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It can be argued that chronic pain is the most ubiquitous disease process in all of medicine. All animals, should they live long enough, will probably experience it. And of all chronic pain syndromes, osteoarthritis (OA) remains the most predictable cause in both dogs and cats. Indeed, in dogs the pathophysiology of OA is commonly heritable and conformational, meaning that the disease process begins at a very young age and is lifelong, with at least 30 to 40 per cent of dogs affected clinically.1 In cats, the aetiopathophysiology is less certain but equally prevalent clinically, and more than 90 per cent of cats over the age of 12 years have radiographic changes consistent with degenerative joint disease.2,3 It follows that the hunt for novel therapy targets to address chronic pain in general and OA in particular needs to remain robust.
One of those targets, nerve growth factor (NGF) and its binding to tropomyosin receptor kinase A (TrkA) receptor, is at the forefront of this hunt. NGF, produced and utilised by many cell types (including epithelium, endothelium, immunoreactive cells and CNS glia), is found in abundance during neonatal and infant development, and gradually downregulates over time.4 However, it upregulates once again with chronic inflammation, among other circumstances, and becomes an integral component of central sensitisation (wind up), spinal cord plasticity and maladaptive pain signalling. This inevitably results in hyperalgesia: lowered thresholds and exaggerated scope, character, duration and field of pain. Therefore, several anti-NGF/TrkA signalling strategies have been investigated for their pain-modifying capabilities and safety. Chief among these …
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