leukoplakia

1. Traumatic lesionsTraumatic lesions
of the oral mucosa .of the oral mucosa .
leukoplakialeukoplakia
Soran ihsan hassanSoran ihsan hassan

2. Chemical Injuries of the OralChemical Injuries of the Oral
MucosaMucosa
 Transient nonkeratotic white lesions of the oral mucosaTransient nonkeratotic white lesions of the oral mucosa
are often a result of chemical injuries caused by aare often a result of chemical injuries caused by a
variety of agents that are caustic when retained in thevariety of agents that are caustic when retained in the
mouth for long periods of time, such as aspirin, silvermouth for long periods of time, such as aspirin, silver
nitrate, formocresol, sodium hypochlorite,nitrate, formocresol, sodium hypochlorite,
paraformaldehyde, dental cavity varnishes, acidetchingparaformaldehyde, dental cavity varnishes, acidetching
materials, and hydrogen peroxide.The white lesions arematerials, and hydrogen peroxide.The white lesions are
attributable to the formation of a superficialattributable to the formation of a superficial
pseudomembrane composed of a necrotic surfacepseudomembrane composed of a necrotic surface
tissue and an inflammatory exudatetissue and an inflammatory exudate

3.  Aspirin Burn. Acetylsalicylic acid (aspirin) is a common source ofAspirin Burn. Acetylsalicylic acid (aspirin) is a common source of
burns of the oral cavity.Usually, the tissue is damaged whenburns of the oral cavity.Usually, the tissue is damaged when
aspirin is held in the mucobuccal fold area for prolonged periodsaspirin is held in the mucobuccal fold area for prolonged periods
of time for the relief of common dental painof time for the relief of common dental pain
 Silver Nitrate. Silver nitrate is commonly used by health careSilver Nitrate. Silver nitrate is commonly used by health care
practitioners as a chemical cautery agent for the treatment ofpractitioners as a chemical cautery agent for the treatment of
aphthous ulcers.It brings about almost instantaneous relief ofaphthous ulcers.It brings about almost instantaneous relief of
symptoms by burning the nerve endings at the site of the ulcer.symptoms by burning the nerve endings at the site of the ulcer.
However, silver nitrate often destroys tissue around theHowever, silver nitrate often destroys tissue around the
immediate area of application and may result in delayed healingimmediate area of application and may result in delayed healing
or (rarely) severe necrosis at the application site (Figure 5-5).Itsor (rarely) severe necrosis at the application site (Figure 5-5).Its
use should be discouraged.use should be discouraged.

6. Frictional (Traumatic) KeratosisFrictional (Traumatic) Keratosis
 CLINICAL FEATURESCLINICAL FEATURES
 Frictional (traumatic) keratosis is defined as a whiteFrictional (traumatic) keratosis is defined as a white
plaque with a rough and frayed surface that is clearlyplaque with a rough and frayed surface that is clearly
related to an identifiable source of mechanical irritationrelated to an identifiable source of mechanical irritation
and that will usually resolve on elimination of theand that will usually resolve on elimination of the
irritant. These lesions may occasionally mimic dysplasticirritant. These lesions may occasionally mimic dysplastic
leukoplakia; therefore, careful examination andleukoplakia; therefore, careful examination and
sometimes a biopsy are required to rule out any atypicalsometimes a biopsy are required to rule out any atypical
changeschanges

8.  Histologically, such lesions show varying degrees ofHistologically, such lesions show varying degrees of
hyperkeratosis and acanthosis.Prevalence rates as highhyperkeratosis and acanthosis.Prevalence rates as high
as 5.5% have been reported.Such lesions are similar toas 5.5% have been reported.Such lesions are similar to
calluses on the skin. Traumatic keratosis has never beencalluses on the skin. Traumatic keratosis has never been
shown to undergo malignant transformation.shown to undergo malignant transformation.
 Lesions belonging to this category of keratosis includeLesions belonging to this category of keratosis include
linea alba and cheek, lip, and tongue chewing. Frictionallinea alba and cheek, lip, and tongue chewing. Frictional
keratosis is frequently associated with rough orkeratosis is frequently associated with rough or
maladjusted dentures and with sharp cusps and edgesmaladjusted dentures and with sharp cusps and edges
of broken teeth.of broken teeth.

