Oral Precancerous Lesions And Conditions Short Notes

Oral Precancerous Lesions and Conditions Question And Answers

Question 1. What is oral precancer?
Answer. Oral cancers are sometimes preceded by some clinically visible lesions, which are noncancerous to begin with and are therefore been termed as “precancers”.

Question 2. Do all cancers develop from pre-existing precancer only?
Answer. No; all cancers do not necessarily originate from precancers.

Read And Learn More: Oral Pathology Short Notes Question And Answers

Question 3. What is a ‘de novo’ lesion?
Answer. When a lesion develops directly in the body and not from any precursor or pre-existing lesion, it is called a ‘de novo’ lesion.

Question 4. Do all precancers eventually turn into cancer?
Answer. No; all precancers do not eventually progress to cancer.

Oral Precancerous Lesions

Question 5. According to WHO oral precancerous states can be divided into how many groups?
Answer. According to World Health Organization (WHO), oral precancerous states are divided into two board groups: (1) precancerous lesions, and (2) precancerous conditions.

Question 6. What is a precancerous lesion?
Answer. Precancerous lesion is defined as a ‘morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart’—WHO, 1978.

Question 7. Give examples of some precancerous lesions.
Answer.

• Leukoplakia
• Erythroplakia
• Stomatitis nicotina
• Chronic candidiasis.

Question 8. What is a precancerous condition?
Answer. A precancerous condition is defied as ‘the generalized state of the body, which is associated with a significantly increased risk of cancer’—WHO,1978

Question 9. Give examples of some common precancerous conditions.
Answer.

• Oral submucous firosis
• Syphilis
• Oral lichen planus
• Sideropenic dysphagia

Oral Precancerous Lesions

Question 10. What is the most important diagnostic procedure in the confirmatory diagnosis of cancers and precancers?
Answer. Histopathological evaluation of the affected tissue.

Question 11.Defie leukoplakia.
Answer. Leukoplakia can be defined as a “white patch” or “plaque” in the oral cavity, which cannot be scrapped off or stripped off easily and which cannot be characterized clinically or pathologically as any other disease”—WHO, 1978.

Question 12. The previous definition is revised fie years later at the international conference; what is the new definition of leukoplakia?
Answer. The new definition states that “leukoplakia is a white patch or plaque in the oral cavity, which cannot be scrapped off or stripped off easily and which cannot be characterized clinically or pathologically as any other disease and moreover, it is not associated with any physical or chemical agents except the use of tobacco”.

Question 13. What is pre-leukoplakia?
Answer. Pre-leukoplakia is a grayish or grayish-white, slightly lobular lesion of oral mucosa with ill-defied borders.

Question 13a.What is the distinct difference between leukoplakia and pre-leukoplakia?
Answer. The whiteness of pre-leukoplakia is much less than that of leukoplakia.

Question 13b.Are pre-leukoplakia and leukoedema same entities?
Answer. No, pre-leukoplakia is a precursor of leukoplakia, whereas leukoedema is a hereditary malformation of the oral mucosa.

Question 13c.What is leukoedema?
Answer. It is a hereditary mucosal condition in which the oral mucosa has a gray, opaque appearance and when the mucosa is stretched the lesion disappears, only to reappear when it is relaxed.

Question 14.Mention the etiologic factors of leukoplakia.
Answer. The etiologic factors of leukoplakia are as follows:
Tobacco (in smoking and smokeless or chewing forms)

• Alcohol
• Candidiasis
• Dietary deficiency
• Syphilis
• Viral infections
• Hormonal imbalance
• Chronic irritation
• Actinic radiation
• Galvanism.

Oral Precancerous Lesions

Question 15. Mention the different forms of use of tobacco.
Answer.

• Tobacco smoking
• Tobacco chewing
• Snuff dipping
• Tobacco as toothpaste.

Question 16.What are the different forms of smoking tobacco?

Answer. For smoking, tobacco is prepared in various smoking forms:

• Cigarette
• Cigar
• Pipe
• Bidis (country-made cigarette)
• Chutta
• Hookah.

Question 17. What is reverse smoking?
Answer. In conventional smoking, the smoker keeps the burning end of the cigarette outside mouth, while the non-burning end is held inside mouth, however in ‘reverse smoking the cigarette is held in the mouth in the opposite direction ( i.e., the burning end of the cigarette kept inside mouth while the non-burning end remains outside mouth).

Question 18. What are the forms of smokeless tobacco?
Answer.

• Pan
• Khaini
• Gutkha
• Jarda
• Snuff
• Gurakhu.

Question 19.How tobacco causes oral leukoplakia?
Answer. During smoking, large amounts of tobacco end products are produced in the oral cavity; which include [aromatic hydrocarbons e.g. benzopyrine and tobacco specific nitrosamines (TsNs), N-nitrosonornicotine (NNN), N-nitroso pyrrolidine (NPYR), N-nitroso-dime thylamine (NDMA)], etc.
These chemicals in association with heat,(generated during smoking) cause severe irritation to the oral mucous membrane and fially results in the development of leukoplakia.

Question 20. Why the incidence of leukoplakia varies from smokers to smokers?
Answer. Because the risk of development of leukoplakia depends not only upon smoking but also on the frequency and duration of the tobacco smoking as well as the age and sex of the smoker concerned.

Question 21. What is the role of alcohol in the development of leukoplakia?
Answer.

• Alcohol acts as a solvent and facilitates penetration of other carcinogens (especially nitrosonornicotine) across the oral mucous membrane
• Alcohol can cause atrophic change in the oral mucosa, which makes the tissue more vulnerable to the effect of other carcinogenic agents.
• This often leads to mutagenic change in the epithelial cells
• The dehydrating effect of alcohol on oral mucosa may further increase the risk of tobacco-related damage
• Long-term alcoholic habit often produces cirrhosis of liver; which in turn increases the risk of development of oral precancers and cancers; simply because the damaged liver cannot detoxify the carcinogenic chemicals in the blood.

