Oral cancer awareness

2. Dr. U. S. Pal
MDS,FICOI,DICOI,(USA)
Professor, Maxillofacial Surgery,
Superintendent (dental) GM & AH
K. G. Medical University , Lucknow
Editor in chief - National Journal of
Maxillofacial Surgery
AWARENESS OF ORAL
CANCER

3. 1. Introduction
2. Epidemiology
3. Cause and prevention
4. Diagnosis
5. PMD (Potentially malignant disorders)
6. Recent advances
7. Conclusion

4. Cancer
• An abnormal growth of cells which tend to
proliferate in an uncontrolled way and, in some
cases, to metastasize (spread)
• Cancer can involve any tissue of the body and
have many different forms in each body area.
Most cancers are named for the type of cell or
organ in which they start
• If a cancer spreads (metastasizes), the new
tumor bears the same name as the original
(primary) tumor

5. 1985 2000 2020
3.9 million
5.4 million
9.3 million
3.7 million
4.7 million
6 million
Chart Title
Developing countries Developed Countries
The Global Cancer Burden is shifting to Developing World
Sarin, caBIG 2009

6. INDIAN SCENARIO
• India has largest number of oral cancer cases
• Fastest rise in tobacco related deaths per year
• Gutka and other non smoking tobacco products are
major contributory factors
• In small positive move SC recently banned sale of
tobacco products from March 2011

7. INCIDENCE
INDIA:
• 2.5 millions new cancer cases/year
• 58,000 die /year
• India has highest number of the oral & throat
cancers in the word
• Every third oral cancer patient in the world is
from India

8. National Institute of Health and Family Welfare
(NIHFW),- India alone accounted for 86 percent of the
total oral cancer figure across the world.
The global incidence of oral cancer is 5,00,000 cases per
year with mortality of 2,70,000 cases.
The incidence of oral cancer in India is 40 % among all
cancer and about 1,00,000.
Oral cancer is responsible for 7% of all cancer deaths in
males while it is3 % in females.

9. Causes of Cancer
• Carcinogens
• Age
• Genetic make up
• Bodyweight, diet and physical activity
• Immune System
• Tobacco smoke
• Sun rays
• Natural and man made radiation
• Work place hazards
• Asbestos
• Viruses
• Bacterial Infection

10. Preventive strategies in cancer
Individual approach
Clinician’s role
Diet and chemopreventive agents
Community and State interventions
Mass media and counter advertising

11. Numerous prospective studies
suggest that
people with higher intake of
Fruits and Vegetables or blood
antioxidant concentrations
have lower risk of some cancers,
coronary heart disease and stroke.
Zino, et al. BMJ 314:1787, 1997.
Diet and Health Risk

12. Preventable Causes of Cancer
• 30% to 40% of all cancers related to diet,
exercise, and weight.
– 20% related to low intake of vegetables and fruits.
– 4%-14% attributable to obesity in men.
– 14%-19% attributable to obesity in women.
• 30% of cancers caused by tobacco.
Food, Nutrition and the Prevention of Cancer: a global perspective, AICR. 1997

13. Dietary Fat and Cancer
• Tennenbaum, 1942, (Cancer Research):
Diet high in fat could promote tumor growth
in animal models.
• National Academy of Science, 1982:
Recommended reduction in fat intake to
30% of calories.

14. Fruit and Vegetable Consumption
and Cancer
• Doll and Peto ( JNCI-1981):
35% all cancers in US may be preventable by
alteration in diet.
• Fruits and vegetables contain antioxidants and
minerals and are good sources of fibre, potassium,
carotenoids, vitamin C, folate and other vitamins.
• World Cancer Research Fund and American
Institute for Cancer Research-1997: found that-
“There is strong and consistent pattern that diets high
in vegetables and fruits decrease the risk of many
cancers”.

15. American Cancer Society:
Dietary Guidelines for Cancer Prevention
• Diets low in fat and high in fibres-
– at least 5 servings of F & V daily.
• Choose whole grains instead of refined, processed grains.
• Limit consumption of red meat, especially processed meat
and those high in fat.
• Select food that help achieve and maintain a healthy weight
• Limit salt and sugar intake.
• Limited consumption of alcoholic beverages.

16. American Institute for Cancer Research
“Diet and Health Guidelines”
for Cancer Prevention
• Choose a diet rich in a variety of plant- based foods.
• Eat plenty of vegetables and fruits.
• Maintain a healthy weight and be physically active.
• Drink alcohol only in moderation, if at all.
• Select foods low in fat and salt.
• Prepare and store foods safely.
• And, always remember... “Do not use tobacco in any form”.

