HPV DNA in clinically different variants of oral leukoplakia and lichen planus
HPV DNA in clinically different variants of oral leukoplakia and lichen planus
复制标题
DOI：
10.1016/j.tripleo.2004.04.012
复制
发表时间：
2004-12-01
期刊：
影响因子：
--
通讯作者：
D'Angelo, M
中科院分区：
文献类型：
--
作者：
Campisi, G;Giovannelli, L;D'Angelo, M
目标。我们的目的是确定口腔白斑(OL)和口腔扁平苔藓(OLP)中人乳头瘤病毒(HPV)感染的流行率，并与健康口腔黏膜进行比较，同时根据患者的年龄、性别、吸烟和饮酒习惯来确定HPV感染是否与口腔白斑或口腔扁平苔藓的特定临床变异有任何可能的联系。对68例口腔扁平苔藓(均质型45例，非均质性23例)和71例口腔扁平苔藓(非萎缩型27例，萎缩型44例)进行HPVDNA检测。用套式聚合酶链式反应(nPCR：MY09-MY11/GP5-GP6)检测口腔黏膜脱落细胞中的HPV DNA，并用DNA直接测序法确定HPV的基因分型。HPV DNA在口腔扁平苔藓、口腔扁平苔藓和对照组中的阳性率分别为17.6%、19.7%和5.6%，两组间HPV感染的风险均有统计学意义(口腔扁平苔藓：P=.01；优势比[OR]=3.64；95%可信区间：1.21~10.80；口腔扁平苔藓：P=0.005；OR=4.17；95%可信区间：1.41~12.18)。人口统计学变量分析显示，唯一显著的相关性是人乳头瘤病毒状态与OL患者当前吸烟(OR‘=3.40；95%CI：1.0-11.59)。HPVDNA在20%的HOL和13%的非HOL中检出，与临床变异无关(P=0.73；OR=0.60；95%CI：0.14~2.48)。HPVDNA在非AE型和AE型OLP中的阳性率分别为18.5%和20.4%，与临床变异无关(P=.84；OR=1.13；95%CI：0.335~3.816)。HPV-18型分别占OLP和OLP的9/12和10/14，其次是HPV-16(2/12 OL和2/14 OLP)、HPV-33(1/12 OL)、HPV-31(1/14 OLP)和HPV-6(1/14 OLP)。在OL和OLP中发现HPV感染的风险增加；然而，没有发现特定的OL或OLP临床变异与HPV感染有关。从口腔扁平苔藓和口腔扁平苔藓的临床特征无法预测HPV感染的可能性。
Objectives. Our objectives were to determine the prevalence of human papillomavirus (HPV) infection in oral leukoplakia (OL) and oral lichen planus (OLP) in comparison with that in healthy oral mucosa, also conditionally to age, gender, smoking, and drinking habits of patients, so as to investigate any possible association of HPV infection with a specific clinical variant of OL or OLP.Study design. We did research on HPV DNA in 68 cases of OL (homogeneous form [H] in 45 cases and nonhomogeneous form [non-H] in 23 cases), and in 71 cases of OLP (nonatrophic/erosive form [non-AE] in 27 cases, atrophic/erosive form [AE] in 44 cases). HPV DNA was investigated in exfoliated oral mucosa cells by nested PCR (nPCR: MY09-MY11/GP5-GP6) and the HPV genotype determined by direct DNA sequencing.Results. HPV DNA was found in 17.6% of OL, in 19.7% of OLP, and in 5.6% of controls, with a statistically significant higher risk of HPV infection in both lesion groups (for OL: P = .01; Odds Ratio [OR] = 3.64; 95% CI: 1.21-10.80; for OLP: P = .005; OR = 4.17; 95% CI: 1.41-12.18). Demographic variables analysis showed that the only significant association was between HPV status and current smoking in OL patients (OR' = 3.40; 95% CI: 1.0-11.59). HPV DNA was found in 20% of H OL and 13% of non-H OL, without any association with the clinical variant (P = .73; OR = 0.60; 95% CI: 0.14-2.48). HPV DNA was found in 18.5% of non-AE OLP and 20.4% of AE OLP, without any significant association with the clinical variant (P = .84; OR = 1.13; 95% CI: 0.335-3.816). HPV-18 was the most frequently detected genotype (9/12 and 10/14 of HPV-positive OL and OLP, respectively), followed by HPV-16 (2/12 OL and 2/14 OLP), HPV-33 (1/12 OL), HPV-31 (1/14 OLP), and HPV-6 (1/14 OLP).Conclusions. An increased risk of HPV infection was found in OL and OLP; however, no specific clinical variant of OL or OLP was noted to be associated with HPV infection. It is not possible to predict the likelihood of HPV infection from the clinical features of OL and OLP.