Vol 50, No 4 (2012)
Original paper
Published online: 2012-12-23
Immunohistochemical expression of apoptotic factors, cytokeratins, and metalloproteinase-9 in periapical and epithelialized gingival lesions
DOI: 10.5603/FHC.2012.0070
Folia Histochem Cytobiol 2012;50(4):497-503.
Abstract
The aim of the study was to assess the involvement of apoptotic factors, cytokeratins and metalloproteinase-
9 in the histogenesis of both Epithelialized Gingival Lesions (EGL) and Periapical Lesions (PAL).
55 consecutive patients, 30 with PAL and 25 with EGL, were selected for the study after clinical and radiological
examinations. The PAL patients had severe periapical lesions and tooth decay with exposure of the pulp chamber.
All PAL and EGL biopsies were surgically extracted, fixed in 10% buffered formalin, and processed for
routine light microscopy. Ten biopsies of each category were processed for immunohistochemistry (IHC). Serial
paraffin sections were stained by IHC with appropriate antibodies to detect cytokeratins (CKs) 1, 5, 8, 10 and 14,
caspase-3 and -9, metalloproteinase-9, and for PCNA and TUNEL assays. Both PAL and EGL showed a high
expression of the cytokeratin 1, 5 and 8 with higher expression in EGL. Moreover, CK10 was markedly less
intense expressed in EGL compared to PAL, while CK14 was almost three times stronger expressed in EGL.
The expression of caspase-3 and -9 was stronger in PAL compared to EGL, however, the difference was only
significant for caspase-9. In PAL apoptosis detected by TUNNEL method and the expression of MMP-9 were
higher than in EGL, whereas PCNA was significantly more expressed in EGL. The results clearly suggest that
both lesions have exclusively an epithelial origin and that epithelial proliferation was correlated with the degree
of apoptosis in both entities. PAL and EGL presented mostly similar cytokeratin expression except for CK10
and CK14, though with marked differences in the distribution and intensity of IHC reactions. Finally, the degradation
of extracellular matrix in both lesions could be partially attributed to the strong presence of MMP-9.
9 in the histogenesis of both Epithelialized Gingival Lesions (EGL) and Periapical Lesions (PAL).
55 consecutive patients, 30 with PAL and 25 with EGL, were selected for the study after clinical and radiological
examinations. The PAL patients had severe periapical lesions and tooth decay with exposure of the pulp chamber.
All PAL and EGL biopsies were surgically extracted, fixed in 10% buffered formalin, and processed for
routine light microscopy. Ten biopsies of each category were processed for immunohistochemistry (IHC). Serial
paraffin sections were stained by IHC with appropriate antibodies to detect cytokeratins (CKs) 1, 5, 8, 10 and 14,
caspase-3 and -9, metalloproteinase-9, and for PCNA and TUNEL assays. Both PAL and EGL showed a high
expression of the cytokeratin 1, 5 and 8 with higher expression in EGL. Moreover, CK10 was markedly less
intense expressed in EGL compared to PAL, while CK14 was almost three times stronger expressed in EGL.
The expression of caspase-3 and -9 was stronger in PAL compared to EGL, however, the difference was only
significant for caspase-9. In PAL apoptosis detected by TUNNEL method and the expression of MMP-9 were
higher than in EGL, whereas PCNA was significantly more expressed in EGL. The results clearly suggest that
both lesions have exclusively an epithelial origin and that epithelial proliferation was correlated with the degree
of apoptosis in both entities. PAL and EGL presented mostly similar cytokeratin expression except for CK10
and CK14, though with marked differences in the distribution and intensity of IHC reactions. Finally, the degradation
of extracellular matrix in both lesions could be partially attributed to the strong presence of MMP-9.
