Kaplan I, Vered M, Moskona D, Buchner A, Dayan D
Department of Oral Pathology and Oral Medicine, Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Israel.
Oral Dis. 1998 Sep;4(3):194-9. doi: 10.1111/j.1601-0825.1998.tb00278.x.
Inflammatory papillary hyperplasia of the palate (IPHP) or the granular type of denture stomatitis, is a non-neoplastic lesion characterized histologically by a significant epithelial hyperplasia and inflammatory infiltrate usually caused by trauma and Candida infection. p53 and proliferative cell nuclear antigen (PCNA) are cell-cycle regulators, that when overexpressed, are considered by many investigators as markers of malignant transformation. The objective of this study was to investigate the immunodetection of p53 and PCNA in IPHP, and to correlate these results with the degree of epithelial hyperplasia and inflammatory infiltrate.
In 12 cases diagnosed clinically as IPHP, Candida was cultured from the denture base and the palatal mucosa. Lesions were biopsied and stained with H&E for histomorphometric analysis of the epithelial width and inflammatory infiltrate. PAS and Gram stains were used for screening of Candida. Sections were immunostained with DO-7 for p53 and PC-10 for PCNA. Fifteen palatal biopsies obtained from autopsies of edentulous subjects with normal palatal mucosa served as controls.
All cultures of swabs from both the palatal mucosa and denture base were positive for Candida. Candidal hyphae could not be identified in PAS stained sections. Small foci of Gram-positive organisms were found in two cases of IPHP. Epithelial width and inflammation were significantly higher in IPHP than in controls (P < 0.001). A three-fold increase in positively stained cells for p53 and a two-fold increase in positively stained cells for PCNA were seen in IPHP compared with controls (P < 0.001).
Although a significant increase in the immunodetection of p53 and PCNA may indicate a malignant potential, IPHP has never been reported to undergo malignant transformation nor is it associated with cytologic signs of dysplasia. The increase in the epithelial width and inflammation degree is probably associated with the colonization of the denture bases with Candida organisms. The increased detection of p53 and PCNA can be a secondary effect of cytokines originating from both the inflammatory cells and the keratinocytes. Thus, immunodetection of p53 and PCNA by current immunohistochemical methods on archival tissues is neither specific nor sensitive enough to be used as indicators for malignant potential in the absence of cytological dysplastic changes or genetic proof of mutated cell cycle genes.
腭部炎性乳头状增生（IPHP）或颗粒型义齿性口炎是一种非肿瘤性病变，组织学特征为显著的上皮增生和炎症浸润，通常由创伤和念珠菌感染引起。p53和增殖细胞核抗原（PCNA）是细胞周期调节因子，当过度表达时，许多研究者认为它们是恶性转化的标志物。本研究的目的是调查IPHP中p53和PCNA的免疫检测情况，并将这些结果与上皮增生程度和炎症浸润情况相关联。
在12例临床诊断为IPHP的病例中，从义齿基托和腭黏膜培养念珠菌。对病变进行活检，并用苏木精-伊红（H&E）染色，用于上皮宽度和炎症浸润的组织形态计量分析。过碘酸雪夫（PAS）染色和革兰氏染色用于念珠菌筛查。切片用DO-7抗体免疫染色检测p53，用PC-10抗体免疫染色检测PCNA。从无牙颌受试者尸检中获取15例腭部活检组织，其腭黏膜正常作为对照。
腭黏膜和义齿基托拭子的所有培养物念珠菌均呈阳性。在PAS染色切片中未发现念珠菌菌丝。在2例IPHP病例中发现革兰氏阳性菌小病灶。IPHP中的上皮宽度和炎症程度显著高于对照组（P < 0.001）。与对照组相比，IPHP中p53阳性染色细胞增加了三倍，PCNA阳性染色细胞增加了两倍（P < 0.001）。
尽管p53和PCNA免疫检测的显著增加可能表明有恶性潜能，但从未有IPHP发生恶性转化的报道，它也与发育异常的细胞学迹象无关。上皮宽度和炎症程度的增加可能与义齿基托被念珠菌定植有关。p53和PCNA检测增加可能是炎性细胞和角质形成细胞产生的细胞因子的继发效应。因此，在存档组织上通过当前免疫组织化学方法对p53和PCNA进行免疫检测，在没有细胞学发育异常变化或细胞周期基因突变的遗传证据的情况下，既不够特异也不够敏感，不能用作恶性潜能的指标。