Question 22. What is tobacco-alcohol synergism?
Answer. In comparison to tobacco, alcohol is not an important risk factor for leukoplakia but if both are taken together (which happens often) then the risk of development of leukoplakia is greatly increased.

Question 23. How does candida-associated leukoplakia differs from non-candidal lesions?
Answer. Candida-associated leukoplakias develop more epithelial dysplasia than the noncandidal lesions.

Question 24. What is the role of vitamin-A deficiency in the development of oral leukoplakia?
Answer. A deficiency of vitamin A causes metaplasia and hyperkeratinization of the oral epithelium,which may eventually result in the development of leukoplakia.

Question 25. Describe the clinical appearance of oral leukoplakia.
Answer. Oral leukoplakia clinically appears as a ‘white patch’; which can be either non-palpable, faintly translucent or can be thick, fisured, indurated or palillomatous in nature.

Question 25a.What is the most common site of oral leukoplakia?
Answer. Buccal mucosa.

Question 26.What is the usual color of leukoplakia lesions in the mouth?
Answer. The lesions are usually white or grayish or yellowish-white in color and in some cases,due to heavy use of tobacco, lesions may take a brownish-yellow color.

Question 27. Describe the symptoms of oral leukoplakia.
Answer. In most of the cases, these lesions are asymptomatic; however, in some cases they may cause pain, a feeling of thickness and burning sensations, etc.

Question 28.Leukoplakia with an ebbing-tide pattern of appearance may be seen in which part of the oral cavity?
Answer. Leukoplakia of the flor of the mouth sometimes has an ebbing-tide pattern of appearance.

Question 29. What are the clinical types of leukoplakia?
Answer. Clinically leukoplakias are of three types:

• Homogenous leukoplakia
• Ulcerative leukoplakia
• Nodular or speckled leukoplakia.

Question 29a. What is the ‘WHO-1980’ clinical classifiation of leukoplakia?
Answer.

• Homogeneous leukoplakia—lesions that are uniformly white; has three subtypes: a)
• Smooth (2) Furrowed (fisured) and (c) Ulcerated
• Non-homogenous leukoplakia—lesions in which part of the lesion is white and rest appears reddened.
• It is also called ‘Non-homogeneous nodule-speckled leukoplakia and has no subtype.

Question 30. Describe the clinical appearance of homogenous leukoplakia.
Answer. Homogenous leukoplakia clinically presents extensive white patch having uniformly white, smooth, flt or corrugated surface with an irregular margin.

Question 31. Which type of tobacco habit is often associated with the development of homogenous leukoplakia?
Answer. These lesions are mostly associated with the oral use of snuff.

Question 32. Name an important clinical characteristic of homogenous leukoplakia.
Answer. These lesions usually maintain a relatively consistent pattern throughout their clinical course.

Question 33. Describe the clinical appearance of ulcerative leukoplakia.
Answer. Ulcerative leukoplakia clinically may be white or mixed red-white in appearance and it has a central ulceration.
The ulcerated area at the center of the lesion appears red and it may have a yellowish firin coating.

Question 34. Describe the clinical appearance of nodular leukoplakia.
Answer. The nodular or speckled leukoplakia clinically presents a mixed red and white lesion; there is an erythematous base within which multiple small, slightly raised, keratotic nodules or granules are scattered here and there.

Question 35.Which clinical type of leukoplakia carries the highest risk of malignant transformation?
Answer. Nodular or speckled leukoplakia carries the maximum risk of malignant transformation.

Question 36.Describe the basic histologic picture of leukoplakia.
Answer. Under microscope leukoplakia generally presents hyperorthokeratinization or hyper parakeratinization or both, with or without the presence of epithelial dysplasia.

Question 37.What is keratin?
Answer. Keratin is a special type of protein, produced by the keratinocytes and it makes a covering on the surface layer of stratum corneum of oral epithelium.

Question 37a.What is orthokeratin?
Answer. Orthokeratin is a homogenous layer of keratin present on the superficial part of the epithelium, which does not contain nuclei, ribosome, mitochondria and keratohyaline granules.

Question 38. What is orthokeratinization?
Answer. The pattern of maturation of the epithelial cells to form anucleated squames of keratin is called orthokeratinization.

Question 39. What is parakeratin?
Answer. Parakeratin is another variety of keratin in which presence of pyknotic nuclei and partially lysed cell organelles are seen.

Oral Precancerous Lesions

Question 40. What is parakeratinization?
Answer. The pattern of maturation of the epithelial cells to form parakeratin is called parakeratinization.

Question 41.Indicate the state of cell maturation when one is producing orthokeratin and the other producing parakeratin.
Answer. The pattern of maturation cells is different; cells producing orthokeratin are more mature in comparison to those producing parakeratin.

Question 42. What is hyperorthokeratinization?
Answer. An abnormal increase in the thickness of orthokeratin layer in the epithelium is called hyperorthokeratinization.

Question 43. What is the relationship between leukoplakia and hyperorthokeratinization of epithelium?
Answer. In case of leukoplakia, hyperorthokeratinization is seen in those areas of epithelium which are keratinized in normal situations. Besides this, some degrees of orthokeratinization may also be seen in the areas of epithelium, which are nonkeratinized in normal situations.

Question 44. What is hyperparakeratinization?
Answer. When there is an abnormal increase in the thickness of parakeratin layer in the epithelium,it is called hyperparakeratinization.

