Oral pathology sheet # 1- Haneen Thnebat

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Oral pathology sheet # 1- Haneen Thnebat

Post by Shadi Jarrar on 23/9/2011, 8:54 pm

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بسم الله الرحمن الرحيم
Oral Pathology 2
White lesions of the oral mucosa

Lect#1

Dr. Faleh Al-swaier

Monday 19/9/2011





We will continue with the oral pathology course, in the same path we have started in summer.lectures notes will be available in the following website:

http://blackboard.ju.edu.jo user name: dent_std

Password: dent_std

Note: the underlined sentences are derived from the oral pathology textbook p.119-122 for further explanation.

This lecture covers the first 5 pages of “White lesions of the oral mucosa” slides.

White lesions

Lesions appear white in the oral cavity due to change in the contexture

(2l nasej) of the tissue(histological changes).The normal color of the oral mucosa is pink due to oxygenated blood vessels in the lamina propria under the epithelium, while the epithelium itself is colorless. The color of normal mucosa depends on the interplay between four factors: vascularity, melanin pigmentation, epithelial thickness, and keratinization.





*What are the factors that cause the lesions to have white appearance???

1) If epithelium thickness increase (Acanthosis, epithelium hyperplasia) it will hide the color of the blood.

2) Increase in formation of keratin on the surface (increase in keratin thickness), also will hide the color of the blood (hyperkeratosis).

3)Hyper parakeratosis.

4) Dense inflammatory cells infiltration that hide the color of the blood.

Orthokeratosis:the superfacial cell layers(squamous) of the epithelium are flattened,anucleate,and have homogenous ,eosinoplilic cytoplasm.

Parakeratosis: the superfacial cell layers(squamous) of the epithelium are flattened, eosinoplilic,but contain pyknotic nuclei.

Hyperkeratosis:increase in the thickness of the keratin layer.

Hyperparakeratosis:increase in the thickness of parakeratin layer.

5) Accumulation of fluid within the cells (intracellular edema) that increase the thickness of the epithelium.

6) Loss of the epithelium so the lesions appear white/gray in color as in oral ulcer. The white lesions here are due to accumulation of fibers on the surface of ulcer, then formation of granulation tissue which will hide the color of the blood so lesions appear white in color.

7) Poor oral hygiene, always be careful that not all white lesions in oral cavity are related to histological changes in the texture of the oral mucosal tissue! Some external factors contribute in whitish lesions, such as poor oral hygiene which is common!!Those patient exhibit accumulation of dental plaque on the gingiva (Tinea Alba)not sure about the term, appears as white lesion.

*You can differentiate Between the White lesions caused by histological changes &those caused by poor oral hygiene by scrapping the lesion using gauze. If the lesion disappeared, then it caused by external factors such as poor oral hygiene (Tinea Alba), but if it’s persist after scrapping then it caused by something within the structure of the mucosa.



Classification:

White lesions classified according to the etiological factors to:

v Hereditary white lesions:

1. _ Oral Epithelial Naevus (White spongy Naevus/WSN).”Common example”.

2. _ Pachyonychia Congenita

3. _ Dyskeratosis Congenita

4. _ Tylosis

5. _ Hereditary Benign Intraepithelial Dyskeratosis

6. _ Follicular Keratosis

7. _ Leukoedema .(more common than WSN)

Lesions #2, 3,4,5,6 are considered as rare hereditary disorders appear as white lesions similar to WSN in clinical manifestations. These lesions will be discussed briefly &you should read it personally &be able to differentiate them from the white spongy naevus (WSN). (You can refer to Box 9.1 p.121 in the textbook).

v Traumatic white Lesions :

Lesions caused by trauma either Mechanical (called frictional keratosis), chemical, thermal trauma.



v Infective white lesions:

§ Candidosis: caused by fungal/candidal infection :

_ Acute Pseudomembranous.

_ Chronic Hyperplastic.

