Spine Centers in Northeastern United States: Assessing Similarities and Disparities to Build more Homogeneity Across the Country.

Ovariohysterectomy (OHE) is one of the most frequently performed elective surgical procedures in dogs and remains a standard clinical model for evaluating perioperative pain and tissue injury (Moxon et al. ). Despite being a routine intervention, OHE involves traction, manipulation and ligation of the ovarian pedicle, recognized sources of substantial noxious stimulation that can trigger pronounced autonomic, endocrine and behavioural responses (del Mar Granados et al. ). This surgical stimulus initiates acute inflammatory and stress pathways, contributing to postoperative discomfort and variation in recovery quality (Flouraki et al. ). Accordingly, recent investigations emphasize the importance of optimizing perioperative analgesia and monitoring, as OHE can still elicit measurable physiological and inflammatory alterations even when performed using modern anaesthetic and surgical techniques (Moxon et al. ; Dalmolin et al. ). Accurate assessment of postoperative pain in dogs remains challenging because most widely used clinical tools rely on behaviour‐based scoring systems that can be influenced by observer interpretation and situational variability (Salichs et al. ). Traditional scales such as numerical rating schemes and composite pain assessments, while commonly applied in clinical practice, exhibit inherent subjectivity and may produce inconsistent results across different observers or clinical environments (Rojsiripornchai et al. ). Furthermore, discrepancies frequently arise between subjective pain scores and more objective physiological or mechanical measures, highlighting the limitations of relying solely on clinician‐observed behaviours to quantify nociception (Hölscher et al. ). These constraints underscore the need for complementary, biologically grounded indicators that may offer a more objective and reproducible understanding of postoperative pain in dogs. Pro‐inflammatory cytokines, such as tumour necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6), play central roles in the early inflammatory cascade triggered by surgical tissue trauma. TNF‐α typically exhibits a rapid and transient rise within the first hour following an inflammatory insult, whereas IL‐6 increases more gradually and sustains elevated concentrations for several hours, reflecting ongoing cytokine‐mediated acute phase activation (Song et al. ). Downstream mediators of this response include acute phase proteins such as haptoglobin (HP) and C‐reactive protein (CRP), both synthesized hepatically under IL‐6 stimulation and recognized as systemic markers of inflammation rather than direct indicators of nociceptive processing (Schmidt and Eckersall ). In dogs, elevations in CRP and circulating cytokines have been documented in various inflammatory and postoperative contexts, though their concentrations often display considerable inter‐individual variability and do not consistently parallel clinical pain manifestations (Gommeren et al. ). Similar biochemical alterations have been reported following OHE, where surgical manipulation induces measurable shifts in inflammatory and stress‐related biomarkers without a predictable relationship to behavioural pain scores (Kang et al. ). Collectively, these findings highlight biological complexity within the postoperative inflammatory response and underscore the need to clarify whether such biomarkers reliably reflect nociceptive experience in dogs.