Question 45. What is the relationship between leukoplakia and hyperparakeratinization of epithelium?
Answer. An important histologic criterion of leukoplakia is the presence of hyperparakeratinization of the normally keratinized epithelium, or some amount of parakeratin deposition in the areas of epithelium which are usually non-keratinized.

Question 46. How epithelial dysplasia in leukoplakia is related to hyperparakeratinization?
Answer. Epithelial dysplasia is more often seen in leukoplakia, where the surface layer is hyperparakeratinized.

Question 47. Is it possible that in a single lesion of leukoplakia both hyperorthokeratinization and hyperparakeratinization can occur?
Answer. Yes; in few lesions of leukoplakia both hyperortho and hyperparakeratinization may be seen.

Question 48. Describe how the thickness of epithelium changes in case of leukoplakia.
Answer. In leukoplakia, the thickness of epithelium is often altered and it occurs in the form of epithelial atrophy or epithelial hyperplasia or acanthosis, etc.

Question 49. What is acanthosis of the epithelium?
Answer. An abnormal increase in the thickness of stratum spinosum of the epithelium is called acanthosis.

Question 50. What is the effect of acanthosis of epithelium in leukoplakia?
Answer. In case of leukoplakia, acanthosis is commonly observed in multiple areas of the epithelium, which often causes elongation, thickening and blunting of the rete-pegs.

Question 51. Mention the precancerous changes in the cellular layer of the epithelium in leukoplakia.
Answer. There are two main changes—development of cellular atypia and epithelial dysplasia.

Question 52. What is cellular atypia?
Answer. When the precancerous changes of leukoplakia involve only at the cellular level in the mucosa, it is known as ‘cellular atypia’. At this situation, the overall alterations in the tissue towards precancerous changes are not fully expressed.

Question 53. What is epithelial dysplasia?
Answer. (Dys—abnormal, plasia—formations) when the precancerous changes in leukoplakia worsen further and the changes (both physical and morphological) begin to express themselves in the overall tissue levels, it is called ‘epithelial dysplasia’.
Here precancerous changes are not limited only to the one or two cells but are affecting the entire thickness of the epithelium as well as the basement membrane and the connective tissue.

Question 54. What is the signifiance of epithelial dysplasia in a lesion of leukoplakia?
Answer. Epithelial dysplasia is the hallmark in the histological changes seen in the epithelium in case of leukoplakia and its presence is an important indicator regarding the precancerous nature of the disease.

Question 55. What is the most important histologic criterion that often determines the malignant potential of a precancerous lesion or condition?
Answer. The most important criterion for evaluating the malignant potential is the microscopic study of “epithelial dysplasia”.

Question 56. What are the features of epithelial dysplasia?
Answer.

• Nuclear hyperchromatism
• Cellular pleomorphism
• Irregular epithelial stratifiations
• Increased nuclear–cytoplasmic ratio
• Poikilocarynosis or division of nucleus without division of cytoplasm
• Loss of polarity of basal cells
• Increased number of mitotic fiures
• Presence of mitotic activity even in the superfiial half of the epithelium
• Individual cell keratinization
• Dyskeratosis
• Enlarged nucleoli
• Diminished intercellular adherence
• Drop-shaped rete-pegs with basal cell hyperplasia
• More than one layer of cells having “basaloid” appearance.

Question 57.What are the different layers present in a normal keratinized epithelium?
Answer. There are four layers of cells:

• The basal cell layer (stratum basale)
• The spinous cell layer (stratum spinosum) (also called the prickle cell layer)
• The granular cell layer (stratum granulosum)
• The keratinized layer (stratum corneum).

Question 58. How the cells morphologically appear in different layers of a keratinized epithelium?
Answer.

• Cells in the basal cell layer—cuboidal or columnar in shape
• Cells in the spinous cell layer—polyhedral in shape
• Cells of the granular cell layer—flttened cells
• Cells of the keratinized layer—flt cells.

Question 58a. Keratohyaline granules are present in which layers of epithelium?
Answer. Stratum corneum and stratum granulosum.

Question 58b. In which layer of the epithelium, melanocytes are present?
Answer. In the basal cell layer.

Question 58c.How the cell layers of mucosa differ from those found in the skin?
Answer. In the skin, there is a fith layer called stratum lucidum, present between stratum corneum and stratum granulosum.

Question 59. What is cellular pleomorphism?
Answer. The epithelial cells have a typical size and shape at different layers of the normal stratifid squamous epithelium; in case of epithelial dysplasia, the size and shape of the cells are altered, which is known as cellular pleomorphism.

Question 60. What is nuclear hyperchromatism?
Answer. In the normal stratifid squamous epithelium, the nuclei are small and uniformly stained with hematoxylin; but in case of epithelial dysplasia the cell nuclei are often large and deeply stained, this change in the nuclei are called nuclear hyperchromatism.

Question 61.What do you mean by irregular epithelial stratification in epithelial dysplasia?
Answer. In the normal keratinized stratifid squamous epithelium, different cell layers are oriented in the following order (from bottom to the surface)—basal cell layer then spinous cell layer then granular cell layer and on the top, the keratinized layer.
However, in epithelial dysplasia, this normal order of orientation (stratification) of cell layers may be disturbed and the phenomenon is called irregular epithelial stratifiations.

Question 62. What do you mean by increased nuclear–cytoplasmic ratio in epithelial dysplasia?
Answer. In normal epithelial cells, the size of nucleus and the volume of cytoplasm is constantly maintained; the ratio, between the two is called ‘nuclear–cytoplasmic ratio’ which is 1:4.
This ratio is often altered (changes to 1:1) in epithelial dysplasia; as there is an increased nuclear–cytoplasmic ratio (size of nucleus increases, and therefore, volume of the cytoplasm decreases).

