ORAL SUBMUCOUS

FIBROSIS
PRESENTED BY GUIDED BY
GOURAB MITRA DR. KEERTHI. R.
IIND YR. MDS PROFESSOR
DEPT. OF OMFS DEPT. OF OMFS 1
 CONTENTS
1. INTRODUCTION
2. DEFINITION
3. CLINICAL MANIFESTATIONS
4. HISTOPATHOLOGICAL FEATURES
5. CLINICAL AND HISTOPATHOLOGICAL STAGING
6. INVESTIGATIONS
7. PATHOGENESIS
8. MALIGNANT TRANSFORMATION
9. MANAGEMENT
10. CONCLUSION
11. REFERENCES
2
 INTRODUCTION
• Growth and development of civilization and industrialization subjected humans to varied amount
of stress and tension.
• To adapt this, humans try psycho- stimulating and euphoria inducing habits such as smoking,
tobacco chewing, drinking alcohol, crippling mental and physical condition.
• In ancient Indian medicine Shusruta described a condition which he named as “Vidasi” presenting
symptom of progressive of mouth, depigmentation of oral mucosa and pain on taking food.
• S. G. Joshi (1953) and D. Lal (1953) were the first Indian workers to described this condition
and termed it as “Submucous fibrosis of palatal pillar”, and “Diffuse oral submucous fibrosis”
respectively.
• Oral submucous fibrosis is one of the devastative conditions resulting from these stress relieving
habits, that leads to progressive reduction in mouth opening, toughening of oral mucosa and
eventually greatly affects lifestyle. 3
 DEFINITIONS

“Insidious, chronic disease affecting any part of the oral cavity and
sometimes pharynx. Although occasionally proceeded by and/or
associated with vesicle formation, it is always associated with juxta-
epithelial inflammatory reaction followed by a fibro- elastic change of
the lamina propria with epithelial atrophy leading to stiffness of
mucosa and causing trismus and inability to eat.”
~ Pindborg J. J & Sirsat S. M. (1966)

4
Other names of the disease suggested are:

• Idiopathic scleroderma of mouth,

• Submucous fibrosis of palate,
• Submucous fibrosis of palate and cheek,
• Idiopathic palatal fibrosis,
• Oral submucous fibrosis,
5
 ETIOLOGY
Local factors:
• Chilli,
• Areca nut,
• Tobacco chewing, Lime,
• Excessive copper consumption,
• Paan chewing,
Systemic factors:
• Genetic susceptibility
• Multi vitamin deficiency,
• Any autoimmune diseases, 6
 CLINICAL MANIFESTATIONS
Symptoms:
• Prodromal symptoms
• Late symptoms

Prodromal Symptoms:
• Burning sensation on mouth when consuming food,
• Appearance of blisters especially on palate, ulceration or recurrent
generalized inflammation of oral mucosa, excessive salivation, detective
gustatory sensation and xerostomia,
• Mucosal blanching are seen and vertical bands become palpable in vertical direction, 7
• Periods of exacerbation and remission are seen along with small blisters or cheeks and palate
• Focal vascular dilations manifest clinical as petechiae in the early stages of the disease.
• Pain in the areas where vertical bands are palpable
• There may be marble- like appearance in the buccal mucosa

Late Symptoms:
Oral mucosa becomes leathery, more blanched, slightly opaque, along with white palpable,
inelastic, bands palpable, and restricted mouth,
Uvula becomes short, shrunken and appears like everted hockey stick, bud- like, or deviated.
Brown or blackish discolouration of the mucosa is seen,
Inability to whistle or blow out a match from a distance of a foot.
8
• The fibrous tissue in the faucial pillars, ranges from a slight submucosal accumulation in both
pillars to a dense fibrosis extending deep into pillars with tonsillar strangulation,
• It is this dense fibrosis involving the buccal mucosa and the pterygomandibular raphe, that causes
varying degrees of mouth opening,
• Slowly the tongue becomes depapilliated, fibrosed , thin, and smaller in size and has restricted
movement,
• Soft palate appears blanched and has no movements on
saying “ah”

9
• This dense fibrosis in more advanced stages starts spreading to pharynx and down to the piriform
fossa, and on palpation circular bands can be felt around the entire rima glottis.
• Also, in more advanced stages the fibrosis involves the nasopharynx, the patient may experience
referred pain to the ear and a nasal voice tone,

In more advanced stages, the following symptoms and signs become appearing:
• Thinning of lips,
• Sunken cheek,
• Masseter muscle hypertrophy.