17. REDUCTION OF CANCER
RISK
• Stopping smoking greatly reduces smoking
related cancers
• A doctor’s study showed half reduction at 50 and
almost all at 30
• It is never too late to quit
• A study showed that who quit even in 60’s can
experience health benefits

18. CHEMICALS IN TOBACCO SMOKE
• Several studies concluded that smokers can
have
– Twice as much cadmium in their blood
– Four times as much polonium-210 in their lungs
– Ten times as much benzene in their breath
– Ten times as much arsenic in their blood
• For most of us much of our exposure comes from
breathing in tobacco smoke

19. TOBACCO AND ALCOHOL
• Alcohol worsen the effect of smoking
• Increases the risk of mouth, esophageal and liver
cancers
• Studies indicate while alcohol does not cause
stomach cancer, it can worsen the risk in
smokers
• Smoking also interacts with many other cancer
risk factors

20. SECOND-HAND SMOKING
• Also causes cancer and kills thousands people every
year
• Many of these chemicals are present, even in higher
concentration than in primary inhalers
• One study estimates passive smoking may kill over
11,000 people each year in UK from cancer and other
diseases
• Second-hand smoking also causes health related
problems as in primary smokers

21. SECOND-HAND SMOKING IN
CHILDRENS
• Particularly at risk because they breath faster
• Similar risk of lung cancer development as in adults
• One study showed children in house where both parents
smoke have a 72% higher risk of respiratory disease
• Another study showed increase risk of bladder cancer as
passive smokers

22. SMOKING IN PREGNANT
WOMEN
• Smoking hinders the blood flow to the
placenta
• Reduces the nutrients that reach the
baby
• Lighter babies than non-smokers

23. SMOKELESS TOBACCO AND
CANCER
• Particularly in South Asian countries
• Greatly increases risk of oral cancer and may cause
pancreatic cancer
• Most dangerous chemicals in smokeless tobacco are
called Tobacco-specific nitrosamines (TSNAs)
• Some studies showed amount of nicotine absorbed
from smokeless tobacco is 3-4 times greater than the
cigarette

24. TOBACCO AND NICOTINE
• About 4000 chemicals, 55 known carcinogen
• Most notable are
Polycyclic aromatic hydrocarbons
N-nitrosamines
Miscellaneous organic compounds
• They form DNA adduct formation, gene mutation and
other sequential events
• Balance between detoxification and metabolic
activation

25. NICOTINE
• Itself not carcinogenic
• Addiction exposes the user to carcinogens
• Minimum of 3 out of 7 diagnostic symptoms
tolerance
withdrawal
greater use than intended
persistent desire to quit
great amount of time spent for smoke
activity reduced
continued smoking despite knowledge of harm

26. SIGN AND SYMPTOMS
Indurated ulcer or crust
Lumps or swelling
Bleeding
Malfiting denture
Restrictions of tongue movements
Change in sensation
Change in taste

27. Process of identifying “at risk” lesions is
fundamental for diagnosis and treatment planning.
Outstanding exception - symptoms and clinical
course at the onset are insidious and mild Pain
and tenderness may be absent for a period of
weeks , sometimes months.

28. Some oral cancers initiate as a De Novo lesion
while some are preceded by Oral premalignant
lesions and conditions.
Practitioners must be able to recognize lesions at
particular risk and several features which help to
assess the likelihood of malignant transformation.

29. HISTORY - DEFINITIONS
• A premalignant lesion is “A morphologically
altered tissue in which oral cancer is more likely to
occur than in its apparently normal counterpart”
-WHO workshop 1978
• Premalignant condition is ‘a generalized state
associated with a significantly increased risk of
cancer’.
-WHO workshop 1978

30. Premalignant lesions Premalignant
conditions
Leukoplakia Oral submucous fibrosis
Erythroplasia Oral lichen planus
Leukokeratosis nicotina
palatinae
Actinic keratosis
Candidiasis Syphilis
Carcinoma in situ Discoid lupus erythematosus
Sideropenic dysphagia

31. PMD (Potentially malignant disorders)
“It is a group of disorders of varying etiologies,
usually tobacco characterized by mutagen associated,
spontaneous or hereditary alterations or mutations in
the genetic material of oral epithelial cells with or
without clinical and histomorphological alterations
that may lead to oral squamous cell carcinoma
transformation”.
(Ref. -Oral potentially malignant disorders: Precising the definition)
- Oral Oncology journal (2012)

32. NEW CLASSIFICATION FOR ORAL
POTENTIALLY MALIGNANT DISORDERS
CLASSIFIED OPMD INTO 4 GROUPS:
Group I: Morphologically altered tissue in which external
factor is responsible for the etiology and malignant
transformation.
Group II: Morphologically altered tissue in which chronic
inflammation is responsible for malignant transformation
(chronic inflammation mediated carcinogenesis).

33. Group III: Inherited disorders that do not necessarily
alter the clinical appearance of local tissue but are
associated with a greater than normal risk of PMD or
malignant transformation.
Group IV: No clinically evident lesion but oral cavity
is susceptible to Oral squamous cell carcinoma.
SARODE, SARODE, KARMARKAR, TUPKARI
(Ref - Oral Oncology xxx, 2011)

34. Group I: Morphologically altered tissue in which external
factor is responsible for the etiology and malignant
transformation.
1. Habit related
a. Tobacco associated lesions
• Leukoplakia
• Tobacco pouch keratosis
• Stomatitis palatine nicotini
b. Betel nut associated
• Oral submucous fibrosis
c. Sanguinaria-associated keratosis

35. 2. Non-habit related
• Actinic cheilosis
• Chronic candidiasis
Certain strains of Candida have been shown to
produce nitrosamines a chemical carcinogen
(external factor) and hence, candidiasis is included
under Group I.

