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Single impact cartilage trauma and TNF-α: Interactive effects do not increase early cell death and indicate the need for bi-/multidirectional therapeutic approaches

  • Authors:
    • Cathrin Hogrefe
    • Helga Joos
    • Vennila Maheswaran
    • Lutz Dürselen
    • Anita Ignatius
    • Rolf E. Brenner

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  • Published online on: August 24, 2012     https://doi.org/10.3892/ijmm.2012.1112
  • Pages: 1225-1232
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Abstract

Blunt trauma of articular cartilage, often resulting from accidents or sports injuries, is associated with local inflammatory reactions and represents a major risk factor for development of post-traumatic osteoarthritis. TNF-α is increased in synovial fluid early after trauma, potentiates injury-induced proteoglycan degradation and may act proapoptotic under permissive conditions. We asked whether TNF-α also influences chondrocyte death, gene expression of catabolic and anabolic markers and the release of proinflammatory mediators in the early post-traumatic phase. Interactive effects of a defined single impact trauma (0.59  J) and TNF-α (100 ng/ml) on human early-stage osteoarthritic cartilage were investigated in vitro over 24 h. Exposure of traumatized cartilage to TNF-α did not increase chondrocyte death. IL-6-synthesis was augmented by trauma, TNF-α and combined treatment. The impact increased the release of PGE2 and PGD2 in the presence and absence of TNF-α to a similar extent while TNF-α alone showed no effect. In contrast, NOS2A-expression and nitric oxide (NO)-release were not affected by trauma but significantly increased by TNF-α. Expression of OPG and RANKL was not affected by TNF-α but modulated by trauma. TNF-α with and without trauma significantly induced MMP1 gene expression. These results indicate that TNF-α does not potentiate early cell death in early-stage osteoarthritic cartilage after blunt injury. However, trauma and TNF-α showed independent and interactive effects concerning prostaglandin and NO release. TNF-α probably contributes to cartilage degradation after trauma by an early induction of MMP1 gene expression. Our study confirms that an anti-TNF-α therapy may have inhibitory effects on catabolic and, partly, on inflammatory processes after a single impact trauma. As TNF-α does not contribute to the loss of chondrocytes in the initial post-traumatic phase, a combination with pharmaco-therapeutic strategies reducing early cell death could be reasonable.
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November 2012
Volume 30 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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  • Journal Metrics
  • Impact Factor: 5.7
  • Ranked Medicine Research and Experimental
    (total number of cites)
  • CiteScore: 12.3
  • CiteScore Rank: Q1: #28/347 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 1.022
  • SCImago Journal Rank (SJR): 1.167
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Spandidos Publications style
Hogrefe C, Joos H, Maheswaran V, Dürselen L, Ignatius A and Brenner RE: Single impact cartilage trauma and TNF-α: Interactive effects do not increase early cell death and indicate the need for bi-/multidirectional therapeutic approaches. Int J Mol Med 30: 1225-1232, 2012.
APA
Hogrefe, C., Joos, H., Maheswaran, V., Dürselen, L., Ignatius, A., & Brenner, R.E. (2012). Single impact cartilage trauma and TNF-α: Interactive effects do not increase early cell death and indicate the need for bi-/multidirectional therapeutic approaches. International Journal of Molecular Medicine, 30, 1225-1232. https://doi.org/10.3892/ijmm.2012.1112
MLA
Hogrefe, C., Joos, H., Maheswaran, V., Dürselen, L., Ignatius, A., Brenner, R. E."Single impact cartilage trauma and TNF-α: Interactive effects do not increase early cell death and indicate the need for bi-/multidirectional therapeutic approaches". International Journal of Molecular Medicine 30.5 (2012): 1225-1232.
Chicago
Hogrefe, C., Joos, H., Maheswaran, V., Dürselen, L., Ignatius, A., Brenner, R. E."Single impact cartilage trauma and TNF-α: Interactive effects do not increase early cell death and indicate the need for bi-/multidirectional therapeutic approaches". International Journal of Molecular Medicine 30, no. 5 (2012): 1225-1232. https://doi.org/10.3892/ijmm.2012.1112