| Objectives:Oral lichen planus (OLP) is chronic nonspecific inflammation of oral mucosa, which is a T cell-mediated autoimmune disease with significant risk of malignant potential. OLP was identified as a precancerous condition by WHO. The prevalence rate reported of OLP varied from 0.14% to 3.17%, and the carcinogenesis rate was 0.14% to 3.17%. The common age affected was between 30 and 60 years old, and with women more frequently.OLP could occur at any part of oral mucosa, but the first common site involved was buccal mucosa, second at tongue (mainly the dorsum), gingiva, labial mucosa, and vermilion of the lower lip. OLP lesions were usually complex and almost always had bilateral, symmetrical distribution. OLP showed small, raised, white, lacy lesions, papules, or plaques, and resembled keratotic diseases such as leukoplakia. Atrophic lesions and erosions were most likely to cause pain.OLP is characterized histologically by dense subepithelial lymphocytic infiltrated and vaculation and liquefaction of epithelial basal cells. The number of intraepithelial lymphocytes is increased and basal cell liquefied and disappeared. At the same time with epithelial cell apoptosis increased, and along with the inherent reduction of inflammatory cells. The basal keratinocytes degenerated and formed colloid or Civatte bodies, which appeared as homogenous eosinophilic globule. The ultrastructure of colloid bodies suggested that they were apoptotic keratinocytes.The incidence of OLP involved in many factors, such as local chronic mechanical damage, drug stimulation, dental materials, oral stimulation and tension, systemic diseases and genetic factors, and it may also be connected with some infection caused by bacteria or virus. A great deal of researches suggested that cell-mediated immune response, the release of cytokines and the abnormal apoptosis perhaps was main responsibility for OLP occurrence and development. So far, the mechanism of OLP incidence is not yet clear.OLP was first reported in 1869, and the different country had the different reports about OLP incidence over recent 100 years. Epidemiological data of domestic and foreign showed that OLP was ranged at the first common disease of oral mucosa except the recurrent ulcer. In 1981, the survey data from"The two diseases of oral leukoplakia and lichen planus"Collaboration Organization showed that the prevalence rate of OLP in some Chinese regions was 0.51%. So far, there is no epidemical information of OLP in Hebei province.Former researches showed that OLP had increased the malignant risk to oral squamous cell carcinoma, it was a potential cancerous oral mucosa lesion. A lot of factors were connected with the occurrence of OLP, the over- expression of Ki-67 and Cox-2 may be related closely to the development of OLP, as well as the mutation of p53 gene. The over-expression of Ki-67 implicated excessive cell proliferation, compared with the conventional proliferation of nuclear antigen PCNA, the background of Ki67 had small interference, and applied in nearly two years with more accurate and reliable to detect the cell proliferation.Cox-2 (cyclooxygenase, Cox-2) is also known as prostaglandin endoperoxide synthase, induced-type membrane protein located at the cell nucleus and endoplasmic reticulum. The expression of Cox-2 could be increased induced by a variety of factors (such as: the toxic, infection factor, growth factor, etc.) and it has a close relationship with apoptosis and tumor carcinogenesis.p53 gene is an important one of the tumor suppressor gene, can initiate apoptosis mechanism. A considerable research showed that: the mutation or inactivation wild-type p53 gene in malignant tumors and precancerous lesions resulted in dysfunction, is an important reason of carcinogenesis. Mutation of p53 gene may be related to the malignant transformation of the benign lesions of oral mucosa. Literatures reported that over-expression of P53 protein is connected with characteristic lesions and carcinogenesis of OLP. Mutation of p53 gene may relate to the incidence and development of OLP.The part I of this subject: Epidemiological investigation by multistage, stratified, quota-sampling method was adopted to evaluate the prevalence, incidence features and space distribution of OLP in Hebei province, so that to find out the more efficient diagnosis and treatment methods for Hebei people involved OLP.The part II of this subject: The clinical and pathological information of 101 patients with OLP were collected from the hospital of stomatology of Hebei Medical University. The expression of Ki-67 and Cox-2 were detected in 100 cases of OLP by immunochemistry, and compared with the normal oral mocusa and oral squamous cell carcinoma. The realationship of Ki-67, Cox-2 and potential carcinogenesis of OLP was discussed.The part III of this subject: The mRNA expression of mutation p53 gene in 60 cases of OLP was detected by RT-PCR, the three samples from each patient were collected by