声带鳞状细胞癌早期改变的病理学观察

Pathologic features of the early change of squamous cell carcimoma in vocal cords

目的探讨声带鳞状细胞癌早期病理学的特点,提高病理诊断水平。方法总结89例声带鳞状细胞癌早期改变病例的病理资料,对其石蜡切片进行HE染色、PAS染色及p53、Ki-67免疫组化染色;以59例声带角化症(分为单纯增生组40例和异型增生组19例)和30例声带浸润癌(浸润深度>3mm的癌)作为对照。结果在HE染色下,声带鳞状细胞癌的早期改变可区分为两种类型:Ⅰ型为上皮全层癌变型,占67.4%(60/89);Ⅱ型为上皮基底层及副基底层癌变型,占32.6%(29/89),又可分为Ⅱa和Ⅱb两个亚型。HE染色显示有可疑微小浸润者52例,PAS染色示其中的43例(83%)的可疑病灶周边基膜样物质消失,有微浸润,Ⅰ型微浸润的比例较Ⅱ型明显偏低(P=0.007)。HE染色下3例(3.4%,3/89)认为无微浸润者经深切证实有浸润,并经PAS染色确认。Ⅰ型和Ⅱ型的p53表达率差异无显著性(P=0.445),而Ki-67阳性率Ⅰ型高于Ⅱ型(P=0.048)。癌早期改变组的p53阳性率高于声带角化症伴单纯增生组(P=0.008),而与声带角化症异型增生组和声带进展癌组之间的差异无统计学意义(P=0.240,P=0.268)。癌早期改变组的Ki-67阳性率明显低于浸润癌组(P=0.000),并明显高于角化症伴单纯增生组(P=0.001),但与角化症伴异型增生组之间差异无显著性(P=0.248)。结论声带鳞状细胞癌早期改变可区分为Ⅰ型和Ⅱ型,Ⅱ型癌变可在不累及上皮全层的情况下,由上皮的基底层和(或)副基底层细胞直接向固有膜内增生及癌变,此型占全部病例的近1/3,早期浸润是Ⅱ型诊断的可靠依据;Ⅱ型的存在提示声带鳞状细胞癌的早期发生和演进可能存在不同的机制;PAS染色和p53、Ki-67免疫组化染色有助于声带鳞状细胞癌Ⅱ型早期的诊断。

Purpose To investigate the clinicopathologic features of squamous cell carcinoma of vocal cords in its early stage for the improvement of its diagnosis. Methods Eighty-nine cases of squamous cell carcinoma of vocal cords in its early stage were collected. The serial sections were reviewed by hematoxylin and eosin staining （HE） ,periodic acid-Schiff （PAS） staining and EnVision immunostaining with anti-p53 ,anti-Ki-67 monoclonal antibody. The control groups included 59 cases of leukoplakia （forty cases with hyperplasia and nineteen with dysplasia） and thirty cases of advanced squamous cell carcinoma of the vocal cords. Results HE sections showed that carcinoma of vocal cords in its early stage had two types. Type Ⅰ had full-thickness epithelial cancerization,accounting for 67.4% （60/89） ;type Ⅱ had basal cell and/or parabasal cell cancerization only,accounting for 32. 6% （29/89） ,which included type Ⅱ a and type Ⅱ b. 52 cases were suspected to have microinvasive lesions, proved by PAS staining, in which 43 cases （83%） were lost of basement membrane-like substance around the cancer nests. The incidents of the microinvasive lesion in type Ⅰ were less than those of type Ⅱ （P = 0. 007）. Three cases, thought to be without microinvasion in HE-stained section, did have the micoinvasive lesions by deep sectioning and PAS staining. There was no difference in the expression of p53 between type Ⅰ and type Ⅱlesions（P =0. 445）. The expression rate of Ki-67 in type Ⅰ was more than that in type Ⅱ （ P = 0. 048）. The expression rate of p53 in squamous cell carcinoma of vocal cords in its early stage was more than hyperplatic group of leukoplakia（ P = 0. 008 ） ,but it was no difference from the dysplastic group of leukoplakia and advanced squamous cell carcinoma （ P = 0. 240, P = 0. 268 ）. The expression rate of Ki-67 in squamous cell carcinoma of vocal cords in its early stage was less than advanced carcinoma （P = 0. 000） and more than the hyperplatic group of leukoplakia （ P = 0. 001 ）, but it was no difference from the dysplastic group of leukoplakia （ P = 0. 248 ）. Conclusions Early change of carcinoma of vocal cords might have two pathologic types. The cancerazation of typeⅡ lesion, not involving in full thickness but in basal and/or parabasal cells, accounts for 1/3 of all the early carcinoma of vocal cords. Existence of early invasion is a dependable feature in the diagnosis of the type Ⅱ lesion. This result indicates that the carcinogenesis and progression of squamous cell carcinoma of vocal cords in its early stage might have different mechanisms. PAS, p53 and Ki-67 staining may play an important role in early detection of the squamous cell carcinoma in vocal cords.