Keratocystic odontogenic tumor (KCOT) is an aggressive lesion with a well-documented predilection for recurrence. This study aims to investigate the reason for the recurrence tendency of KCOT.
Material and Methods: The materials were 80 KCOTs in 58 patients. All 80 KCOTs were reviewed histopathologically, and 45 of them in 23 patients were examined immunohistochemically by means of monoclonal antibodies against proliferating cell nuclear antigen (PCNA) ,Ki-67, interleukin-1
α (IL-1
α ) ,and podoplanin.
Results:1. Comparison of sporadic KCOTs with lesions of nevoid basal cell carcinoma syndrome (NBCCS)
(1) Histopathologically, the proportion of lesions showing budding proliferation, islands of odontogenic epithelium and daughter cysts was higher for NBCCS than for sporadic KCOTs.
(2) Immunohistochemically, the ratio of Ki-67-positive cells in NBCCS lesions was higher than in sporadic KCOTs. The intensity of PCNA immunoreactivity was higher in the basal layer of NBCCS lesions than in KCOTs. However, there was no significant difference in the ratio of IL-1
α -positive cells between NBCCS and sporadic KCOTs.
(3) The podoplanin immunoreactivity in NBCCS lesions was more intense than in sporadic KCOTs.
2. Comparison of recurrent and non-recurrent lesions after enucleation
(1) Histopathologically, the proportion of lesions showing odontogenic epithelial islands was higher in recurrent KCOTs (45.5%) than in non-recurrent (11.6%) KCOTs.
(2) Immunohistochemically, the positivity ratios were higher in recurrent KCOTs than in non-recurrent KC4.4% and 2.8%) and PCNA (55.6% and 44.6%).
(3) In sporadic KCOTs, the podoplanin immunoreactivity in recurrent primary lesions was more intense than in non-recurrent lesions.
3. Comparison of the primary KCOTs with or without recurrence and the secondary KCOTs after recurrence
(1) Histopathologically, only one lesion of secondary KCOT showed a slight sign of inflammation, in contrast to the high ratio (63.6%) in primary KCOTs.
(2) Immunohistochemically, the ratio of IL-1
α -positive cells in secondary KCOTs that showed almost no inflammation was higher than that in primary KCOTs.
(3) There were no significant differences in podoplanin immunoreactivity between primary KCOTs and secondary KCOTs after recurrence.
Conclusion: The experimental results suggest that any residual epithelial tissue left behind after surgery on the KCOT has a potential to cause proliferation and recurrence. Furthermore, this immunohistochemical study of reactivity for podoplanin supports the contention that KCOT is a benign cystic neoplasm but becomes aggressive when associated with NBCCS.
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