36. Group II: Morphologically altered tissue in which
chronic inflammation is responsible for malignant
transformation
(chronic inflammation mediated carcinogenesis).
Group II a. Chronic inflammation caused by internal
derangement.
• 1. Lichen planus
• 2. Discoid lupus erythematosus

37. II b: Chronic inflammation caused by external factors.
1. Chronic mucosal trauma
2. Lichenoid reactions
3. Poor oral hygiene
4. Chronic infections
• Chronic bacterial infections
• Chronic viral infections
• Chronic fungal infections
5. Other pathologies associated with prolonged
untreated chronic inflammation of the oral cavity.

38. • Group III: Inherited disorders that do not necessarily
alter the clinical appearance of local tissue but are
associated with a greater than normal risk of PMD or
malignant transformation.
1. Inherited cancer syndromes
• Xeroderma pigmentosum
• Ataxia telangiectasia
• Fanconi’s anemia
• Li Fraumeni syndrome

39. 2. Dyskeratosis congenita
3. Epidermolysis bullosa
4. White sponge nevus
5. Darier’s disease
6. Hailey–Hailey disease

40. Group IV: No clinically evident lesion but oral
cavity is susceptible to Oral squamous cell carcinoma.
1. Immunosupression
• AIDS
• Immunosupression therapy (for malignancy or
organ transplant)
2. Alcohol consumption and abuse
3. Nutritional deficiency
• Sideropenic dysphagia
• Deficiency of micronutrients

41. ORAL SUBMUCOUS
FIBROSIS

42. • This condition was first described by Joshi
(1952) and by Schwatz among East Indian
Women.
• This is an insidious chronic disease affecting
any part of oral cavity including pharynx. It
is considered to be POTETIALLY
MALIGNANT DISORDER .

43. (J.J Pindborg and Sirsat 1966)
“ It is an insidious chronic disease affecting any part of
the oral cavity and sometimes the pharynx. Although
occasionally preceded by or associated with vesicle
formation, it is always associated with juxta-epithelial
inflammatory reaction followed by a fibro-elastic changes
of the lamina propria with epithelial atrophy leading to
stiffness of the oral mucosa and causing trismus and
inability to eat.”
DEFINITION

44. EPIDEMIOLOGY
• OSMF is a crippling fibrotic disorder seen commonly in
India and Indian subcontinent. Sporadic cases are seen in
Malaysia, Nepal, Thailand and South Vietnam.
• Population between 20 to 40 years of age are most
commonly affected .
• Incidence of OSMF in India is 0.2-0.5% of population.

45. Etiology of OSMF:
Exact etiology is unknown. The predisposing factors are,
1. Chronic Irritation
- Chilies, Lime, Areca nut, Tobacco.
2. Defective iron metabolism
3. Bacterial Infection
4. Collagen disorder
5. Immunological disorders
7. Genetic disorder.

46. Chronic irritation:-
• Pathogenesis of OSMF lies in the continuous action of mild
irritants.
Chillies:-
• "Capsaicin" an active extract from capsicum.
• The active principle irritants of chillies (Capsicum annum
and Capsicum frutescence) .

47. Areca nut –
It contains,
• ARECOLINE, ARECAIDINE
-Fibroblast proliferation
-Stimulate collagen synthesis
• TANNIN, CATHECHIN-
- Makes collagen fibrils resistant to
collagenase.

48. CLINICAL FINDINGS
• The data regarding the sex predilection is conflicting.
Earlier it was thought to be common in females.
• But at present, study ratio shows 2.3: 1=M:F
• Age group - 2nd to 4th decade of life.

49. Prodromal symptoms
Initial symptoms Later
Burning sensation on eating
spicy food
Blisters on the palate
Ulceration or recurrent
stomatitis
Defective gustatory sensation
Dryness of mouth.
Difficulty in opening mouth
Inability to whistle, blow
Difficulty in swallowing
Referred pain to the ear
Changes in tone of the voice
due to vocal cord involvement
Sometimes deafness due to
occlusion of eustachian tubes

50. COMMON SITES INVOLVED-
• Buccal mucosa, faucial pillars, soft palate, lips and hard palate.
• The fibrous bands in the buccal mucosa run in a vertical
direction, sometimes so marked that the cheeks are almost
immovable.
• In the soft palate the fibrous bands radiate from the
pterygomandibular raphe or the faucial pillars and have a scar
like appearance.

51. • The uvula is markedly involved, shrinks and appears as a
small fibrous bud.
• The faucial pillars become thick, short, and extremely hard.
• The tonsils may be pressed between the fibrosed pillars.
• The lips are often affected and on palpation, a circular band
can be felt around the entire lip mucosa.
• When gingiva is affected, it is fibrotic, blanched and devoid
of its normal stippled appearance.

52. SHRUNKEN UVULA GIVING HOCKEY STICK
APPEARANCE

53. PALE AND BALD TONGUE

54. Trismus

55. Staging of OSMF:
• Stage I : Stage of stomatitis & vesiculation
• Stage ll : Stage of fibrosis
• Stage III :Stage of sequelae and complication
(Ref -Pindborgh JJ-1989)

56. Stage I : Stomatitis & vesiculation
Stomatitis includes erythmatous mucosa,
vesicles, mucosal ulcers,melanotic mucosal
pigmentation.