10
 CLINICAL STAGING

Wahi et al (1966), classified OSMF into three clinical groups on the basis of clinical feature,
severity and extent of involvement.
(i) Group 1- Usually there are no symptoms referable to mucosal involvement. This lesion affect
one or other commonly involved anatomic sites, are focal in character, show pallor or whitish
discolouration, wrinkling of mucosa, and minimal induration.
(ii) Group 2- Soreness of mucosa, or increased sensitivity to spicy food, along with diffuse,
sensitive, white, indurated lesion, involving one or more anatomic sites,
(iii) Group 3- Symptoms are mainly due to restricted mouth opening, stretching at the labial
commissures and altered pronunciation, firm mucosal bands with surface ulceration or fissuring.

11
Ahuja and Agarwal (1971), classified OSMF clinically based on the extent and type of fibrosis:

• Class I: Localized fibrotic bands in the cheek, extending vertically from vestibular fornix on both
the sides.
In the order of frequency, these bands are usually located on the lips, in the premolar region and in
the 2nd molar region.
• Class II: Generalized diffuse hardening of subepithelial tissues extending from cheek and hard
palate to the soft palate, uvula, and pillar of fauces, and can extend to pharynx.
• Class III: Combination of the above two types, where the fibrous bands are associated with
generalized diffuse form of submucous fibrosis.
12
Gupta et al (1980): Clinically classified four stages of submucous fibrosis according to increasing
intensity of trismus:
1. Very early stage: Patient complaints of burning sensation in the mouth or ulceration without
any difficulty in opening the mouth.
2. Early stage: Along with the symptoms of burning sensation, there is slight difficulty in mouth
opening.
3. Moderately advanced stage: Marked trismus to the extent that patient can’t open mouth more
than fingers width, associated with difficulty in mastication too.
4. Advanced stage: Patient is undernourished, anaemic and shows marked trismus ad/or other
symptom, as mentioned.

13
Haider et al (2000), staged the disease both clinically and functionally:
Clinical Staging
• Stage I: Faucial bands only,
• Stage II: Faucial and buccal bands,
• Stage III: Faucial and labial bands,
Functional staging
• Stage A: Mouth opening~ 13- 20mm
• Stage B: Mouth opening~ 10-12 mm
• Stage C: Mouth opening <10 mm.
They concluded that the bands are common at the posterior region and are extension of the bands in
labial parts , increases the severity of the disease.
14
Kerr et al (2011): Proposed a disease grading system, consisting of five grades:
• Grade I: Mild, any features of the disease like (burning, depapillation, blanching, leathery
mucosa) and interincisal opening ~ 35 mm.
• Grade II: Moderate; the above features , with interincisal opening of ~ 35- 20 mm,
• Grade III: Severe, the above features, with interincisal opening of ~ 20 mm,
• Grade IV:
- Grade IV a: OSMF along with other potentially malignant disorder on clinical examination,
- Grade IV b: OSMF along with any grade of oral epithelial dysplasia on biopsy,
• Grade V: OSMF along with confirmed oral carcinoma.

15
16
17
 HISTOPATHOLOGICAL FEATURES
Epithelial changes:
• Early stage: Epithelial hyperplasia,
• Late stages: Epithelial atrophy, associated with and increased tendency for keratinizing
metaplasia, with reduced stratum spinosum, and Stratum Basale atypia can also be seen,

18
Subepithelial changes:
• Presence of submucosal edema,
• Loss of normal rete peg structure
• Juxta epithelial collagen is non- bifringent under polarized
light , amorphous, non- bundular,, and stains greyish pink
rather than the typical deep red appearance that normal
collagen have with Rinehart stain.
• Narrow blood vessels first in more superficial layer and then to more deeper layer.
• Infiltration of submucous layer with mast cells, lymphocytes and plasma cells.

