Seventy samples of
odontogenic cysts samples were immunohistochemically stained to detect
claudin-1, -4, and -7 expression. Patient information and OKC recurrence data were recorded. The staining was analyzed semiquantitatively and categorized based on the pattern and percentage of positively stained cystic epithelial cells.
STATISTICAL ANALYSIS: Expression of different
claudins between groups was analyzed using the Kruskal-Wallis test with Dunn's test, followed by post hoc pairwise comparison. The association between
claudin expression and OKC recurrence was analyzed by the Mann-Whitney U test. Correlations among
claudin expression were examined with Spearman's correlation coefficient. Level of significance was at p < 0.005.
RESULTS: Claudin-1 was widely expressed in every
odontogenic cyst. Most DCs (50%) expressed
claudin-1 in more than 75% of cells, as did RCs (65%), while most OKCs (50%) expressed
claudin-1 in 26 to 50% of cells. Most COCs (50%) expressed
claudin-1 in 51 to 75% of cells. Every sample of OKC and RC was positive for
claudin-4, but no sample showed staining in more than 51% of cells. Every
odontogenic cyst was positive for claudin-7. DCs (35%), OKCs (55%), and RCs (40%) mostly showed staining in 26 to 50% of cells. High
claudin-1 expression was shown in COCs, DCs, and RCs, while low expression of
claudin-4 was shown in every
odontogenic cyst. For claudin-7, the expression is high only in COCs.
Claudin-1 and -4 was significantly different among each
odontogenic cyst. High expression of
claudin-1 was correlated with OKC recurrence. The correlations of
claudin-1 with claudin-7 expression and
claudin-4 with claudin-7 expression were significant in DCs. In COCs,
claudin-1 and claudin-7 expression was significantly correlated.
CONCLUSIONS: The expression of
claudin-1, -4, and -7 was present in every
odontogenic cyst, but the proportion of positive staining cells was different. Expression of
claudin-1 is associated with OKC recurrence. Dysregulation of
claudin expression may play a pathogenic role in
cyst pathogenesis.