

elongated and widened like a drop , its constricted

above and widened toward the basal layer, and this is

because of more and more proliferation in basal area .

4. Disturbed polarity of basal cells or loss of cellularorientation , you wont see the basal layer normally a

lined or side by side next to each other , it ll be poorly

oriented and extended suprabasaly to the superficial


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layer , this may be by increasing of the proliferation in

the basal area .

5. Increase in nuclear/cytoplasmic ratio , in this casewell see nucleus as big and the cytoplasm is less than

normal cells . if we go up from the basal layer well

see big nucleus and less cytoplasm , so it can be seen

in the middle and superficial layers not just in the

basal .

6. Nuclear hyperchromatism, well see some nucleisdeeply blue because they take stain more than others

because they are hyperchromatised . now

hyperchromatic cells are restricted to the basal layer ,

but here we see it in the middle so its abnormal .


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7. Prominent and enlarged nucleoli , as we can see its a

nucleus and inside it prominent nucleoli . this feature

in many tumors .

8. Irregular epithelial stratification or disturbedmaturation , in normal epithelium we havecuboidal basal layer ,above it flattened pickledcell layer ,and at the top will be more flattened

and thin. This stratification is lost in dysplasia,everything is looking the same all of them arecuboidal and hyper chromatic. Also maturationwill be disturbed, when epithelial cells becomemature it starts forming keratin .so we cant see


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any granular layer because all layers like eachother . this is an architectural feature andthats mean I cant say its atypia because its

just in individual cell , but we can say itsdysplasia because it involves atypia andarchtictural features .

9.Nuclear and cellular pleomorphism , you can see

variation in shape and stain of the cells . the nucleus may

show slight change in size and shape like to be

polyhedral , round several shapes .

10.Abnormal keratinization , keratin as we know ll be in

the superficial and top layer (surface) , but sometime we

can see it even below the granular layer. So this is

abnormal maturation .


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11.Loss or reduction of intercellular adhesion , it ll be

decreased so we can see a spaces between cells . so thistell us the dysplasia is coming soon .

Now ,

Sometime the epithelial dysplasia may be seen in a

reactive area like candidoses or inflammation , so the

dysplasia here ll be considered as reactive because when

we give an antifungal or vaccine it can be reversed .

In some studies theres a rate up to 14% that leaukoplakia

ll transform to carcinoma . this transition depend on the

location in the oral cavity , some have high risk like

ventral of the tongue, Floor Of the Mouth, lingual aspect


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of lower alveolar mucosa. These sight show high

malignant transformation even there is any medical

treatment or vaccine . these lesions are called sublingual

keratosis , it have a high risk of transformation tosquamous cell carcinoma even though 25% will

transform .

If leaukoplasia has a hyperkeratosis alone there ll be no

risk to transform . while leaukoplakia that carry

dysplastic features ll has high risk .

The majority of dysplastic lesions remain unchanged

during observation period.

We cant leave our patient go home with leaukoplakia

without take a biopsy because of high percentage of

having transformation .

Sometimes we see white areas in the corner of the

smokers mouth and it cant be removed by scrubbing ,

but when we give them antifungal theyll be improved so

its a candida infection . in this infection there is 30% to

transform .

-Dysplastic leukoplakia have higher rate to progress than

non neoplastic (10-30%)

-More severe dysplasia higher risk

-Majority of dysplasia remain unchanged

May progress or improve

- No clear corelation between histology and clinical:


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-Sublingual keratosis even with mild dysplasia is

high risk

There is a feature that ll indicate transformation itsthe DNA content . the normal DNA content is diploid ,

so if the leaukoplakia carry diploid there ll be low risk .

but if it carry tetraploid ( double of the normal ) it ll

have intermediate risk . and if it carry aneuploid

( abnormal amount of DNA even less than normal or

more) it ll have the highest risk to transform .

The risk assessment is based on:1. Size ( bigger have higher risk )

2. Site

3. Clinical appearance ( speckled vs homogenous vs

erythroplakia )

4. Degree of epithelial dysplasia.

**Note : the dr said the percentage is included , so youshould know it .

We said the causes of white lesions in the oral cavity

are :- traumatic causes ( mechanical , chemical and

thermal )

- hereditary causes ( sponge nevus )

- idiopathic causes ( leaukoplakia )

- and now terminological causes (Lichen Planus and

Lupus Erythematosus)


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* Lichen Planus :

It may present in the skin and oral cavity . usually if the

patient has Lichen Planus in the skin , 50% there ll be

in the oral cavity . if the patient has it in the oral cavity,

10% there ll be in the skin .

