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.