Abstract
Category:
Basic Sciences/Biologics
Introduction/Purpose:
The aim of current study was to investigate the pathological characters and relative molecular pathogenesis of the cartilages damage in diabetic neuropathic osteoarthropathy (DNOAP) patients.
Methods:
The articular cartilages of ankle joint, subtalar joint and talonavicular joint of 8 patients with DNOAP from March 2017 to June 2018 were selected as DNOAP group. And the articular cartilage of matched joints from 8 amputation patients were selected as control group. Masson staining and safranine O/fixed green staining were used to observe the histopathological characteristics of cartilage, and the ultrastructural changes of chondrocytes were observed by electron microscopy. Chondrocyte culture was carried out in DNOAP group and control group. Western blot was used to detect the expression of RANKL, OPG, IL-1ß, IL-6, TNF-a, Aggrecan protein in chondrocyte. DCFH-DA probe was used to detect the level of reactive oxygen species in chondrocyte. Flow cytometry was used to detect the apoptotic rate of chondrocyte.
Results:
In DNOAP group, chondrocytes decreased, subchondral bone proliferated, structure disordered and osteoclasts formed in a large number in subchondral bone area. Under transmission electron microscopy, mitochondrial and endoplasmic reticulum swelling were observed in DNOAP chondrocytes. The chromatin was partially broken and concentrated at the edge of nuclear membrane. The ROS fluorescence intensity of chondrocyte in DNOAP group was higher than that in normal control group (28.1±2.3 VS 11.9±0.7, P<0.05). The relative expression of RANKL, TNF-a, IL-1ß and IL-6 protein in DNOAP group was higher than that in normal control group, while the relative expression of OPG and Aggrecan protein was lower than that in normal control group (both P < 0.05). Flow cytometry showed that the apoptotic rate of chondrocyte in DNOAP group was 3.3%±0.2%, which was higher than that in normal control group (1.2%±0.1%, P<0.05).
Conclusion:
Serious destruction of chondrocytes and organelles structure was the pathological characteristics of DNOAP. Inflammation plays a role in promoting the pathogenesis of DNOAP.
