Campisi Giuseppina, Giovannelli Lucia, Aricò Pietro, Lama Anna, Di Liberto Chiara, Ammatuna Pietro, D'Angelo Matteo
School of Dentistry, Pontifical University Catholic, Porto Alegre, Brazil.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Dec;98(6):705-11. doi: 10.1016/j.tripleo.2004.04.012.
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.
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.
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).
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.
我们的目的是确定口腔白斑(OL)和口腔扁平苔藓(OLP)中人类乳头瘤病毒(HPV)感染的患病率,并与健康口腔黏膜中的患病率进行比较,同时根据患者的年龄、性别、吸烟和饮酒习惯进行条件分析,以调查HPV感染与OL或OLP的特定临床变体之间是否存在任何可能的关联。
我们对68例OL(45例均质型[H]和23例非均质型[非H])以及71例OLP(27例非萎缩/糜烂型[非AE]和44例萎缩/糜烂型[AE])的HPV DNA进行了研究。通过巢式PCR(nPCR:MY09-MY11/GP5-GP6)在脱落的口腔黏膜细胞中检测HPV DNA,并通过直接DNA测序确定HPV基因型。
在17.6%的OL、19.7%的OLP和5.6%的对照中发现了HPV DNA,两个病变组中HPV感染的风险在统计学上显著更高(对于OL:P = 0.01;优势比[OR]=3.64;95%置信区间:1.21-10.80;对于OLP:P = 0.005;OR = 4.17;95%置信区间:1.41-12.18)。人口统计学变量分析表明,唯一显著的关联是OL患者中HPV状态与当前吸烟之间的关联(OR' = 3.40;95%置信区间:1.0-11.59)。在20%的H型OL和13%的非H型OL中发现了HPV DNA,与临床变体无任何关联(P = 0.73;OR = 0.60;95%置信区间:0.14-2.48)。在18.5%的非AE型OLP和20.4%的AE型OLP中发现了HPV DNA,与临床变体无任何显著关联(P = 0.84;OR = 1.13;95%置信区间:0.335-3.816)。HPV-18是最常检测到的基因型(分别在HPV阳性的OL和OLP中占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感染风险增加;然而,未发现OL或OLP的特定临床变体与HPV感染相关。无法根据OL和OLP的临床特征预测HPV感染的可能性。