Oral submucous fibrosis

gift to all the students learning oral maxillofacial surgery

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. Areca nut

5. chillies

6. GENETIC AND IMMUNOLOGICAL

7. PATHOGENESIS

8. PATHOGENESIS Not well established Multifactorial Areca nut chewing Ingestion of chillies ( capsacian ) Genetic and immunologic processes Nutritional deficiencies Collagen disorders

9. 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

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

11. 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

12. INTERFERON GAMMA

13. I mmunoglobulins

14. I mmunoglobulins

15. SYMPTOMS

16. Early symptoms

17. Early symptom Pigmentation

18. Excessive Salivation(EARLY SYMPTOM)

19. Dry mouth (early symptom)

20. SYMPTOMS

21. Late symptoms

22. Late symptoms

23. Late symptoms

24. trismus

25. Flattening of palate

26. LATE STAGE

27. D eafness

28. Tongue protrusion difficulty(late stage)

29. 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

30. 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

31. 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

32. HISTOPATHOLOGY(mucosal changes) Thinning of epithelium Loss of rete ridges Saw toothing Liquefaction degeneration of basal layer Pigment incontinence Superficial ulceration Areas of ulceration replaced by granulation tissue Hyperplastic changes ( hyperkeratosis,acanthosis,parakeratosis,basal cell hyperplasia,papillomatosis,psudoepithliomatous hyperplasia) 9. Dysplastic changes

33. Rete ridges

34. histopathology

35. SAW TOOTHING

36. 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

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

38. 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.

39. TREATMENT Preventive measures Medical treatment Physical therapy Surgical treatment

40. PREVENTIVE MEASURES

41. Medical treatment

42. Immune modulation

43. 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.

44. Fibrotic bands excision

45. EXCISION OF FIBROTIC BANDS

46. BUCCAL FAT PAD

47. 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

48. 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

49. NASOLABIAL FLAP

50. NL FLAP INSERTION ORAL CAVITY

51. SUTURED FLAP

52. Oral stents

53. THE END