|Year : 2021 | Volume
| Issue : 1 | Page : 12-17
Epidemiological and clinicopathological analysis of oral leukoplakia in Patna
Madhuresh Kumar, Manisha Singh, S Suwasini
Department of Oral Pathology and Microbiology, Buddha Institute of Dental Sciences and Hospital, Patna, Bihar, India
|Date of Submission||20-Feb-2020|
|Date of Acceptance||09-Sep-2020|
|Date of Web Publication||31-Dec-2020|
158-A, Anandpuri, West Boring Canal Road, Patna, Bihar
Source of Support: None, Conflict of Interest: None
Background: The early detection of oral potentially malignant disorder can reduce the transformation risk to oral squamous cell carcinoma, thereby reducing cancer morbidity and mortality. Aim: To obtain epidemiological information of oral leukoplakia (OL) and distribution of this disease in Patna. Subjects and Methods: Data were collected and analyzed for prevalence of OL among gender, age group, various oral sites, habits, and clinical and histopathological basis. Results: The overall prevalence shows high incidence of homogenous leukoplakia along with mild dysplasia in middle age male persons. Conclusion: Appropriate steps should be taken for early intervention, as it is the key to effective prevention.
Keywords: Epidemiology, leukoplakia, oral potentially malignant disorder
|How to cite this article:|
Kumar M, Singh M, Suwasini S. Epidemiological and clinicopathological analysis of oral leukoplakia in Patna. Indian J Dent Sci 2021;13:12-7
|How to cite this URL:|
Kumar M, Singh M, Suwasini S. Epidemiological and clinicopathological analysis of oral leukoplakia in Patna. Indian J Dent Sci [serial online] 2021 [cited 2021 Jun 20];13:12-7. Available from: http://www.ijds.in/text.asp?2021/13/1/12/305972
| Introduction|| |
Oral potentially malignant disorder (OPMD) is defined as “the risk of malignancy being present in a lesion or condition either during the time of initial diagnosis or at a future date.” Multiple conditions fall under OPMDs including leukoplakia, oral submucous fibrosis, lichen planus, and erythroplakia. Oral leukoplakia (OL) is one of the most common OPMD entity defined by the WHO as “a white plaque of questionable risk having excluded other known disease or disorders that carry no increased risk for cancer.” OL is more prevalent in men and presents clinically as white, hyperkeratotic, and well-defined plaques, which could be homogeneous or nonhomogeneous.
The early detection of OPMD can reduce the transformation risk to oral squamous cell carcinoma, thereby reducing cancer morbidity and mortality. Nevertheless, OPMD epidemiological and clinical spectrums may vary in different geographical districts within the same country. Multiple epidemiological studies on OPMD have been conducted previously in different parts of India. This study was conducted to determine the epidemiological profile and clinicopathological characteristics of OL among the population of Patna, Bihar, in 6 months of duration.
To obtain epidemiological information of the most common potentially malignant disorders leukoplakia and distribution of this disease in Patna with comparison among age, gender, site, and clinical and histopathological basis.
| Subjects and Methods|| |
This study was carried out on the data collected from selected patients reported in our consultancy and different associated private dental clinics of various locations of Patna and in 6 months of duration from June 2019 to November 2019. A total number of 200 patients diagnosed with OL were taken in the study. After taking informed consent, a proper clinical examination and essential investigation was carried out and final diagnosis was based on histopathological established.
A final analysis for the prevalence of OL was done among gender, age group, various oral sites, habits, and clinical and histopathological grade.
| Results|| |
The total number of cases taken was 200 and the age of the patients ranged from 20 to 75 years (mean age 53.83 years) [Table 1] and [Graph 1].
|Table 1: Mean age of study participants with minimum, maximum and standard deviation|
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Among all 200 patients, 160 were male and 40 were female. Gender distribution shows more common in males than females (ratio 4:1) [Table 2].
A high prevalence rate (93 out of 200) was observed amongst patients in 5th and 6th decade of life. [Table 3] .
Age and gender comparison shows high prevalence in females in the 5th and 6th decades [Table 4] and [Graph 2].
Habit distribution data showed that khaini and gutkha were the most common causes, followed by smoking, alcohol, and pan [Table 5] and [Graph 3].
The most frequent site for OL was found to be buccal and labial mucosa, followed by gingival, tongue, and floor of the mouth [Table 6] and [Graph 4].
