Indian Journal of Dental Research

ORIGINAL RESEARCH
Year
: 2007  |  Volume : 18  |  Issue : 3  |  Page : 106--111

Oral submucous fibrosis: A clinico-histopathological study in Chennai


K Kiran Kumar1, TR Saraswathi2, K Ranganathan2, M Uma Devi2, Joshua Elizabeth2,  
1 Department of Oral and Maxillofacial Pathology, SDM Collage of Dental Science and Hospital, Sattur, Dharwad - 580 007, India
2 Department of Oral and Maxillofacial Pathology, Ragas Dental Collage and Hospital, Chennai, India

Correspondence Address:
K Kiran Kumar
Department of Oral and Maxillofacial Pathology, SDM Collage of Dental Science and Hospital, Sattur, Dharwad - 580 007
India

Abstract

Background: Oral submucous fibrosis (OSF) is a precancerous condition associated with the use of areca nut in various forms. There are very few reports to correlate the clinical stage to histopathological grading in OSF. Materials and Methods: A hospital-based study was conducted on 75 OSF cases who visited our hospital in Chennai from 2000-2003. A detailed history of each patient was recorded along with a clinical examination. Biopsy was performed for histopathological correlation. Clinical stage of the disease in terms of the ability to open one«SQ»s mouth was correlated with histopathological grading. Results: The male to female ratio of OSF cases was 6:1. All forms of areca nut products were associated with OSF. Chewing of paanmasala was associated with early presentation of OSF as compared to chewing of the betel nut. Out of 57 cases, which were in clinical stage II, 91.2% had histological grading of I and II in equal proportions and 8.8% had histological grade III. Out of 13 cases that showed a clinical stage of III, 52% showed a histological grade of II, 40% grade III and 8% grade I. Conclusion: In the present study, there was no direct correlation between clinical stages and histopathological grading. The possibility of difference in the severity and extent of fibrosis in different regions of the oral mucosa and involved muscles were considered as contributory factors for this variation.



How to cite this article:
Kiran Kumar K, Saraswathi T R, Ranganathan K, Uma Devi M, Elizabeth J. Oral submucous fibrosis: A clinico-histopathological study in Chennai.Indian J Dent Res 2007;18:106-111


How to cite this URL:
Kiran Kumar K, Saraswathi T R, Ranganathan K, Uma Devi M, Elizabeth J. Oral submucous fibrosis: A clinico-histopathological study in Chennai. Indian J Dent Res [serial online] 2007 [cited 2022 Jun 28 ];18:106-111
Available from: https://www.ijdr.in/text.asp?2007/18/3/106/33785


Full Text

Oral sub mucous fibrosis (OSF) is a disease, which predominantly occurs in Indians and South East Asians. [1] OSF is an insidious, chronic disease affecting any part of the oral cavity and sometimes the pharynx and oesophagus. [2] It is characterized by a mucosal rigidity of varying intensity due to the fibroelastic changes of the juxtaepithelial layer, resulting in a progressive inability to open the mouth.

It has been suggested that consumption of chillies, nutritional deficiency, chewing of areca nut, genetic susceptibility, altered salivary constituents, autoimmunity and collagen disorders may be involved in the pathogenesis of this condition. [3] OSF is a well-recognized, potentially premalignant condition. Malignant transformation rates as high as 7.6% have been reported from the Indian subcontinent over a 17 year period. [4]

Over the past several decades, dental researchers reported different aspects of OSF, either as simple case reports, population-based studies or hospital-based case control studies. In addition, animal experiments and in vitro human fibroblast culture studies were carried out to analyse the aetiopathogenesis of OSF. [5] Histopathological studies with light microscopy and transmission and scanning electron microscopy were also done. [6] Yet, there is a paucity of studies, which correlates the clinical features to the various histopathological changes of OSF. The present study was undertaken to correlate the ability to open the mouth to the histopathological features seen under a light microscope.