Question 63.What is poikilocarynosis?
Answer. During normal mitotic cell division both cell nucleus and the cytoplasm divide; however,in some cases of epithelial dysplasia, division of nucleus occurs without division of the cell cytoplasm and this phenomenon is called poikilocarynosis.

Question 64. What is loss of polarity of basal cells?
Answer. In normal stratified squamous epithelium, the basal cells are always placed at the bottom layer; however, in case of epithelial dysplasia these cells may be found in other top cell layers too; this abnormal change in position of basal cells in the dysplastic epithelium is called ‘loss of polarity of basal cells’.

Question 65.What is dyskeratosis?
Answer. In normal keratinized epithelium, the keratinization occurs at the surface layer; however in epithelial dysplasia, there can be abnormal expression of keratin production in the superfiial as well as in the deep layers of epithelium and this phenomenon is called ‘dyskeratosis’.

Question 65a. Name the most abundant glycoprotein present in the basement membrane of epithelium.
Answer. Laminin.

Question 66. What are the types (degrees) of epithelial dysplasia?
Answer. Depending on the degree and the extent to which the dysplastic changes have taken place in a lesion of leukoplakia; epithelial dysplasias may be divided into three categories,namely the:

• Mild epithelial dysplasia
• Moderate epithelial dysplasia
• Severe epithelial dysplasia.

Question 66a.What is the modifid OLEP classification oral leukoplakia?
Answer. It is presented by van der Waal et al. (2000), in which the size of the leukoplakia and the presence or absence of epithelial dysplasia are taken into account.

Question 66b.Describe the modifid classifiation and staging system for oral leukoplakia.
Answer.

• L Size of leukoplakia:
• L1—size of leukoplakia is < 2 cm
• L2—size of leukoplakia is 2–4 cm
• L3—size of leukoplakiais >4 cm
• Lx—size of leukoplakia is not specifid
• P—Pathology:
• PO—No epithelial dysplasia
• P1—Distinct epithelial dysplasia
• Px—Dysplasia not specifid in pathology report.

Question 66c. Describe the modifid OLEP staging system for oral leukoplakia.
Answer. Altogether four stages are recognized:

• Stage I—L 1 PO
• Stage II—L2 PO
• Stage III—L3 PO or L1 L2 PI
• Stage IV—L3 P1.

Question 67. Why it is important to evaluate the degree of epithelial dysplasia?
Answer. The degree of dysplasia is of immense value in predicting the malignant potential of a precancerous lesion such as leukoplakia.
For example, severe dysplasia in a lesion means it has more chances of undergoing malignant transformation and likewise, mild dysplasia in a lesion means it has least chance of undergoing malignant transformation.

Question 67a.Can malignant transformation occur in a non-dysplastic leukoplakia?
Answer. Yes (Rajendran R. Oral leukoplakia (leukokeratosis): Compilation of facts and fiures. J Oral Maxillofac Pathol. 2004;8:58-68).

Question 68. Does the degree of epithelial dysplasia change in a lesion with time?
Answer. Yes, the degrees of epithelial dysplasia in a lesion may change in both ways (good and bad) with time. If intensity of the predisposing factors are increased, a lesion with mild dysplasia may turn towards moderate to severe, similarly if the predisposing factors are removed, the dysplastic cells can turn back towards normal.

Question 69. Name the factors determining the degree of epithelial dysplasia.
Answer.

• Age and sex of the patient
• Frequency and duration of oral habits
• Types of oral habits (tobacco, alcohol, snuff, etc.)
• Types of tobacco used and mode of consumption (smoking, chewing or others)
• Any synergism (combination) of multiple habits
• Location of the lesion in the oral cavity (lips, tongue, flor of the mouth)
• Secondary infections (candidacies, syphilis, HPV or HSV)
• Systemic health.

Question 70. What is the signifiance of secondary candidal infection in leukoplakia?
Answer. The candida-associated leukoplakias may have an increased tendency for malignant transformation.

Question 71.How the thickness of basement membrane of epithelium in leukoplakia changes with change in the severity of epithelial dysplasia?
Answer. There is gradual reduction in the thickness of basement membrane with increase in the severity of the epithelial dysplasia.

Question 72. Name the special investigations done in leukoplakia for confimatory diagnosis and to evaluate its malignant potential.
Answer.

• Histochemistry
• Enzyme histochemistry
• Immunohistochemistry
• Exfoliative cytology
• Cell proliferation study
• Stereological techniques
• DNA histograms.

Question 73. What is the rate of malignant transformation in leukoplakia?
Answer. According to WHO, the overall malignant transformation rate of leukoplakia is about 3 to 6 percent.

Question 73a.Leukoplakia at which intraoral site shows maximum risk of malignant transformation?
Answer. Floor of the mouth.

Question 74. Name the lesions commonly included in the differential diagnosis of leukoplakia.
Answer.

• Lichen planus
• Candidiasis
• Frictional keratosis
• Verrucous carcinoma
• White sponge nevus
• Chemical burns
• Leukoedema.

Question 75. Patient belonging to which gender will have more tendencies for malignant transformation?
Answer. Women carry higher risks of malignant transformation if they have leukoplakia as compared to men.

Question 76. Which clinical type of leukoplakia will have maximum risk of malignant transformation?
Answer. Usually, the nodular leukoplakias have maximum risk of malignant transformation among all the clinical types.

Question 77. Which clinical type of leukoplakia will have minimum risk of malignant transformation?
Answer. Homogenous leukoplakia.

Question 78. Leukoplakia of which part of mouth shows least chance of malignant transformation?
Answer. Leukoplakias of the palate have least chances of malignant transformation.

