Pathophysiology and treatment of pain in joint disease

Author(s): Schaible HG1, Schmelz M, Tegeder I

Abstract

Deep somatic pain originating in joints and tendons is a major therapeutic challenge. Spontaneous pain and mechanical hypersensitivity can develop as a consequence of sensitization of primary afferents directly involved in the inflammatory process, but also following sensitization of neuronal processing in the spinal cord (central sensitization) or higher centres. Inflammatory pain is linked to sensitization of sensory proteins at the nociceptive endings whereas pain originating from nerve damage (neuropathic pain) has been linked to changes in axonal ion channels producing ectopic discharge in nociceptors as a source of pain. New targets for analgesic therapy include sensory proteins at the nociceptive nerve endings such as the activating TRPV and ASIC channels, but also inhibitory opioid and cannabinoid receptors. Therapeutic targets are also found among the axonal channels that set membrane potential and modulate discharge frequency such as voltage sensitive sodium channels and various potassium channels.

Similar Articles

Ankle osteoarthritis scale

Author(s): Domsic RT1, Saltzman CL

Clinical rating systems for the ankle-hindfoot, midfoot, hallux, and lesser toes

Author(s): Kitaoka HB1, Alexander IJ, Adelaar RS, Nunley JA, Myerson MS, et al.

Unipedal stance testing as an indicator of fall risk among older outpatients

Author(s): Hurvitz EA1, Richardson JK, Werner RA, Ruhl AM, Dixon MR

Efficacy of intra-articular botulinum toxin type A in painful knee osteoarthritis: a pilot study

Author(s): Boon AJ1, Smith J, Dahm DL, Sorenson EJ, Larson DR, et al.

Neurogenic aspects of inflammation

Author(s): Schaible HG1, Del Rosso A, Matucci-Cerinic M

Reduced muscle function in patients with osteoarthritis

Author(s): Fisher NM1, Pendergast DR