9. Smokeless Tobacco–InducedSmokeless Tobacco–Induced
KeratosisKeratosis
 Chewing tobacco is an important establishedChewing tobacco is an important established
risk factor for the development of oralrisk factor for the development of oral
carcinoma in the United States.carcinoma in the United States.
 Habitually chewing tobacco leaves or dippingHabitually chewing tobacco leaves or dipping
snuff results in the development of a well-snuff results in the development of a well-
recognized white mucosal lesion in the area ofrecognized white mucosal lesion in the area of
tobacco contact, called smokeless tobaccotobacco contact, called smokeless tobacco
keratosis, snuff dipper’s keratosis, or tobaccokeratosis, snuff dipper’s keratosis, or tobacco
pouch keratosispouch keratosis

11.  While these lesions are accepted as precancerous, they areWhile these lesions are accepted as precancerous, they are
significantly different from true leukoplakia and have a muchsignificantly different from true leukoplakia and have a much
lower risk of malignant transformation.This habit was oncelower risk of malignant transformation.This habit was once
almost universal in the United States and is very common amongalmost universal in the United States and is very common among
certain other populations, most notably in Sweden, India, andcertain other populations, most notably in Sweden, India, and
Southeast Asia.Southeast Asia.
 Smokeless tobacco use among white males in the United StatesSmokeless tobacco use among white males in the United States
has shown a recent resurgence.The estimated proportion of adulthas shown a recent resurgence.The estimated proportion of adult
men in the United States who regularly use “spit” tobacco rangesmen in the United States who regularly use “spit” tobacco ranges
from 6 to 20%.This range is attributed to significant geographic,from 6 to 20%.This range is attributed to significant geographic,
cultural, and gender variations in chewing habits.The cumulativecultural, and gender variations in chewing habits.The cumulative
incidence for smokeless tobacco use was highest for non-incidence for smokeless tobacco use was highest for non-
Hispanic white males.Unfortunately, the habit starts relativelyHispanic white males.Unfortunately, the habit starts relatively
early in life, usually between the ages of 9 and 15 years, and isearly in life, usually between the ages of 9 and 15 years, and is
rarely begun after 20 years of age.rarely begun after 20 years of age.

13. LeukoplakiaLeukoplakia
(leuko-white; plakia-patch)(leuko-white; plakia-patch)
 Oral leukoplakia is defined by the WHO as “a whiteOral leukoplakia is defined by the WHO as “a white
patch or plaque thatpatch or plaque that cannotcannot be characterized clinicallybe characterized clinically
or pathologically as any other disease”.or pathologically as any other disease”.
 Thus a diagnosis byThus a diagnosis by exclusionexclusion..
 The term is strictly aThe term is strictly a CLINICALCLINICAL one and doesone and does notnot
imply a specific histopathologic tissue alteration.imply a specific histopathologic tissue alteration.
 Leukoplakia is the most common oral precancer.Leukoplakia is the most common oral precancer.

14. Leukoplakia: Why is it White?Leukoplakia: Why is it White?
 The clinical color (white) results from aThe clinical color (white) results from a
thickened surface keratin layer (which appearsthickened surface keratin layer (which appears
white when wet) or a thickened spinous layer,white when wet) or a thickened spinous layer,
which masks the normal vascularity (redness) ofwhich masks the normal vascularity (redness) of
the underlying connective tissue.the underlying connective tissue.

16. Leukoplakia: A Premalignant orLeukoplakia: A Premalignant or
Precancerous LesionPrecancerous Lesion
 Risk of malignant transformation is greater in aRisk of malignant transformation is greater in a
leukoplakic lesion than that associated withleukoplakic lesion than that associated with
normal or unaltered mucosa.normal or unaltered mucosa.

17. LeukoplakiaLeukoplakia
In fact, dysplastic epithelium or invasive carcinomaIn fact, dysplastic epithelium or invasive carcinoma
is found in only 5 to 25 % of the biopsy samplesis found in only 5 to 25 % of the biopsy samples
of leukoplakia.of leukoplakia.

18. Leukoplakia: MalignantLeukoplakia: Malignant
Transformation PotentialTransformation Potential
 Overall, the malignant transformation potentialOverall, the malignant transformation potential
of leukoplakia is 4 % (estimated lifetime risk).of leukoplakia is 4 % (estimated lifetime risk).

19. Leukoplakia: How Common Is It?Leukoplakia: How Common Is It?
 Leukoplakia is by far the most common oral precancer,Leukoplakia is by far the most common oral precancer,
accounting for 85 % of such lesions.accounting for 85 % of such lesions.

