We do not understand posttraumatic arthritis. Preliminary research with preclinical models is under way to better understand the postinjury intra-articular cascade that leads to posttraumatic arthritis. Certainly clarification of the pathways would allow modulation of healing and perhaps identify targets in the chain for therapeutic approaches. We have had little success for many reasons: lack of a good preclinical model, paucity of research, lack of controls, failure to differentiate between systemic and local conditions, and no large clinical trials, among others. We absolutely need the information that Haller et al. sought in the clinical setting.

Haller et al. evaluated inflammatory cytokine concentrations in human synovial fluid following acute tibial plateau fractures. Their hypothesis was that there would be an elevated inflammatory response following intra-articular fracture and that the inflammatory response would be greater after high-energy injuries than after low-energy injuries. Fractures heal through inflammation, and supposedly higher-energy trauma results in more inflammation. The difficulty is in specifying which marker shows up and when it appears. We are also not sure whether there are missing markers or temporal relationships between markers that may affect the cascade.

The authors quantified the concentrations of interferon-gamma (IFN-γ), interleukin-1 beta (IL-1β), interleukin-1 receptor antagonist (IL-1RA), IL-2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12 (p70), IL-13, IL-17A, tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1 beta (MIP-1β) with multiplex assays (see glossary below). They were hoping that the large grab bag of inflammatory markers would provide insight into the pathways of healing or arthritis.