This document discusses oral submucous fibrosis (OSF), a chronic condition characterized by fibrosis of the submucosal tissues and epithelial atrophy of the oral cavity. It causes stiffness of the oral mucosa and trismus. The condition is caused by chewing areca nut and ingesting spicy foods. The pathogenesis involves increased collagen production and decreased breakdown due to areca nut compounds, as well as genetic and immunological factors. Symptoms progress from pigmentation and salivation to dry mouth and trismus. Treatment involves preventing habits, medical management, physiotherapy, and surgery such as excision of fibrous bands and use of flaps like buccal fat pad or nasolabial flaps to

1. ORAL SUBMUCOUS FIBROSIS
DR JAMEEL KIFAYATULLAH
DENTIST KHYBER COLLEGE OF
DENTISTRY PESHAWAR PAKISTAN

2. ORAL SUBMUCOUS FIBROSIS
• Chronic, complex, potentially premalignant
condition of the oral cavity, characterized by
juxta-epithelial inflammatory reaction and
progressive fibrosis of the submucosal tissues
(the lamina propria and deeper connective
tissues) and epithelial atrophy leading to
stiffness of oral mucosa causing trismus and
inability to eat.

3. Oral submucous fibrosis (WHO
DEFINITION)

5. Areca nut

6. chillies

7. GENETIC AND IMMUNOLOGICAL

8. PATHOGENESIS

10. PATHOGENESIS
Not well established
Multifactorial
1. Areca nut chewing
2. Ingestion of chillies (capsacian)
3. Genetic and immunologic processes
4. Nutritional deficiencies
5. Collagen disorders

11. ARECA NUT
• Arecoline (alkaloid) undergoes hydrolysis to active form
arecadainestimulates fibroblasts to increase production
of collagen by 150%
• Inhibits metalloproteinases decreasing overall breakdown
of tissue collagen
• Flavanoid, catechin,tannin: cross linking of collagen
fibers less susceptible to collagenase degradation
• Therefore increases fibrosis by causing increased collagen
production and decreased collagen breakdown.
• Areca nuthigh copper content  stimulates fibrogenesis
through upregulation of copper dependent lysyl oxidase
activity

13. Chillies Ingestion
• Hypersensitivity reaction to chillies contribute
to oral submucous fibrosis
• Capsacian in chillies stimulates widespread
palatal fibrosis

14. Genetic and immunologic process
• following levels increased in these patients.
• Increased frequency of HLA-A 10,HLA-B7, HLA-
DR3, increased CD4 TO CD8 cells, increased
levels of proinflammatory cytokines,
decreased antifibrotic interferon gamma(IFN
Gamma).
• Increased IgA, IgG, IgM serum levels

17. INTERFERON GAMMA

18. Immunoglobulins

19. Immunoglobulins

20. SYMPTOMS

22. Early symptoms

23. Early symptom Pigmentation

24. Excessive Salivation(EARLY SYMPTOM)

25. Dry mouth (early symptom)

27. SYMPTOMS

28. Late symptoms

29. Late symptoms

30. Late symptoms

31. trismus

32. Flattening of palate

33. LATE STAGE

34. Deafness

35. Tongue protrusion difficulty(late stage)

38. CLASSIFICATION
PINDBORG J.J
• Oral submucous fibrosis is clinically divided into three
stages:
• Stage 1: Stomatitis
• Stage 2: Fibrosis
– a- Early lesions, blanching of the oral mucosa
– b- Older lesions, vertical and circular palpable fibrous
bands in and around the mouth or lips, resulting in a
mottled, marble-like appearance of the buccal mucosa
• Stage 3: Sequelae of oral submucous fibrosis
– a- Leukoplakia
– b- Speech and hearing deficits

39. SYED MEHMOOD HAIDER CLINICAL
AND FUNCTIONAL STAGING
Clinical Stage
• Faucial bands only
• Faucial and buccal bands
• Faucial,Buccal and labial bands
• Functional stage
• Mouth opening ≥ 20 mm
• Mouth opening 11-19 mm
• Mouth opening ≤ 10 mm

40. KHANNA AND ANDRADE
CLASSIFICATION 1995
Developed a group classification for the surgical
management of trismus
• Group I: Earliest stage without mouth opening
limitations with interincisal distance> 35 mm.
• Group II: interincisal distance of 26-35 mm.
• Group III: Moderately advanced case with interincisal
distance of 15-26 mm.
• Group IV A: ADVANCED CASES: Trismus is severe
,interincisal distance 2-15 mm and extensive fibrosis of
all the oral mucosa.
• Group IV B: ADVANCED CASES WITH MALIGNANT AND
PREMALIGNANT CHANGES

41. HISTOPATHOLOGY(mucosal changes)
1. Thinning of epithelium
2. Loss of rete ridges
3. Saw toothing
4. Liquefaction degeneration of basal layer
5. Pigment incontinence
6. Superficial ulceration
7. Areas of ulceration replaced by granulation tissue
8. Hyperplastic changes
(hyperkeratosis,acanthosis,parakeratosis,basal cell
hyperplasia,papillomatosis,psudoepithliomatous
hyperplasia)
9. Dysplastic changes

42. Rete ridges

43. histopathology

44. SAW TOOTHING

45. Histopathology( submucosal changes)
• Fibrosis (mild,moderate,severe)
• Diffuse chronic inflammatory infilterate
• Atrophy of minor salivary gland
• Skeletal muscle atrophy
• Band like infiltrate
• Edema and congestion
• Vesicle formation

46. Hall mark of histopathology
• Diffuse fibrosis in submucosa with chronic
inflammatory infiltrate

49. TREATMENT
• depends on the level of clinical involvement.
At a very early stage, cessation of the habit is
adequate. Medical/surgical treatment is
necessary for moderate to severe cases.
Surgical treatment is the method of choice in
patients with marked limitation of mouth
opening or in patients not responding to the
conservative management.

50. TREATMENT
• Preventive measures
• Medical treatment
• Physical therapy
• Surgical treatment

51. PREVENTIVE MEASURES

53. Medical treatment

54. Immune modulation

55. Surgical treatment
The treatment protocols
• Step 1: Excision of fibrotic bands with scalpel or
using lasers.
• Step 2: Coverage of the mucosal defect using flaps,
grafts and collagen membranes.
• Step 3: Adjunctive procedures intraoperatively
included coronoidectomies and masticatory muscle
myotomies.
• Step 4: Post operative oral physiotherapy, dietary
supplementation and other medications.

56. Fibrotic bands excision

57. EXCISION OF FIBROTIC BANDS

58. BUCCAL FAT PAD

59. Disadvantages of BFP
• Severe atrophy of buccal fat pads in patients
with chronic disease
• Anterior reach of buccal pad inadequate
• Region anterior to the cuspid required to be
left raw.
• Raw areas heal by secondary intention and
subsequently fibrosis leads to gradual relapse

60. NASOLABIAL FLAP
• Extended nasolabial flaps is raised from the tip of
nasolabial fold to the inferior border of mandible
in the plane of the superficial
musculoaponeurotic system from both terminal
points to the region of the central pedicle. The
pedicle is 1 cm lateral to the corner of mouth and
the diameter of the pedicle is roughly 1 cm. The
flap is transposed intraorally through a small
transbuccal tunnel near the commissure of the
mouth, with no tension and sutured over
intraoral defect

61. NASOLABIAL FLAP

62. NL FLAP INSERTION ORAL CAVITY

63. SUTURED FLAP

65. Oral stents

66. THE END