_ Chronic Mucocutaneous.

§ Syphilitic Leukoplakia:caused by syphilis(bacterial infection).

§ Hairy Leukoplakia:caused by Viral infection.

v Dermatological

Skin disease that may appear in oral cavity as whitish lesion, ex:

_ Lichen Planus

_ Lupus Erythematosus

v Idiopathic (Leukoplakia)

Premalignant lesion, white in color without known causes, so the term leukoplakia mean white lesion of unknown causes.

v Neoplastic

Cancers lesions may appear white such as Squamous cell carcinoma; also premalignant lesion may appear whitish such as Carcinoma-in-situ.


Hereditary White lesions

Ø Oral epithelium Naevus(white sponge naevus).

- One of the imp characteristic that this lesion presents in child.

- Autosomal dominant.

- Delay in appearance until adolescence age may take place (may not appear after birth immediately but delay for some years).

- So generally it’s a white lesion in a child with a family history.

- Caused by mutation in the genes coding for keratin type 4 or 13(so it’s a genetic disorder).So any mutation in keratin type 4 or 13 will lead to white spongy Naevus.





**Clinically:

-White lesion as a sponge, so it’s thick, soft, white, asymptomatic, translucent & irregularly thickened lesion.

-Usually diffuse affecting mostly the buccal mucosa (usually bilateral), sometimes may appear all over the oral cavity but rarely involved the gingival margin &the dorsum if tongue.

-Border: the margins usually show a gradual transition to normal (change gradually until become normal in color).

-Thickness: irregular (some area appear thin, other appear thick).

- So the presence of asymptomatic white lesion in young child simplifies the diagnosis.

-Other sites: An important Feature of the WSN is the involvement of other mucousal membrane (other than the oral cavity mucosa). Other membrane will be affected in the same period in which the oral cavity is affected.

** Histology:

-Hyperplasia of the epithelium (Acanthosis/thick epithelium).

- Moderate-marked Hyperparakeratosis.

- Marked intracellular (not intercellular) edema, you can see sites of vacuoles ,this edema occur exactly in Prickle cell layer& superficial cell layer(parakeratin layer).

-Folds appear as cleft in epithelium but not in the whole epithelium thickness. (Still above the basal cell layer).

-This Histological section of superficial hyperkeratosis layer and fluid within cells indicate the term (Basket wave appearance) for the epithelium.

**Cytology:

-If you scrap the lesion and investigate the cells under the microscope, you will find large cells with cytoplasm, condense area around the nucleus in the cytoplasm, these are the characteristic of white spongy Naevus in cytology.

-White spongy Naevus don’t exhibit a dysplasia so it’s not a pre-malignant lesion or potentially malignant lesion (will not develop to squamous cell carcinoma) that’s why, the white spongy lesion consider as good prognosis in the affected child.

-No inflammation in the lamina propria under the epithelium, which ensure that’s an epithelium disorder lesion (defect in gene coding for keratin/ lamina propria isn’t involved).

Now discussion for the other lesions briefly:

Ø Pachyonychia Congentita:

-It’s mean a thick nails

-Whitish Hereditary (autosomal dominant) lesion in the oral cavity with extremely thick nails, in very young stage is indication of Pachyonychia Congenita.

-Clinically &histologically similar to white spongy Naevus.

Ø Dyskeratosis Congenita:

-Mode of inheritance isn’t clear.

- Pigmentation of skin.

-opposite to the Pachyonychia Congenita , as here we’ve dystrophy in the nails(very thin nails).

-Oral lesion: those patients have destructed periodontitis .

-It’s a premalignant lesion! , unlike white spongy naevus, so may develop to oral cancer, that’s why it’s important to be differentiated from white spongy naevus.





Ø Tylosis:

-very thick superficial layer(hyperkeratosis)in palms and planter /very thick keratin ”Palmoplanter hyperkeratosis”

-Whitish lesion in the oral cavity (oral hyperkeratosis).