Question 79. Leukoplakia of which part of mouth shows highest chance of malignant transformation?
Answer. Leukoplakias of flor of the mouth and ventral surface of tongue carry the highest risk for malignant transformation.

Question 80. Name the lesion which results from malignant transformation in leukoplakia.
Answer. Squamous cell carcinoma.

Question 81. What is oral hairy leukoplakia?
Answer. Oral hairy leukoplakia is a HIV-associated mucosal disorder and is considered as a reliable marker for the presence of HIV virus in the body and is also a precursor of full blown AIDS.

Question 82. In ‘hairy leukoplakia’, why the disease is named so?
Answer. The lesion characteristically exhibits numerous linear vertical folds or projections on its surface and these projections are sometimes so marked that they resemble “hairs” (hence the name hairy leukoplakia is given).

Question 83. Which groups of individuals often suffer from oral hairy leukoplakia?
Answer. There are two categories:
Homosexual men with HIV (human immnunodefincey virus) infection
Other HIV/AIDS risk individuals like patients with hemophilia and other common transfusion recipients.

Question 84. Name the common sites for development of oral hairy leukoplakia.
Answer.

• Most common sites—lateral borders and ventral surface of tongue
• Less common sites—flor of mouth, buccal or labial mucosa and palate

Question 85. Describe the brief clinical appearance of oral hairy leukoplakia.
Answer. Clinically hairy leukoplakia appears as a slightly raised, white plaque with vertically corrugated, irregular surface. There are numerous fie linear vertical folds or projections on the surface of the lesion, which resemble “hairs”.

Question 86. What is the chance of malignant transformation in oral hairy leukoplakia?
Answer. There is no evidence of malignant transformation in this form of leukoplakia.

Question 87. Describe the histological appearance of oral hairy leukoplakia.
Answer. In oral hairy, leukoplakia the parakeratin layer is thick and is often colonized by candidial organisms. A very characteristic fiding is presence of large, pale staining ‘balloon cells’ below the keratin layer; these are cytopathically altered keratinocytes.

Question 88. What special investigation is done in oral hairy leukoplakia?
Answer. Hairy leukoplakia is diagnostically confimed by using DNA in situ hybridization with an EB virus molecular probe; on processed tissue section.

Question 89.Define Leukoedema.
Answer. Leukoedema is an alteration of the oral epithelium characterized by intracellular accumulation of flid (edema) within the spinus cell layer.

Question 90. What is the other name of leukoedema?
Answer. Preleukoplakia (However, now they are considered separate entities.

Question 91. What is the clinical appearance of leukoedema?
Answer. The disease clinically exhibits an asymptomatic, diffuse, translucent, grayish–white area in the oral mucosa with a fimy appearance.

Question 92. Describe a typical clinical characteristic of leukoedema.
Answer. When the mucosa is stretched, the lesion disappears.

Question 93. Describe the histopathological characteristics of leukoedema.
Answer. Histologically leukoedema presents thickening of epithelium with mild degree of parakerotosis and acanthosis. Large amount of intracytoplasmic flid and glycogen are often present within the spinus cell layer.

Question 94. What is carcinoma in situ?
Answer. Carcinoma in situ is a laterally spreading, intra-epithelial type of superficial carcinoma; which mostly occurs over the skin and sometimes in the mucosa including that of the oral cavity.

Question 95. What is the most important characteristic of carcinoma in situ?
Answer. It is the most severe stage of epithelial dysplasia, which involves the entire thickness of the epithelium; however the basement membrane is intact, and therefore, dysplastic epithelial cells do not invade into the underlying connective tissue stroma.

Question 96. Which categories of people suffer from carcinoma in situ more often?
Answer. Elderly males.

Question 97. Name the common intraoral areas where carcinoma in situ develops often?
Answer. Floor of the mouth, tongue or lips.

Question 98. Describe the clinical features of carcinoma in situ.
Answer. Clinically, the lesion appears either as a white plaque or as an ulcerated, eroded or red area over the oral mucosa. Some lesions produce combined features of both leukoplakia and erythroplakia.

Question 99. What are the histological features of carcinoma in situ?
Answer. Histologically the lesion shows hyperplastic epithelium with pronounced epithelial dysplasia involving almost every layer of the epithelium.
Loss of orientation and loss of polarity of the dysplastic epithelial cells are very characteristic features and since the basement membrane is intact, there is no invasion of the neoplastic cells into the underlying connective tissue.

Question 100. What is the keratinization potential of dysplastic cells in carcinoma in situ?
Answer. The features like individual cell keratinization and keratin pearl formation, etc. are exceedingly rare in carcinoma in situ. In fact if keratin pearls are found, invasive carcinoma should be suspected rather than carcinoma in situ.

Question 101. Define erythroplakia.
Answer. Erythroplakia is a clinical term, which refers to “a red patch or plaque in the oral mucosa that cannot be characterized clinically or pathologically as any other condition and which has no apparent cause” (WHO,1978).

Question 102. What is the signifiance of oral erythroplakia?
Answer. Oral erythroplakias represent the most severe type among all oral precancerous lesions and histologically they almost always exhibit dysplastic changes.

Question 103.What are the most common sites for oral erythroplakia in males?
Answer. Floor of the mouth and retromolar areas.

Question 104. What are the most common sites for oral erythroplakia in females?
Answer. Gingiva and alveolar ridge.

Question 105. Describe the clinical features of erythroplakia.
Answer. Clinically erythroplakia appears as a small or extensive, red, velvety lesion with clearly defied margins.

Question 106. What are the clinical types of erythroplakia?
Answer. Erythroplakia has three distinct clinical types:

• Homogenous erythroplakia
• Erythroplakia interspersed with patches of leukoplakia
• Speckled erythroplakia.

