ArticleJournal of orthopaedics and traumatology : official journal of the Italian Society of Orthopaedics and Traumatology2015
Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures.
Article in Journal of orthopaedics and traumatology : official journal of the Italian Society of Orthopaedics and Traumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Protective Effects of Spirulina Supplementation on Chondrocytes Under Moderate Acute Dynamic Compression.Cartilage · 2026Article
- Membrane stretch as the mechanism of activation of PIEZO1 ion channels in chondrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A flexible and highly sensitive organic electrochemical transistor-based biosensor for continuous and wireless nitric oxide detection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Articular Cartilage Friction, Strain, and Viability Under Physiological to Pathological Benchtop Sliding Conditions.Cellular and molecular bioengineering · 2021Article
- Mitochondrial dependent pathway is involved in the protective effects of carboxymethylated chitosan on nitric oxide-induced apoptosis in chondrocytes.BMC complementary medicine and therapies · 2020Article
- Anti-inflammatory role of TPCA-1 encapsulated nanosomes in porcine chondrocytes against TNF-α stimulation.Inflammopharmacology · 2019Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe primary goal of this study was to identify nitric oxide (NO)-induced apoptosis in traumatized chondrocytes in intra-articular lower extremity fractures and the secondary goal was to identify the timeline of NO-induced apoptosis after injury. MATERIALS AND
methodsThis is a prospective collection of samples of human cartilage harvested at the time of surgery to measure apoptotic cell death and the presence of NO by immunohistochemistry. Three patients met the criteria for control subjects and eight patients sustained high-energy intra-articular fractures and were included in the study. Subjects who sustained intra-articular acetabular, tibial, calcaneal and talus fracture had articular cartilage harvested at the time of surgical intervention. All 8 patients underwent open reduction and internal fixation of the displaced intra-articular fractures. The main outcome measures were rate of apoptosis, degree of NO-induced apoptosis in chondrocytes, and the timeline of NO-induced apoptosis after high-energy trauma.
resultsThe percentage of apoptotic chondrocytes was higher in impacted samples than in normal cartilage (56 vs 4 %), confirming the presence of apoptosis after intra-articular fracture. The percentage of cells with NO was greater in apoptotic cells than in normal cells (59 vs 20 %), implicating NO-induction of apoptosis. The correlation between chondrocyte apoptosis and increasing time from injury was found to be -0.615, indicating a decreasing rate of apoptosis post injury.
conclusionsThe data showed the involvement of NO-induced apoptosis of chondrocytes after high-energy trauma, which decreased with time from injury.
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