57. Stage II: (Fibrosis):-
• There is inability to open mouth completely and stiffness in
mastication. As disease advances there is difficulty in blowing
out cheek & protruding tongue. Sometimes pain in ear and
speech is affected. On examination there in increasing amount
of fibrosis in the submucosa. This causes blanching of mucosa.
• Lips & checks become stiff & lose their normal resistance.
Shortening & disappearance of uvula in advanced cases.
• Mucosa of floor of mouth show blanching & stiffness

58. Stage III (Sequelae & Complication)
• Patient presents with all the complaints as in stage II. Also
there may be evidence of leukoplakia.
• Changes in mucosa are whitish or brownish black.
• Pindborg et al (1967) found that OSMF was found in 40%
cases of oral cancer than in general population (1.2%).

59. Recent classification for OSMF
- Chandramani More et al 2011• Clinical staging –
S1 -Stomatitis or blanching of oral mucosa
S2 –Presence of fibrous bands over buccal
mucosa, oropharynx with or without
stomatitis.
S3 - Presence of fibrous bands over buccal
mucosa, oropharynx and any part of oral
cavity with or without stomatitis.

60. • S4 a –
Anyone of above stage with potentially
malignant disorders
Eg- leukoplakia, erythroplakia.
• S4 b –
Anyone of above stage with oral
carcinoma

61. Recent classification for OSMF
- Chandramani More et al 2011
Functional staging -
M1- Interincisal mouth opening upto or > 35 mm
M2- Interincisal mouth opening between 25-35 mm
M3 - Interincisal mouth opening between 15-25 mm
M4 - Interincisal mouth opening <15 mm

62. DIAGNOSIS IS BASED ON :
 Clinically appreciable blanching and pallor.
 Palpable bands and restriction-of mouth opening.
 Severe burning sensation of mouth, aggravated by use of
even moderate spicy food.
 Biopsy report.

63. Histopathological findings -
• Atrophic Oral epithelium.
• Loss of rete pegs .
• Epithelial atypia may be observed.
• Hyalinization of collagen bundles.
• Fibroblasts decreased and blood vessels obliterated.

64. MANAGEMENT -
Various modalities of treatment have been tried.
1.Restriction of habits/ Behavioral therapy.
2.Non-surgical therapy.
3.Surgical therapy.
4.Oral Physiotherapy.

65. Restriction of habits/behavioral therapy-
 The consumption of pan, betel nut, chillies, spices, &
commercially available, pan masalas, guthkas with or
without tobacco is increasing in India. So people should be
encouraged to stop these habits.
 Affected patients should be explained about the disease and
possible malignant potential of OSMF.
 Possible irritants should be removed.
 Nutritional supplements.

66. NON-SURGICAL THERAPY:-
• Antioxidants
• Intralesional injections of hyaluronidase. Hydrocortisone
• Use of Placentrix 2ml solution at interval of 3 days.
• Topical application -
1. Triamcinolone acetonide
2. 5 Fluorouracil

67. Systemic administration of immunomodulators -
• Levamisole 150mg for 3 weeks ,orally
• Dapsone 75 mg O.D for 90 days, orally

68. SURGICAL TREATMENT -
Fibrotomy (scalpel, electrocautery, laser)
Coronoidectomy & Temporalis myotomy
• Extraction of third molars
Reconstruction
(Bilateral nasolabial flaps, Pedicled tongue flaps, Buccal fat pad, Split
thickness skin grafting, Collagen membrane & Temporalis fascia)
(Ref -Oral submucous fibrosis, a new concept in surgical management. Report of
100 cases.J. N. Khanna & N. N. Andrade: IJOMS)

69.  Cryosurgery
 Laser treatment

70. Leukoplakia
Oral leukoplakia, as defined by the WHO, is
“ A predominantly white lesion of the oral mucosa
that cannot be characterised as any other definable
lesion.”
(Ref – WHO workshop 2012)
J Oral Pathol Med (2012) 36: 575–80

71. Etiology -
• The exact etiology is unknown.
• But some predisposing factors can be identified
that are
• PREDISPOSING FACTORS ARE BEST
REMEMBERED AS 6 S
Smoking , Spirit , Sharp tooth , Spicy food ,
Syphilis, Sepsis

72. A. SMOKING
B. CHEWING
Most important causative factor
• Roed-Petersen & co-workers found a strong correlation between bidi
smoking and presence of leukoplakia in the residents of Bombay. 20% of the
smokers in the age group of 60-89yrs had leukoplakia whereas 5% of non-
smokers of the same age group were affected.
• Pindborg & colleagues pointed out that tobacco produces a specific effect on
the oral mucosa, leading to a characteristic appearance of pumice stone .
Similar lesions are seen in patients who apply snuff to the labial sulcus.
TOBACCO

73. • Alcohol- Heavy consumption of alcohol is second most
important risk factor, it acts synergistically with tobacco.
• Candida infection- Candida albicans infection (chronic
hyperplastic candidiasis) may play a role in the etiology of
leukoplakia.
• Human papilloma viruses-HSV1, HPV, HHV6, HHV8
(HHV = Human Herpes Viruses)
(HSV = Herpes Simplex Viruses)
(HPV = Human Papilloma Virus)

74. • Syphilis :
Hobaeck, Cooke and Renstrup found that this has a
minor role. There is a higher incidence of leukoplakia
among patients of syphilitic glossitis than non-
syphilitic background.
• Vitamin Deficiency :
Vit A deficiency will cause metaplasia and
keratinization of epithelial structures (particularly
glands).

