The prevalence of oral leukoplakia in 138 patients with oral squamous cell carcinoma

OBJECTIVES: To determine the relationship between oral leukoplakia (OL) and oral squamous cell carcinoma (OSCC), and to evaluate possible differences between those carcinomas with and without associated leukoplakia. MATERIAL AND METHODS: A total of 138 patients were studied at the Stomatology Service of the University General Hospital, Valencia, Spain. These patients were divided into two groups: group 1, patients with oral cancer and leukoplakia, and group 2, patients with OSCC but with no associated premalignant lesions. The relationship between this precancerous lesion and the OSCC was evaluated, as well as the possible clinical and histological differences between the tumours of the two groups. RESULTS: Leukoplakia was detected in 27 (19.56%) patients with OSCC. No differences were found between the two groups regarding age and tumour location. However, statistically significant differences were observed with respect to the form, tumour stage and the presence of adenopathies in the cancers with and without leukoplakia; in that the tumours associated with leukoplakia were diagnosed as being at a more initial stage. CONCLUSIONS: Those patients with OL associated with oral cancer presented with tumours at a less advanced stage than those where no associated leukoplakia existed.     

不同癌基因在口腔白斑和鳞癌中表达的研究

目的 研究正常口腔黏膜，口腔黏膜白斑及口腔鳞癌组织中不同癌基因的表达。方法 通过HE染色确定口腔黏膜组织类型，提取组织中RNA，采用RT－PCR的方法研究不同组织中c-myc、ras、cyclinD1及bcl-2基因的表达。结果 正常口腔黏膜中未见c-myc、ras、cyclinD1及bcl-2基因表达；轻、中、重度异常增生白斑和鳞癌组织中c-myc、ras、cyclinD1及bcl-2基因表达显著增加。结论 c-myc、ras、cyclinD1及bcl-2基因的表达增加与口腔黏膜白斑及鳞癌的发生相关。     

Midkine expression in oral squamous cell carcinoma and leukoplakia

J Oral Pathol Med (2012) 41 : 21–26 Background: Midkine (MK), a 13‐kDa heparin‐binding growth factor, is overexpressed in various human cancers. However, its role in the development and progression of oral cavity squamous cell carcinoma (OCSCC) is still unclear. Thus, the aim of this study was to evaluate the expression of MK in samples of OCSCC, leukoplakia, and healthy oral mucosa (control). Methods: Surgically excised specimens from patients with primary OCSCC (n = 28) were immunostained for MK, Ki‐67, PCNA, p53, bcl‐2, Bax, and CD31. Besides this, MK expression was also investigated in leukoplakia and normal oral mucosa. The relationship of MK⁺ cells with clinical parameters (tumor location, tumor size, lymph node metastasis, and survival) and microscopic parameters (WHO histological grading, intensity of inflammation, proliferation index, apoptosis, and angiogenesis) was also evaluated. Results: The results showed that MK expression was increased in OCSCC in relation to leukoplakia and normal mucosa. Furthermore, MK expression was increased in late‐stage tumors (T3/T4) compared with early‐stage lesions (T1/T2). MK‐positive lesions also showed increased expression of the anti‐apoptotic protein bcl‐2. Conclusion: OCSCC, particularly late‐stage tumors, exhibits increased MK expression, which may be involved in tumor progression via upregulation of anti‐apoptotic genes, as shown by the augmented bcl‐2 positivity in MK‐positive tumors.     

