ArticleJournal of molecular medicine (Berlin, Germany)2025
Nintedanib reduces severity of post-traumatic joint contracture by modulating fibrosis and inflammation.
Article in Journal of molecular medicine (Berlin, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Prophylactic Effects of Combined Bosentan and Nintedanib on Early Post-Traumatic Joint Contracture Formation in a Rat Model.Journal of clinical medicine · 2026Article
- Development of a novel external fixation device for inducing knee arthrofibrosis in rats.Scientific reports · 2026Article
- Nintedanib Enhances the Antibacterial Activity of Bedaquiline Against Non-Tuberculous Mycobacteria: In vitro and in Mice Models.Infection and drug resistance · 2026Article
- Dual Endothelin Receptor Inhibition with Bosentan Does Not Prevent the Early Formation of Post-Traumatic Joint Contracture in a Rat Model.Journal of clinical medicine · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
This study investigates the potential of nintedanib, a tyrosine kinase inhibitor with antifibrotic and anti-inflammatory properties, to mitigate post-traumatic joint contracture (PTJC) in a rat model. Given the lack of effective pharmacological treatments for this debilitating condition, this study aims to address the unmet need for non-surgical interventions by targeting the underlying fibrotic and inflammatory processes. A total of 26 male Sprague-Dawley rats were subjected to standardized knee trauma and immobilization for 2 weeks. Rats were randomized into two groups: a nintedanib treatment group (5 mg/kg taken twice daily, n = 13) and a placebo group (n = 13). Joint mobility was evaluated biomechanically by measuring the contracture angle (CA) and resistance to extension. Posterior joint capsule tissues were analyzed histologically and via qPCR for profibrotic gene expression, including α-Sma, Il-6, Tgf-β1, Nf-κb, and Ctgf. Nintedanib treatment significantly reduced CA compared to placebo (68.1° ± 12.6° vs. 84.8° ± 11.1°, p < 0.01), indicating improved joint mobility. Knee extension in the nintedanib-treated rats required less force, particularly at lower extension angles (p < 0.05). Molecular analysis showed a marked reduction in α-Sma expression, a myofibroblast marker, in the nintedanib group compared to placebo (11-fold decrease, p < 0.05). Histological examinations revealed relatively fewer myofibroblasts in the posterior joint capsule of rats treated with nintedanib. Nintedanib effectively mitigates fibrosis and inflammation in a rat model of PTJC, enhancing joint mobility and reducing profibrotic gene expression. These findings support further exploration of nintedanib as a pharmacological therapy for PTJC in clinical settings. KEY MESSAGES: Nintedanib is a promising candidate for the prevention of post-traumatic joint contracture. Oral administration of nintedanib (5 mg twice daily) over a period of 2 weeks improves joint mobility in post-traumatic joint contracture (PTJC). Nintedanib reduces the relative number of myofibroblasts. A significant reduction in α-SMA expression levels under the influence of nintedanib indicates a slowed transition of fibroblasts to myofibroblasts.
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