19
STAGE HISTOPATHOLOGICAL FEATURES
I. • Fine fibrillar collagen with marked edema,
(Early) • Strong fibroblastic response,
• Blood vessels are normal but sometimes dilated and congested,
• Inflammatory cells are neutrophils and occasional eosinophils.
II. • Juxta epithelial hyalinization.
(Moderate) • Plump young fibroblasts in moderate no.,
• Collagen is separate with plump young fibroblasts.
• Blood vessels are dilated, and congested
• Submucous infiltration of neutrophils, eosinophils and plasma cells are present.
III. • Collagen is moderately hyalinized,
(Moderately • Fibroblastic response is less marked, with greater no. of adult fibrocytes,
Advanced) • Blood vessels are congested,
• Submucous infiltration of lymphocytes and plasma cells are seen.
IV. • Collagen completely hyalinized.
(Advanced) • Hyalinized areas are devoid of fibroblasts.
• Blood vessels are completely and narrowed and obliterated.
• Lymphocytes and plasma cells are predominant with loss of pigmentation. 20
 PATHOGENESIS
Basic mechanisms involved in the pathogenesis of OSF can be divided into four steps:

1. Occurrence of the chronic inflammation at the site of betel quid placement

2. Increased collagen synthesis

3. Collagen cross-linking

4. Decreased collagen degradation

21
22
23
24
 NUTRITIONAL DEFICIENCIES

• Hydroxyproline is an amino acid found only in collagen and is incorporated in collagen in

hydroxylated form (4 hydroxyl proline),
• This reaction requires iron and ascorbic acid,
• The decrease in iron levels may be due to utilization of iron in fibrosis.
• Lack of iron causes improper vascular channel formation and concomitant decrease in
vascularity, which makes percolation of esters of arecoline easier.
• Also for normal epithelium maturation iron containing enzyme cytochrome oxidase is required.
• In iron deficiency, levels of this enzyme is low and consequent atrophy of epithelium results,
which leads to burning sensation and ulcerations of oral cavity in areca chewers.
25
 COLLAGEN- RELATED GENES

• OSMF is a disease of dysregulation in collagen metabolism,

• Different enzymes such as collagenase, lysyl oxidase along with cytokine TGF-β have been
implicated,
• The genes COL1A2, COL3A1, COL6A1, COL6A3 have been linked with the progression of
the disease,
• Also polymorphism of gene coding for TNF- α has been reported in OSMF which in turn
inhibits collagen phagocytosis,
• The altered auto- antigen released from areca nut ingredient and damaged cells may induce
antibody production.
26
MALIGNANT TRANSFORMATION

27
 DIAGNOSIS
1. Habit history, and clinical features,
2. Blood Investigations:
Increased ESR, Mild increase in eosinophil count,
Microcytic and hypochromic RBCs,
Decreased serum iron, and TIBC,
Increased serum LDL, VLDL,
Increased gammaglobulins,
3. Immunofluorescence,
4. Incisional biopsy,
28
5. Neural network based pathological stage detection .
 TREATMENT
The exact causative factor for OSMF is a matter of conflict, but still some treatment options are
available to be considered:
1. Habit counselling,
2. Medical management,
3. Nutritional support,
4. Physiotherapy,
5. Microwave diathermy,
6. Ultrasound therapy,
7. Surgical treatment.
29
Medical Management

1. Corticosteroids

• Inhibits the production of inflammatory factor,

• Increases the apoptosis of inflammatory cells,
• Inhibits the proliferation of fibroblasts,
• Up-regulation of collagen synthesis,
• Down-regulation of collagenase production.