75. CLINICAL FEATURES
• Male predilection
• Mostly occurs in 4th to 7th decade of life.
• Oral leukoplakias are found on the Upper and lower
alveolus(36%) buccal mucosa(22 %) , lips (11%),
palate (11%), floor of mouth (9%), gingiva(8%),
Tongue(7%), retromolar trigone(6%).
(Ref -Oral potentially malignant disorders: Precising the definition)
Otorhinolaryngology clinics – may-sept. 2009

76. Leukoplakia

77. • Leuko means white & Plakia means plaque.( Greek term)
• The term is strictly a clinical one and does not imply a
specific histopathologic tissue alteration.
• It makes the diagnosis dependent not so much on definable
appearances but on the exclusion of other entities that
appear as oral white lesions.

78. Clinical Types
1. Homogenous
2. Non-homogenous

79. HOMOGENOUS-
• Uniform white patch lesion with smooth or
corrugated surface sometimes, slightly raised
mucosa. Usually plaque like, some are smooth,
may be wrinkled or criss-crossed by small crack
or fissure.
• Malignant transformation – 1 to 7%.
• Types –
1. Smooth
2. Furrowed
3. Ulcerative

80. NON-HOMOGENOUS LEUKOPLAKIA
TYPES -
1. Ulcerative or Erosive
2. Verrucous (proliferative verrucous leukoplakia) or
Nodular
3. Speckled (High malignant transformation)
(Ref- WHO workshop 1994)

81. • Ulcerative- Red ulcerative lesion (Atrophic epithelium ) with small white
specks or nodules over it.
• Verrucous -Warty surface (white lesion with hyperplastic surface) or
Heaping up of the surface or like a nodule on an erythematous background.
white lesion with a granular surface is associated with candida.
• Speckled- Mixed red and white patches on an irregular surface.

82. • Hairy leukoplakia is a condition that is characterised by
irregular white patches on the side of the tongue and
occasionally elsewhere on the tongue or in the mouth.
Etiology -
It is a form of leukoplakia often arises in response to
chronic irritation. Hairy leukoplakia is associated with
Epstein-Barr virus (EBV) and occurs primarily in HIV-
positive individuals.
Hairy leukoplakia

83. Clinical features
• Male predilection
• Most common in 40 – 60 years of age
(Recent studies show higher incidences in young
adults)
It occurs on the lateral
margins of the tongue
often bilaterally. The
lesions are white,
sometimes corrugated
and may be proliferative
to produce a shaggy
carpet like appearance

84. Clinical Staging
• A clinical staging system for oral leukoplakia
(OL-system) on the lines of TNM staging was
recommended by WHO in 2005 taking the size (L)
and the histopathological features (P) of the lesion
into consideration.

85. Clinical Staging
• Lx: Size not specified.
• L1: Single or multiple lesions together <2 cm.
• L2: Single or multiple lesions together 2-4 cm.
• L3: Single or multiple lesions together >4 cm.
• Px: Epithelial dysplasia not specified.
• P0: No epithelial dysplasia.
• P1: Mild to moderate epithelial dysplasia.
• P2: Severe epithelial dysplasia.
• Stage I: L1 P0.
• Stage II: L2 P0.
• Stage III: L3 P0 or L1/ L2 P1.
• Stage IV: L3 P1 or Lx P2.

86. Histopathology
• Leukoplakia is purely a clinical terminology and
histopathologically it is reported as epithelial
dysplasia.
• WHO in 2005 proposed five grades of epithelial
dysplasia based on architectural disturbances and
cytological atypia.

87. HISTOLOGICAL GRADING OF LEUKOPLAKIA
• 1. Squamous Hyperplasia –
• 2. Mild Dysplasia – better prognosis.
• 3. Moderate Dysplasia.
• 4. Severe Dysplasia.
• 5. Carcinoma in-situ – poor prognosis.
• It has been recently proposed to modify the above 5-tier
system into a binary system of ‘high risk’ and ‘low risk’
lesions to improve clinical management of these lesions.

88. Diagnosis
• A provisional diagnosis of leukoplakia is made
when a predominantly white lesion at clinical
examination cannot be clearly diagnosed as any
other disease or disorder of the oral mucosa .
A biopsy is mandatory.
A definitive diagnosis is made when any
aetiological cause other than tobacco/areca nut use
has been excluded and histopathology has not
confirmed any other specific disorder.

89. Differential diagnosis
• White sponge nevus
• Acute pseudomembranous candidiasis
• Leukoedema
• Lichen planus (plaque type)

90. TREATMENT AND PROGNOSIS
• The first step in treatment is to arrive at a definitive
histopathologic diagnosis.
• Therefore, a biopsy is mandatory and will guide the
course of treatment. Tissue to be obtained for biopsy,
should be taken from the clinically most "severe" areas
of involvement .
• Multiple biopsies of large or multiple lesions may be
required.