Now Skin lesions:

-Violaceous, itchy papules, may have white streaks on

surface that we call it Wickhams striae. Usually appear

along the scratch

-Variable patterns for papules: discrete, linear, annular,bullous, or widespread rash

-Predilection to flexor surface of wrist.

10% with nail involvement in the form of vertical ridges.

-Lesions develop slowly and 85% resolve within 18months, sometimes with recurrence.

Now oral lesions : it ll show a white striations on the

buccal mucosa and mostly affect it , oral lesions show a


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much more chronic course sometimes extending over

many years.

-may also affect tongue, gingiva , palate and lips.

-Bilateral (most of the time bilateral) and wide spectrumof presentations, alone or in combination.

**Non-erosive type:

- reticular or annular, papular, plaque-like.

- usually asymptomatic.

**Erosive/atrophic types:

- red glazed appearance with areas of superficialulceration which may take several weeks to heal.

- occasionally, ulcers are preceded by bullae (bullous

type).

- often associated with typical areas of non-erosive

lichen planus.

- pain and discomfort may be severe.


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Why the atrophic type ll take the higher risk ?

Because the epithelium ll be thin and the barrier is

impaired ( we concern about epithelium as a barrier also ,so when the epithelium is atrophic the insult ll be more

effective and the barrier is less .

When the Lichen planus involve the gingiva often presents

as a desquamative gingivitis. But its not the marginal

gingiva ( the gingiva at the margin of the tooth and gingiva

that lies above it attached gingiva attach to the bone .** I

think we took about these two concepts briefly in a figure

in oral histo course ** .

What are the Histopathologic Features? :

- hyper keratosis para or ortho ( white areas)

-Epithelial atrophy especially in red areas (so epitheliumthickness and keratosis ll reflect the color ) or

acanthosis (sawtooth pattern of rete ridges).


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- the most important well-defined band of subepithelial

mononuclear infiltrate immediately below the

epithelium , its component is lymphocyte mainly

CD8+ type that is cytotoxic T-cells. These cells llattack the epithelium and ll cause Liquefactive

degeneration of basal layer so we cant see the

basement membrane . may be the attack occure

because of high activity or infection ( we can say like

the antigen of epithelium like the virus antigen so itll

be attacked ). Sometime by this the fluid ll

accumulate and sometime bullae ll be there or not .

- we may see Civatte bodies , its hyaline shrunken

bodies representing apoptotic cells. And by this the

basal layer wont appear .

the causes of the Lichen planus :

not fully understood but it can be due to :-Widely accepted that cell-mediated immune responses

to an external antigen, or internal antigenic changes in

epithelial cells, are involved.


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-Response resembles type IV hypersensitivity.

-Cytotoxic lymphocytes damage basal epithelium

-In most cases the precipitating factors are unknown andwhen the cause is removed it ll be better.

-May be hypersensitivity to drugs and dental materials

-Association with systemic conditions: Hepatitis C

-Graft versus host reaction that present when the patient

has transplant and the body reject it so this rejection ll

affect the skin and the oral cavity , so the body ll reject

the organ and also ll attack the oral mucosa and othersand its fatal sometimes .

-In some patients, lesions are triggered by

hypersensitivity to drugs or dental materials.

-In such cases the condition resolves upon withdrawal ofthe offending agent.

-Such lesions are referred to as lichenoid reactions to

distinguish them from idiopathic lichen planus.

**** Slide 56 so important and the dr just read it

We forgot to say females are affected more than males

with lichen planus.

The last disease for today :


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Lupus erythmatosus

Two types :

1. Chronic discoid :more localized, rounded area on the

face ll show white and purple scaly likekeratosis.intra orally we may have areas that is white

but with some atrophic red parts and some striations

that are more prominent than systemic(sle) ( so by this

we can differentiate between them and by biopsy also ,

or even examining the patient for antinuclear antibody

may help). These areas wont go away by any topical

cream

Most common is a discoid area of erythema or ulcerationsurrounded by white keratotis border sometimes with

radiating striae

--butterfly appearance : more common in sle ( sys lopus

eryth) not in discoid because the most common in

discoid is round .

2. Systemic LE: disseminated.

A variety of autoantibodies are present in SLE,

e.g. antinuclear antibodies (ANA)

Females are affected more than males.

" )

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*** important note: after you read this script I advice you

to refer to the slides because the dr didnt mention all the

things in the slide , the record wasnt good enough to giveme support to cover all the lecs information and the drs

voice sometimes was too low . so I hope that the record ll

be better for you for the next lec script.

Forgive me if theres any mistake

Best wishes for all ^_^

Done by :

Yahya al Omary

Oral Patho 3

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