Prevalence of oral leukoplakia and lichen planus in 1167 Iranian textile workers

OBJECTIVE: To evaluate the prevalence of oral precancerous lesions in textile workers. MATERIALS AND METHODS: A cross-sectional study was undertaken to assess a total of 1167 textile factory workers randomly selected from a total of 6947. An overall 97 women and 1070 men aged 18-69 years (mean=31.8 years) were studied. Regular smoking during the past 6 months was considered as the smoker group. Leukoplakia lesions were classified in accordance to Axell criteria [Axell T, Pindborg JJ, Smith CJ and Van-der-waal I (1996). J Oral Pathol Med 25: 49]. RESULTS: The results showed that 115 workers (9.9%) had red and white lesions. Among these 43 positive detections (3.7%) had leukoplakia and six cases (0.5%) had lichen planus. The smoking habits of the workers were limited to cigarette smoking. There was a statistically significant positive correlation between tobacco smoking and oral leukoplakia (P<0.001). CONCLUSION: There was a statistically significant positive correlation between tobacco smoking and leukoplakia in this relatively young cohort with generally mild tobacco use. The prevalence of leukoplakia had an inverse relationship with the level of education.     

Incidence rates for oral leukoplakia and lichen planus in a Japanese population

BACKGROUND: Data on the incidence rates of potentially malignant diseases of the oral cavity in different populations is meagre. This is the first study to report on the age-specific incidence of oral leukoplakia and oral lichen planus from an industrialized country. METHODS: Annual screening for oral cancer and pre-cancer was undertaken in Municipal Health Centres in Tokoname city, Japan from 1995 to 1998. A total of 9536 volunteers aged 40-95 years participated in this programme. A cohort of 6340 (67%) subjects attended annual mouth examinations following a negative screen result at entry, allowing 13 072 person-years of observations. Some associated risk factors (tobacco and alcohol misuse) and health-related variables were also evaluated. RESULTS: Over a 4-year follow-up period, 18 new oral leukoplakias (all homogenous; 11 idiopathic and seven tobacco-associated) and 24 oral lichen planus (22 reticular, one erythematous and one ulcerative) were detected at screening and confirmed by re-examination at specialist units. The age-adjusted incidence rate for leukoplakia was 409.2 (95% CI: 90.6-727.9) in male and 70.0 (95% CI: 17.9-121.8) in female per 100,000 person-years observations. For lichen planus, the corresponding rates were 59.7 (95% CI: 7.4-112.1) and 188.0 (95% CI: 96.0-280.1). The age-adjusted incidence rate for tobacco-associated leukoplakia in males was almost 12 times compared with female (560.3 vs. 45.2 per 100,000). Age-specific incidence rates for oral leukoplakia varied by age groups. New oral leukoplakias were more prevalent on gingival/alveolar ridge (33.3%) than in other oral sites, and lichen planus at buccal site (33.3%). Prevalence of smoking habits among those positive for leukoplakia (38.9%) was higher compared with the screen-negatives (26.4%) but these differences did not reach statistical significance (P = 0.232). Regular drinking was not related to occurrence of either oral leukoplakia or oral lichen planus. In cases with diabetes mellitus, relative risk for oral lichen planus adjusted by logistic regression was 6.4 (95% CI: 2.4-17.6), suggesting an association. CONCLUSIONS: The reported incidence rates for oral leukoplakia in this Japanese population are somewhat higher to those reported from India, the risk habits of the two groups being markedly different. The reported rates for oral leukoplakia and lichen planus allow estimation of service needs in specialist oral medicine clinics and for the training of primary care dentists. A high incidence of idiopathic leukoplakia found in this study raises challenges to the strategy of screening high-risk populations aimed at conserving resources.     

Incidence of oral candidiasis and oral hairy leukoplakia in HIV-infected adults in North Carolina

OBJECTIVES: To establish incidence rates and risk factors for HIV-associated oral candidiasis (OC), oral hairy leukoplakia (OHL), and any HIV-associated oral diseases (HIV-OD). DESIGN: This prospective, cumulative case-control study followed 283 initially oral disease-free HIV-1-infected men and women for 2 years. Incidence rate ratios (IRR) and incidence proportions for OC, OHL, and HIV-OD were estimated. Multivariable analyses using Poisson regression determined the most parsimonious best-fitting model explaining the outcomes. RESULTS: Incidence rate (per 1000 person-months) was 9.3 for OC, 6.8 for OHL, and 13.5 for HIV-OD. Incidence of OC was associated with low CD4 count (adjusted IRR = 3.0 (95% CI = 1.7, 5.1)), smoking (IRR = 1.9 (1.0, 3.8)) and combination antiretroviral therapy (IRR = 0.3 (0.1, 0.8)). Incidence of OHL was associated with low CD4 count, conditional upon smoking status. Conclusions Low CD4 count and smoking are important risk factors for HIV-associated OC and OHL. Antiretroviral medications are protective for OC but not for OHL.     

