This document provides information about precancerous lesions and conditions of the oral cavity. It begins with an introduction by Dr. Bhavik Miyani and is guided by several other doctors. The document discusses the definition and classification of potentially malignant disorders. It provides details on the history, etiology, clinical features and types of oral leukoplakia. Diagnosis, treatment options including photodynamic therapy and prognosis are also summarized. Histopathological grading and staging of oral leukoplakia are described.

1. DR. BHAVIK MIYANI, IIND YEAR
OMFS, NPDCH
GUIDED BY,
DR. ANIL
MANAGUTTI,
DR. SHAILESH
MENAT,
DR. RUSHIT PATEL,
DR. JIGAR PATEL.
PRECANCEROUS LESIONS &
CONDITIONS

2. CONTENTS…
 Introduction
 History
 Definition
 Classification
 Potentially malignant disorders
 Recent advances
 Conclusion
 References
205-04-2019

3. INTRODUCTION…
Oral cancer constitutes an important entity in
the field of Oral and Maxillofacial surgery. 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 patients
suffer from oral cancer in any year.
Oral cancer is responsible for 7% of all cancer
deaths in males while it is 3 % in females.
Some oral cancers initiate as a De Novo
lesion while some are preceded by Oral
premalignant lesions and conditions.
305-04-2019

4. Various premalignant lesions, particularly red
lesions(erythroplakias) and some white lesions
(leukoplakias) have a potential for malignant
change. In that, risk of erythroplakias is
exceedingly high.
Practitioners will see many oral white lesions
but few carcinomas. However they must be able to
recognize lesions at particular risk and several
features which help to assess the likelihood of
malignant transformation.
The accuracy of such predictions about
premalignant lesions and conditions is low but the
process of identifying “at risk” lesions is
fundamental for diagnosis and treatment planning.05-04-2019 4

5. Currently confusion came up between these
two terminologies and many opinioned that the
prefix ‘pre’ quotes that all precancerous lesions
become cancer, whereas studies found this to be
untrue.
Hence it was recommended in WHO workshop
of 2005 to abandon the distinctions between
precancerous lesions and conditions and to use the
term “Potentially Malignant Disorders” instead,
incorporating both the terminologies.
The latest WHO monograph on head and neck
tumors (2005) used the term “Epithelial precursor
lesions” and defined it as “Altered epithelium with an
increased likelihood for progression to squamous05-04-2019 5

6. HISTORY…
Oral candidiasis in infants was recognized
first by Hippocrates (400 B.C.)
The terms premalignant (pre-preliminary and
malignant-cancerous) lesions and conditions were
coined by Romanian physician Victor Babeş in1875.
In 19th century, Trousseus called Oral Thrush
as “ Disease of the diseased”
Plummer-Vinson syndrome is one
manifestation of iron deficiency anaemia and was
first described by Plummer in 1914 and by Vinson
in 1922 under the term ‘hysterical dysphagia’
05-04-2019 6

7. The term leukoplakia was coined by
shwimmer in 1877 & In 1994,it was classified by
the WHO.
Oral submucous fibrosis was first described
by Joshi and Schwartz among East Indian Women in
1952.
Tissue therapy in oral submucous fibrosis , as
a new method of therapy was introduced by Filatov
in 1933 and later developed in 1953.
In oral submucous fibrosis ,The attendant
trismus is a result of juxta-epithelial hyalinisation
and secondary muscle involvement. Muscular05-04-2019 7

8. DEFINITION
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
05-04-2019 8

9. Premalignant condition ‘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.’
-WHO workshop 2005
05-04-2019 9

10. 05-04-2019 10

11. 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”
Oral potentially malignant disorders: Precising the definition) - Oral
Oncology journal (2012)
05-04-2019 11

12. NEW CLASSIFICATION FOR ORAL
POTENTIALLY MALIGNANT DISORDERS
Sarode, sarode, karmarkar, tupkari (ref - oral oncology xxx, 2011) 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).
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.05-04-2019 12

13. 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 nicotine
b. Betel nut associated
• Oral submucous fibrosis
c. Sanguinaria-associated keratosis
2. Non-habit related
• Actinic cheilosis
• Chronic candidiasis
05-04-2019 13

14. 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
Group 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.
05-04-2019 14

15. 1. Inherited cancer syndromes
• Xeroderma pigmentosum
• Ataxia telangiectasia
• Fanconi’s anemia
• Li Fraumeni syndrome
2. Dyskeratosis congenita
3. Epidermolysis bullosa
4. White sponge nevus
5. Darier’s disease
6. Hailey–Hailey disease
05-04-2019 15
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.