30
Modalities of corticosteroids used in the treatment
Topical:
• Triamcinolone acetonide 0.1% (Kenacort)
• Betamethasone – 0.5% (Betnesol)
Systemic :
• Prednisolone – 20 mg/day (Wysolone)
• Dexamethasone – 4mg/day (Dexona)
• Triamcinolone – 12mg/day (Kenacort)
Intralesional :
• Dexamethasone – 4mg/ml (Inj. Dexona)
• Triamcinolone - 40 mg/ml (Inj. Kenacort)
• Hydrocortisone – 25 mg/ml (Inj. Wycort) 31
• Short acting drugs: Hydrocortisone intralesional injection 1.5cc given once a week for a
duration of 12 weeks have proven to be beneficial.
Systemic corticosteroids were found to be useful in only early and mild cases.

• Intermediate acting drugs: Topical triamcinolone acetonide 0.1% and local injection of
triamcinolone acetonide can be used in very early and early cases.

• Long acting drugs: Dexamethasone 4mg intralesional injections, is given biweekly. Also if
given in combination with hyaluronidase gives better long term results. Betamethasone is given
as 4mg/ml intralesional injections biweekly.

32
2. Enzymes
(i) Chymotrypsin
Chymotrypsin, an endopeptidase, hydrolyses ester and peptide bonds and is used as a proteolytic and
anti-inflammatory agent,
Dosage: Chymotrypsin (5000 IU), twice weekly submucosal injections for 10 weeks.

(ii) Hyaluronidase
• Acts by depolymerizing hyaluronic acid, which is the ground substance in connective tissue,
lowering the viscosity of the intercellular cement substance, and decreasing collagen formation.
• Reduces burning sensation and trismus,
Dosage: Intralesional injections of 1500 IU of hyaluronidase mixed with 2% lignocaine twice daily
for 10 weeks.
33
(iii) Collagenase
• A lysosomal enzyme, capable of degrading phosphate esters, proteins, polysaccharides,
glycosides, and sulphate esters,
• Submucous proliferation, persistently good vascularization and a mild increase in thickness
usually are noticed 1 months after collagenous treatment,
Dosage: 2mg of collagenase materials dissolved in 1ml of distilled water for injection
purposes.

34
3. ANTIOXIDANTS
Antioxidants act by reducing the free radical reaction that can cause DNA mutations and
changes in lipid peroxidation of cellular membranes and changes in enzymatic activities
(i) Lycopene
Obtained from tomatoes,
• Shows abnormal fibroblast inhibition,
• Regulates lymphocyte response to stress,
• Interfere with adverse reaction to excessive local cytokine and growth factor secretion,
• Inhibit dysplastic cell proliferation,
• Exhibits highest physical quenching rate constant with singlet oxygen,
Dosage: 16mg of lycopene daily in 2 divided doses for 2 months, or,
2mg daily for 3 months.
35
(ii) Beta Carotene
A precursor of Vitamin A,
Antioxidant and radical trapping agent,
It:
• Maintains epithelial integrity,
• Improves cellular turnover rate,
• Dysplastic cellular growth are arrested,
• Increases immune response that retards neoplastic development,
• Decreases free radical damage,
• Increases T- lymphocytes and retard development of dysplastic cells,
36
(iii) Alpha- Lipoic Acid
Also called as thioctic acid is a sulphur containing substance, acts as a coenzyme in Krebs cycle
in decarboxylation of pyruvate and alpha- keto acids claimed to be the near-perfect antioxidant.
It:
• Removes hydroxyl radicals and hydrochlorous acid and thus terminates singlet oxygen
molecules,
• Indirectly maintain cellular antioxidant state by enhancing synthesis of endogenous low
molecular wt. antioxidant and reduces their uptake,
• Increases glutathione uptake.
Dosage: Alpha-lipoic acid 100 mg,
1 capsule per day for 30 days has shown reduction in burning sensation and improved
mouth opening
37
(iv) α- Tocopherol
Vitamin E (α- isoform), as in human only α- tocopherol is retained,
It:
• Has the antioxidant activity,
• Inhibits cell proliferation,
• Decreases platelet aggregation,
• Decreases monocyte adhesion.

Antioxidant potential ranking:

Lycopene > Vitamin E > α- Carotene > cryptoxanthin > β- Carotene
38
ELEMENTS

(i) Zinc
• Increases immune efficiency by increasing function of cell mediated innate immunity,
neutrophils, and NK cells,
• Increases macrophages, phagocytosis, intracellar killing and cytokine production,
• Needed for DNA synthesis, RNA transcription, and activation,

Generally Zn levels are educed in OSMF patients, which indicates utilization of Zn by neoplastic
cells causing Zn deficiency.

