IADR Abstract Archives
Langerhans Cells in Odontogenic Keratocysts
Objectives: Langerhans cells (LCs) are antigen-presenting cells. This study assessed the LC counts in odontogenic keratocysts (OKCs).
Methods: 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 immunostained with anti-S100 antibodies.
Results: The mean LC counts in the lining epithelia and subepithelial connective tissues increased significantly from no inflammation (0.5±0.4 and 0.7±0.6 cell/high-power field or HPF, respectively) through mild/moderate inflammation (5.9±2.7 and 5.0±3.5 cells/HPF, respectively) to severe inflammation OKC sites (14.7±5.3 and 13.3±6.8 cells/HPF, respectively; all P<0.001). OKC sites with inflammation had thicker lining epithelia than those without inflammation. Moreover, the mean LC counts in the lining epithelia and subepithelial connective tissues of OKCs were significantly higher in the thicker lining epithelium (>100μm) group (7.7±5.6 and 6.5±5.8 cells/HPF, respectively) than in the thinner lining epithelium (≦100μm) group (1.0±2.0 and 1.4±2.6 cells/HPF, respectively; both P<0.001).
Conclusions: A significant association of inflammation grade with the number of LCs in OKCs is found. The paucity of finding 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.
Methods: 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 immunostained with anti-S100 antibodies.
Results: The mean LC counts in the lining epithelia and subepithelial connective tissues increased significantly from no inflammation (0.5±0.4 and 0.7±0.6 cell/high-power field or HPF, respectively) through mild/moderate inflammation (5.9±2.7 and 5.0±3.5 cells/HPF, respectively) to severe inflammation OKC sites (14.7±5.3 and 13.3±6.8 cells/HPF, respectively; all P<0.001). OKC sites with inflammation had thicker lining epithelia than those without inflammation. Moreover, the mean LC counts in the lining epithelia and subepithelial connective tissues of OKCs were significantly higher in the thicker lining epithelium (>100μm) group (7.7±5.6 and 6.5±5.8 cells/HPF, respectively) than in the thinner lining epithelium (≦100μm) group (1.0±2.0 and 1.4±2.6 cells/HPF, respectively; both P<0.001).
Conclusions: A significant association of inflammation grade with the number of LCs in OKCs is found. The paucity of finding 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.