 Materials and Methods



The cases were collected from the patients attending the department of Oral and Maxillofacial pathology in Ragas Dental College, Chennai during the period 2000-2003. A total of 75 cases were selected. This included cases reported during 2000 and 2001, both prospective and retrospective cases. For the latter type of cases, all clinical details and histopathology slides were retrieved from files of the oral and maxillofacial pathology department. For the other cases, case history was taken and clinical examination was done in visible light using a mouth mirror and a probe.

Clinical criteria for the diagnosis of OSF were difficulty in opening the mouth and associated blanched oral mucosa with palpable fibrous bands. Cases complaining of difficulty in opening the mouth due to other reasons like inflammation etc were excluded from the study. The distance between the interincisal edges was measured in mm for assessing the ability to open the mouth. Incision biopsy was done with the patient's consent. OSF cases were clinically categorized into three clinical stages according to their ability to open the mouth as given below:

Stage I - Mouth opening ≥ 45 mm

Stage II - Restricted mouth opening 20-44 mm

Stage III - Mouth opening ≤ 20 mm

The biopsy tissue was processed for paraffin embedding. Sections of 5 micrometer thickness were used for haematoxylin and eosin (H and E) staining. The sections were studied under a binocular light microscope.

The following histological details were recorded and graded:

Epithelium: Type of keratinization-para / orthokeratosis

Thickness-atrophic / hyperplastic

Dysplasia-mild / moderate / severe

Connective tissue: Type of fibrous tissue-loose / dense

Hyalinization-partial / complete

Inflammatory cells: Acute / Chronic; focal / diffuse; juxtaepithelial / perivascular

The histopathological grading is given below:

Patients' chewing habits are categorized as follows:

Betel nut: Use of betel / areca nut like kalipakku, kottai pakku or seeval; Betel quid: Use of betel leaf, lime and betel nut along with tobacco; Paanmasala: Various commercial brands in which the main ingredient is areca nut, to which sweetening and flavoring agents are added.

Statistical analysis

Data analysis and database management were done using SPSS (Statistical Package for Social Science) version 10.05. Person's Chi-square test was done to determine the association between variables. Student t-test was utilized to find out the mean age difference between genders. Measurement of agreement between clinical and histopathological grading was done using Kappa statistics. Due to the nonnormality of frequency / day and duration / year of the habits, the Kruskal-Wallis test was used to determine the significance of associations between the habits. A significance level of P et al.[7] in India. We also observed a male predominance and the male to female ratio was 6:1. Half of the study population was in the age group of 20-29 years. This observation is different from that of Pindborg et al. who reported the maximum number of OSF cases in the age group of 40-49 years in their study. Increase in the chewing habit of the areca nut without any tobacco and the use of various commercial products containing areca nut may explain the decrease in the age of OSF cases due to various chewing habits. The mean age of occurrence was lower in males than in females and the difference was statistically significant (P [1],[3],[8] In recent years, commercial preparations like paanmasala have become available in India and abroad. The main ingredient of these products is areca nut along with lime and catechu wrapped in a betel leaf with or without tobacco. Many patients with OSF give a history of chewing paanmasala.

In our study group, the patients had the habit of chewing either raw areca nut or the commercial areca nut products. Forty (81%) patients chewed paanmasala. Shah et al. reported that paanmasala chewing produced OSF changes in a shorter period of time than betel quid chewing. In our study, we observed that the mean duration of the habit in those who chewed betel quid was ten years while it was six years for betel nut chewers and five years for paanmasala chewers. We also found that the patients who used paanmasala with a greater frequency / day developed OSF with a shorter duration of the habit. This was consistent with the observation made by Shah et al.[9] who stated that the total duration of the chewing habit was not significantly correlated to OSF. This means that the exposure to the total burden of various harmful substances in a given period, i.e., daily consumption was more significant that the total duration of the habit. A similar observation was also reported by Maher et al. who stated that the daily consumption rate appears to be much more significant with respect to risk than the lifelong duration of the habit. [10]

It is well-documented that in OSF, there is a progressive inability to open the mouth and tongue movement gets restricted to varying degrees depending up on the severity of the disease process. In a study of 800 normal patients in South India conducted by Ranganathan et al., [11] it is reported that the average size of the mouth opening was 47.5 mm and 44.6 mm in males and females respectively. Based on interincisal distance, we grouped our OSF patients into three clinical stages. Seventy-five per cent of the males and 80% female OSF patients were in stage II (mouth opening 20 mm). This could be due to the fact that the majority of our patients reported for treatment only after the onset of restriction in their ability to open their mouths.

