ArticlePloS one2016
Sodium Thiosulfate Prevents Chondrocyte Mineralization and Reduces the Severity of Murine Osteoarthritis.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 32 citations in OpenAlex.
- Hydrogen sulfide generated by cystathionine gamma lyase inhibits lysyl oxidase and protects against calcific tendinopathy.Journal of orthopaedic translation · 2026Article
- Clinical Potential of Hydrogen Sulfide in Peripheral Arterial Disease.International journal of molecular sciences · 2023Review
- The Gasotransmitter Hydrogen Sulfide (HAntioxidants (Basel, Switzerland) · 2021Article
- Xanthine Oxidoreductase Is Involved in Chondrocyte Mineralization and Expressed in Osteoarthritic Damaged Cartilage.Frontiers in cell and developmental biology · 2021Article
- Assessment of sodium thiosulfate neutralizing effect on micro-hardness of dentin treated with sodium hypochlorite.BMC oral health · 2020Article
- The protective role of the 3-mercaptopyruvate sulfurtransferase (3-MST)-hydrogen sulfide (HArthritis research & therapy · 2020Article
- The role of the gasotransmitter hydrogen sulfide in pathological calcification.British journal of pharmacology · 2020Review
- CD11b Signaling Prevents Chondrocyte Mineralization and Attenuates the Severity of Osteoarthritis.Frontiers in cell and developmental biology · 2020Article
- Calcium crystal deposition diseases - beyond gout.Nature reviews. Rheumatology · 2018Review
- Disease-Associated Particulates and Joint Inflammation; Mechanistic Insights and Potential Therapeutic Targets.Frontiers in immunology · 2018Review
- Osteoarthritis-associated basic calcium phosphate crystals activate membrane proximal kinases in human innate immune cells.Arthritis research & therapy · 2017Article
- Revisiting the Role of Interleukin-1 Pathway in Osteoarthritis: Interleukin-1α and -1β, and NLRP3 Inflammasome Are Not Involved in the Pathological Features of the Murine Menisectomy Model of Osteoarthritis.Frontiers in pharmacology · 2017Article
- Comparison of Meniscal Cell-Mediated and Chondrocyte-Mediated Calcification.The open orthopaedics journal · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCalcium-containing crystals participate in the pathogenesis of OA. Sodium thiosulfate (STS) has been shown to be an effective treatment in calcification disorders such as calciphylaxis and vascular calcification. This study investigated the effects and mechanisms of action of STS in a murine model of OA and in chondrocyte calcification.
methodsHydroxyapatite (HA) crystals-stimulated murine chondrocytes and macrophages were treated with STS. Mineralization and cellular production of IL-6, MCP-1 and reactive oxygen species (ROS) were assayed. STS's effects on genes involved in calcification, inflammation and cartilage matrix degradation were studied by RT-PCR. STS was administered in the menisectomy model of murine OA, and the effect on periarticular calcific deposits and cartilage degeneration was investigated by micro-CT-scan and histology.
resultsIn vitro, STS prevented in a dose-dependent manner calcium crystal deposition in chondrocytes and inhibited Annexin V gene expression. In addition, there was a reduction in crystal-induced IL-6 and MCP-1 production. STS also had an antioxidant effect, diminished HA-induced ROS generation and abrogated HA-induced catabolic responses in chondrocytes. In vivo, administration of STS reduced the histological severity of OA, by limiting the size of new periarticular calcific deposits and reducing the severity of cartilage damage.
conclusionsSTS reduces the severity of periarticular calcification and cartilage damage in an animal model of OA via its effects on chondrocyte mineralization and its attenuation of crystal-induced inflammation as well as catabolic enzymes and ROS generation. Our study suggests that STS may be a disease-modifying drug in crystal-associated OA.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.