39
(ii) Selenium
An anticarcinogenic
It:
• Represents an active site of GSH peroxidase,
• Is an antioxidant, which inhibits unwanted cellar growth by eliciting methylated Se-
metabolites and Seleno- proteins.

Se levels are decreased OSMF patients,

40
Combination Antioxidant Drugs
Rationale for the Combination epidemiological studies have shown carcinogenesis occurs by
generation of ROS which act by initiating lipid peroxidation (LPO). Prevention against LPO
mediated damage is done by non-enzymatic antioxidants, especially β-carotene and vitamin E.
Since, there is an increase demand for antioxidants a combination therapy of all these
antioxidants is necessary.

Antoxid tablet: Containing beta-carotene 50 mg, Vitamin A palmitate 2500 IU, Vitamin E
acetate 10 IU along with Vitamin C, zinc, manganese and copper
Dosage: Thrice daily for 6 weeks has been shown to cause significant clinical improvement in
patients with oral submucous fibrosis

41
PERIPHERAL VASODILATORS
In OSF the deposition of collagen fibres can cause occlusion of blood vessels resulting in
restriction of nutrients substances from reaching the affected areas,
These drugs are used to improve the circulation and hemorheology.
(i) Pentoxifylline
A methylxanthine derivative having vasodilating properties,
It:
• Increases mucosal vascularity,
• Have anti inflammatory properties like altering fibroblast physiology, suppressing
leucocyte function and stimulating fibrinolysis.
• Produces increased RBC flexibility,
• Inhibits T- cell, B- cell activation
• Decreases RBS and platelet levels 42

Dose: (SR) 400mg given t.i.d. for 7 months

(ii) Nylidrin hydrochloride
• Produces vasodilation of arterioles of skeletal muscles,
• And also a peripheral vasodilator which affects the tissues in diffuse fibrosis to a noticeable
degree by relieving the local ischemic effects and also helps the nutritional and therapeutic
substances to reach the affected tissues.
• Effective only in oral reparation;
Dosage: 6mg
(iii) Buflomedil
• A vasoactive agent, acts on the microcirculation, relieves the ischemic effect and thus helps the
nutritional and therapeutic substances reach the affected tissues.
• Can be used as effective adjunct drug both in early and advanced cases of OSF.
43
Placental Extracts
• It is an aqueous extract of human placenta that contains nucleotides, enzymes, vitamins,
amino acids and steroids.
• They can be divided into four different fractions such as aqueous extracts, lipoidal extracts,
immune gamma globulins and tissue coagulants.
• Only the aqueous extracts of placenta acts as biogenic stimulators in the cellular metabolism
regulating the absorption of epithelium and increasing the physiological actions of the organs.
Aqueous extract of fresh human placenta contains:
a. Enzymes: alkaline and acid phosphatase, glutamic oxaloacetic acid transaminase, glutamic
acid and pyruvate transaminase.
b. Nucleotides: ribonucleic acid and deoxy ribonucleic acid, adenosine triphosphate.
44
c. Vitamins: Vit E, B1, B2, B4, B6, Pantothenic acid, Nicotinic acid, P-amino benzoic acid, Folic
acid, Choline, Inositol.
d. Amino acids: Alanine, Aspargic Acid, Cysteine, Glutamic Acid, Glycine, Histidine, Leucine,
Lysine, Phenyl Alanine, Proline, Serine, Threonine, Tryptophan, Tyrosine , Valine.
e. Steroids: 17- ketosteroids, cholesterol , cholesterol, cholesterol ester.
f. Fatty acids: linoleic acid, Linolenic acid, oleic acid and palmitic acid.
g. Trace elements: cadmium, potassium, calcium, magnesium, Copper, iron, phosphorous and
silicone,
Main effects: Anti- inflammatory effect, analgesic, local increase in blood flow, arrest of local
tissue growth.
Dosage: 2cc of placentrix injection intralesional at weekly intervals for 10 weeks was found to be
superior to cortisone. 45
Recombinant Human Interferon Gamma (γ- IFN)
Induces:
• Epithelial regulatory effect,
• Upregulation of antifibrotic cytokines in basal cellular layer and lamina propria,
• Down regulation of fibroblast proliferation and collagen synthesis,
Dosage: Intralesional injection of γ-IFN (0.01- 10.0 U/mL) 3 times daily for 6 months.