16. 1. Immunosuppression
• AIDS
• Immunosuppression therapy (for malignancy or
organ transplant)
2. Alcohol consumption and abuse
3. Nutritional deficiency
• Sideropenic dysphagia
• Deficiency of micronutrients
05-04-2019 16
GROUP IV: No clinically evident lesion but oral cavity is
susceptible to Oral squamous cell carcinoma.

17. LEUKOPLAKIA
Oral leukoplakia (Leuko = white; plakia =
patch) is defined by the World Health Organization
(WHO) as "a white patch or plaque that cannot be
characterized clinically or pathologically as any
other disease.“
(Ref – WHO workshop 2012) J Oral Pathol Med (2012) 36: 575–80
05-04-2019 17

18. 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
05-04-2019 18

19. TOBACCO
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.
05-04-2019 19

20. ALCOHOL
Heavy consumption of alcohol is
second most important risk factor, it acts
synergistically with tobacco.
05-04-2019 20

21. CANDIDA INFECTIONS
Candida albicans infection (chronic
hyperplastic candidiasis) may play a role in
the etiology of leukoplakia.
05-04-2019 21

22. HUMAN PAPILLOMA VIRUSES
HSV1, HPV, HHV6, HHV8
(HHV = Human Herpes Viruses)
(HSV = Herpes Simplex Viruses)
(HPV = Human Papilloma Virus)
05-04-2019 22

23. 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 nonsyphilitic
background.
05-04-2019 23

24. VITAMIN DEFICIENCY
Vit A deficiency will cause metaplasia and
keratinization of epithelial structures(particularly
glands).
05-04-2019 24

25. 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%)
Otorhinolaryngology clinics –An International journal may-sept. 2009
05-04-2019 25

26. 05-04-2019 26

27. 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.
05-04-2019 27

28. CLINICAL TYPES
1. Homogenous
2. Non-homogenous
05-04-2019 28

29. HOMOGENOUS LEUKOPLAKIA
Uniform white patch lesion with smooth or
corrugated surface sometimes, slightly raised
mucosa. Usually plaque like, some are smooth,
may be wrinkled or crisscrossed by small crack or
fissure.
• Malignant transformation – 1 to 7%.
• Types –
1. Smooth
2. Furrowed
3. Ulcerative05-04-2019 29

30. NON-HOMOGENOUS
LEUKOPLAKIA
• 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.
05-04-2019 30

31. HAIRY LEUKOPLAKIA
Hairy leukoplakia is a condition that is
characterized 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.
05-04-2019 31

32. 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 carpet05-04-2019 32

33. 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.
05-04-2019 33

34. 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.
05-04-2019 34

35. 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.05-04-2019 35

36. 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.
05-04-2019 36

37. DIFFERENTIAL DIAGNOSIS
1) White sponge nevus
2) Acute pseudomembranous candidiasis
3) Leukoedema
4) Lichen planus (plaque type)
05-04-2019 37

38. 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.
05-04-2019 38

39. A. 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.
• 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.05-04-2019 39

40. PHOTODYNAMIC THERAPY
05-04-2019 40

41. 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 beta-carotene
has been reported to reduce or eliminate some
leukoplakic lesions in short term studies.
• 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.05-04-2019 41

42. B. SURGICAL TREATMENT
1. Scalpel excision / Stripping
2. Electrocautery
3. Cryotherapy
4. CO2 Laser therapy
05-04-2019 42

43. 1. SCALPEL EXCISION /
STRIPPING
The traditional method.
• The area is outlined including few millimeters of
normal tissue. It is incised with scalpel and patch
(leukoplakia) is undermined by scalpel or by blunt
dissection to a depth of 2 to 4 mm. This allows
leukoplakia to be removed in one piece. The
mucosal defect if small is closed primarily or it is
covered by transported local mucosal flaps. Larger
defects are grafted with split thickness skin graft.
• Advantages –
Whole of patch can be taken in one piece for
histopathological examination and in addition no
special equipment are required.05-04-2019 43

44. • 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 %
05-04-2019 44

45. 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.
05-04-2019 45

46. CRYOTHERAPY
• 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
3minutes freezing.
05-04-2019 46

47. 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.
05-04-2019 47

48. DISADVANTAGES
1. There is no surgical specimen for
histopathological examination.
2. The zone of tissue elimination is variable
resulting in inaccurate margin of destruction.
Postoperatively there is marked oedema.
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).
05-04-2019 48

