Abstract
BackgroundPatients with intra-articular fractures tend to develop post-traumatic osteoarthritis (PTOA). The initial inflammatory response with elevation of inflammatory cytokines following joint trauma might be responsible for triggering cartilage catabolism and degradation. We aimed to identify and quantify cytokine levels in fractured and healthy knee joints and the correlation of these cytokines with clinical outcomes.MethodsIn this prospective cohort study, synovial fluid and plasma were collected from 12 patients with proximal intra-articular tibia fractures before surgery. The concentration of sixteen inflammatory cytokines, two cartilage degradation products and four metabolic mediators where measured, comparing the acute injured knee with the healthy contralateral knee. Patients were evaluated 3- and 12-months after surgery with clinical parameters and radiographical scanning. Non-parametrical Wilcoxon rank-sum and Spearman tests were used for statistical analysis, and a P-value below 0.05 was considered significant.ResultsWe found an elevation of the pro-inflammatory cytokines IL-1β, IL-2, IL-6, IL-8, IL-12p70, TNF-α, IFN-y, MMP-1, MMP-3, and MMP-9 and a simultaneous elevation of the anti-inflammatory cytokines IL-1RA, IL-4, IL-10, and IL-13 in the injured knee. Several pro- and anti-inflammatory cytokines and metabolic mediators were correlated with clinical outcomes 12 months after surgery, especially with pain perception.ConclusionsOur results support that an inflammatory process occurs after intra-articular knee fractures, which is characterized by the elevation of both pro- and anti-inflammatory cytokines. There was no sign of cartilage damage within the timeframe from injury to operation. We found a correlation between the initial inflammatory reaction with clinical outcomes 12 months after surgery.
Highlights
Patients with intra-articular fractures tend to develop post-traumatic osteoarthritis (PTOA)
Twelve patients with proximal intra-articular tibia fractures were included in this prospective cohort
We found that IL-8, IL-1β, Tumor necrosis factor (TNF)-α, and Matrix metalloproteinase (MMP)-1 had a higher ratio than the other cytokines measured (212, 40, 20, and 74) compared to levels in the healthy knee (Table 3)
Summary
Patients with intra-articular fractures tend to develop post-traumatic osteoarthritis (PTOA). The initial inflammatory response with elevation of inflammatory cytokines following joint trauma might be responsible for triggering cartilage catabolism and degradation. Up to 40% of patients with joint-affecting trauma develop OA within 10 years, and OA has been associated with previous biomechanical treatment [1, 3]. Previous studies indicate that the initial inflammatory response following joint trauma might be responsible for triggering cartilage catabolism and cartilage degradation [3, 5]. The exact inflammatory mechanism(s) and level of cytokine involvement that lead to the progression from initial injury to post-traumatic OA (PTOA) requires further investigation before we can supplement current surgical practice to improve outcomes following intra-articular fractures [2, 6, 7]
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