Abstract
ABSTRACT By immunohistochemistry the expression of a pan-cadherin antibody that recognizes a wide variety of cadherins in chondrocytes from normal and tibial dyschondroplasia (TD) growth plates was compared. Surprisingly, an upregulated expression that was not expected in TD lesion chondrocytes was observed. The reason for this apparent upregulation is not clear. The increased expression may simply be due to the particular phenotype of lesion chondrocytes, and cadherin may be involved in apoptosis of chondrocytes of TD lesion. Another possibility, is that a low level of calcium in the lesion may be responsible for the observed upregulation. The results of the present study suggest that the formation of the dyschondroplastic lesion is not merely due to the impaired terminal differentiation of lesion chondrocytes and that other mechanisms are probably involved in TD etiology. Further studies will be necessary to provide insight into the precise nature of the condition. Keywords: tibial dyschondroplasia, cadherin, immunohistochemistry
Highlights
By immunohistochemistry the expression of a pan-cadherin antibody that recognizes a wide variety of cadherins in chondrocytes from normal and tibial dyschondroplasia (TD) growth plates was compared
An upregulated expression that was not expected in TD lesion chondrocytes was observed
The increased expression may be due to the particular phenotype of lesion chondrocytes, and cadherin may be involved in apoptosis of chondrocytes of TD lesion
Summary
As caderinas expressam-se em muitos tipos celulares, incluindo as células ósseas e cartilaginosas, e sabe-se que têm uma participação ativa nos processos de condrogênese e de osteogênese (Helfrich e Horton, 1999; DeLise et al, 2000; Marie, 2002). A marcação foi mais evidente nos condrócitos da zona de hipertrofia, com uma sobre-expressão nas placas de crescimento discondroplásicas (91.2%), sendo a percentagem de células positivas significativamente mais elevada nestas do que nas placas de crescimento normais (34,8%) (Tab. 1, Fig. 1).
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