Our study shows that the maximum numbers of cases are of homogenous leukoplakia, followed by ulcerative and nodular type. [Table 7] [Figure 1], [Figure 2], [Figure 3], [Figure 4].
|Table 7: Distribution of clinical features of lesion among study participants|
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The study data reveal that maximum cases were of mild dysplasia, followed by moderate and severe dysplasia. [Table 8] [Figure 5], [Figure 6], [Figure 7], [Figure 8].
|Table 8: Distribution of histological features of lesion among study participants|
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Distribution of clinical types in different age groups reveals high incidence of ulcerative and nodular leukoplakia in the 5th and 6th decades of life [Table 9] and [Graph 5].
Analysis of age-wise distribution of histological features reveals high incidence of moderate and severe dysplasia seen in the 5th and 6th decades of life [Table 10] and [Graph 6].
Gender-wise analysis of clinical and histological features shows nonsignificant distribution of cases among males and females [Table 11] and [Table 12].
| Discussion|| |
OL is a white patch or plaque that cannot be rubbed off, cannot be characterized clinically or histologically as any other condition, and is mostly associated with the chemical causative agent tobacco products. Therefore, a process of exclusion establishes the diagnosis of the disease. The term leukoplakia implies only the clinical feature of a persistent, adherent white plaque and therefore reserves the term for idiopathic lesions when investigations fail to reveal any cause. Histopathologically, OL is characterized by hyperkeratosis of ortho- or parakeratotic type along with different grades of epithelial dysplasia. However, histopathological features per se are not sufficient to establish the diagnosis; clinical features combined with histopathological changes establish the diagnosis.
It is well established that all leukoplakias do not progress to cancer, but they have a higher risk of malignant transformation unless diagnosed early and treated.
This study was conducted to assess the prevalence of Leukoplakia and determining the potential risk factors for its development in Patna population. The limitation of the study was a smaller sample size as more number of patients can provide more accurate data and better representation from all sections of the society. The results of this study showed that males were affected more often than females (M: F ratio 4:1). This finding is in concordance with Mishra et al., Dietrich et al., and Liu et al., showing increased incidence among males. This can be explained by a higher incidence of habit-related abuse in males.
Our findings show high prevalence of OL in the age group of the 5th and 6th decades of life. This findings were very much correlating with the study of Scott and Cheah and Waldron and Shafer who found the sixth and seventh decades as the most common age of occurrence. One of the salient finding of this study was increased number of cases in 3rd and 4th decades of life.
In clinical findings, it has been found that homogenous leukoplakia was most commonly seen and nodular was least prevalent. Similar findings and similar spectrum of distribution of OL were detected in a study conducted by Mishra et al.
In habits distribution it was observed that many patients were having more than one habit. Tobacco in both smokeless and smoked form along with gutkha and alcohol is the most frequent causative factors. These findings are in concordance with the existing literature. Iype et al. reported that 56.4% of patients with OPMDs were habituated to either tobacco chewing, smoking, or alcohol, while Khandekar et al. observed that 71.3% of patients were habituated to tobacco. 63.3% of patients were habituated to tobacco in the form of cigarettes or beedis. In a number of other studies, tobacco abuse, as well as alcoholic consumption, was found to be a causative factor for both oral premalignant lesions and oral cancer.
The study reveals that the most frequent site for OL is buccal and labial mucosa, followed by gingival, tongue, and floor of the mouth. This finding is very much similar along the study done by Mishra et al. They reported maximum number of cases present on buccal mucosa (52.26%), followed by tongue (31.23%), lips (11.7%), and palate (2.22%).
Our study data reveal that maximum cases were of mild dysplasia, followed by moderate and severe dysplasia. Lee et al., conducted a large scale analysis of 1046 patients with OL between 1997 and 2004 and found that 408 cases were of epithelial hyperplasia and hyperkeratosis. They reported 477 cases (45.6%) showing epithelial dysplasias of various degrees. Mild dysplasia was seen in 200 cases (19.12%), moderate in 234 (22.37%), and severe in 43 (4.11%) cases in their findings.
| Conclusion|| |
The overall prevalence of OPMD s was found to be 13.7% with OL to be more predominant in the Indian population. The consumption of tobacco and consumption of areca nut were identified as risk factors for the development of this disease. Individuals who have already developed this disorder may be advised to reduce the exposure to this risk factor which may prevent further progression of this disorder. Appropriate steps should be taken for early intervention, as it is the key to effective prevention.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12]