Question 107.Describe the clinical appearance of homogenous erythroplakia.
Answer. Homogenous erythroplakia appears as bright red, velvety, soft area on the oral mucosa,with an irregular but well-defied margin.

Question 108. What is the clinical appearance of erythroplakia interspersed with patches of leukoplakia?
Answer. This type of erythroplakia presents multiple, irregular erythematous areas in the oral mucosa along with few white leukoplakic patches.

Question 109. What is the clinical appearance of speckled erythroplakia?
Answer. These lesions are similar to the speckled leukoplakias and are characterized by the presence of soft, irregular, raised, erythematous areas in the epithelium with a granular surface. There are some tiny, focal white plaques distributed all over the red surface.

Question 110.What is the histological appearance erythroplakia?
Answer. Histologically erythroplakia often exhibits features of invasive epidermoid carcinoma or carcinoma in situ or at least severe epithelial dysplasia.

Question 111. What is the cause of redness of oral mucosa in erythroplakia?
Answer. Redness in erythroplakia is due to three reasons:

• Atrophy of the epithelium
• Reduction in keratin production
• Connective tissue pegs projecting too high into the epithelium and too close to the surface.

Question 112. Name the lesions included in the differential diagnosis of erythroplakia.
Answer.

• Erosive lichen planus
• Early squamous cell carcinoma
• Atrophic candidiasis
• Kaposi’s sarcoma
• Stomatitis associated with nutritional deficiency or denture irritation
• Contact allergy
• Palatal erythema due to heavy smoking.

Question 113.What is treatment of erythroplakia?
Answer. Deep and wide surgical excision of the lesion is the treatment of choice.

Question 114. What is stomatitis nicotina?
Answer. Stomatitis nicotina (smoker’s keratosis) is a tobacco-related keratosis of the oral mucosa and is commonly seen in the palate of the excessive pipe or cigar smokers.

Question 115. What is the site for stomatitis nicotina?
Answer. The hard and soft palate.

Question 116. Stomatitis nicotina represents two separate abnormalities simultaneously; what are they?
Answer.

• Hyperkeratosis of the epithelium
• Inflammatory swelling of the palatal mucous glands.

Question 117. Describe the clinical features of stomatitis nicotina.
Answer.

• Initially the palatal mucosa becomes red (due to intense heat and irritation from tobacco as a result of pipe smoking)
• Later on it becomes rough and white due to increased thickening and hyperkeratosis
• Few red, dot-like areas surrounded by elevated, white keratotic rings are seen, which represent the inflmed duct openings of the palatal minor salivary glands
• In severe cases, the entire palatal mucosa may become ulcerated.

Question 117a. Is stomatitis nicotina a reversible condition?
Answer. Yes, the condition is reversible and it subsides to a great extent once the pipe smoking habit is discontinued.

Question 117b. A diffuse white lesion having few red dots within, present in the palate of a pipe smoker; it is probably?
Answer. Stomatitis nicotina.

Question 118. Describe the histological features of stomatitis nicotina.
Answer.

• Hyperorthokeratosis and acanthosis of surface epithelium with swelling and inflmmation of the palatal mucous glands.
• Squamous metaplasia of the ductal epithelium of the minor gland.
• Moderate inflammatory cell infitration in the connective tissue adjacent to the palatal minor salivary glands.
• Occasional dysplastic changes may be in the palatal mucosa or in the ductal epithelium of the salivary glands.

Question 119. Define oral submucous firosis (OSF).
Answer. Oral submucous firosis is the most predominant precancerous condition and is characterized by juxta-epithelial inflammatory reaction in the oral mucosa, followed by a firoelastic transformation of the lamina propria leading to mucosal atrophy, rigidity and trismus.

Question 120. Name the common sites of origin of submucous firosis.
Answer. Oral cavity, oropharynx, nasopharynx and esophagus, etc.

Question 121. When the disease (OSF) was fist reported?
Answer. The condition was fist reported by Schwartz (1952) in the name of “Atrophia idiopathica (tropica) mucosae oris”.

Question 122. Who gave the present name to the disease?
Answer. The present name oral submucous firosis was coined by Dr Joshi from Bombay in the year 1953.

Question 123. In which part of the world the disease oral submucous firosis is more prevalent?
Answer. The disease is more common among the people of South-East Asian countries, especially the Indians, Bangladeshis, Nepalese, Burmese, Vietnamese and South Africans, etc.

Question 124. Why it is more prevalent especially in these regions?
Answer. The extreme climatic conditions in these regions and likings of the people for more spicy foods are believed to be the main reasons behind the higher incidence of the disease.

Question 125. What is consequence of malignant transformation in the pre-existing oral submucous firosis?
Answer. Oral submucous firosis may undergo malignant transformation and develop squamous cell carcinoma in the mouth.

Question 126. Enumerate the etiologic factors of oral submucous firosis.
Answer.

• Excessive consumptions of red chillies
• Excessive “areca nut” chewing
• Nutritional defiiency
• Immunological factors
• Genetic factors
• Excessive use of chewable tobacco
• Defiiency of micronutrients.

Question 127. Describe the outline of pathogenesis in oral submucous firosis.
Answer.

Question 128. What is the common age of occurrence of oral submucous firosis?
Answer. The common age of occurence is 20 to 40 years.

Question 129.Oral submucous firosis is more prevalent in which gender?
Answer. It is more prevalent in females.

Question 130.What are the intraoral sites for oral submucous firosis?
Answer. Buccal mucosa, retromolar area, uvula, soft palate, palatal fauces, tongue, lips, etc.

Question 131. What are the other sites for oral submucous firosis besides oral cavity?
Answer. Oropharynx, nasopharynx and esophagus.

