口腔上皮變異中蘭格罕氏細胞數量及其與臨床病理參數之相關性

Abstract

背景：蘭格罕氏細胞是由骨髓來之抗原呈現細胞，口腔病變中較高之蘭格罕氏細胞數目，表示口腔病變患者對該病變之免疫監視能力有明顯增加。口腔上皮變異是一種癌前病變，它可能轉變成口腔癌。 方法：本研究利用免疫組織化學染色法，探討58例口腔上皮變異（21例輕度，18例中度，19例重度上皮變異）和10例正常口腔黏膜之上皮及上皮下方結締組織中之蘭格罕氏細胞數目。 結果：我們發現於上皮中之平均蘭格罕氏細胞數目，從正常口腔黏膜之14 ± 3細胞/高倍視域，至輕度口腔上皮變異之32 ± 12細胞/高倍視域，中度口腔上皮變異之40 ± 12細胞/高倍視域，至重度口腔上皮變異之49 ± 13細胞/高倍視域，有隨著上皮變異程度的增加，而呈現統計學上有意義增加的情形 (P < 0.001)。統計分析的結果也顯示，上皮下方結締組織中之平均蘭格罕氏細胞數目，從正常口腔黏膜之5 ± 2細胞/高倍視域，至輕度口腔上皮變異之24 ± 12細胞/高倍視域，中度口腔上皮變異之33 ± 12細胞/高倍視域，至重度口腔上皮變異之47 ± 17細胞/高倍視域，亦有隨著上皮變異程度的增加，而呈現統計學上有意義增加的情形 (P < 0.001)。另外上皮中之平均蘭格罕氏細胞數目，也隨著口腔上皮變異病變中上皮層厚度及上皮下方結締組織中發炎帶寬度之增加而增加。另外上皮下方結締組織中之平均蘭格罕氏細胞數目，也隨著口腔上皮變異病變中上皮下方結締組織中發炎帶寬度之增加而增加。我們也發現9例有惡性轉變口腔上皮變異病變（包括5例重度，3例中度及1例輕度口腔上皮變異病變），比49例無惡性轉變口腔上皮變異病變，其上皮及上皮下方結締組織中平均蘭格罕氏細胞數目明顯較低。 結論：蘭格罕氏細胞數目從正常口腔黏膜經由輕度和中度口腔上皮變異至重度口腔上皮變異，呈現有意義之逐漸增加，此表示口腔上皮變異患者之免疫監視能力於口腔癌生成之早期即有明顯增加。口腔上皮變異中較低之蘭格罕氏細胞數目，可能表示口腔上皮變異患者對變異細胞部分喪失免疫監視能力，此情況下有利於口腔上皮變異病變進一步惡性轉變成口腔癌。

BACKGROUND: Langerhans cells (LCs) are bone marrow-derived antigen presenting cells. The high LC number in oral lesion may suggest an increase in immunosurveillance ability in patients with that oral disease. Oral epithelial dysplasia (OED) is a precancerous lesion that may develop into an oral cancer. METHODS: This study examined the LC counts in the epithelium and in the subepithelial connective tissue of 58 specimens of OED (21 mild, 18 moderate, and 19 severe OED cases), and 10 specimens of normal oral mucosa (NOM) by immunohistochemistry. RESULTS: We found that the mean LC counts in the epithelia increased significantly from NOM (14 ± 3 cells/high-power field [HPF]) through mild OED (32 ± 12 cells/HPF) and moderate OED (40 ± 12 cells/HPF) to severe OED samples (49 ± 13 cells/HPF, P < 0.001). Moreover, the mean LC counts in the subepithelial connective tissues also increased significantly from NOM (5 ± 2 cells/HPF) through mild OED (24 ± 12 cells/HPF) and moderate OED (33 ± 12 cells/HPF) to severe OED samples (47 ± 17 cells/HPF, P < 0.001). In addition, a significant correlation was found between the higher mean LC counts in the dysplastic epithelia of OED samples and OED lesions with thicker epithelial layers (P < 0.001) or wider inflammatory zones (P < 0.001) as well as between the higher mean LC counts in the subepithelial connective tissues of OED samples and OED lesions with wider inflammatory zones (P < 0.001). Moreover, the 9 OED lesions (including 5 severe, 3 moderate and one mild OED lesions) with malignant transformation had a significantly lower mean LC count in the dysplastic epithelia or subepithelial connective tissues than 49 OED lesions without malignant transformation. CONCLUSIONS: The significant and gradual elevation in LC count from NOM through mild and moderate OED to severe OED lesions suggests an upregulation of immunosuveillance ability in OED patients during the early oral carcinogenesis process. The low LC count in OED lesions may suggest the partial loss of immunosurveillance ability against the dysplastic cells; this in turn favors the malignant transformation of an OED lesion into an OSCC lesion.