-All of these patients (approximately 90%) will develop esophageal cancer when reach 70 years old.

-Autosomal dominant disease.



Ø Hereditary Benign Intraepithelial Dyskeratosis:

-Dyskeratosis mean that epithelium normally keratinized, but you can see cells with early keratinization within the prickle cell layer, so half of the epithelium cells start to form keratin (premature keratinization).

-Those patient may become blind due to sever conjunctivitis!

-Also they develop an oral white lesion (folds &plaque).

-Autosomal dominant inheritance.



Ø Follicular Keratosis (Darier’s disease):

-Occasionally sporadic (no family history), other cases are autosomal dominant.

-Appears as white lesion.

** Histology:

-Supra basal clefting (clefting in epithelium)/intraepithelial acantholytic clefts).

-heavily keratotic papules(coalescing and infected) in skin of forehead, scalp,face,trunk,ears.

-Intraorally: small whitish papules on keratinized mucosa mainly hard palate and gingival)

-we will re-discuss it under the vesiculobullous disease topic.



Ø Leukoedema: (important)

-More common, seen in 50% of people, especially in advanced age patient.

-In black people, it may reach 90-100%, so it’s imp to be differentiated and distinguished from Fordyce granules, (White spongy Naevus/WSN), and other oral lesions.

-Seen as grayish, translucent ,membrane in buccal mucosa with some white threads.

-How to confirm??

By Stretch the buccal mucosa, the whitish lesion will disappear and back to normal.

-Why the lesions disappear upon stretching??

Because this lesion (Leukoedema) is just an accumulation of fluid within the epithelium so by stretching test it will disappear immediately! (an important difference from WSN& other white lesions.

-So in this lesion, the presence of little keratin (no or little Parakeratosis) explain why the lesion vanishing upon stretching.

-It’s thought to be a variation of normal, because it’s widely distributed among people mostly in black. Also a significant rate has been identified among white people & people in our countries (between white& black).

-Site: Mostly in Buccal mucosa bilaterally, and to less extent in the Lateral border of the tongue (grayesh ,translucent membrane).



** Clinically:

- Asymptomatic, Diffuse,translucent,grayish-white,firmly appearance.

-Identified by stretch test.

** Histology:

-Decreased Keratosis&Parakeratosis(Mild Parak&acanthosis).

-Intracellular (not intercellular) edema as in WSN.

-No inflammation in Lamina propria so normal LP.





white spongy naevus
Leukoedema
Sever Parakeratosis
Moderate Parakeratosis
Clear white lesion
Grayish white lesion(due to in Keratin)
Clefting in the epithelium
No clefting
No inflammation in lamina propia
No inflammation in lamina propia



Traumatic Keratosis:

A) Mechanical Trauma:

Oral cavity may affected by many types of trauma, due to teeth, appliances (Complete denture, RPD, Orthodontic appliance) , tooth brushing……

o If the trauma was sever & acute, it will cause ulcer.

o If the trauma was mild/friction (chronic) and continue over a long period of time, it may cause hyperplasia & hyperkeratosis in the epithelium.

So here, we’ve the same principle of connective tissue hyperplasia that was discussed in summer, in which, the chronic mild irritation lead to granulation tissue formation and then fibro epithelial polyps. Hyperparakeratosis may occur at the surface, so the fibro epithelial polyp appears white in color.



A chronic irritation by (sharp tooth, cheek biting, prolonged wearing of ill-fitting denture) lead to epithelium hyperkeratosis and hyperplasia, appear as white lesion called(frictional keratosis).Frictional because it’s occur due to friction.



Again!! The etiological factor is prolonged mild abrasion caused by sharp tooth, rough surface, restoration, Denture, habits (common in person who suffers from stress, anxiety. They used to bite on their tongue, lip, and cheek mildly &frequently which lead to Hyperkeratosis&hyperplasia.