49. • 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.
05-04-2019 49

50. 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.
05-04-2019 50

51. • 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.
05-04-2019 51

52. 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.
05-04-2019 52

53. 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.
05-04-2019 53

54. ERYTHROPLAKIA
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”.
05-04-2019 54

55. ETIOLOGY
1. Unknown
2. Contributing factors include tobacco use,
alcohol consumption.
05-04-2019 55

56. INCIDENCE
It is more common in males and occurs more
frequently in the 6th and 7th decade of life.
05-04-2019 56

57. 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
05-04-2019 57

58. • 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.
05-04-2019 58

59. DIAGNOSIS
• Appearance; History of tobacco/alcohol use.
• Biopsy results.
05-04-2019 59

60. DIFFERENTIAL DIAGNOSIS
• Erythematous (atrophic) candidiasis
• Kaposi’s sarcoma
• Ecchymosis
• Contact stomatitis
• Vascular malformation
• Squamous cell carcinoma
• Geographic tongue/ erythema migrans
05-04-2019 60

61. 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.
05-04-2019 61

62. ORAL SUBMUCOUS FIBROSIS
• 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 .
05-04-2019 62

63. DEFINITION
“ 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.”
(J.J Pindborg and Sirsat 1966)
05-04-2019 63

64. 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.
05-04-2019 64

65. ETIOLOGY
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
6. Genetic disorder.
05-04-2019 65

66. 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) .
05-04-2019 66

67. ARECA NUT
ARECOLINE, ARECAIDINE
-Fibroblast proliferation
-Stimulate collagen synthesis
TANNIN, CATHECHIN-
-Makes collagen fibrils resistant to
collagenase.
05-04-2019 67

68. 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.
05-04-2019 68

69. PRODROMAL SYMPTOMS
05-04-2019 69

70. 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.
• 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.
05-04-2019 70

71. SHRUNKEN UVULA GIVING HOCKEY
STICK APPEARANCE
05-04-2019 71

72. PALE AND BALD TONGUE
05-04-2019 72

73. TRISMUS
05-04-2019 73

74. STAGING
Stage I : Stage of stomatitis &
vesiculation
Stage ll : Stage of fibrosis
Stage III :Stage of sequelae and
complication
(Ref -Pindborgh JJ-1989)
05-04-2019 74

75. STAGE I : STOMATITIS &
VESICULATION
Stomatitis includes
erythmatous mucosa, vesicles,
mucosal ulcers,melanotic mucosal
pigmentation.
05-04-2019 75

76. 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 &
stiffness05-04-2019 76

77. STAGE III : SEQUALAE AND
COMPLICATIONS
• 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%).
05-04-2019 77

78. RECENT CLASSIFICATION
FOR OSMF
• 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.
S4 a –
Anyone of above stage with potentially malignant
disorders
Eg- leukoplakia, erythroplakia.
S4 b –
Anyone of above stage with oral carcinoma05-04-2019 78
Chandramani More et al
2011

79. 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
05-04-2019 79

80. 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.
05-04-2019 80

81. HISTOPATHOLOGICAL
FINDINGS
• Atrophic Oral epithelium.
• Loss of rete pegs.
• Epithelial atypia may be observed.
• Hyalinization of collagen bundles.
05-04-2019 81

82. MANAGEMENT
1.Restriction of habits/ Behavioral
therapy.
2.Non-surgical therapy.
3.Surgical therapy.
4.Oral Physiotherapy.
05-04-2019 82

83. 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.
05-04-2019 83

84. NON SURGICAL THERAPY
Antioxidants
• Intralesional injections of hyaluronidase.
Hydrocortisone
• Use of Placentrix 2ml solution at interval of 3
days.
• Topical application -
1. 4% Acetic acid (At PH 6.5) 3 times daily.
2. 5 Fluorouracil
05-04-2019 84

85. Systemic administration of
immunomodulators -
• Levamisole 150mg for 3 weeks ,orally
• Dapsone 75 mg O.D for 90 days,
orally
05-04-2019 85

86. 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)05-04-2019 86

87. • Cryosurgery
• Laser treatment
05-04-2019 87

88. CANDIDIASIS
• 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).
05-04-2019 88

89. 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.05-04-2019 89

90. Chronic
• Atrophic (erythematous): painful red patches; organism
difficult to identify by culture, smear, and biopsy.
• “Denture-sore mouth” : a form of atrophic candidiasis
associated with poorly fitting dentures; mucosa is red and
painful on denture-bearing surface.
• Median rhomboid glossitis: a form of hyperplastic
candidiasis seen on midline dorsum of tongue anterior to
circumvallate papillae.
• Perleche: chronic Candida infection of labial
commissures; often coinfected with Staphylococcus
aureus.
• Hyperplastic/chronic hyperplastic: a form of
hyperkeratosis in which Candida has been identified;
usually buccal mucosa near commissures; cause and
effect not yet proven.
• Syndrome associated: chronic candidiasis may be seen
in association05-04-2019 90