Question 132.According to the common belief, oral submucous firosis initiates from which part of the oral cavity?
Answer. It is believed that the disease initiates from the posterior part of the oral cavity and then it gradually spreads to the anterior locations.

Question 133.What are the initial complaints in a patient of oral submucous firosis?
Answer. Burning sensations in the mouth, particularly during taking hot and spicy foods and formation of multiple vesicles over the palate or ulcers in other parts of the oral mucosa.

Question 134.What are the early changes in the mucosa in oral submucous firosis?
Answer. In the initial phases of the disease oral mucosa elicits a “wet-leathery” feeling, there are many petechial spots and mucous membrane is very painful upon palpation.

Question 135.What is the most striking change in the mucosa in advanced oral submucous firosis?
Answer. The most important striking change is the gradual stiffening of the oral mucosa with progressive reduction in the mouth opening (trismus).

Question 136. What are the other signs and symptoms seen in advanced oral submucous firosis?
Answer.

• Blanched opaque (white marble-like) appearance of the oral mucosa
• Occasional presence of leukoplakic or erythroplakic patches in mouth
• Thick vertical white firous bands on buccal mucosa
• Diffiulty in deglutition
• Referred pain in the ear or deafness
• Nasal intonation of voice
• Depapillation of tongue with glossitis
• ‘Bud-like’ shrunken uvula
• Microchelia.

Question 137.How salivary secretion changes in OSF?
Answer. There can be either excessive salivation or decreased salivation (xerostomia).

Question 138. Describe the histopathological features of oral submucous firosis.
Answer.

• The oral epithelium is hyperkeratinized and atrophic; it shows flttening and shortening of rete-pegs
• Variable degrees of cellular atypia or epithelial dysplasia seen
• Underlying connective tissue shows “homogenization” and “hyalinization” of the collagen fiers
• Narrowing or obliteration of the blood vessels due to ‘perivascular firosis’
• Degeneration of the muscle fiers and chronic inflmmatory cell (lymphocyte and plasma cell, etc.) infitration in the stroma.

Question 139.Define sideropenic dysphagia.
Answer. Sideropenic dysphagia occurs primarily due to chronic iron defiiency and this disease is often associated with a high risk of cancer of the oral cavity and the aerodigestive tract.

Question 140. What are the other names given to this condition?
Answer. Paterson-Brown-Kelly syndrome or Plummer-Vinson syndrome.

Question 141. Which category of people often suffer from sideropenic dysphagia?
Answer. Sideropenic dysphagia occurs more often among the middle-aged females.

Question 142. What are the general manifestations of sideropenic dysphagia?
Answer. Patients often suffer from weakness and generalized fatigue along with diffiulty in swallowing, which is a common problem and it occurs due to formation of esophageal webs.

Question 143. Describe the oral manifestations of sideropenic dysphagia.
Answer.

• Angular cheilosis
• Mucosal pallor with atrophy
• Tongue is depapillated, smooth and glossy
• Buccal mucosa is pale and atrophic.

Question 144. What is the common hematological fiding in sideropenic dysphagia?
Answer. Often there is presence of severe iron defiiency anemia.

Question 145. What are the histological changes in oral mucosa in sideropenic dysphagia?
Answer. Histological examination of oral mucosa often exhibits mucosal atrophy and increased mitotic activity.

Question 146.Why there is an increased risk of malignant transformation in oral and aerodigestive tract mucosa in sideropenic dysphagia?
Answer. It is believed that chronic iron defiiency in sideropenic dysphagia causes atrophic changes in the mucosa and also causes suppression of the reparative potential of the mucosal tissue. This results in an increased susceptibility of the tissue towards malignancy when it is subjected to common irritants.

Question 147.Define Lichen planus.
Answer. Lichen planus is a common chronic mucocutaneous disease, which probably arises due to an abnormal immunological reaction and has some tendency to undergo malignant transformation.

Question 148. Describe the brief pathogenesis of lichen planus.
Answer. The disease occurs as a result of an autoimmune reaction developing due to abnormal recognition and expression of basal keratinocytes of the epithelium as foreign antigens by the langerhans cells. This eventually causes ‘liquefaction degeneration’ of basal keratinocytes by cytotoxic T lymphocytes.

Question 149. What is the role of emotional stress in lichen planus?
Answer. Emotional stress often aggravates the condition.

Question 150. Name the areas of body, where cutaneous lesions of lichen planus often occur.
Answer.

• Flexor surface of the wrist and forearms
• Inner aspect of the knee and thigh
• Upper part of the trunk
• Scalp and nail beds
• Genitalia.

Question 151. Name the common sites of oral lichen planus.
Answer. Buccal mucosa, vestibule, tongue, lips and gingiva, etc.

Question 151a. What is the commonest oral site for lichen planus?
Answer. Buccal mucosa.

Question 152. Name the intraoral sites, which are least affected by lichen planus.
Answer. Palate and flor of the mouth are the least affected sites.

Question 153. Name one interesting clinical fiding in lichen planus.
Answer. Many lesions occur bilaterally.

Question 154. Describe the clinical appearance of cutaneous lesions of lichen planus.
Answer. The cutaneous lesions of lichen planus often appear as clusters or diffuse areas of raised, purplish or reddish papules, which are covered by a white glistening scale (or a white keratotic “cap”).

Question 155. What is Koebner phenomenon?
Answer. It refers to the development of skin lesions of lichen planus, which are extending along the areas of injury or irritation.

Question 156. What is the clinical feature of typical oral lichen planus?
Answer. Oral lichen planus clinically exhibits numerous interlacing white keratotic lines, which often produce a typical ‘lace-like’ or ‘annular’ pattern, against an erythematous base. A tiny white elevated dot-like structure is frequently present at the point of intersection of the white lines, which is known as “striae of Wickham”.