ANTI HELMINTHIC DRUGS

Levamisole
an immunomodulator which modifies both cellular and humoral immunity.
In OSF it reduces the level of IgG, IgA and IgM thus slow down the chronic inflammatory process.
Dosage: 150mg, three times daily for three consecutive days in a week for three alternate weeks or in
combination with two capsules of anoxid daily for six weeks showed symptomatic improvement. 46
COMBINATIONS:

1. 1.5 ml (37.5 mg) hydrocortisone mixed with 1500 IU of hyaluronase intralesional half dose
on each side at weekly interval for 22 week
2. Triamcinolone (10mg/ ml) combined with hyaluronase (1500IU) intralesional once in 15
days for a total of 11 injections,
3. Combination of dexamethasone, hyaluronase, and placental extract; about 2 ml of soln. to be
deposited at interval for 3 days in divided doses; and this course can be repeated after a
week.

47
IMMUNIZED MILK
Immunised milk is a type of skim milk produced from cows immunised with multiple human
intestinal bacteria, containing modest amounts of Vitamin A, C, B1, B2, B6, B12, nicotinic acid,
pantothenic acid, folic acid, iron, copper and zinc, and 20-30% higher concentration of IgG type
I antibody.
It has good anti-inflammatory effect, which can suppress the inflammatory reaction and
modulate cytokine production.
Tai et al advocated 45gms of immunised milk powder twice a day, for 3 months and observed
significant improvement in symptoms of OSF

48
 STEM CELL THERAPY
Stem cells are defined as immature or undifferentiated cells that are capable of generating
daughter cells identical to themselves or of differentiating into diverse cellular phenotypes.

49
Sankaranarayanan et al. have demonstrated the effectiveness of stem cell treatment in OSMF
patients by injecting 0.5–1 ml of marrow-derived stem cell concentrate into labial and buccal
mucosa and tongue under local anesthesia.

They found:
• Reduction in blanching,
• Improved suppleness of the mucosa,
• Decrease in the burning sensation while consuming spicy food,
• Significant increase in the mouth opening.

The results were found to be sustained in the follow-up period from 6 months to 5 years. 50
 PHYSICAL THERAPY
1. Kneading:
Gentle stretch over the buccal region in side the mouth with mild stretching over the fibrous
bands with in tolerable pain limits, and TMJ mobilization by Antero-inferior glides to improve
jaw depression.

2. Forceful Mouth- opening:

May be helpful to prevent further restriction of mouth movements and to prevent relapse.
Can be performed using clinically using, Hyster mouth gag, ezbite device,
Also home exercise with ballooning of mouth, hot water gargling, and ice-cream stick exercises,
can be performed,
Ice- cream stick exercises by placing ice-cream sticks between the jaws and increasing one by
51
one to provide stretch and maintaining for 3-5 minutes for 2-3 times a day can be performed.
3. Micro wave diathermy:
Utilized EM wave at 915 to 2456 MHz,
It acts by physiofbrinolysis of bands by selective heating of juxta epithelial connective tissue.
Unique features:
• Specifically absorbed in tissue with high water contain,
• Very minimal scattering.
Gupta D.S. et al, used microwave diathermy at 2450 MC/s daily for 20 mins at each site of the
lesion with 20 to 25 watts of energy, with 15 sittings given reported, the use of microwave
diathermy of great significance for moderately advanced stages but in very advanced cases
results were very poor.