云南地区成年人类免疫缺陷病毒感染患者口腔毛状白斑发病情况分析

目的探讨云南地区成年人类免疫缺陷病毒（HIV）感染患者口腔毛状白斑（OHL）的发病情况、临床特点及其与免疫状态的关系。方法以2008年1月-2010年6月收治的1 060例成年HIV感染患者为研究对象,收集信息包括每位患者的年龄、性别、教育程度、HIV阳性确诊时间、传播途径、口干症、口腔念珠菌病、临床高效抗逆转录病毒药物的使用及CD4细胞计数等,并通过口腔检查记录OHL的发病情况,分析OHL发病与CD4细胞计数的关系。结果1 060例HIV感染者中,检出OHL患者94例（8.9%）,其平均年龄为（39.33±10.45）岁。90%的OHL发生在舌的两侧缘,70.2%的患者其CD4细胞计数低于200 mm-3。结论OHL经常发生在严重的免疫抑制的患者中,与CD4细胞计数下降有关。     

Langerhans cells in candidal leukoplakia

Using histochemical and immunohistochemical methods, we examined specimens of candidal leukoplakia from the oral mucosa of 5 smokers to determine the morphological relationships between Candida and Langerhans cells (LC) in tissue sections. LC were fairly evenly distributed in control sections, but had a patchy distribution in lesions. Fewer LC were found in lesions than in control tissue, but the difference was not statistically significant. Candidal antigens were not detected on LC by the methods used, but we found ATPase-positive LC among, or at least near, intraepithelial candidal hyphae. However, sections double-reacted with anti-Candida and T6 antibodies to label candidal antigens and LC, respectively, showed a clear zone of epithelium between the T6-positive LC and the candidal hyphae. The difference in distribution of ATPase-positive and T6-positive LC may indicate locations of 2 subtypes of LC, or a change in T6 antigen expression by the LC closest to the candidal hyphae.     

Langerhans cells in candidal leukoplakia

Using histochemical and immunohistochemical methods, we examined specimens of Candidal leukoplakia from the oral mucosa of 5 smokers to determine the morphological relationships between Candida and Langerhans cells (LC) in tissue sections. LC were fairly evenly distributed in control sections, but had a patchy distribution in lesions. Fewer LC were found in lesions than in control tissue, but the difference was not statistically significant. Candidal antigens were not detected on LC by the methods used, but we found ATPase-positive LC among, or at least near, intraepithelial candidal hyphae. However, sections double-reacted with anti- Candida and T6 antibodies to label candidal antigens and LC. respectively, showed a clear zone of epithelium between the T6-positivc LC and the candidal hyphae. The difference in distribution of ATPase-positive and T6-positive LC may indicate locations of 2 subtypes of LC, or a change in T6 antigen expression by the LC closest to the candidal hyphae.     

Malignant transformation in oral leukoplakia

Abstract – A retrospective study on the incidence of malignant transformation in oral leukoplakia was performed covering the period from 1970 to 1980. Carcinoma developed in 11 of the 157 patients, and this 7% incidence increased to 8.9% when the same patients were followed prospectively for 6 more years. Dysplasia was fotind in biopsies from 51 patients (31.8%), and was significantly more frequent in women than men ( P <0.05). Dysplasia grade and cancer development were related to updated clinical and etiological parameters.     

Malignant transformation in oral leukoplakia

A retrospective study on the incidence of malignant transformation in oral leukoplakia was performed covering the period from 1970 to 1980. Carcinoma developed in 11 of the 157 patients, and this 7% incidence increased to 8.9% when the same patients were followed prospectively for 6 more years. Dysplasia was found in biopsies from 51 patients (31.8%), and was significantly more frequent in women than men (P less than 0.05). Dysplasia grade and cancer development were related to updated clinical and etiological parameters.     

Apoptosis-associated proteins in oral hairy leukoplakia

OBJECTIVE To test the hypothesis that the anti-apop totic ability of Epstein-Barr virus (EBV) may result in altered expression of apoptosis-associated proteins in oral hairy leukoplakia (HL), we evaluated HL tissue and normal epithelium for these proteins by immunohistochemistry.
MATERIALS AND METHODS Twenty formalin-fixed, paraffin-embedded specimens of HL lesions and six spedmens of normal control mucosa were selected from archived tissue specimens. Bcl-2. Bcl-x, Bax and p53 apoptoris-associated proteins were evaluated in immu-nohistochemically stained tissue sections according to staining intensity and pattern. The percentage of p53-positive burl cells was estimated in sequential fields.
RESULTS: Generalty, there were only slight differences in the expression of Bcl-2 and Bcl-x proteins in the epithelium of HL and control tissue. The staining for Bcl-2 was weaker in keratinocytes than in putative melano-cytes and Langerhans cells. Equivocal diffuse cytoplasmic staining of prickle cells was also noted. Keratinocytes throughout the epithelium stained positively for Bcl-x protein, although upper layers were more weakly stained. The 'balloon' keratinocytes in HL were infrequently positive for Bcl-x. Bax staining in HL differed from that in control tissue in being more heterogeneous. The staining reaction in HL was weak to negative in upper epithelial levels where 'balloon' keratinocytes were located. Weak to moderate nuclear p53 protein staining was detected in a mean of 25.3% of basal keratinocytes in all but one of the HL specimens; weak staining was seen in only two control specimens.
CONCLUSIONS: We found only slight immunohistochemid evidence that expression of the apoptosis-associated proteins is altered in HL. p53 appears to be over-expressed in HL; we speculate that this may be related to upregulation or stabilization of wild-type p53 protein related to EBV infedon.