Keratoses and Related Disorders of Oral Mucosa

Introduction: Normal Oral Mucosa

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The color of normal mucosa is kind of pink, This color result from interplay of factors which are the : vascularity , epithelium and melanin The epithelium itself depend on the thickness of epithelium , and the keratin layer of the epithelium in that area

looking at the picture on the left we can see brownish area and we think that we have here more melanin than we have in the pic on the right because of the brown\black appearance

Some time we have white appearing mucosa in those case the problem will be in the epithelium itself ,,, that the epithelium may be thicker than normal, or the keratin layer is thicker Some time we have pale mucosa in that situation the : vascularity is less than normal In smokers the melanin pigmentation layer will increase and we will have certain area in oral cavity with brownish appearance this appearance not because the epithelium is altered

Where do we have the melanocytes ? in the basal layer of the epithelium it will produce melanin

keratin layer

Epithelium

Blood vessels

 Kertinaization of the oral cavity

o o We have keratinized, and Non-keratinized mucosa Actually all oral mucosa in the oral cavity will have a keratin layer but some area are more keratinized than others so they well known as keratinized and the rest as non keratinized

Non keratinized areas lower labial epithelium , the buccal epithelium of mucosa , the soft palate , part of the hard palate ,floor of the mouth ,ventral surface of the tongue and the lateral lateral border of it are non keratinized. ** although these tissue are not keratinized but we will see keratin layer microscopically but its very minimal

The keratinized areas the dorsum of the tongue, the gingiva the attached gingival because removable gingival will be non keratinized up in the sulcus , and the hard palate mainly the anterior part roughe area are keratinized areas

Introduction: White Patches

white patch , maybe result of either of the increase of the thickness of epithelium itself, or the production of the keratin itself, or having abnormal keratin

why is that ?
increase in keratin will give us white appearance because you will not see the blood vessels in the underlining mucosa the reflection of light over the blood vessels will not be normal you will see it as white and especially that when kertin absorbed saliva or water it will appear whitish we will not have the normal pink appearance . When the keratin increase in thickness we cannot remove it be scrapping, if u scrapped it with tongue depressor it will not wiped off . while if u have debris food debris or necrotic tissue e.g due to burn it can be wiped off easily even if it because Candida infection it can be removed be scrapping but increase in keratin thickness it will not whipped off Debris , necrotic tissue , infection of Candida like the acute candidosis it can be scraped off

Why some time do we have debris accumulating on the tongue to give this whitish appearance especially in patient who are ill or having tonsillitis or fever? Because there will be lack of mechanical stimulation of the tongue so there will be no movement of the tongue the patient doesnt have appetite doesnt eat doesnt speak like normal , so stimulation will be less than normal and there will be no sloughing of the debris especially when they silvery flow is low .

Definition of Histopathological Terms

Orthokeratosis: superficial keratinized squames are flattened, anucleate, with homogeneous, acidophilic cytoplasm.

Parakeratosis: superficial keratinized squames are flattened, with homogeneous, acidophilic cytoplasm, but contain pyknotic nuclei

Hyperkeratosis: increased thickness of keratin layer where its normally present Keratosis: keratinization of epithelium that is not normally keratinized Hyperparakeratosis: increased thickness of parakeratin layer Hyperorthokeratosis: increased thickness of orthokeratin layer Acanthosis is increase in thickness of the epithelium in general {close to hyperplasia in the epithelium} but mainly its in the prickle cell layers , and when we say hyperplastic we mean all layer of the epithelium - when there is acanthosis there will be elongation of the rete ridges

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rete ridges

Epithelial atrophy: decrease in thickness of epithelium

Celluler atypia changes affecting certain cells that may mean premalignant lesion. - we said may mean because some time the change is due to inflammation . Epithelial dysplasia a term describing epithelium when features of cellular atypia are present - in these term we describe the whole epithelium not a certain cells , because sometime we will have cells without atypia but the whole surface of the whole epithelium is dysplastic but not all the epithiulm are showing the a typical features

So epithelial dysplasia refers to epithelia itself including celluer atypia and architecture changes while Cellular atypia refers to specific cells If we have a white lesion in oral cavity it will be classified according to this table

