Abstract
Osteoarthritis (OA) pain is associated with peripheral and central sensitization in humans and results in widespread increased sensitivity across the body. Sensitization contributes to the OA-associated pain (OAP) state. We recently identified increased levels of an endogenous neurotrophic factor, artemin (ARTN), in dogs with OAP compared to healthy pain-free controls. Circulating ARTN released from damaged tissues in OA, may play a central role in widespread sensitivity and pain. However, the relationship between ARTN and somatosensory sensitivity remains unknown. The study aimed to assess the relationship between serum ARTN concentrations and measures of sensitivity in dogs with OAP using quantitative sensory testing. We hypothesized that there would be a positive association between circulating ARTN and increased sensitivity to mechanical and thermal stimuli in dogs with OAP. We used linear and logistic regression models to assess the relationship between ARTN, sensitization, and pain within a cohort of 43 dogs with spontaneous OAP. Serum ARTN was not associated with the degree of sensitization within dogs with OAP. Further, across dogs with varying OAP severity, we did not find any association between ARTN, and clinical measures of joint pain and disability. Although a relationship between ARTN and joint pain was not ruled out.
Highlights
Osteoarthritis (OA) pain is associated with peripheral and central sensitization in humans and results in widespread increased sensitivity across the body
Data from subjects whose owners failed to complete the Liverpool Osteoarthritis in Dogs (LOAD) and the Canine Brief Pain Inventory (CBPI) surveys successfully were excluded from the clinical metrology instruments (CMIs) analysis
The main objective of this study was to evaluate the association between serum ARTN concentrations and measures of somatosensory sensitivity using quantitative sensory testing (QST) in dogs with spontaneously occurring OA-associated pain (OAP)
Summary
Osteoarthritis (OA) pain is associated with peripheral and central sensitization in humans and results in widespread increased sensitivity across the body. Generalized sensitivity in long-standing pain states such as OAP can arise from a wide variety of underlying mechanisms It can be associated with one or more of the following: sensitization of the peripheral primary afferent neurons 8, algoplastic changes within the spinal cord or brain 8, or decreased function of the endogenous pain modulation system 3. In conditions such as OAP, the GS state is likely established and maintained by peripheral input generated by sensitized and hyperresponsive peripheral afferents. Canine spontaneous OA and OAP closely resembles human OA, and client-owned dogs with OA show GS in association with OAP 23 as humans do [3,21]
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