It’s common to see a horizontal white line in buccal mucosa parallel to occlusal plane called “Linea Alba”. The term (Linea Alba) means white line. ”fig. #3 /slide#4 or( fig.9.4) p.121 in the textbook”

Linea Alba occurs due to:

1) Friction of the mucosa with the teeth at the site of biting.

2) Suckling of the buccal mucosa which leads to white fold (elevation).

All these lesions called Linea Alba which is an example of frictional keratosis.

As the other types of frictional keratosis, Linea Alba is common in people who have habit such Bruxism, grinding of teeth, under stress.

Clinically:

Linea Alba appears as dense white patch with rough surface.



Sometimes, the frictional keratosis caused by cheek biting (which differs from Linea Alba!).In cheek biting, the patient intends to bite a region of the buccal mucosa as a habit, he don’t bite on a line (limited area) as Linea Alba, but on a more diffuse area ”back to fig.#4 in slide#4 or to fig.9.3 / p.121 in the textbook”

The most important feature of cheek biting, is that this lesion don’t distribute toward the vestibule (don’t involve the vestibule), as the patient can’t bite the vestibule area! So the presence of this feature, provide a confirmation that this white lesion caused by cheek biting. Whenever you deal with a white lesion that reaches the vestibule, always exclude the cheek biting habit as a cause& start to think about other causes(taking a biopsy is recommended).

Those people may press on their cheek from outside, the cheek bind toward the oral cavity and then they bite!!This biting sometimes may remove part of the cheek oral mucosal texture, so the surface exhibit roughness, some area have thick keratin& other with completely removed epithelium(erosion),unlike the surface of White spongy naevus in which the surface is smooth & homogenous.

Mechanical trauma also may occur by tooth brushes, hard incorrect brushing that cause chronic mild irritation to the gingival (frictional keratosis).Doctor displayed a fig show an incorrect tooth brushing that lead to gingival recession & whitish lesion in the canine area.



The alveolar mucosa of Patient with missing (extracted) teeth, will exposed to a high friction during mastication(trauma/chronic mild irritation) which explain the whitish area seen on the alveolar ridge of edentulous space that wasn’t replaced by any dental appliance. Trauma to these edentulous spaces is considered to be a type of frictional keratosis.

**Dx (Differential diagnosis):

How to diagnose& confirm that this white lesion caused by trauma??

1) Source of the trauma/chronic irritation must be identified. It’s caused by rough surface, restoration, denture, tooth brush, habit?

2) Cause of the trauma must fit with size& shape &site of the lesion. Ex: Fractured restoration in canine &whitish lesion in retromolar pad area!!(Not fit with the site)

3) White lesions due to trauma are reversible. Once the source of irritation is removed, the lesion will resolve after certain time(approximately 3 weeks) .The severity of the lesion decrease then it will completely disappear(gradual disappearance).



4) Traumatic lesion isn’t a premalignant lesion.



If you face a white lesion and you suspect to be traumatic and remove the source of irritation, if the patient comes back after a month with the same white lesion, then it’s not a traumatic lesion! you must start to think about other causes(don’t consider any persistence lesion with removed source of irritation as a friction).

**Histology:

-it’s just a hyperplasia & hyperkeratosis (parakeratosis or orthokeratosis).

- No dysplasia.

-Irritation in LP (lamina proprai)/chronic inflammation in LP under epithelium/Scattered chronic inflammatory cell infiltration in LP.

-If the irritation was concentrated in certain area in the buccal mucosa, polyps such as fibro epithelial polyp may appear.

B) Chemical Trauma:

Chemicals may cause white lesions in the oral cavity, but with a different mechanism than the mechanical one. Here it’s not keratosis. Which mean that if the mucosa was insult by acid or any chemical irritant, no hyperkeratosis or hyperplasia will occur, instead, necrosis & sloughing &ulceration will take place.

