齒源性角化囊腫及含齒囊腫中之蘭格罕氏細胞數目及其與臨床病理參數之相關性

Abstract

背景：蘭格罕氏細胞是主要存在於上皮內的抗原呈遞細胞，本研究評估齒源性角化囊腫(OKC)及含齒囊腫(DC)中之蘭格罕氏細胞(LC)數目。 方法：本研究主要利用anti-CD1a及anti-S100蛋白質免疫組織化學染色法，評估於60例OKC標本及80例DC標本中之蘭格罕氏細胞數目及其與臨床病理參數之相關性。於60例OKC標本中，評估60個無發炎部位，39個輕度或中度發炎部位，13個重度發炎部位之蘭格罕氏細胞數目；於80例DC標本中，評估80個無發炎部位，33個輕度或中度發炎部位，9個重度發炎部位之蘭格罕氏細胞數目。 結果：60例OKC樣本中，在內襯上皮和上皮下方結締組織中之平均CD1a陽性或S100陽性之LC細胞數目，從無發炎部位至輕度/中度發炎部位，及至重度發炎部位，其蘭格罕氏細胞數目皆逐步顯著增加（P值皆< 0.001）。有發炎之OKC部位比無發炎之OKC部位，具有較厚之內襯上皮。此外，在厚內襯上皮（> 100 μm）組之OKCs中，內襯上皮和上皮下結締組織中之平均CD1a陽性或S100陽性之LC細胞數目，皆明顯高於薄內襯上皮（≤ 100 μm）組之OKCs (P值皆< 0.001）。於80例DC樣本中，也可發現在內襯上皮和上皮下方結締組織中之平均CD1a陽性或S100陽性之LC細胞數目，從無發炎部位至輕度/中度發炎部位，及至重度發炎部位，其蘭格罕氏細胞數目皆逐步顯著增加（P值皆< 0.001）。有發炎之DC部位比無發炎之DC部位，具有較厚之內襯上皮。此外，在厚內襯上皮（> 50 μm）組之DCs中，內襯上皮和上皮下結締組織中之平均CD1a陽性或S100陽性之LC細胞數目，皆明顯高於薄內襯上皮（≤ 50 μm）組之DCs (P值皆< 0.001）。 結論：本研究發現發炎之等級與OKC中之LC數量，有顯著相關。在無發炎OKC的內襯上皮中，只可發現極少量之LC，此表示OKC內襯上皮細胞之免疫監視能力明顯喪失，這可解釋為什麼OKC具有強大臨床侵犯性、強大細胞增殖潛力和高的復發率。此外在DC研究中，LC數量之增加與高發炎程度和厚內襯上皮有顯著相關。在無發炎DC之內襯上皮中，只發現極少數之LC，也表明DC患者之內襯上皮細胞免疫監視能力明顯下降。然而，需要進一步研究來確認上皮免疫監視能力之降低和DC之囊腫增大是否有關。

Background/Purpose: Langerhans cells (LCs) are antigen-presenting cells that reside mainly within the epithelium. This study assessed the LC counts in odontogenic keratocysts (OKCs) and dentigerous cysts (DCs). Methods: This study used anti-CD1a and anti-S100 protein immunostains to assess the LC counts in 60 OKCs and 80 DCs and the correlations of LC counts with clinicopathological parameters of 60 OKCs and 80 DCs. The LC numbers in the lining epithelia and subepithelial connective tissues were counted at 60 OKC sites without inflammation, 39 OKC sites with mild/moderate inflammation, and 13 OKC sites with severe inflammation from 60 OKC specimens as well as at 80 DC sites without inflammation, 33 DC sites with mild/moderate inflammation, and 9 DC sites with severe inflammation from 80 DC specimens. Results: For 60 OKC cases, the mean CD1a-positive or S100-positive LC counts in the lining epithelia and subepithelial connective tissues increased significantly from no inflammation through mild/moderate inflammation to severe inflammation OKC sites (all P-values < 0.001). OKC sites with inflammation had thicker lining epithelia than those without inflammation. Moreover, the mean CD1a-positive or S100-positive LC counts in the lining epithelia and subepithelial connective tissues of OKCs were significantly higher in the thicker lining epithelium (> 100 μm) group than in the thinner lining epithelium (≦ 100 μm) group (both P-values < 0.001). For 80 DC cases, the mean CD1a-positive or S100-positive LC counts in the lining epithelia and subepithelial connective tissues also increased significantly from no inflammation through mild/moderate inflammation to severe inflammation DC sites (all P-values < 0.001). DC sites with inflammation had thicker lining epithelia than those without inflammation. Moreover, the CD1a-positive or S100-positive mean LC counts in the lining epithelia and subepithelial connective tissues of DCs were significantly higher in the thicker lining epithelium (> 50 μm) group than in the thinner lining epithelium (≦ 50 μm) group (both P-values < 0.001). Conclusion: A significant association of inflammation grade with the number of LCs in OKCs is found in this study. The finding of scare LCs in the lining epithelia of OKCs without inflammation indicates the loss of immunosurveillance ability against the OKC lining epithelial cells; this can explain why OKCs have aggressive clinical behavior, a great growth potential, and a high recurrence rate. Moreover, the increased LC number in DCs is also associated with high-grade inflammation and thick lining epithelium. The finding of few LCs in the lining epithelia of DCs without inflammation also indicates the reduced immunosurveillance ability against DC lining epithelial cells in DC patients. However, it needs further studies to confirm the role of reduced lining epithelial cell immunosurveillance in the enlargement of the DC.