Hereditary

Oral epithelial nevus Oral manifestations of other rare genodermatoses Leukoedema

Traumatic

Mechanical (frictional keratosis) Chemical Thermal Candidosis: - acute psuedomembranous - chronic hyperplastic - chronic mucocutaneous Syphilitic leukoplakia Hairy leukoplakia Leukoplakia Lichen planus Lupus erythematosus Carcinoma in situ Squamous cell carcinoma

Infective

Idiopathic Dermatological Neoplastic

 Heredity conditions

White sponge nevus Featuers o We have white lesion in oral cavity in different position for example buccal and labial mucosa o The patient is having a white lesion which cant be removed be scrapping o These spot appear in child hold because its heredity so its genetically determinant early stages of life o The problem here in keratin genes 13 and 4 - We have 20 genes only two of them are mutated and we will have this net result which is white sponge nevus appearance of the mucosa The border of the lesion are usually ill defined there continuation between the lesion and the adjacent normal epithelium o The other feature not only the oral cavity is involved but the soft palate the esophagus nose , nasal mucosa and other mucosal surfaces are involved with this mutation Histologicaly o

We have hyper keratosis and we have edematous intra cellularly inside the epithelium we have spaces which are edematous and also we have small piknotic nucleus which is important because its is not seen in leuko edema >>>> in which we have intracellular edema we have glycogen accumulation but there is no specific feature of the nuclei So when u have empty cytoplasm and when u have prominent cell borders and small nucleus it will look like the basket weave just the cellular border are obvious while the cytoplasm is empty {empty in appearance} This edema is in the super facial prickle cell layer and also it may extend to the parakertinazed layer

hyper keratosis

acanthosis and edema

What is the concern of these white patches is it malignant potential ?

no , Its just esthetic appearance it does not have any other feature of concern like pre malignant potential While luka plasia is a pre malignant has pre malignant potential

Lukoedema

It may be familial , it apper as white milky appearance in the buccal mucosa that disappear upon starching its appear more in dark people and smokers

Histologicaly the lukoedema will show intercellular edema and glycogenic accumulation inside the cell in addition to the intra cellular edema there is also increase in the thickness of the prickle cell layer we dont have hyper keratosis so it should be easy for us to differentiate between white sponge nevus and lukoedema

Traumatic

What are the tube of trauma mechanical , thermal and chemical Some time in mechanical irritation we have ulcer or erosion of surface epithelium and some mechanical irritation will give us white lesion whats the difference ?

It depends on the severity of the trauma ,For example if we had a bite from a sharp cusp acute bite with a considerable force we will have ulcer or erosion ,But if I have a sharp cusp which is chronically irritating the buccal mucosa in low grade force for example while talking .. in this situation the body will have enough time to increase the thickness of epithelium or to form keratin so I will have white lesion of frictional keratosis in low grade friction of the cusp .while I will have ulcer if I accidently had a bite to my buccal mucosa and this bite was sharp o In traumatic keratosis | or frictional keratosis I need to identified a cause so I can call it frictional keratossis and this cause should match the size and the site of the lesion . for example if I have a sharp cusp this sharp cusp should be on the site of the lesion if the lesion in the left buccal mucosa and the cusp is in the right buccal mucosa its not the cause both should be in the left side in addition if I have for example 5 cm lesion and the is only 3cm so its not the cause Another feature that when I remove the cause or when I correct it , the lesion should show a sign of healing within 2 weeks and reevaluate the patient if the lesion shows a sign of healing so its the cause friction keratosis and epithiluim this is the granular cell layer which show granuolsis which is the top layer before the keratinized layer usually we have this granular layer in orthokeratosis

In epithiluim We have basal layer prickle cell layer- granular cell layer then keratin layer the keratin will be flattened cells whith piknotic nucli or without nucli, and then we will have keratin production by the surface epithiluim and ussally we this granular cell layer when we have orthokerstosis

In this histopathological picture I have thick layer of keratin production . But usually we dont have dysplasia no cellular atypia no dysplasia except increase in keratin thickness and some time increase in the thickness of prickle cell layer or the whole epithelium acanthoses I may have acanthosis and hyperkeratosis or hyper keratosis alone for frictional keratosis

Chemical trauma

Done by mohammad elwir