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Elevation of Pro-Inflammatory Cytokine Levels Following Intra-Articular Fractures-A Systematic Review

Publikation: Bidrag til tidsskriftReviewForskningpeer review

DOI

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  • That Minh Pham
  • Julie Ladeby Erichsen
  • Justyna Magdalena Kowal
  • Søren Overgaard
  • Hagen Schmal
Vis graf over relationer

Introduction: Intra-articular fractures are a major cause of post-traumatic osteoarthritis (PTOA). Despite adequate surgical treatment, the long-term risk for PTOA is high. Previous studies reported that joint injuries initiate an inflammatory cascade characterized by an elevation of synovial pro-inflammatory cytokines, which can lead to cartilage degradation and PTOA development. This review summarizes the literature on the post-injury regulation of pro-inflammatory cytokines and the markers of cartilage destruction in patients suffering from intra-articular fractures. Methods: We searched Medline, Embase, and Cochrane databases (1960-February 2020) and included studies that were performed on human participants, and we included control groups. Two investigators assessed the quality of the included studies using Covidence and the Newcastle-Ottawa Scale. Results: Based on the surveyed literature, several synovial pro-inflammatory cytokines, including interleukins (IL)-1β, IL-2, IL-6, IL-8, IL-12p70, interferon-y, and tumor necrosis factor-α, were significantly elevated in patients suffering from intra-articular fractures compared to the control groups. A simultaneous elevation of anti-inflammatory cytokines such as IL-10 and IL-1RA was also observed. In contrast, IL-13, CTX-II, and aggrecan concentrations did not differ significantly between the compared cohorts. Conclusions: Overall, intra-articular fractures are associated with an increase in inflammation-related synovial cytokines. However, more standardized studies which focus on the ratio of pro- and anti-inflammatory cytokines at different time points are needed.

OriginalsprogEngelsk
Artikelnummer902
TidsskriftCells
Vol/bind10
Udgave nummer4
Antal sider9
ISSN2073-4409
DOI
StatusUdgivet - 14 apr. 2021

Bibliografisk note

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This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine

ID: 66310609