The epithelium in chemical trauma’s white lesion is necrotic (no keratosis).if you scrap the lesion by gauze, the epithelium will get out with the gauze ,in addition to Erosion, redness, bleeding in that lesion.

1) A common example, insulting of the oral mucosa produced by topical use of aspirin (aspirin burn), some people (Especially, those with irreversible pulpitis) thought that the placement of aspirin tablets in the vestibule near the sore tooth is more effective & will alleviate the pain!! Actually the aspirin is an acid & will lead to epithelium necrosis.

Erosion, bleeding and pain are common in the area of aspirin placement.

2) Some dental material may cause erosion (chemical burns appear as necrotic epithelium), such H2O2 (Hydrogen peroxide), itching solution, composit, acid solution such formalin benzole(not sure about the term).

3) Cinnamon القرفة : continuous using oftoothpaste or chewing gum that contains cinnamon, may cause chemical irritation(Whitish area in the lateral border of the tongue ).

4) Tobacco: In Tobacco, 2 factors contribute to white lesions: chemical and thermal irritation.

All form of tobacco (Cigarettes, Cigar, Pipe, chewing gum), may cause white lesions.

In people with chronic habit of chewing Tobacco, white lesions usually appear in buccal mucosa and buccal vestibule.



Tobacco leads to hyperkeratosis& hyperplasia. These lesions are premalignant lesions so may involve dysplasia.



C) Thermal Trauma:

-Thermal trauma can cause white lesions in the oral cavity.

-Very hot drinks, food will insult the oral cavity and lead to necrosis (shown as white lesions).

- In the fig. showed by the doctor, a very hot fork caused necrosis (white lines) on the lip!

- As we said, smoking contributes to white lesion due to heat &chemicals as well.

-In cigarette smoking, the white lesions appear all over the oral cavity (all the oral cavity mucosa has tendency to look white rather than normal pink color) due to hyperkeratosis and hyperplasia. Whitish discoloration may appear in the lip also!! As the smokers continue to smoke until the last part of the cigarette (dangle the cigarette from the lip) so the lip will insult by heat and look white in color.

- In Pipe smokers, white lesions have more tendencies to appear in the tongue and palate.

***Reverse smoking: Type of smoking in which the smoker reverse the orientation of the cigarette (the fired part placed intraorally)!! High temperature intraorally will insult all over the oral cavity especially the palate. Later on, converting to oral cancer such ssq ( squamous cell carcinoma) may take place.

The palate considered as a rare site of ssq except in reverse smoking, where a palate cancer may occur.



-Regular smoking may cause a lesion at the junction of hard and soft palate called nicotinic stomatitis due to heat generated by smoking.

Nicotinic means caused by nicotine (smoking)

Stomatitis means inflammation in the oral cavity.

Nicotinic stomatitis means long term pipe smokers (not necessary pipe! Cigars and cigarettes are involved also).



**Clinically:

“back to fig.#4 in slide#5 or fig 9.8 p.122 in the textbook”



In the palate region of heavy smokers (not any smokers), you can see the whitish area with red spots in the posterior Part of the palate. These red spots are the opening of the minor salivary glands which undergo inflammation due to heat, so appear as red spots surrounded by white area due to hyperplasia&hyperkeratosis.



Nicotinic stomatitis isn’t a premalignant lesion (will not convert to cancer) except those caused by reverse smoking where the Nicotinic stomatitis will develop to cancer.

So Nicotinic stomatitis is just an alarm that you’re dealing with heavy smokers and he’s more susceptible to oral cancer than other normal individuals ”the doctor exact words, although he mention that it’s not a premalignant lesion!!!”



**Histology:

-White areas due to hyperkeratosis & hyperplasia.

-Red spots due to dilated ducts of minor salivary glands surrounded by inflammation and have a prominent vascularity.




Done By
Haneen Thnebat





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Shadi Jarrar
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