Oral submucous fibrosis

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Oral submucous fibrosis
Classification and external resources
ICD-10 K13.5
DiseasesDB 33590

Oral submucous fibrosis (OSF) is a chronic, complex, irreversible, highly potent pre-cancerous condition characterized by juxta-epithelial inflammatory reaction and progressive fibrosis of the submucosal tissues (lamina propria and deeper connective tissues). As the disease progresses, the jaws become rigid to the point that the sufferer is unable to open his mouth.[1][2] The condition is linked to oral cancers and is associated with areca nut chewing, the main component of betel quid. Areca nut or betel quid chewing, a habit similar to tobacco chewing, is practiced predominantly in Southeast Asia and India, dating back thousands of years.

History[edit]

In 1952, J. Schwartz coined the term atrophica idiopathica mucosa oris to describe an oral fibrosing disease he discovered in five Indian women from Kenya.[3] S.G. Joshi subsequently coined the termed oral submucous fibrosis (OSF) for the condition in 1953.[4]

Classification[edit]

Oral submucous fibrosis is clinically divided into three stages:[5]

  • 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

Khanna and Andrade in 1995 developed a group classification system for the surgical management of trismus:[6]

  • Group I: Earliest stage without mouth opening limitations with an interincisal distance of greater than 35 mm.
  • Group II: Patients with an interincisal distance of 26-35 mm.
  • Group III: Moderately advanced cases with an interincisal distance of 15-26 mm. Fibrotic bands are visible at the soft palate, and pterygomandibular raphe and anterior pillars of fauces are present.
  • Group IVA: Trismus is severe, with an interincisal distance of less than 15 mm and extensive fibrosis of all the oral mucosa.
  • Group IVB: Disease is most advanced, with premalignant and malignant changes throughout the mucosa.

Pathogenesis[edit]

Chronic exposure to betel nuts, chili, pepper and prolonged deficiency of iron and zinc may lead to an alteration in oral mucosa, which causes hypersensitivity to these irritants.

This hypersensitivity reaction may often results in a juxta-epithelial inflammation that leads to increased fibroblastic activity resulting in formation of collagen fibres in lamina propria.

These collagen fibers are non degradable and the phagocytic activity is minimized.

Symptoms[edit]

In the initial phase of the disease, the mucosa feels leathery with palpable fibrotic bands. In the advanced stage the oral mucosa loses its resiliency and becomes blanched and stiff. The disease is believed to begin in the posterior part of the oral cavity and gradually spread outward.

Other features of the disease include:

  • Xerostomia
  • Recurrent ulceration
  • Pain in the ear or deafness
  • Nasal intonation of voice
  • Restriction of the movement of the soft palate
  • A budlike shrunken uvula
  • Thinning and stiffening of the lips
  • Pigmentation of the oral mucosa
  • Dryness of the mouth and burning sensation
  • Decreased mouth opening and tongue protrusion

Causes[edit]

Dried products such as paan masala and gutkha have higher concentrations of areca nut and appear to cause the disease. Other causes include:

  • Immunological diseases
  • Extreme climatic conditions
  • Prolonged deficiency to iron and vitamins in the diet

Common sufferers[edit]

The incidence of the disease is higher in people from certain parts of the world including South-East Asia, South Africa and the Middle East.[7]

Treatment[edit]

Biopsy screening is mandatory before treatment. Treatment includes:

  • Abstention from chewing areca nut (also known as betel nut) and tobacco
  • Minimizing consumption of spicy foods, including chiles
  • Maintaining proper oral hygiene
  • Supplementing the diet with foods rich in vitamins A, B complex, and C and iron
  • Employing a dental surgeon to round off sharp teeth and extract third molars

Treatment also includes following:

  • The prescription of chewable pellets of hydrocortisone (Efcorlin); one pellet to be chewed every three to four hours for three to four weeks
  • Forgoing hot fluids like tea, coffee
  • Forgoing alcohol
  • Submucosal injections of hydrocortisone 100 mg once or twice daily depending upon the severity of the disease for two to three weeks
  • Submucosal injections of human chorionic gonadotrophins (Placentrax) 2-3 ml per sitting twice or thrice in a week for three to four weeks
  • Surgical treatment is recommended in cases of progressive fibrosis when interincisor distance becomes less than 2 centimetres (0.79 in). (Multiple release incisions deep to mucosa, submucosa and fibrotic tissue and suturing the gap or dehiscence so created by mucosal graft obtained from tongue and Z-plasty. In this procedure multiple deep z-shaped incisions are made into fibrotic tissue and then sutured in a straighter fashion.)
  • Pentoxifylline (Trental), a methylxanthine derivative that has vasodilating properties and increases mucosal vascularity, is also recommended as an adjunct therapy in the routine management of oral submucous fibrosis.

The treatment of patients with oral submucous fibrosis depends on the degree of clinical involvement. If the disease is detected at a very early stage, cessation of the habit is sufficient. Most patients with oral submucous fibrosis present with moderate-to-severe disease. Moderate-to-severe oral submucous fibrosis is irreversible. Medical treatment is symptomatic and predominantly aimed at improving mouth movements.

Stem cell therapy for oral submucosal fibrosis[edit]

Recently scientists have proven that intralesional injection of autologous bone marrow stem cells is a safe and effective treatment modality in oral sub mucosal fibrosis. It has been shown autologous bone marrow stem cell injections induces angiogenesis in the area of lesion which in turn decreases the extent of fibrosis thereby leading to significant increase in mouth opening.[8][9]

See also[edit]

References[edit]

  1. ^ Cox SC, Walker DM (Oct 1996). "Oral submucous fibrosis A review". Aust Dent J. London 41 (5): 294–9. 
  2. ^ Aziz SR (Spring 1997). "Oral submucous fibrosis: an unusual disease". J N J Dent Assoc 68 (2): 17–9. 
  3. ^ Schwartz J (1952). "Effects of the medicinal mushroom Agaricus blazei Murill on immunity, infection and cancer.". Atrophia Idiopathica Mucosae Oris. London. 
  4. ^ Joshi SG (1952). "Fibrosis of the palate and pillars". AIndian J Otolaryngol 4 (1). 
  5. ^ Pindborg JJ. Oral submucous fibrosis: a review. Ann Acad Med Singapore. 1989 Sep;18(5):603-7. View Abstract
  6. ^ Khanna JN, Andrade NN. Oral submucous fibrosis: a new concept in surgical management. Report of 100 cases. Int J Oral Maxillofac Surg. 1995 Dec;24(6):433-9.
  7. ^ http://emedicine.medscape.com/article/1077241-overview
  8. ^ Sankaranarayanan S, Padmanaban J, Ramachandran CR, Manjunath S, Baskar S, Senthil Kumar R, Senthil Nagarajan R, Murugan P, Srinivasan V, Abraham S (June 2008). "Autologous Bone Marrow stem cells for treatment of Oral Sub-Mucous Fibrosis - a case report". Sixth Annual Meeting of International Society for Stem Cell Research (ISSCR), Philadelphia, PA USA. 
  9. ^ Abraham S, Sankaranarayanan S, Padmanaban J, Manimaran K, Srinivasan V, Senthil Nagarajan R, Murugan P, Manjunath S, Senthil Kumar R, Baskar S (June 2008). "Autologous Bone Marrow Stem Cells in Oral Submucous Fibrosis – Our experience in three cases with six months follow-up". 8th Annual Meeting of Japanese Society of Regenerative Medicine, Tokyo, Japan 68 (12): 233–55. 

External links[edit]