91. I . NON-SURGICAL TREATMENT
• Photodynamic Therapy
• Chemoprevention
• L-Ascorbic Acid (Vitamin C)
• α-Tocoferol (Vitamin E)
• Retinoic Acid (Vitamin A)
• Vitamin A derivative, isotretinoin, and 13-cis retinoic acid:
28,500IU per day.

92. • Beta-carotene 150,000 IU of beta-carotene
twice per week for six months.
• Bleomycin-Topical bleomycin in treatment
of oral leukoplakia was used in dosages of
0.5%/day for 12 to 15 days or 1%/day for
14 days.

93. Photodynamic therapy

94. Chemoprevention
• Chemoprevention may also be useful, but it remains
primarily experimental.
• Isotretinoin (13-cis-retinoic acid, a form of vitamin A)-
alone or in combination with betacarotene has been reported
to reduce or eliminate some leukoplakic lesions in short
term studies.

95. • However, to date there is insufficient evidence from well-designed
clinical trials to support the effectiveness of such medical therapies in
treating oral dysplasia or preventing the progression of oral dysplasia
to squamous cell carcinoma.

96. II. Surgical Management
• SURGICAL MANAGEMENT:
FOUR methods are available for the removal of leukoplakia
patches of the oral mucosa
1. Scalpel excision / Stripping
2. Electrocautery
3. Cryotherapy
4. CO2 Laser therapy

97. Scalpel Excision
• Traditional method .
• The area outlined including few millimetres of normal tissue.
• Incised with scalpel and patch (leukoplakia) is undermined by scalpel or by
blunt dissection to a depth of 2 to 4 mm.
• Allows leukoplakia to be removed in one piece.
• The mucosal defect if small is closed primarily or covered by transported
local mucosal flaps.
• Larger defects grafted with split thickness skin graft.
• Advantages –
whole of patch can be taken in one piece for histopathological examination
and in addition no special equipments are required.

98. • Disadvantages -
• Persistent bleeding, which makes accurate excision difficult. In the floor of
mouth care has to be taken for submandibular duct and lingual artery.
• There is contraction and scarring resulting in restricted movement of oral
soft tissues.
• The skin grafts when used remains white and masks any recurrence of
leukoplakia.
• Recurrence rate - 20 to 35 %

99. Electrocautery ( Fulguration )
Fulguration with electrocautery appliance is another
treatment of leukoplakia. This procedure requires
local or general anaesthesia. The healing process is
slow and painful.
Procedure -
Here multiple areas of the lesion are pierced with
electrocautery and left to heal.

100. Cryotherapy is a method of superfreezing
tissue in order to destroy it.
Procedure –
• Cryotherapy is done using a cotton swab that has been
dipped into liquid nitrogen or a probe that has liquid
nitrogen flowing through it. The technique involves
freezing the mucosa with the cryoprobe for 1.5 to 2
minutes, then waiting for 2 minutes, followed by further
freezing of 1.5 to 2 minutes. Thicker lesions may require
2 to 3 minutes freezing.
Cryotherapy-

101. Advantages -
1. Simple, Painless, out-patient procedure, well tolerated by patients including the
elderly.
2. During the healing phase there is absence of infection and pain and the wound is
cleaner without foul odour.
3. General anaesthesia is not required.
4. There is little scar formation,
5. There is no intra or post operative bleeding and the procedure may be repeated on
several occasions.

102. Disadvantages
1. There is no surgical specimen for histopathological
examination.
2. The zone of tissue elimination is variable resulting
in inaccurate margin of destruction. Post-
operatively there is marked edema.
3. There is unpleasant delayed necrosis of the treated
area which separates as a slough and it might
stimulate epithelial changes (particularly in cases
of advanced stages of pre-malignant state).

103. • Soko and colleagues found a recurrence rate of 20% in
patients who are treated by cryotherapy .
• Long-term follow-up after removal is extremely important
because recurrences are frequent, additional types of
leuloplakias may develop. This is especially true for the
verruciform or granular types, 83% of which recur and
require additional removal or destruction.

104. CO2 Laser Therapy :
• This destroys soft tissue in a unique manner and is ideal
means of removing leukoplakia.
• CO2 laser beam wavelength - 10.6μ
• Well absorbed by water and hence by soft tissues.
• The absorbed energy causes vaporisation of the intra and
extra cellular fluid and destruction of cell membrane. The
cell debris are released and burned in the laser beam,
depositing a carbonised layer on the tissue surfaces.

105. • There are two techniques which are used to remove the
leukoplakia using CO2 laser
1. Excision.
2. Vaporisation
• To excise a patch of leukoplakia, the laser is used to cut
around the margins, which can be held in tissue forceps
while the laser undermines the leukoplakic patch.
• Vaporisation of leukoplakia is by moving the laser beam
back and forward across the surface of lesion. It has the
risk of leaving small bits of abnormal tissue which are
deep under thickly keratinized tissue.

106. Advantages
1. There is excellent visibility and precision when
dissecting through the tissue planes.
2. There is little contraction or scarring.
3. Patients usually feel less pain when compared
with scalpel excision.