52
Ultrasound Therapy
Frequency used is ~ 17000 Hz,
Ones used of therapeutic purpose has frequency of 0.8- 1 MHz and an intensity of 0.5- 3 W/sq.
cm,
Mechanism:
• Cell membrane permeability is increased by altering sodium and potassium ions,
• It also induces vasodilation, and causes increased lymph flow and improves metabolism
• Provides pain relief,
• Accelerated healing,
• Increases extensibility of collagen fibres

53
Dosage:
A 5 mm diameter transducer, should be used for 3- 4 mins on each side of cheek for 15
consecutive days with permissive one day off each week.

NUTRITIONAL SUPPORT
The rationale of giving nutrients in OSF patients is to correct deficiency states and promote
normal cellular processes,
Supplementing the diet with foods rich in vitamins A, B complex, and C and iron
• Advice green leafy vegetables, red tomatoes, fresh fruits.
• Advice Green tea
• High protein diet
54
 SURGICAL TREATMENT

• Surgical treatment is the treatment of choice in patients who have a severe trismus,

• The primary motive behind surgical treatment of OSMF is to release the fibrous bands to increase
the mouth opening, and to make sure that the increased mouth opening is maintained afterwards,

• Initially surgeons aimed at surgical elimination of the fibrotic bands which showed further scar
formation and recurrence of trismus, to prevent which, they started using various interpositional
graft materials

55
Fibrotomy and reconstruction with buccal fat pad flap

56
FIBROTOMY AND RECONSTRUCTION BY TEMPORALIS FLAP

57
Complications:
1. Flap necrosis- Caused by:
- Inadvertent trauma to pedicled flap development,
- If there is excessive tension in the flap, zygomatic bone can be
permanently taken out to relieve some tension.

2. Restricted mouth opening:

- Most likely due to postoperative edema,
- May be due to defect with retromolar area.

3. Temporal hollowing,
58
4. Facial nerve palsy- Generally seen in ~ 10 % of the cases, caused mainly by retraction, and
inexperience with anatomy
It is important to dissect in subperiosteal plane during zygomatic
dissection,

59
FIBROTOMY FOLLOWED BY RECONTRCTION WITH NASOLABIAL
FLAP

60
Inferiorly based Nasolabial Flap

61
Main disadvantages of inferiorly based nasolabial flap:

• Oro-cutaneous fistula,

• Bulkiness of the flap, and

• Delayed healing.

62
EXTENDED NASOLABIAL FLAP

63
Advantages of extended nasolabial flap over inferiorly based nasolabial flap:

• Robust vascularity,

• Better aesthetics,

• More available flap tissue for reconstruction,

64
Complications:

1. Partial flap necrosis, usually at the distal aspect of the flap,

2. Flap dehiscence,

65
FIBROTOMY AND RECONTRUCTION WITH TONGUE FLAP

66
Tongue Flap:

• Dorsal Tongue Flap

• Ventral tongue flap
• Double- and Single-Door Tongue Flap
• Lateral Tongue Flap
• Sliding and Island Tongue Flaps

67
Complication:

1. Altered tongue contour, which can lead to speech deformity,

2. Premature detachment (in case of double- door tongue flap), caused by either excessive
tongue movement, or inadequately securing the flap,
Remedy- Placement of Barton's bandage,
Use of K- wire to restrict tongue movement postoperative,
3. Rarely, flap necrosis can be seen due to excessively tight suturing of the muscles in the flap
in the distal end of the flap,

68
 CONCLUSION
OSMF is a commonly occurring and widely spread premalignant condition increasingly
affecting the youth.
The occurrence of OSMF in gutkha chewers is far more faster and more severe as compared in
other forms of areca nut products chewers. The easy availability and promotions of these areca
nut products specially gutkha and pan masala outside the schools colleges and social places has
impacted younger population in India which has led to the increased occurrence of OSMF a
premalignant condition and malignancies like SCC.
Now it is a time call to have a control on use of areca nut and its products in various forms
specially gutkha and pan masala.