following regions: OLP lesion,adjacent tissue and normal tissue. The mRNA expression of mutation p53 gene of OLP was compared with oral squamous cell carcinoma in order to reveal the potential carcinogenesis risk of OLP, and provided a reliable basis for the early diagnosis, treatment and prevention of OLP.Methods1 The epidemiological investigation of OLP in Hebei province Based on"The Third National Oral Health Investigation Criteria", OLP was surveyed by using multistage, stratified, quota-sample methods estimated by the overall sample. Thirty-six regions were selected by random from three cities and three counties in Hebei province, the two age groups of 742 people were surveyed, the ratio of male and female was 1:1, a total of 1548 people were investigated. OLP diagnostic criteria: the diagnostic criteria of OLP according to the"Third national epidemiological survey of oral health programme". All data was dealt statistically with SPSS 10.0. 2 The relationship between the potential carcinogenesis risk of OLP and the expression of Ki-67 and Cox-2A total of 101 cases of OLP and 10 cases of oral cancer sample were enrolled. Additional 10 normal oral mocusa were used as the control. The expression of Ki-67 and Cox-2 were detected by immunochemistry (SP method). All data was dealt statistically with SPSS 10.0.by single-factor analysis of variance.3 The detection of mRNA expression of mutant p53 gene in OLP Sixty cases of OLP and 30 cases of oral cancer were confirmed by pathology. Twenty cases of normal oral mucosa were collected from the tissue around injury wound acted as the control. The mRNA expresstion of mutant p53 gene was detected by one-step RT-PCR. All data was dealt statistically with SPSS 10.0.by usingχ2–test.4 The detection of mRNA expression of p53 gene mutant in OLP and the adjacent tissues of the lesionThirty cases of OLP were confirmed by pathology. Three samples from the same patient were collected by the following three regions: OLP lesion,adjacent tissues and normal tissues, and 90 samples in total. The distance of the adjacent tissue far from OLP lesion was more than 0.5cm; the distance of the normal tissues far from OLP lesion was more than 1cm. All samples were obtained by patient agreement with the knowledge. The mRNA expression of mutant p53 gene was detected by one-step RT-PCR. All data was dealt statistically with SPSS 10.0.by usingχ2–test.Result1 The prevalence of oral lichen planus was 0.82% in the investigated people of Hebei province. The result was slightly higher than that of"The two diseases of oral leukoplakia and lichen planus"Collaboration Organization. It suggested that the prevalence rate of OLP of Hebei province was 95%, confidence interval was 0.38% to 1.26%.2 This epidemiological investigation showed that the statistically significant difference of the proportions of all kinds of oral mucosa disease, at present OLP was ranged the first common disease of oral mucosa except the recurrent oral ulcer.3 OLP was easy to happen on cheek, the illness had a tendency to increase with the age. There was no difference in rural areas and urban areas.4 Clinic-pathological features: One hundred and one cases of OLP were enrolled in this study, including 39 males and 62 females, age ranged from 21 to 78, with an average age of 48.8. The ratio of male and female was 1:1.6, there were more women than men. The most common site for the onset in cheek was of 81 cases, followed by the tongue of 11 cases; 5 cases in other gingival, 4 cases in lip.5 The pathological change of 101 cases of OLP: Epithelial hyperplasia and / or atrophy, basal cells were liquefied and disappeared, the band infiltrating lymphocytes were observed closely subepithelium. Epithelial hyperplasia was of 48 cases; epithelial atrophy of 22 cases; both epithelial hyperplasia and atrophy of 23 cases. Fifteen cases were with vesicle and 19 cases with epithelial erosion and ulcers. Mild epithelial dysplasia was involved in 7 cases and epithelial carcinogenesis in 1 case. The histopathology of oral squamous cell showed: the special-shaped tumor cells were of the polyhedral cells arranged nest, tended to keratosis with cancer beads.6 The expression of Ki-67 in OLP: Ki-67 was expressed in all 10 normal oral mucosa. The positive cells scattered distributed in the basal cell, the ratio of positive cells was 15.2%. Ki-67 was expressed in 93 cases out of 101 cases of OLP which located in epithelial hyperplasia or atrophy epithelial cells in the basement and adjacent cells, the ratio of positive cells was 37.1%. OLP with epithelial dysplasia, the ratio of positive cells was 47.0%. OLP with squamous cell carcinoma, the ratio of positive cells was 61.0%. Ki-67 was expressed in all cases of oral squamous cell carcinoma, the positive cells increased markedly with the up-regulated atypical basal cells and basal-like cells, the ratio of positive cells was 62.5%. Statistical analysis showed that the positive rate of OLP was higher than that of normal oral