Short description of each disease with images.

1. PRESENTED BY:- DR.AKSHAY SHETE

2. Definition:
“A morphologically altered tissue in
which cancer is more likely to occur than in its
apparently normal counterpart”
-WHO 1978

3. Premalignant condition
Definition:
‘a generalized state associated with a
significantly increased risk of cancer’.
-WHO 1978

4. Premalignant lesions Premalignant
conditions
Leukoplakia Oral submucous fibrosis
Erythroplakia Oral lichen planus
Leukokeratosis nicotina
palatinae
Actinic keratosis
Candidiasis Syphilis
Carcinoma in situ Discoid lupus
erythematosus

5. Leukoplakia
Definition:
“A predominantly white lesion of the oral
mocosa that cannot be characterized as any other
definable lesion”
-WHO

6. Etiology:
 Tobacco
 Alcohol
 Chronic irritation
 Candidiasis
 Electromagnetic reaction
 Vitamin deficiency
 Nutritional deficiency
 Xerostomia
 Idiopathic

7. Clinical Feature:
 Sex & age: Occurs more in 35 to 45 years old and above age
group ,males>females.
 Common site: Commonly involved-Buccal mucosa
Lip lesion more common in men
Tongue lesion more common in women
-Also involved: Palate,Alveolar ridge,Floor of mouth,Soft
palate nd Gingiva.
 Sunlingual keratosis
 Ebbing tide type
 Colour:White or Yellowish white.

8. Buccal mucosa
involvement
Tongue
Involvement
Lip

9.  Symptoms: Increased thickness of mucosa with uclerated and
nodular type may complain of burning sensation.
 Size and margin: Raised plaque varying in size with irregular
edges.

10. Homogenous
Leukoplakia
Non-homogenous
Leukoplakia
Completely whitish lesion
Smooth surface
Corrugated-Ebbing tide
Pumice like with a pattern
of fine lines
Wrinkled- Dry,cracked
surface
Nodular or Speckled
Verrucous-Slow growing
Ulcerated
Lesion is partly white and
partly reddish

11. Homogenous Leukoplakia
Non-homogenous Leukoplakia

12. Homogeneous
Speckled/Nodular
Ulcerative

13. Hairy Leukoplakia
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 –
Associated With Epstein-barr Virus (EBV)
And Occurs Primarily In Hiv-positive Individuals.

14. Clinical features
 Male predilection
 Most common in 40 – 60 years of age

15. Malignant Transformation
 Development of oral cancer from pre-existing
leukoplakia
 Occurs in 0.3% to 10% of cases
 Higher in women (6%) than men (3.9%).
 Higher rate of transformation- chewing tobacco
habit
 Buccal mucosa-1.8%
 Lip and tongue-16% to 38.8%

16. Differential diagnosis
 Leukoedema
 Lichen planus
 Chemical burn
 Lupus erythematosus
 White sponge nevus

17. Treatment
A)Elimination of etiological factor
 Prohibition of smoking or Tobacco
 Removal of chronic irritant(To remove sharp broken down
teeth)
B)Conservative treatment
 Vitamin Therapy
a)Vit. A(topically)with podophyllin solution
b)Vit A+Vit E:- To inhibit metabolic degradation
c)13-cis-retinoic Acid:-High dose of 1.5 to 2mg/kg of
body wt for 3 months
d)Vit B complex:- for lingual lesion

18.  Antioxidant therapy:-beta carotene supplementation
 Nystatin therapy:-Given in Candidal leukoplakia
C)Surgical Management
 Scalpel excision / Stripping
 whole of patch can be taken in
one piece

19.  Electrocautery ( Fulguration )
 The healing process is slow and painful.

20. 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

21.  CO2 Laser Therapy :
Two techniques which are used to remove the leukoplakia using
CO2 laser
1. Excision.
2. Vaporisation
1.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.
2.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.

22. Erythroplakia
Definition:
“Any lesion of the oral mucosa that presents as a bright
red velvety patch or plaque, which cannot be characterized
clinically or pathologically as any other recognizable
condition”

23. Etiology
 Idiopathic
 Alcohol and smoking
 Candida infection
CLINICAL FEATURE
 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.

24. Male predilection and most common in 6th & 7th
decade of life

25. Treatment-
 The treatment is same as that for invasive carcinoma like surgery,
radiation and cauterisation.
 Surgical excision if proven dysplastic/ malignant.

26. Smoker’s Palate
“Leukokeratosis Nicotina Palati”
 It is tobacco induced white lesios
 Some of these lesions may transform into cancer
Etiology
 Tobacco

27. Treatment
Cessation of Smoking

28. Candidiasis
Candidosis,Moniliasis,Thrush
Etiology
 Infection with a fungal organism of the Candida species, usually
Candida albicans.
 Other Species- Candida Tropicalis,C.Parapsilosis,C.Krusei etc.
 Associated with predisposing factors: most commonly,
immunosuppression, diabetes mellitus, antibiotic use, or xerostomia (due
to lack of protective effects of saliva).

29. Clinical Presentation
 Acute (oral thrush)
 Pseudomembranous-most common form
 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.

