Advances in the pharmaceutical treatment options for canine osteoarthritis

Abstract

Canine osteoarthritis is a significant cause of pain in many dogs and can therefore compromise animal welfare. As the understanding of the biology and pain mechanisms underpinning osteoarthritis grows, so do the number of treatments available to manage it. Over the last decade, there have been a number of advances in the pharmaceutical treatment options available for dogs with osteoarthritis, as well as an increasing number of clinical trials investigating the efficacy of pre-existing treatments. This review aims to examine the current evidence behind pharmaceutical treatment options for canine osteoarthritis, including non-steroidal anti-inflammatory drugs, piprants, monoclonal antibodies, adjunctive analgesics, structure modifying osteoarthritis drugs and regenerative therapies.

FIG 1

Illustration of an osteoarthritic knee joint showing the four main stages of the pain pathway in osteoarthritis and the targets of certain drugs. Transduction is the conversion of a nociceptive stimulus into electrical impulse. Transmission is the electrical impulse transmitted from peripheral sensory nerves to the central nervous system (CNS). Modulation is how the nociceptive stimulus is processed by the CNS and includes the endogenous opioid system, as well as ascending input and descending inhibitory pathways. Perception is how the brain (particularly the somatosensory cortex) interprets nociceptive inputs resulting in conscious perception of pain. Adapted from Yamaoka & Auckburally (2014)

FIG 2

Targets of corticosteroids, COX‐inhibiting NSAIDs and piprants on the pathway of arachidonic acid metabolism. Corticosteroids inhibit phospholipase A2, preventing the conversion of phospholipids to arachidonic acid. NSAIDs inhibit cyclooxygenase, therefore preventing the production of prostaglandins from arachidonic acid. Piprants selectively antagonise the prostaglandin‐E₂ EP4 receptor. Adapted from Monteiro & Steagall (2019)