Szarka K, Tar I, Fehér E, Gáll T, Kis A, Tóth E D, Boda R, Márton I, Gergely L
Department of Medical Microbiology, Medical and Health Science Center, University of Debrecen, H-4032 Debrecen, Nagyerdei krt. 98, Hungary.
Oral Microbiol Immunol. 2009 Aug;24(4):314-8. doi: 10.1111/j.1399-302X.2009.00516.x.
We investigated the potential role of human papillomaviruses (HPVs) in potentially malignant oral disorders, oral leukoplakia (OL) and oral lichen planus (OLP), and in oral squamous cell cancer (OSCC) in an Eastern Hungarian population with a high incidence of OSCC.
Excised tumor samples (65 OSCC patients) and exfoliated cells from potentially malignant lesions (from 44 and 119 patients with OL and OLP, respectively) as well as from healthy controls (72 individuals) were analysed. OLPs were classified based on clinical appearance, 61 patients had erosive-atrophic lesions (associated with higher malignancy risk, EA-OLP) and 58 had non-erosive non-atrophic lesions (with lower risk of becoming malignant, non-EA-OLP), respectively. Exfoliated cells collected from apparently healthy mucosa accompanied each lesion sample. HPV was detected by MY/GP polymerase chain reaction (PCR) and genotyped by restriction analysis of amplimers. Copy numbers in lesions were determined using real-time PCR. Prevalence rates, copy number distributions, and association with risk factors and diseases were analysed using chi-square test, t-test, and logistic regression, respectively.
We detected HPVs significantly more frequently in lesions than in controls (P < or = 0.001 in all comparisons). HPV prevalence increased gradually with increasing severity of lesions (32.8, 40.9, and 47.7% in OLP, OL, and OSCC, respectively). Copy number distribution patterns roughly corresponded to prevalence rates, but OLP and OL were comparable. HPV prevalence differed significantly between EA-OLP and non-EA-OLP groups (42.6 vs. 22.4%); EA-OLP group showed a prevalence similar to that found in OL.
HPVs may be involved in the development or progression of not only OSCC but also of potentially malignant oral lesions.
我们在口腔鳞状细胞癌(OSCC)发病率较高的匈牙利东部人群中,研究了人乳头瘤病毒(HPV)在潜在恶性口腔疾病、口腔白斑(OL)和口腔扁平苔藓(OLP)以及口腔鳞状细胞癌(OSCC)中的潜在作用。
分析了切除的肿瘤样本(65例OSCC患者)以及潜在恶性病变的脱落细胞(分别来自44例OL患者和119例OLP患者)和健康对照(72人)。OLP根据临床表现进行分类,61例患者有糜烂萎缩性病变(与较高恶性风险相关,EA-OLP),58例有非糜烂非萎缩性病变(恶变风险较低,非EA-OLP)。每个病变样本均采集了明显健康黏膜的脱落细胞。通过MY/GP聚合酶链反应(PCR)检测HPV,并通过扩增子的限制性分析进行基因分型。使用实时PCR测定病变中的拷贝数。分别采用卡方检验、t检验和逻辑回归分析患病率、拷贝数分布以及与危险因素和疾病的关联。
我们在病变中检测到HPV的频率显著高于对照组(所有比较中P≤0.001)。HPV患病率随病变严重程度增加而逐渐升高(OLP、OL和OSCC中分别为32.8%、40.9%和47.7%)。拷贝数分布模式大致与患病率相对应,但OLP和OL相当。EA-OLP组和非EA-OLP组的HPV患病率差异显著(42.6%对22.4%);EA-OLP组的患病率与OL中的相似。
HPV可能不仅参与OSCC的发生或发展,还参与潜在恶性口腔病变的发生或发展。