91. 05-04-2019 91

92. 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
05-04-2019 92

93. DIFFERENTIAL DIAGNOSIS
1) Leukoplakia
2) Erythroplakia
3) Atrophic lichen planus
4) Histoplasmosis
5) White lesion due to denture irritation
05-04-2019 93

94. 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).05-04-2019 94

95. 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
05-04-2019 95

96. LICHEN PLANUS
• ETIOLOGY:-
• Unknown.
• Autoimmune. T cell–mediated disease
targeting basal keratinocytes.
• Lichenoid changes associated with galvanism,
graft-versushost
• disease (GVHD), certain drugs, contact
allergens.
05-04-2019 96

97. INCIDENCE
1. Up to 3 to 4% of Indian population has oral
lichen planus
2. 0.5 to 1% of population has cutaneous lichen
planus; 50% also have oral lesions.
3. More common in White females (60%)
4. Occurs in 4th to 8th decades of life.
05-04-2019 97

98. CLINICAL PRESENTATIONS
• 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)
05-04-2019 98

99. 05-04-2019 99

100. DIAGNOSIS
• Examination of oral mucosa, skin
• H/O galvanism, GVH disease.
• Biopsy
• Direct immunofluorescence–fibrinogen and
cytoid bodies at interface help confirm
05-04-2019 100

101. DIFFERENTIAL DIAGNOSIS
1) Lichenoid drug eruptions
2) Erythema multiforme
3) Lupus erythematosus
4) Contact stomatitis
5) Mucous membrane pemphigoid
05-04-2019 101

102. TREATMENT
• Mild to moderate: topical corticosteroids
• Severe: systemic immunosuppression, chiefly
prednisone.
• Topical tacrolimus ointment
05-04-2019 102

103. INTRAEPITHELIAL
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.
05-04-2019 103

104. 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.
05-04-2019 104

105. TREATMENT
The lesions are surgically excised,
irradiated or cauterised.
05-04-2019 105

106. 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.
05-04-2019 106

107. 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.
05-04-2019 107

108. SMOKELESS TOBACCO KERATOSIS
(SNUFF POUCH)
• Etiology
Persistent habit of holding ground tobacco
within the mucobuccal vestibule.
05-04-2019 108

109. 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.
05-04-2019 109

110. 05-04-2019 110

111. DIFFERENTIAL DIAGNOSIS
1) Leukoplakia (idiopathic)
2) Mucosal burn (chemical/thermal)
05-04-2019 111

112. TREATMENT
1) Discontinuation of habit.
2) If dysplasia is present, stripping of mucosal
site.
05-04-2019 112

113. PROGNOSIS
1) Generally good with tobacco cessation.
2) Malignant transformation to squamous cell
carcinoma or verrucous carcinoma occurs
but less frequently.
05-04-2019 113

114. 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 lesion05-04-2019 114

115. 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.
05-04-2019 115

116. • 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.
05-04-2019 116

117. RECENT ADVANCES
• Temporalis myofascial flap for reconstruction in
OSMF.
• Dr. S. Sankara Narayanan, at the Stem Cell
Therapy Unit of KMC Hospital, Trichy, in Tami
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.
05-04-2019 117

118. • 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.
05-04-2019 118

119. 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.
05-04-2019 119

120. • 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.
05-04-2019 120

121. REFERENCES
Books -
[1] R.A.Cawson’s essentials of Oral Pathology and Oral
Medicine . 7th Edition
[2] Burkitts Oral Pathology 5th Edition
[3] Shafer, Hine & Levy: A textbook of oral pathology.
4th
edition.
05-04-2019 121

122. REFERENCES
Articles –
1. Nanotechnology : A new era in dentistry JADA 2012
2. Oral potentially malignant disorders: Precising the
definition.
Otorhinolaryngology clinics –An International journal may-
sept. 2009
4. Classification of OSMF. Swati Gupta, Jigar joshi , JIAOMR
5. NEW CLASSIFICATION FOR ORAL POTENTIALLY
MALIGNANT DISORDERS
S. SARODE, SARODE, KARMARKAR, TUPKARI (Ref - Oral
Oncology xxx, 2011)
6. Precancerous lesions of oral cavity. -Uday pawar, Pankaj05-04-2019 122

123. THANK
YOU...
123
A SMOOTH SEA,
NEVER MADE A SKILLED SAILOR
05-04-2019