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ORAL SUBMUCOUS FIBROSIS
DR JAMEEL KIFAYATULLAH
DENTIST KHYBER COLLEGE OF
DENTISTRY PESHAWAR PAKISTAN
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.
Oral submucous fibrosis (WHO
DEFINITION)
Areca nut
chillies
GENETIC AND IMMUNOLOGICAL
PATHOGENESIS
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
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
Chillies Ingestion
• Hypersensitivity reaction to chillies contribute
to oral submucous fibrosis
• Capsacian in chillies stimulates widespread
palatal fibrosis
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
INTERFERON GAMMA
Immunoglobulins
Immunoglobulins
SYMPTOMS
Early symptoms
Early symptom Pigmentation
Excessive Salivation(EARLY SYMPTOM)
Dry mouth (early symptom)
SYMPTOMS
Late symptoms
Late symptoms
Late symptoms
trismus
Flattening of palate
LATE STAGE
Deafness
Tongue protrusion difficulty(late stage)
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
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
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
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
Rete ridges
histopathology
SAW TOOTHING
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
Hall mark of histopathology
• Diffuse fibrosis in submucosa with chronic
inflammatory infiltrate
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.
TREATMENT
• Preventive measures
• Medical treatment
• Physical therapy
• Surgical treatment
PREVENTIVE MEASURES
Medical treatment
Immune modulation
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.
Fibrotic bands excision
EXCISION OF FIBROTIC BANDS
BUCCAL FAT PAD
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
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
NASOLABIAL FLAP
NL FLAP INSERTION ORAL CAVITY
SUTURED FLAP
Oral stents
THE END

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Oral submucous fibrosis

  • 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)
  • 4.
  • 9.
  • 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
  • 12.
  • 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
  • 15.
  • 16.
  • 21.
  • 25. Dry mouth (early symptom)
  • 26.
  • 36.
  • 37.
  • 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
  • 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
  • 47.
  • 48.
  • 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
  • 52.
  • 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.
  • 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
  • 62. NL FLAP INSERTION ORAL CAVITY
  • 64.

Editor's Notes

  1. Loss of rete ridges
  2. enables closure of oral defects up to 3 × 5 cm and 6 mm in thickness