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Chondrocyte apoptosis in rat mandibular condyles induced by dental occlusion due to mitochondrial damage caused by nitric oxide.

Abstract：

OBJECTIVE:Chondrocyte apoptosis is a pathological manifestation of osteoarthritis. The goal of this report was to explore the role of nitric oxide in chondrocyte apoptosis in osteoarthritic mandibular condylar cartilage. DESIGN:This study used our reported experimental unilateral anterior crossbite in vivo rat model and chondrocyte fluid flow shear stress in vitro model. In the in vivo model, apoptosis in the mandibular condylar cartilage was assessed by detection of the TUNEL-positive cells, the expression levels of inducible nitric oxide synthase (iNOS), caspase-9, and caspase-3. In the in vitro model, mitochondrial injury was evaluated, the nitric oxide and superoxide dismutase (SOD) production levels were measured, and the cytochrome C (Cyt C) expression level was detected. The expression levels of apoptosis-related proteins B cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3, and poly-ADP-ribose polymerase 1 (PARP1) were analyzed in both in vivo and in vitro models. The effects of iNOS inhibitor on chondrocyte apoptosis were also investigated. RESULTS:The data indicated that the unilateral anterior crossbite induced cartilage degeneration with enhanced cell apoptosis and stimulated the expression of caspase-3/-9 and iNOS. The fluid flow shear stress upregulated the expression of iNOS, SOD, and nitric oxide, reduced mitochondrial membrane potential, and promoted Cyt C to enter the cytoplasm. All of these changes were reversed by iNOS inhibitors. CONCLUSION:The abnormal occlusion stimulated mitochondrial damage and apoptosis of the chondrocytes in the mandibular condylar cartilage mediated by nitric oxide. Inhibiting nitric oxide production could be a therapeutic strategy.

journal_name

Arch Oral Biol

journal_title

Archives of oral biology

authors

Ren H,Yang H,Xie M,Wen Y,Liu Q,Li X,Liu J,Xu H,Tang W,Wang M

doi

10.1016/j.archoralbio.2019.03.006

subject

Has Abstract

pub_date

2019-05-01 00:00:00

pages

108-121

eissn

0003-9969

issn

1879-1506

pii

S0003-9969(18)30844-6

journal_volume

101

pub_type

杂志文章

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