Evidence of cellular proliferation in the spinal cord and hippocampus in an animal model of osteoarthritis

Abstract

Osteoarthritis is a degenerative joint disease that involves articular cartilage destruction, local inflammatory response, pain and hypersensitivity to mechanical and thermal stimulation. Sensitization in the joint has been shown to change the dynamics of central neural networks leading to nociceptive behaviors, learning and adaptation. In this study, we hypothesize that perturbation of local equilibrium, caused by flooding of excitatory neurotransmitters and neuropeptides from sensitized primary afferents, has the potential to induce cellular proliferation in the dorsal horn of the spinal cord and dentate gyrus of the hippocampus prompting reorganization of nociceptive circuits. Using an animal model of osteoarthritis, our findings have shown that knee joint inflammation induced by intra-articular injection of kaolin/carrageenan (K/C) can spark off an increase in the number of bromodeoxyuridine (BrdU)-positive neurons both in the dorsal horn of the spinal cord and the DG of the hippocampus, concomitant with nociceptive behaviors. This new evidence of cellular proliferation in the CNS may provide a new road map for the treatment of arthritic pain.

Keywords

• Hippocampus
• Neurogenic inflammation
• Osteoarthritis
• Pain
• Spinal cord