107. Disadvantages
1. High cost of equipment.
2. Requires protection of patient’s as well as
surgeon’s eye,
3. There is delayed wound healing.
4. Frame and colleague reported a 20 %
recurrence rate following removal of
leukoplakia by CO2 laser therapy.

108. Erythroplasia
• Also known as ERYTHROPLASIA OF QUEYART
• This was first described by Queyart in 1911 as a
lesion occurring on glans-penis.
• It is clinically similar to conditions such as candidiasis,
tuberculosis, histoplasmosis and non-specific
conditions such as denture irritation.
WHO definition :-
• A fiery red patch that cannot be characterized
clinically or pathologically as any other definable
disease.

109. Etiology
1. Unknown
2. Contributing factors include tobacco use,
alcohol consumption.

110. Incidence -
It is more common in males and occurs more frequently
in the 6th and 7th decade of life.

111. Clinical Presentation-
Red, often velvety, well-defined patches.
Most commonly present on
floor of mouth, retromolar
trigone area, lateral tongue.
• Usually asymptomatic.
• May be smooth to nodular.

112. • Homogenous form which appears as a bright red, soft velvety
lesion with straight or scalloped well demarcated margins, often
quite extensive in size, commonly found on the buccal mucosa
and sometimes on the soft palate, more rarely on the tongue
and floor of the mouth.
• Speckled leukoplakia / erythroplakia which is soft, red lesions
that are slightly elevated with an irregular outline and a granular
or fine nodular surface speckled with tiny white plaques.

113. Diagnosis-
• Appearance; History of tobacco/alcohol use.
• Biopsy results.
Differential Diagnosis-
• Erythematous (atrophic) candidiasis
• Kaposi’s sarcoma
• Ecchymosis
• Contact stomatitis
• Vascular malformation
• Squamous cell carcinoma
• Geographic tongue/ erythema migrans

114. Treatment-
• The treatment is same as that for invasive carcinoma or
carcinoma-in-situ like surgery, radiation and cauterisation.
• Surgical excision if proven dysplastic/ malignant.

115. Candidiasis
Etiology
• Infection with a fungal organism of the Candida species,
usually Candida albicans.
• Associated with predisposing factors: most commonly,
immunosuppression, diabetes mellitus, antibiotic use, or
xerostomia (due to lack of protective effects of saliva).

116. Clinical Presentation
• Acute (oral thrush)
• Pseudomembranous.
• Painful white plaques representing fungal colonies on
inflamed mucosa.
• Erythematous (acute atrophic): painful red patches caused
by acute Candida overgrowth and subsequent stripping of
those colonies from mucosa.

117. Clinical Presentation-
 Chronic
• Atrophic (erythematous): painful red patches; organism
difficult to identify by culture, smear, and biopsy.
• “Denture-sore mouth”
• Median rhomboid glossitis
• Perleche:
•

119. Diagnosis-
 Microscopic evaluation of lesion smears
• Potassium hydroxide preparation to demonstrate hyphae
• Periodic acid–Schiff (PAS) stain
• Culture on proper medium (Sabouraud’s, corn meal, or
potato agar)
• Biopsy with PAS, Gomori’s methenamine silver (GMS), or
other fungal stain of microscopic sections

120. • Differential Diagnosis
• Leukoplakia
• Erythroplakia
• Atrophic lichen planus
• Histoplasmosis
• White lesion due to denture irritation

121. Treatment-
• Topical or systemic antifungal agents.
• For immunocompromised patients: routine topical agents after
control of infection is achieved, usually with systemic azole
agents.
• Correction of predisposing factor, if possible.
• Some cases of chronic candidiasis may require prolonged
therapy (weeks to months).
Prognosis-
• Excellent in the immunocompetent host.

122. Topical therapy
• Nystatin oral suspension (100,000 units/mL); rinse 5 mL and swallow
4 times/day
• Clotrimazole (Lotrimin) solution 1%; rinse 5 mL and swallow 4
times/day
Systemic therapy
• Fluconazole (Diflucan) 100 mg #15; 2 tablets on the first day, 1 tablet
days 2–7, 1 tablet every other day for days 8–21
• Ketoconazole (Nizoral) 200 mg #21; 1 tablet every day with breakfast
× 21 d

123. Lichen Planus
Etiology-
• Unknown.
• Autoimmune. T cell–mediated disease targeting basal
keratinocytes.
• Lichenoid changes associated with galvanism, graft-versus-
host disease (GVHD), certain drugs, contact allergens.

124. Incidence -
• Up to 3 to 4% of Indian population has oral lichen planus
• 0.5 to 1% of population has cutaneous lichen planus; 50%
also have oral lesions.
• More common in White females (60%)
• Occurs in 4th to 8th decades of life.
Clinical Presentation-
• Variants: reticular (most common oral form); erosive
(painful); atrophic, papular,(plaque types); bullous (rare)
• Bilateral and often symmetric distribution
• Oral site frequency: buccal mucosa (most frequent), then
tongue, then gingiva, then lips (least frequent)

125. Lichen Planus

126. Diagnosis-
• Examination of oral mucosa, skin
• H/O galvanism, GVH disease.
• Biopsy
• Direct immunofluorescence–fibrinogen and cytoid bodies
at interface help confirm
Differential Diagnosis-
• Lichenoid drug eruptions
• Erythema multiforme
• Lupus erythematosus
• Contact stomatitis
• Mucous membrane pemphigoid

127. Treatment of Oral Lichen Planus-
• Mild to moderate: topical corticosteroids
• Severe: systemic immunosuppression, chiefly prednisone.
Topical tacrolimus ointment

128. INTRA EPITHELIAL CARCINOMA
This occurs frequently on the skin(Bowen’s disease) but
also on mucous membrane.
Incidence -
• Shafer also found the occurrence as 23% in floor of
the mouth, 22% on the tongue, 20% on the lip.
• It is more common in elderly men.