20. Leukoplakia: Who Develops It?Leukoplakia: Who Develops It?
 There is a strong male predilection (70%),There is a strong male predilection (70%),
except in parts of the country where females useexcept in parts of the country where females use
tobacco products more than males.tobacco products more than males.
 In general, leukoplakia is diagnosed moreIn general, leukoplakia is diagnosed more
frequently now than in the past, probablyfrequently now than in the past, probably
because of enhance awareness.because of enhance awareness.

21. Leukoplakia: EtiologyLeukoplakia: Etiology
 The cause of leukoplakia remainsThe cause of leukoplakia remains unknownunknown..
 Over the years the following have beenOver the years the following have been
considered: tobacco, alcohol, ultravioletconsidered: tobacco, alcohol, ultraviolet
radiation, microorganisms and trauma.radiation, microorganisms and trauma.

22. Etiology of Leukoplakia: The RoleEtiology of Leukoplakia: The Role
of Tobaccoof Tobacco
 The habit of tobacco smoking appears most closelyThe habit of tobacco smoking appears most closely
associated with leukoplakia development.associated with leukoplakia development.
 80 % of patients with leukoplakia are smokers.80 % of patients with leukoplakia are smokers.
 Smokers are much more likely to have leukoplakia thanSmokers are much more likely to have leukoplakia than
non-smokers.non-smokers.
 Heavier smokers have greater numbers of and largerHeavier smokers have greater numbers of and larger
lesions than light smokers.lesions than light smokers.
 A large proportion of leukoplakias in persons who stopA large proportion of leukoplakias in persons who stop
smoking either disappear or become smaller soon aftersmoking either disappear or become smaller soon after
discontinuing the habit.discontinuing the habit.

23. Etiology of Leukoplakia: The RoleEtiology of Leukoplakia: The Role
of Alcoholof Alcohol
 Alcohol, which seems to have a strong synergistic effectAlcohol, which seems to have a strong synergistic effect
with tobacco in oral cancer development, haswith tobacco in oral cancer development, has notnot beenbeen
associated with leukoplakia.associated with leukoplakia.

24. Etiology of Leukoplakia: The RoleEtiology of Leukoplakia: The Role
of Ultraviolet Radiationof Ultraviolet Radiation
 Ultraviolet radiation has been associated withUltraviolet radiation has been associated with
leukoplakia of the vermilion of the lower lip.leukoplakia of the vermilion of the lower lip.
 This leukoplakia is usually associated with actinicThis leukoplakia is usually associated with actinic
cheilosis.cheilosis.

25. Etiology of Leukoplakia: The RoleEtiology of Leukoplakia: The Role
of Microorganismsof Microorganisms
 Treponema pallidumTreponema pallidum has been implicated inhas been implicated in
leukoplakia of the dorsal surface of the tongueleukoplakia of the dorsal surface of the tongue
in patients with syphilis.in patients with syphilis.
 Candida albicansCandida albicans has been demonstratedhas been demonstrated
histologically in the hyperplastic/dysplastichistologically in the hyperplastic/dysplastic
epithelium of lesions termed candidalepithelium of lesions termed candidal
leukoplakia and candidal hyperplasia.leukoplakia and candidal hyperplasia.

26. Etiology of Leukoplakia: The RoleEtiology of Leukoplakia: The Role
of Microorganisms Continuedof Microorganisms Continued
 Human papillomavirus (HPV), particularlyHuman papillomavirus (HPV), particularly
subtypes 16 and 18, have been identified insubtypes 16 and 18, have been identified in
some oral leukoplakias.some oral leukoplakias.
 However, HPV has also been demonstrated inHowever, HPV has also been demonstrated in
normal oral epithelial cells.normal oral epithelial cells.

27. Etiology of Leukoplakia: The RoleEtiology of Leukoplakia: The Role
of Traumaof Trauma
 Several keratotic lesions, which until recentlySeveral keratotic lesions, which until recently
have been viewed as variants of leukoplakia, arehave been viewed as variants of leukoplakia, are
now considerednow considered notnot to be premalignant.to be premalignant.
 Included in this group are lesions termedIncluded in this group are lesions termed
nicotine stomatitis and frictional keratosis.nicotine stomatitis and frictional keratosis.
 The keratoses are readily reversible after theThe keratoses are readily reversible after the
elimination of the trauma or chronic irritation.elimination of the trauma or chronic irritation.

