Changes in proinflammatory cytokines, neuropeptides, and microglia in an animal model of monosodium iodoacetate-induced hip osteoarthritis.

The aim of this study was to investigate the local production of proinflammatory cytokines, pain-related sensory innervation of dorsal-root ganglia (DRG), and spinal changes in a rat model of induced hip osteoarthritis (OA). Seventy-five Sprague-Dawley rats were used, including 25 controls and 50 injected into the right hip joints (sham group, injected with 25 µl of sterile saline: N = 25; and monosodium iodoacetate (MIA) group, injected with 25 µl of sterile saline with 2 mg of MIA: N = 25). We measured the local production of TNF-α, immunoreactive (-ir) neurons for calcitonin gene-related peptide (CGRP), and growth associated protein-43 (GAP-43) in DRG, and immunoreactive neurons for ionized-calcium-binding adaptor molecule-1 (Iba-1) in the dorsal horn of spinal cord, on post-induction days 7, 14, 28, 42, and 56 (N = 5 rats/group/time point). For post-induction days 7-42, the MIA group presented significantly elevated concentrations of TNF-α than the other groups (p < 0.01), and a higher expression of CGRP-ir in FG-labeled DRG neurons than the sham group (p < 0.01). MIA rats also presented significantly more FG-labeled GAP-43-ir DRG neurons than the sham group on post-induction days 28, 42, and 56 (p < 0.05), and a significantly higher number of Iba-1-ir microglia in the ipsilateral dorsal horn than the other groups, on post-induction days 28, 42, and 56. The results suggest that in rat models, pain-related pathologies due to MIA-induced hip OA, originate from inflammation caused by cytokines, which leads to progressive, chronic neuronal damage that may cause neuropathic pain.