129. CLINICAL STUDY:
• Shafer found that 45% of the lesions of
carcinoma –in-situ were leukoplakic, 46%
were erythroplakic, 9% were a
combination of leukoplakic and
erythroplakic patches, 13% were ulcerated
lesions, 5% were white ulcerated lesions,
1% were red ulcerated lesions and 11%
didn’t have specific appearance.

130. TREATMENT:
• The lesions are surgically excised, irradiated
or cauterised.

131. ACTINIC (SOLAR) KERATOSIS,
ELASTOSIS AND CHELITIS
• Actinic keratosis is also potentially malignant disorder
associated with long term exposure to radiation and may be
found on the vermilion border of the lips as well as other
exposed skin surfaces.
• Clinical features -
• On the skin surfaces and the vermilion border of the lip, the
lesion is crusted and keratotic.
• On the labial mucosa exposed to sun, a white area of
atrophic epithelium develops with underlying scarring of the
lamina propria referred to as elastosis. When this atrophic
tissue abrades or ulcerates, it is called actinic chelitis.

132. Treatment
• 5 flurouracil is found to be effective.
But dysplastic changes in epithelium remains.
So adequate follow-up is required unless
surgical removal is done.

133. Smokeless Tobacco Keratosis
(Snuff Pouch)
Etiology
• Persistent habit of holding ground tobacco within
the mucobuccal vestibule.

134. Clinical Presentation-
• Usually in men in Western countries and India.
• Mucosal pouch with soft, white, fissured appearance.
• Leathery surface due to chronic tobacco use over many
years.

136. Differential Diagnosis-
• Leukoplakia (idiopathic)
• Mucosal burn (chemical/thermal)

137. Treatment
• Discontinuation of habit.
• If dysplasia is present, stripping of mucosal site.
Prognosis
• Generally good with tobacco cessation.
• Malignant transformation to squamous cell carcinoma or
verrucous carcinoma occurs but less frequently.

138. DISCOID LUPUS ERYTHEMATOSIS
• WHO has defined the oral lesions of DLE as
“circumscribed, slightly elevated, white patches that may
be surrounded by a (red) telengiectatic halo. A radiating
pattern of very delicate white lines is usually observed.
The oral lesion may or may not be accompanied by skin
lesion.”
• Clinical differentiation from leukoplakia and lichen planus
is difficult. Immunofluorenscent techniques usually show a
good correlation between the clinical appearance of the
oral lesion and their histologic counterpart.
•

139. • The incidence of malignant transformation is
very less.

140. SIDEROPENIC DYSPHAGIA (PLUMMER VINSON
SYNDROME)
• Iron deficiency anaemia is one manifestation of
Plummer-Vinson syndrome and was first
described by Plummer in 1914 and by Vinson in
1922 under the term ‘hysterical dysphagia’.
• Iron deficiency anaemia occurs especially in
women.

141. • The clinical features are pale skin and
mucous membrane, spoon shaped nails
(Koilonychia), atrophic glossitis, tongue is
smooth and glazy. It is accompanied by
dysphagia and oesophageal webs.
• Laboratory findings show hypochromic
microcytic anaemia of varying degree.
• The patients respond well to iron therapy
and high protein diet.

142. Recent advances
• Dr. S. Sankara Narayanan, at the Stem Cell Therapy Unit of KMC
Hospital, Trichy, in Tamil Nadu has reportedly developed a non-
surgical form of treatment using Autologous Bone Marrow Stem
Cells-Stem Cell Therapy- to treat OSMF and to change the
malignant potential. The doctor along with his associates claimed
they have successfully treated 3 patients with OSMF by using this
medical technology.

143. Nano particles for oral cancer diagnosis are more
accurate and less invasive to the body. Many cancer cells
have a protein, epidermal growth factor receptor (EGFR),
non cancer cells have much less of this protein. By attaching
gold nano particles to an antibody for EGFR, researchers
have been able to bind the nanoparticles to the cancer cells
which show different light scattering and absorption spectra
than benign cells. Pathologist can thereafter use these results
to identify malignant cells in biopsy sample.

144. CONCLUSION
Patient presenting with Potentially malignant disorders
should undergo a careful examination to identify any
causative factors, which are best eliminated at the first stage
of the treatment. However, many patients may not have any
obvious causative factor. A biopsy of the lesion is necessary
to demonstrate the histological features of the lesion and
detect any existing invasive carcinoma. Frequent monitoring
of histopathological changes is essential to obtain an accurate
assessment of histological activity of the lesion and to try to
predict its future behavior. The subsequent management of
the patient depends on how “high risk” the lesion is.

145. THANK YOU