Question 157.What is striae of Wickham?
Answer. In oral lichen planus, numerous interlacing white keratotic lines are seen, which intersect with each other; striae of Wickham is the tiny white elevated dot-like structure which is frequently present at this point of intersection of these white lines.

Question 158. Name the common symptoms of oral lichen planus?
Answer. Oral lesions are generally asymptomatic, although few lesions can cause pain and burning sensation while taking hot or spicy foods.

Question 159. Name one typical characteristic of oral lichen planus.
Answer. Lesions normally occur in a bilaterally symmetrical pattern.

Question 160. Name the other mucosal lesions, which may occur simultaneously with oral lichen planus?
Answer. Oral submucous firosis and leukoplakia.

Question 161. Name the different clinical types of oral lichen planus.
Answer. There are several types of oral lichen planus, which are as follows:

• Reticular type
• Erosive type
• Bullous type
• Ulcerative type
• Plaque type
• Atrophic type.

Question 162. What is the clinical appearance of reticular lichen planus?
Answer. It usually consists of numerous raised, thin, snowy-white lines, which produce a lacework or a reticular appearance and the lines radiate from a central erythematous area.

Question 163. Describe the clinical appearance of erosive lichen planus.
Answer. Clinically the lesion presents shallow irregular, erythematous, ulcerated areas in the oral mucosa; which are often covered with a yellowish-white pseudomembrane. A faint white radiating striae is frequently seen at the periphery of the lesion.

Question 164. What is ‘desquamative gingivitis’?
Answer. When erosive lichen planus is confied only to the gingival area, the condition is referred to as ‘desquamative gingivitis’.

Question 165. Describe the symptoms of ‘desquamative gingivitis’.
Answer. Severe pain and burning sensation in the mouth; especially at the time of taking hot or spicy foods or during taking alcoholic beverages.

Question 166. What is the clinical appearance of plaque type of lichen planus?
Answer. The plaque type of lichen planus clinically presents a raised or flttened, white area on the oral mucosa; which often clinically resembles leukoplakia.

Question 167. What is the common location of plaque type of lichen planus in oral cavity?
Answer. Dorsal surface of the tongue.

Question 168. Describe the clinical appearance of atrophic type of lichen planus.
Answer. Atrophic lichen planus clinically presents smooth, poorly defied, erythematous, painful area on the oral mucosa with or without the presence of peripheral radiating striae.

Question 169. What is the clinical appearance of bullous type of lichen planus?
Answer. This rare form of lichen planus is characterized by formation of large vesicle or bullae on the oral mucosa, within an erythematous base. Bullous lichen planus usually have peripheral radiating striae.

Question 170. Describe the clinical appearance of ulcerative type of lichen planus.
Answer. Ulcerative lichen planus is a rare variant of lichen planus presenting with chronic, painful bullae and ulceration; ulcers exist often within the hyperkeratotic areas of existing lesions and sometimes there may be no white radiating striae.

Question 171. Name the common lesions enlisted in the differential diagnosis of lichen planus.
Answer.

• Leukoplakia
• Candidiasis
• Mucous membrane pemphigoid
• Discoid lupus erythematosus
• Syphilis.

Question 172. Describe the histological appearance of lichen planus.
Answer. Histologically lichen planus presents the following features:

• Hyperortho or hyperparakeratinization of the epithelium
• Thickening of the granular cell layer and acanthosis
• Necrosis and liquefaction degeneration of the basal cell layer of the epithelium
• Thick ‘band-like’ infitration of chronic inflmmatory cells at the juxta-epithelial region.

Question 173. What is ‘saw-tooth’ appearance and in which type of lichen planus it is mostly seen?
Answer. In lichen planus, the-rete pegs of the epithelium are often short and pointed; as a result it often produces a so called “saw-tooth” appearance. This appearance is not often seen in histologic sections of oral lesions of lichen planus rather it is more commonly seen in the skin lesions.

Question 174. What happens to the epithelium because of “liquefaction degeneration” of basal cells?
Answer. Due to liquefaction degeneration of the basal cell layer, the epithelium becomes thin and more importantly, the spinus cell layer comes in direct contact with the underlying connective tissue.

Question 175. What is so interesting in the histological picture of erosive lichen planus?
Answer. In erosive lichen planus, the epithelium is often extremely thin and it shows areas of complete loss of rete-peg formation. Moreover, chronic inflmmatory cells may often extend into the middle or upper layer of the epithelium.

Question 176. What are colloid or civatte bodies?
Answer. In lichen planus few round or ovoid, amorphous, eosinophilic bodies are sometimes present within the epithelium, which are known as “colloid or civatte bodies”. They probably originate from apoptotic (dead) basal keratinocytes due to degeneration of basal cells.

Question 177.In lichen planus, a thick ‘band-like’ infiltrations of chronic inflammatory cells are seen; What type of cell they are?
Answer. The cells are predominantly lymphocytes.

Question 178.The thick ‘band-like’ infiltrations of chronic inflammatory cells are seen in which area?
Answer. These are seen at the juxta-epithelial region.

Question 179. What is a macrophage?
Answer. Macrophage is a large white blood cell, occurring principally in connective tissue and in the bloodstream that ingests foreign particles and infectious microorganisms by phagocytosis.

Question 180. Macrophages are produced by the differentiation of which blood cells?
Answer. lt is produced by the differentiation of monocytes in tissues.

Question 181. What is mast cell?
Answer. It is a tissue cell, containing histamine and heparin granules; which has got some structural and functional similarity to the basophil.

Question 182. What are the functions of mast cell?
Answer. It has the main role in precipitating allergy and anaphylaxis; its good role includes wound healing and protection against microorganisms.