28. Leukoplakia: Clinical FeaturesLeukoplakia: Clinical Features
 Individual lesions vary in clinical appearance andIndividual lesions vary in clinical appearance and
tend to change over time.tend to change over time.
 Early/mild lesions usually appear as slightlyEarly/mild lesions usually appear as slightly
elevated gray or gray-white plaques, which mayelevated gray or gray-white plaques, which may
appear translucent, fissured or wrinkled and areappear translucent, fissured or wrinkled and are
typically soft and flat.typically soft and flat.
 Early/mild lesions are usually well demarcatedEarly/mild lesions are usually well demarcated
but may blend into the surrounding normalbut may blend into the surrounding normal
mucosa.mucosa.

32. Leukoplakia: HistopathologicLeukoplakia: Histopathologic
FeaturesFeatures
 Leukoplakia is characterized by a thickenedLeukoplakia is characterized by a thickened
keratin layer (hyperkeratosis) with or without akeratin layer (hyperkeratosis) with or without a
thickened spinous layer (acanthosis).thickened spinous layer (acanthosis).
 Some leukoplakias show surface hyperkeratosisSome leukoplakias show surface hyperkeratosis
but with atrophy or thinning of the underlyingbut with atrophy or thinning of the underlying
epithelium.epithelium.
 Variable numbers of chronic inflammatory cellsVariable numbers of chronic inflammatory cells
are typically noted within the underlyingare typically noted within the underlying
connective tissue.connective tissue.

33. Leukoplakia: HistopathologicLeukoplakia: Histopathologic
Features ContinuedFeatures Continued
 While most leukoplakias show no dysplasia onWhile most leukoplakias show no dysplasia on
biopsy, some 5 to 25 % of the cases do showbiopsy, some 5 to 25 % of the cases do show
evidence of epithelial dysplasia (or squamous cellevidence of epithelial dysplasia (or squamous cell
carcinoma).carcinoma).
 The histopathologic alterations of dysplasticThe histopathologic alterations of dysplastic
epithelial cells are outlined in the next slide.epithelial cells are outlined in the next slide.

34. Histopathologic Alterations ofHistopathologic Alterations of
Dysplastic Epithelial CellsDysplastic Epithelial Cells
 Enlarged nuclei and cells.Enlarged nuclei and cells.
 Large and prominent nucleoli.Large and prominent nucleoli.
 Increased nuclear-cytoplasmic ratio.Increased nuclear-cytoplasmic ratio.
 Hyperchromatic (dark-staining) nuclei.Hyperchromatic (dark-staining) nuclei.
 Pleomorphic (abnormally shaped) nuclei and cells.Pleomorphic (abnormally shaped) nuclei and cells.
 Dyskeratosis (premature keratinization)Dyskeratosis (premature keratinization)
 Increased mitotic activity and abnormal mitotic figuresIncreased mitotic activity and abnormal mitotic figures

35. Histopathologic Alterations ofHistopathologic Alterations of
Dysplastic Epithelium ContinuedDysplastic Epithelium Continued
 Bulbous or teardrop-shaped rete ridges.Bulbous or teardrop-shaped rete ridges.
 Loss of polarity (lack of progressive maturationLoss of polarity (lack of progressive maturation
toward the surface).toward the surface).
 Keratin or epithelial pearls.Keratin or epithelial pearls.
 Loss of typical epithelial cell cohesiveness.Loss of typical epithelial cell cohesiveness.

41. Erythroplakia: DefinitionErythroplakia: Definition
 Erythroplakia is defined as a red patch thatErythroplakia is defined as a red patch that
cannotcannot be clinically or pathologically diagnosedbe clinically or pathologically diagnosed
as any other condition.as any other condition.
 Erythroplasia is occasionally used as a synonymErythroplasia is occasionally used as a synonym
for erythroplakia although it was originally usedfor erythroplakia although it was originally used
by Queyrat to describe a precancerous red lesionby Queyrat to describe a precancerous red lesion
of the penis.of the penis.

42. ErythroplakiaErythroplakia
 Almost all true erythroplakias demonstrateAlmost all true erythroplakias demonstrate
significant epithelial dysplasia, carcinomasignificant epithelial dysplasia, carcinoma in situin situ
or invasive squamous cell carcinoma.or invasive squamous cell carcinoma.
 The cause (s) of erythroplakias are unknown butThe cause (s) of erythroplakias are unknown but
presumed to be the same as those associatedpresumed to be the same as those associated
with squamous cell carcinoma.with squamous cell carcinoma.