69
 REFERENCES
1. BURKETT'S ORAL MEDICINE,
2. ORAL SUBMUCOUS FIBROSIS- MADAN KAPRE , SUDHANSHU KOTHE,

3. RAVI KIRAN ONGOLE

4. OPERATIVE ORAL AND MAXILLOFACIAL SURGERY (2ND EDITION)- JOHN LAGDON, MOHAN PATEL
5. ORAL SUBMUCOUS FIBROSIS: AN UPDATE (2015): UWE WOLLINA ET AL,

6. ORAL SUBMUCOUS FIBROSIS- CURRENT CONCEPTS OF AETIOLOGY & ITS MANAGEMENT- MANAS
GUPTA, PANKAJ MISHRA,
7. CLINICAL STAGING OF ORAL SUBMUCUOUS FIBROSIS- SHIVAKUMAR G. C.
8. IMMUNOLOCALIZATION OF CYTOKINES AND GROWTH FACTORS IN ORAL SUBMUCOUS FIBROSIS

M.F. HAQUE ET AL,

9. ORAL SUBMUCOUS FIBROSIS: ETIOLOGY, PATHOGENESIS, AND FUTURE RESEARCH- R. RAJENDRAN ET AL,
70
10. NON SURGICAL APPROACHES IN TREATMENT OF OSF USHA DAYANARAYANA,
11. RECENT ADVANCEMENTS IN ORAL SUBMUCOUS FIBROSIS MANAGEMENT: AN OVERVIEW M GUPTA
ET AL,
12. LITERATURE REVIEW ON STEM CELL TREATMENT & ORAL SUBMUCOUS FIBROSIS (OSMF) PRATHIPATY
JAMES SUDHAKAR1, P. B. KAMESWARARAO, P. B. KAMESWARARAO , P. B.,
13. ETIOPATHOGENESIS AND CLINICAL MANIFESTATIONS OF ORAL SUBMUCOUS FIBROSIS, A
POTENTIALLY MALIGNANT DISORDER: AN UPDATE ARTICLE IN INTERNATIONAL JOURNAL OF CURRENT
RESEARCH, AUGUST 2018: NAMAN RAJESHKUMAR RAO,
14. ORAL SUBMUCOUS FIBROSIS: CORRELATION OF CLINICAL GRADING TO VARIOUS HABIT FACTORS:
VANAJA REDDY ET AL,
15. THE CLINICO- HISTOPATHOLOGIC STUDY OF ORAL SUBMUCOUS FIBROSIS: A NEW STAGING
SYSTEM WITH TREATMENT STRATEGIES: YESHA V JANI, BHAVIN B DUDHIA,
16. PATHOGENESIS OF ORAL SUBMUCOUS FIBROSIS (REVIEW): SABA KHAN, LAXMIKANTH CHATRA,
17. SURGICAL INTERVENTIONS IN ORAL SUBMUCOUS FIBROSIS: A SYSTEMATIC ANALYSIS OF THE
LITERATURE: VENKATESH V. KAMATH,
18. ORAL SUBMUCOUS FIBROSIS: REVIEW ON MECHANISMS OF PATHOGENESIS AND MALIGNANT
TRANSFORMATION: RASIKA PRIYADHARSHANI EKANAYAKA AND WANNINAYAKE MUDIYANSELAGE 71

TILAKARATNE,
19. ORAL SUBMUCOUS FIBROSIS AS A PRECANCEROUS CONDITION: J. J. PINDBORG*, P. R. MURTI, R. B.
BHONSLE,
20. DRUG TREATMENT OF ORAL SUB MUCOUS FIBROSIS – A REVIEW: REVANT H. CHOLE, RANJIT KUMAR
P.A.,

21. PHYSIOTHERAPY IN TREATMENT OF ORAL SUBMUCOUS FIBROSIS RELATED RESTRICTED MOUTH

OPENING: ASHA V, NEVICA BARUAH,
22. AN APPROACH TO MANAGEMENT OF ORAL SUBMUCOUS FIBROSIS: CURRENT STATUS AND REVIEW
OF LITERATURE: RAMESH FRY ET AL,
23. PHYSIOTHERAPY FOR IMPROVING MOUTH OPENING & TONGUE PROTRUTION IN PATIENTS WITH
ORAL SUBMUCOUS FIBROSIS (OSMF): M VIJAY KUMAR,

24. ORAL AND MAXILLOFACIAL CLINICS,

72
THANK
YOU
73