Seventy-five per cent of the patients in stage II had a habit of chewing commercially available areca nut products-"Paanmasala" and 50% of the total study population were in the age group of 20-29 years. It has been documented that paanmasala chewing was preferred by people in younger age groups (11-30 years). [12] In addition, onset of OSF changes occurred earlier with paanmasala chewing compared with areca nut / quid chewing. Absence of betel leaf, which has anti-oxidant properties and a consequently higher dry weight proportion of areca nut were responsible for early development of OSF. These findings are of great concern because younger individuals are at greater risk as it has been well established that OSF is a premalignant and crippling condition of the oral mucosa. [13]

OSF is a disease of altered collagen metabolism. The lesion is characterized by increased collagen fiber formation in the initial stages followed by formation of dense collagen fiber bundles and different degrees of hyalinization. This alters the flexibility of the mucosal tissue leading to restriction in the ability to open one's mouth. The histopathological grading followed in the study is as follows: loose, thin and thick fibres constituted grade I, loose or thick fibres with partial hyalinization grade II and sections that showed complete hyalinization grade III.

In our study, we did not find any association between clinical staging and histopathological grading. There were 57 cases in clinical stage II while there were 26 (45.6%) patients with a histological grade of II. Similarly, we had 13 patients in clinical stage III of whom one case (7.7%) had a histological grading of III, seven (53.8%) cases grade II and five (38.5%) cases grade I.

Haider et al.[14] who studied the clinical and functional grading of 228 OSF patients concluded that the bands formed initially in the fauces, followed by the buccal and labial areas. This is accompanied by an increase in the severity of the disease as measured by restriction in the ability to open the mouth. In our study, the site of biopsy was in the anterior buccal region, a site accessible to the surgeon to perform an incision biopsy. Patients with histopathological grading II could have had more collagenous bands in the posterior region, which could have been fewer in the anterior region. This may be the reason for the shift of some of the patients in clinical stage II to histopathological grade I and of some patients in clinical stage III to histopathological grades I and II.

Oral submucous fibrosis shows characteristic histopathological features consisting of an atrophic epithelium with juxtaepithelial hyalinization and collagen of varying density. Pindborg in his study of 53 biopsies found atrophy of the epithelium in 71.4% of the OSF patients. [15] Eighty per cent of all the histological grade III cases in our study showed epithelial atrophy. We observed mild epithelial dysplasia in 46%, moderate dysplasia in 52% and severe dysplasia in 2.0% of the cases. However, although we observed epithelial dysplasia, we did not have any case of OSF with features of malignant transformation.

It has been postulated by Caniff et al. that areca nut products exacerbate the submucosal fibrosis initiated by chronic inflammation. [16] The inflammatory cells seen predominantly were lymphocytes and plasma cells. The presence of a large number of lymphocytes and the production of cytokines play significant roles in the tissue reaction in OSF. In our study, 64% of the cases had diffuse chronic inflammation of which 54% had histological grade I, 39% histopathological grade II and 7% had histopathological grade III. Although chronic inflammatory cell infiltrate is a common feature in all three histopathological grades, it shows a reduced presence in histopathological grade III as a result of the stabilisation of the lesion and reduction in levels of proinflammatory mediators.

 Conclusion



In this study, the occurrence of OSF was higher in the younger age group of 20-29 years. The prevalence of OSF was more in males than in females with a ratio of 6:1. The number of patients with a paanmasala chewing habit (68.0%) was higher than the number of patients with betel nut (17.4%) or betel quid chewing habits (14.6%). The chewing of paanmasala was associated with earlier presentation of OSF as compared to betel nut chewing. Significant and direct correlation to the manifestation of OSF was seen with frequency rather than duration of chewing.