mucosa, lower than that of the oral squamous cell carcinoma (P<0.05), there was significant difference. There was no significant difference between the OLP (36.1%) and OLP with epithelial dysplasia (47.0%) (P> 0.05); there was significant difference between the OLP and OLP with carcinoma.7 The expression of Cox-2 in OLP: Cox-2 was not expressed in all 10 normal oral mucosa. Cox-2 was expressed in 36 cases out of 101 cases of OLP, the positive ratio was 35.6%, which both pathological changes showed Cox-2 over-expressed in the cytoplasm of stratum spinosum cells and stratum granulosum cells, basal cells submitted negative expression. OLP with epithelial dysplasia, the positive spinosum cells increased markedly with slight malignancy. OLP with carcinoma, the positive tumor cells infiltrated the mesenchyme. In the 36 cases of OLP positive, 16 cases were with the epithelial dysplasia, 9 cases with epithelial atrophy, 4 cases with both epithelial hyperplasia and atrophy, 6 cases with epithelial dysplasia, 1 case with epithelial carcinogenesis. Cox-2 was expressed in 2 out of 10 cases of carcinoma, which tumor cells grew infiltrated and showed obviously malignancy, the ratio of positive cells was 20.0%. There was significant difference among the normal (0%), OLP (36.1%) and OLP with epithelial dysplasia (47.0%) (P<0.05). There was no significant difference between OLP(35.6%)and oral squamous cell carcinoma(20.0%)(P>0.05).8 The results of mRNA expression of mutant p53 gene of OLP showed:There were 13 positive cases out of 60 cases of OLP, the positive rate was 21.67% (13/60). There were 16 positive cases out of 30 cases of oral cancer, the positive rate was 53.3% (16/30). There was 1 positive case out of 20 cases of oral normal mucosa, the positive rate was 5% (1/20). There were significant differences (P<0.017) between OLP and oral cancer in the positive rate of mutant p53 gene mRNA. There was no significant differences(P>0.05) between OLP and oral normal mucosa in the positive rate of mutant p53 gene mRNA. There were significant differences (P<0.017) between oral normal mucosa and oral cancer in the positive rate of mutant p53 gene mRNA.9 The detection of mRNA expression of p53 gene mutant in OLP and the adjacent tissues, the results showed: In the total of 90 samples from 30 cases of OLP, including OLP lesions, adjacent tissue and normal tissue of each case, 3 cases the mRNA of mutant p53 gene in 9 samples were all positive, accounting for 10% of all patients (3/30). Three cases the mRNA of mutant p53 gene in adjacent tissue were positive, but negative in OLP lesion and normal tissue, accounting for 10% of all patients (3/30). One case the mRNA of mutant p53 gene in OLP lesion was positive, but negative in adjacent tissue and normal tissue, accounting for 3.33 % of all patients (1/30). One case the mRNA of mutant p53 gene in OLP lesion and adjacent tissue were positive, but negative in normal tissue, accounting for 3.33 % (1/30).Conclusion1 The prevalence of oral lichen planus was 0.82% among the investigated persons in Hebei province. The 95% confidence interval of the prevalence rate of OLP in Hebei province was 0.38% to 1.26%.2 This investigation results showed that the significant difference of the proportions existed the all kinds of oral mucosa diseases, OLP was the first common disease in oral mucosa except the recurrent oral ulcer.3 The clinical pathology analysis showed that: The carcinogenesis rate of OLP was 0.9%, the incidence of precancerous lesions was 6.9%, implicated that OLP has potential carcinogenesis.4 The positive rate of Ki-67 expression increased from the normal oral mucosa to OLP and oral cancer in turn, the difference among the three groups was significant (P<0.05), The result suggested that the abnormal proliferation and atypical differentiation of epithelial cells were the mechanism of the carcinogenesis of OLP.5 There was no significant difference between OLP and OLP with epithelial dysplasia (P>0.05); but there was significant difference between OLP and OLP with carcinoma (P<0.05). The result implicated that there was a leap process of quantitative change from epithelial hyperplasia and malignant transformation to squamous cell carcinoma.6 The expression of Cox-2 showed significantly increased in the early stages of OLP with precancerous lesions, suggested that Cox-2 promoted and played a catalytic role in the carcinogenesis.7 There were significant differences (P<0.017) between OLP and oral cancer in the positive rate of mutant p53 gene mRNA. There was no significant differences between OLP and oral normal mucosa in the positive rate of mutant p53 gene mRNA (P>0.05). There was significant differences (P<0.017) between oral normal mucosa and oral cancer in the positive rate of mutant p53 gene mRNA.8 The potential mutation of p53 gene and carcinogenesis existed in the regions both OLP lesions and the normal oral mucosa within 1cm around OLP lesions .
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