The pathophysiology of pain in Tibialis posterior tendon dysfunction (TPTD) is not well understood. It has been theorized that TPTD is a degenerative process unrelated to inflammation. However, we hypothesize that inflammation is a key component of TPTD. The purpose of this study was to determine if inflammatory cytokines, matrix metalloproteases (MMPs), and glutamate were elevated in diseased TPTs.
Matched torn TPT, TPT insertion, and flexor digitorum longus (FDL) samples were collected from 21 patients with TPTD. The samples were individually incubated in media for 48 hours. The conditioned media was analyzed for inflammatory cytokines, MMPs, and glutamate. Histology was performed on the samples. Statistical analysis was performed with Friedman’s test and Wilcoxon-signed-rank post-hoc tests with Bonferroni correction (α = 0.0167). Spearman’s ρ was used to determine non-parametric correlations between histology and cytokine, MMP, and glutamate concentrations.
Diseased TPT and TPT insertion groups were significantly elevated compared to healthy FDL for inflammatory cytokines IL-1β, IL-6, IL-8, IL-10, and TNF-α and MMPs MMP-1, MMP-2, and MMP-3 (p<0.005). Differences in glutamate concentrations were also significant, but only the diseased TPT group was significantly elevated compared to the healthy FDL tendons (p<0.01). Histologic grading correlated with inflammatory cytokine levels.
Diseased TPT and the TPT insertion demonstrated significantly elevated levels of inflammatory cytokines and MMPs compared to healthy FDL controls, suggesting a role for inflammation in the disease process. The amount of inflammation correlated with increased tendon degradation. The TPT, but not the insertion, contained significantly larger amounts of glutamate.