Behavioral and inflammatory changes in the nervous system as a tool for studying monoiodoacetate-induced osteoarthritis

Abstract

Objective: This study aims to elucidate the mechanisms underlying neuroinflammation and behavioral changes in the MIA-induced OA model. Methodology: PubMed and Science Direct databases were used, employing the descriptors MIA, Osteoarthritis, Neuroinflammation, Rat, Monoiodoacetate-induced Osteoarthritis, and Boolean operators AND and OR, and studies published between 2019 and 2023 were included. Review articles, studies in humans, animal models of joint destabilization, meniscectomy-induced osteoarthritis, fracture-induced osteoarthritis, or intra-articular compression-induced osteoarthritis were excluded from the analysis. Results: the 16 articles considered in this study highlight the roles of various inflammatory cytokines acting in the central nervous system (CNS) and peripheral nervous system (PNS) that synergistically facilitate nociception and behavioral disorders correlated with anxiety and depression. The main factors involved in the neuroinflammatory process in OA induced by MIA involve pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, sensitizing nerves in the PNS, in dorsal root ganglia (DRG), and sciatic nerve. Neuroinflammation affects different parts of the CNS, namely: the spinal cord, the hippocampus, and the prefrontal cortex. In the CNS and PNS, inflammatory cytokines facilitate the transmission of the nociceptive signal and increase microglial and astrocytic activity, inducing persistent hypernociception, anxiety, and depressive behaviors. Conclusion: in the MIA-induced OA model, neuroinflammation in the PNS and CNS is responsible for persistent nociception, as well as brain changes that generate behavioral conditions related to anxiety and depression.