43. ErythroplakiaErythroplakia
 Erythroplakia is far less common thanErythroplakia is far less common than
leukoplakia but has a much greater potential toleukoplakia but has a much greater potential to
be severely dysplastic at the time of biopsy or tobe severely dysplastic at the time of biopsy or to
develop invasive malignancy at a later time.develop invasive malignancy at a later time.
 Erythroplakia can occur in conjunction withErythroplakia can occur in conjunction with
leukoplakia and has been found concurrentlyleukoplakia and has been found concurrently
with a large proportion of early invasive oralwith a large proportion of early invasive oral
carcinomas.carcinomas.

44. Erythoplakia: Clinical FeaturesErythoplakia: Clinical Features
 It is predominantly a disease of older males with a peakIt is predominantly a disease of older males with a peak
prevalence between the ages of 65 and 74 years.prevalence between the ages of 65 and 74 years.
 The floor of the mouth, tongue and soft palate are theThe floor of the mouth, tongue and soft palate are the
most commonly involved sites.most commonly involved sites.
 Multiple lesions may occur.Multiple lesions may occur.
 Early erythroplakias appear as well-demarcatedEarly erythroplakias appear as well-demarcated
erythematous macules or plaques with a soft velvetyerythematous macules or plaques with a soft velvety
texture.texture.
 Unfortunately, it is usually asymptomatic.Unfortunately, it is usually asymptomatic.

47. Plummer-Vinson SyndromePlummer-Vinson Syndrome
(Paterson-Kelly Syndrome)(Paterson-Kelly Syndrome)
 This is an uncommon condition characterizedThis is an uncommon condition characterized
by an iron-deficiency anemia with an associatedby an iron-deficiency anemia with an associated
glossitis and dysphagia.glossitis and dysphagia.
 It is of significance because of its associationIt is of significance because of its association
with a high frequency of oral and esophagealwith a high frequency of oral and esophageal
squamous cell carcinoma.squamous cell carcinoma.

48. Plummer-Vinson Syndrome: ClinicalPlummer-Vinson Syndrome: Clinical
Features ContinuedFeatures Continued
 Another sign involves the nails, which are oftenAnother sign involves the nails, which are often
spoon-shaped (koilonychia) and may be brittle.spoon-shaped (koilonychia) and may be brittle.
 The symptoms of anemia such as fatigue,The symptoms of anemia such as fatigue,
shortness of breath and weakness often lead theshortness of breath and weakness often lead the
patient to seek medical care.patient to seek medical care.

49. Plummer-Vinson Syndrome:Plummer-Vinson Syndrome:
Laboratory & Microscopic FeaturesLaboratory & Microscopic Features
 Hematologic studies show a hypochromic,Hematologic studies show a hypochromic,
microcytic anemia consistent with iron-microcytic anemia consistent with iron-
deficiency anemia.deficiency anemia.
 Biopsy of the oral mucosa reveals epithelialBiopsy of the oral mucosa reveals epithelial
atrophy with submucosal inflammation.atrophy with submucosal inflammation.
 In advanced case one may see epithelial atypia,In advanced case one may see epithelial atypia,
dysplasia, carcinomadysplasia, carcinoma in situin situ or frank squamousor frank squamous
cell carcinoma.cell carcinoma.

50. Plummer-Vinson Syndrome:Plummer-Vinson Syndrome:
Treatment and PrognosisTreatment and Prognosis
 Treatment centers on correcting the iron-Treatment centers on correcting the iron-
deficiency anemia and if this is successful, thedeficiency anemia and if this is successful, the
glossodynia and esophageal symptoms improve.glossodynia and esophageal symptoms improve.
 Patients should be evaluated periodically forPatients should be evaluated periodically for
oral, pharyngeal and esophageal cancer.oral, pharyngeal and esophageal cancer.
 The frequency of malignancy in these patientsThe frequency of malignancy in these patients
has ranged from 5 to 50 % in the literature.has ranged from 5 to 50 % in the literature.

53. BENIGN TUMORSBENIGN TUMORS
 pyogenic granuloma is a highly vascular pedunculated lesion,pyogenic granuloma is a highly vascular pedunculated lesion,
usually occurring in the gingiva of children, young adults, and,usually occurring in the gingiva of children, young adults, and,
commonly, pregnant women (pregnancy tumor). The surface ofcommonly, pregnant women (pregnancy tumor). The surface of
the lesion is typically ulcerated and red to purple in color.the lesion is typically ulcerated and red to purple in color.

54. Squamous cell carcinoma

55. Schematic representation of the sites of origin of
squamous cell carcinoma of the oral cavity, in
numerical order of frequency.

57. THANK YOU