30.  Occur at any age
 Soft,white,slightly elevated plaque mostly on Buccal mucosa and
tongue
 Also in palate,gingiva and floor of mouth

31. Plaque described as milk curds
Wiped off white membrane

32. Differential Diagnosis
 Leukoplakia
 Erythroplakia
 Atrophic lichen planus
 Histoplasmosis
 White lesion due to denture irritation

33. Treatment-
 Topical or systemic antifungal agents.
 Correction of predisposing factor, if possible.
 Some cases of chronic candidiasis may require prolonged therapy (weeks to months).
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


34. Systemic therapy
 Fluconazole (Diflucan) 100 mg ; 2 tablets on the first day, 1 tablet days 2–7, 1 tablet
every other day for days 8–21
 Ketoconazole (Nizoral) 200 mg; 1 tablet every day with breakfast × 21 d

35. ORAL SUBMUCOUS FIBROSIS

36. 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.”

37. Etiology
1. Chronic Irritation
- Chilies, Lime, Areca nut(Betel nut), Tobacco.
2. Defective iron metabolism
3. Bacterial Infection
4. Collagen disorder
5. Immunological disorders
6. Nutritional deficiency
7. Genetic disorder.

38. CLINICAL FINDINGS
 Age group - 2nd to 4th decade of life.
 Earlier it was thought to be common in females, But at present, study
ratio shows male:female 2.3:1
 COMMON SITES INVOLVED-Buccal mucosa, 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
 Pain in areas where submucosal fibrotic bands are developing,palpation
is useful test.
 Petechie observed in 22% of OSMF mostly on tongue followed by labial
and buccal mucosa.
 It is dense fibrosis,involving tissue around the pterygomandibular
raphe,that causes varying degrees of difficulty in mouth opening

39. Restricted mouth
opening
Fibrosi
s

40. Prodromal symptoms
Initial symptoms Later
1)Burning sensation on eating
spicy food
2)Blisters on the palate
3)Ulceration or recurrent
stomatitis
4)Excessive salivation
5Defective gustatory
sensation
6)Dryness of mouth.
1)Difficulty in opening mouth
Inability to whistle, blow
2)Difficulty in swallowing
3)Referred pain to the ear
5)Sometimes deafness due to
occlusion of eustachian tubes

41. Staging of OSMF:
 Stage I : Stage of stomatitis & vesiculation
 Stage ll : Stage of fibrosis
 Stage III :Stage of sequelae and complication

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

43. 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

44. 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%).

45. 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.

46. MANAGEMENT
A)Stoppage of habit
Affected patients should be explained about the disease and its
possible malignant potential.
Improvement in clinical features like gradual increase in the inter-
incisal opening has been observed in most of patients who discontinue the
habit
B) Medicinal therapy
• Vitamin rich diet
• Iodine B complex preparation:- intramuscular injection Ranodine, is
responsible for stimulation of metabolic process and enzymatic process
within the body, 2ml ampule daily . The course of 5 injections is repeated
after 7 days.each 2ml consists of
• Methyltrioxyethyl iodomine
• Vitamin B1:-1.0mg,vitaminB6:-0.3mg,vitaminB2:-
0.6mg,nicotinamide:-15.0mg,calcium pantothenate:-1.0 mg

47. Steroids
Local:-
Hydrocortisone injection along with procaine hydrochloride injection locally in
the area of Fibrosis.
Systemic:-
Therapy with hydrocortisone 25 mg tablet dose 100 mg/day is useful in
relieving burning sensation without effects.this is supplemented with local injection of
hydrocortisone 25 mg at biweekly intervals at the affected site.anti-allergic and anti-
inflammatory action of corticosteroid.
The Fibrosis is prevented by decreasing fibroblastic production and
the deposition of collegen
Hyaluronidase: Decreases cell formation by virtue of its action on hyaluronic acid
,Which plays an important role in collagen formation.

48. Vitamin E:-
Surgical treatment
A)Conventional:-
• Indication:- Surgical treatment is method of choice when there is
marked limitation of opening of the mouth in cases where biopsy reveals
neoplastic changes and when there is marked trismus and dysplasia
• Flap as graft:-
Excision of fibrous bands followed by use of tongue flap
as a graft gives good results because tongue flap is highly vascular and
resists further Fibrosis. It is done in patients who have got mouth
opening less than 1.5 cm, in case of failure of conservative treatment and
absence of any other pathology like ulceration infection and leukoplakia.

49. B)Implantation of fresh human placenta
C)Nasolabial flap:- The excision of fibrotic bands is followed by reconstruction
using bilateral full thickness Nasolabial flap
D)Bilateral palatal flap :-
E)Oral stent:- a stent is an appliance made up of acrylic having posterior vertical
stops bilaterally.
Made for decrease mouth opening and to allow the tissue to heal at new
height.
F) Laser:-
Technique :- under general anaesthesia a co2 laser is used to
incise the buccal mucosa and vaporize the submucosal connective tissue to the
level of buccinator muscle.
Hemostasis is provided by lased surface itself and the mouth opening
increases immediately.

