Journal of Southern Medical University ›› 2014, Vol. 34 ›› Issue (12): 1785-.

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Comparison of the expression profiles of cell death factors in articular cartilage between
Kashin-Beck disease and osteoarthritis

  

  • Online:2014-12-20 Published:2014-12-20

Abstract: Objective To compare the expressions of programmed cell death 5 (PDCD5) and early growth response protein-1
(EGR-1) in the articular cartilage between Kashin-Beck disease (KBD) and primary osteoarthritis and the roles of these factors
in KBD cartilage. Methods Cartilage specimens were collected from 10 confirmed KBD patients, 15 osteoarthritic patients and
6 healthy subjects. The expression levels of PDCD5 and EGR-1 in the cartilage were detected by immunohistochemistry
staining, and the positive chondrocyte counts were recorded in the different layers of KBD and OA cartilages. Results The
KBD cartilages contained a significantly higher percentage of PDCD5-positive chondrocytes in the middle layer [(41.35 ±
2.97)%] than OA cartilages [(26.48±2.04)%, P=0.001] and normal cartilages [(19.02±1.88)%, P=0.000] with also obvious PDCD5
over-expression in the deeper layer compared to OA (P=0.000) and normal cartilages (P=0.029), but PDCD5 expression in the
superficial layer of the cartilages showed no significant difference among the 3 groups(P>0.05). The average EGR-1 positivity
rate in the superficial layer of the cartilage was significantly higher in KBD patients than in OA patients (P=0.000) and healthy
controls (P=0.000), but in the middle layer, its positivity rate in KBD patients was higher than that in the normal control (P=
0.017) but lower than that of OA cartilage (P=0.002); EGR-1 expression in the deeper layer was comparable in KBD and OA
cartilages but both was higher than that in normal cartilages. PDCD5 and EGR-1 expressions were not correlated in either KBD
or normal cartilages, but were positively correlated in the superficial layer of OA cartilages. Conclusions KBD cartilages show
a significantly increased PDCD5 expression in the deeper layer and enhanced EGR-1 expression in both superficial and deeper
layers, suggesting the involvement of PDCD5 and EGR-1 in the pathogenesis of KBD.