Concomitant leukoplakia in patients with oral squamous cell carcinoma

OBJECTIVE: There is an ongoing debate on the prevalence of premalignant lesions, in particular leukoplakia, at the time of diagnosis of an oral squamous cell carcinoma (OSCC). The aim of the present study was to determine the presence of concomitant leukoplakia in 100 patients with OSCC, and to evaluate possible differences in clinical and histopathological parameters of the OSCC between those with or without concomitant leukoplakia.PATIENTS AND METHODS: One hundred consecutive patients, 61 men and 39 women, with a histologically proven OSCC were screened on the presence of leukoplakia. Four groups were distinguished: (I) leukoplakia adjacent to the OSCC, (II) combination of leukoplakia adjacent to the OSCC, and leukoplakia at another oral site, (III) leukoplakia present at another oral site, but not adjacent to the OSCC, and (IV) no leukoplakia present.RESULTS: In 47 (47%) patients with OSCC the presence of concomitant leukoplakia was observed. Thirty-six (36%) patients had a leukoplakia adjacent to the OSCC (groups I and II), of which eight (8%) patients (group II) also had a leukoplakia present at another oral site. Eleven (11%) patients (group III) had no leukoplakia adjacent to the OSCC, but a leukoplakia present at another oral site. Fifty-three (53%) patients (group IV) with OSCC had no concomitant leukoplakia present. No differences were noted between men and women, nor was there any preference for an oral subsite with regard to the carcinoma. There were no statistically significant differences in clinical and histopathological presentation of OSCC's between those with or without concomitant leukoplakia.CONCLUSION: Almost 50% of oral squamous cell carcinomas are presumably associated with or preceded by leukoplakia. Early detection and active management of patients with oral leukoplakia may prevent the true development of a number of oral squamous cell carcinomas.     

单核苷酸多态性芯片在口腔白斑癌变监测中的应用

目的：运用单核苷酸多态性芯片检测口腔白斑（OLK）及鳞癌（OSCC）的DNA变化。方法：利用SNP6．0Array基因芯片对906,660个SNP（单核苷酸多态性）位点进行分型检测,对946,000位点进行拷贝数变异检测,DNA序列分析验证。结果：OLK和OSCC中存在复杂的遗传变异,主要位于染色体3、5、7、8、9、11、13、14、15、17、18上。结论：微阵列比较基因组杂交是研究OLK发病机制的新方法,多个基因参与OLK癌变的发生发展。     

白斑及鳞癌9p微卫星位点改变及与病理的关系

目的:探讨口腔白斑及鳞癌染色体9p上4个微卫星位点改变的状况及其与临床病理诊断的关系。方法:选择微卫星位点D9S171、D9S175 2、D9S1748和IFNA ,应用聚合酶链式反应-变性聚丙烯酰胺凝胶电泳-银染方法,检测3 9例口腔白斑及12例鳞癌,分析其微卫星不稳定(MSI)及杂合性缺失(LOH)状况。结果:不同病理组别间4个位点MSI及LOH总的检出率有显著性差异(P <0 .0 1)。其中LOH检出率在不同临床病理组别之间有显著性差异(P <0 .0 5 ) ;而MSI的检出率在不同临床病理组别之间无显著性差异(P >0 .0 5 )。不同病理组别间单个位点的MSI及/或LOH无显著性差异(P >0 .0 5 )。结论:口腔癌的发生是多阶段多基因共同作用的结果。4个微卫星位点附近可能存在与口腔鳞癌发生发展相关的抑癌基因。MSI在口腔癌前病变癌变早期即已发生,而LOH发生频率则随口腔癌前病变癌变的发生发展逐渐增高     

Proliferative verrucous leukoplakia and its progression to oral carcinoma: a review of the literature

BACKGROUND: Proliferative verrucous leukoplakia (PVL) is a distinct clinical form of oral leukoplakia defined by its progressive clinical course, changing clinical and histopathological features, and potential to develop into cancer. PVL behaves in a more aggressive and relentless manner than the more innocuous white oral lesions that it can resemble clinically. METHODS: A PubMed search was conducted which identified studies that examined patients with PVL and reported data meeting inclusion criteria. RESULTS: PVL is seen much more frequently in females and most often diagnosed after the sixth decade of life. Tobacco use is not strongly linked to the presence of PVL (63% of patients did not use tobacco products). Most (74%) of the patients with PVL progressed to oral carcinoma. CONCLUSION: PVL is a persistent and progressive oral lesion that requires very close follow-up along with early and aggressive treatment to increase the chances of a favorable outcome.