50. Nasolabial flap

51. Vertical incision in nasolabial flap

52. Cryosurgery
It is method of local destruction of tissue by freezing it.
Oral physiotherapy
Oral exercises for advised in early and moderately
advanced cases.
This includes mouth opening and Ballooning of mouth. Forceful
mouth opening have been tried with mouth gag and acrylic surgical
screw
Diathermy

53. Lichen planus
Erasmus Wilson described it in 1869.
It is the probable precancerous condition.

54. Clinical features
• Sites:- common sites are buccal mucosa(84%) and to extent tongue,
lips,gingiva,floor of mouth and palate
• Symptoms:- burning sensation of oral mucosa
• Appearance:- radiating white and grey velvety thread-like papules in a
linear,angular retiform arrangement
• Wickham's striae:- tiny white elevated dots present at the intersection of white
lines.
• Age and sex:- male is 35-44years and female 45-54 years.more predilection for
females.
• 25% lichen planus have only oral lesion
• The chief complaint is usually intense pruritus. Itching provokes rubbing off the
region rather than scratching.

55. Buccal mucosa
involvement
Tongue involvemen

56. Six Ps of lichen planus
Planar,polygonal,purple,pruritic,papules and plaques
Vaginogingival syndrome:-
Oral lesions coexisting which genital mucosal lesions known as
Vaginogingival syndrome
Colour:-
Red but soon takes reddish purple.
Later,dirty brown color develops.
Complication:-
Post inflammatory hyperpigmentation,malignancy from oral
lesions,dystrophy.

57. Etiology
1. Cell mediated immune response
2. Auto immunity:- the activated t lymphocytes also secret Gamma
interferon which induce keratinocytes to produce HLA-DR and increase
their rate of differentiation with formation of thickened surface.
3. Immunodeficiency:- decreased serum levels of IgG,IgA or IgM in
lichen planus, but at the same time, reports of normal concentrations of
IgA and IgM are found, therefore the role of immunodeficiency is
questionable.
4. Genetic factors:- Familial cause might be environmental and related to
infection,rather than genetics.
5. Infection:- bacterial etiology maybe there but results are not confirmed.

58. Psychogenic factor:- stress and neurogenic basis is suggested. Observation
mostly in nervous and highly stressed person is associated with emotional upset,
overwerk and some form mental strain.
Habits:- habit of chewing tobacco and betel.
Smoking may play a role in initiating oral lichen planus of plaque type.
Types:-
Reticular,papular,plaque,atrophic,classical,erythematous,ulcerative,hyper
trophic,erosive,bullous,hypertrophied,annular,actinic,follicular,linear.

59. Reticular type
OLP
Plaque type
OLP

60. Management
• Removal of cause
• Steroids:- in most patients with erosive and ulcerative lesion steroids
are commonly used. Full steroid dose is required.
• Steroid spray:- small and moderate sized painful lesions can be
treated with beclomethasone dispropionate spray,triamcinolone
acetone in gel or cream base.
• Topical delivery regimen:- Topical delivery QID,for 3or more
weeks,once a week intralesional injection, for 3weeks(usually 0.5-
1.5mL). Systemic steroid(prednisolone 5mgtab)
• Topical application:-Topical application of fluocinolone acetonide
for 4 weeks

61. Combination of Prednisolone and levamisole:- Prednisolone 5mg and
levamisole 50mg tablets for first three days of rest and this schedule to be followed for
two to three more weeks
Topical application of antifungal agent:- Nystatin and ketoconazole.
Vitamin A(retinoid)analogy:-
Topical vitamin A Acid cream(0.1%)
Cyclosporine:-
5ml rinse TID for 8 weeks
Surgical therapy
Psychotherapy
Dapsone therapy

62. Lichenoid reaction
Lichenoid reactions where differentiated from lichen
planus on the basis of association of lichenoid reaction
with administration of drugs and systemic disease and their
resolution when the drug was discontinued.

63. Etiopathogenesis:-
1. Disorders:- lichen planus,lupus erythematous,erythema multiform,fixed drug
eruption,secondary syphilis.
2. Drugs and chemical:-
- Antimicrobial:- Dapsone,para-aminosalicylate,streptomycin and
tetracycline
-Anti-parasitic:- Chloroquine and quinacrine
-Antihypertensives:-
Chlorothiazide,hydrochlorothiazide,labetalol,methyldopa,mercurial diuretic
and practolol.
-Anti-arthritis:-Aurothioglucose and gold sodium thiosulfate
-Oral hypoglycemic agents of sulfonylureas type:-Tolbutamide
and chlorpropamide.

64. Clinical features
• Lichenoid mucositis:- Lesion of mucosa similar to lichen planus due
to drugs
• Lichenoid dermatitis:- when lesion presents on the skin
• Lichenoid foreign body gingivitis:- occurs due to foreign material
• Lichen planus type lesion can be seen in oral cavity

65. Lichenoid dermatitis
Lichenoid reaction

66. Diagnosis
Lichen planus type lesion with drug history will Diagnosis lichenoid
reaction
Management
Majority of it are resolved after discontinuation of drug

67. Thank You