The maximum number of patients (74.3%) as well as most of the paanmasala chewers were in clinical stage II. Although various degrees of epithelial dysplasia were observed, malignant transformation was not seen. There was no correlation between clinical staging to histopathological grading. This observation could be explained by the fact that patients with higher histopathological grading could have had more collagenous bands in the posterior region, which restricted the mouth opening. Chronic inflammatory cell infiltrate was observed in a large number of cases in histopathological grade I but less so in higher histopathological grades, possibly due to a stabilisation of the lesion and a decrease in the levels of proinflammatory mediators.

References

1Neville BW, Allen CM, Damm DD, Bouquot JE. Oral and Maxillofacial pathology. WB Saunders Company: Philadelphia; 1995. p. 291.
2Shafer WG, Hine MK, Levy BM. A text book of oral pathology. WB Saunders Publication: Philadelphia; 1983. p. 109.
3Murthi PR, Bhonsle RB, Gupta PC, Daftary DK, Pindborg JJ, Mehta FS. Etiology of Oral submucous fibrosis with special references to the role of areca nut chewing. J Oral Pathol Med 1995;24:145-52.
4Murti PR, Bhonsle RB, Pindborg JJ, Daftary DK, Gupta PC, Mehta FS. Malignant transformation rate in oral submucous fibrosis over a 17-year period. Community Dent Oral Epidermol 1985;13:340-1.
5van Wyk CW, Oliver A, Hoal Van Helden EG, Grobler Rabie AF. Growth of oral and skin fibroblasts from patients with oral sub mucous fibrosis. J Oral Pathol Med 1995;24:349-53.
6van Wyk CW, Seedat HA, Phillips VM. Collagen in oral submucous fibrosis: An Electron microscopic study. J Oral Pathol Med 1990;19:182-7.
7Sinor PN, Gupta PC, Murthi PR, Bhonsle RB, Daftary DK, Mehta FS, et al. A case control study of oral sub mucous fibrosis with special reference to the etiologic role of areca nut. J Oral Pathol Med 1990;19:94-8.
8Canniff JP, Harvey W, Harris M. Oral submucous fibrosis: Its pathogenesis and management. Br Dent J 1986;21:429-34.
9Shah N, Sharma PP. Role of chewing and smoking habits in the etiology of oral submucous fibrosis: A case control study. J Oral Pathol Med 1998;28:475-9.
10Maher R, Lee AJ, Warnakulasuriya KA, Lewis JA, Johnson NW. Role of areca nut in the causation of Oral submucous fibrosis: A case control study in Pakistan. J Oral Pathol Med 1994;23:65-9.
11Ranganathan K, Uma Devi M, Elizabeth Joshua, Arun Bhardwaj, Rooban T, Viswanathan R. Mouth opening, cheek flexibility and tongue protrusion parameters of 800 normal patients in Chennai, south India - A base line study to enable assessment of alteration in oral sub mucous fibrosis. JIDA 2001;72:78-80.
12Anil S, Beena VT. Oral submucous fibrosis in a 12 year old girl: Case report. Pediatr Dent 1993;15:120-2.
13Pindborg JJ, Bhonsle RB, Murti PR, Gupta PC, Daftary DK, Mehta FS. Incidence and early forms of oral sub mucous fibrosis. Oral Surg Oral Med Oral Pathol 1980;50:40-4.
14Haider SM, Merchant AT, Fikree FF, Rahbar MH. Clinical and functional staging of oral submucous fibrosis. Br J Oral Maxillofac Surg 2000;38:12-5.
15Pindborg JJ, Mehta FS, Daftary DK. Occurrence of epithelial atypia in 51 Indian villages with oral submucous fibrosis. Br J Cancer 1970;24:253-7.
16Canniff JP, Harvey W. The aetiology of oral submucous fibrosis: The stimulation of collagen synthesis by extracts of areca nut. Int J Oral Surg 1981;10:163-7.