Langerhans cell counts in odontogenic keratocysts and dentigerous cysts and their correlations with clinicopathological parameters

• Main Authors: Chun-Han Chang, 張君涵
• Other Authors: 江俊斌
• Format: Others
• Language: en_US
• Published: 2017
• Online Access: http://ndltd.ncl.edu.tw/handle/wx9gqn

博士 === 國立臺灣大學 === 口腔生物科學研究所 === 106 === 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.