Eric Troncy

Chronic pain (CP) associated with canine osteoarthritis (OA), remains under-detected, under-diagnosed, and insufficiently managed, while the early signals prompting owners to consult a veterinarian are poorly characterized. This narrative review draws on self-determination theory (SDT) to explore how the experience of OA-associated CP reshapes the self-determination capacities within owner–dog dyads. It describes the deco-construction of dyadic co-construction induced by the apparition and progression of OA-associated CP, followed by its reco-construction after the veterinary diagnosis, integrating a pivotal moment: the owner’s rupture point. Its objectives are twofold: (1) from a SDT perspective, to conceptualize these processes when the dog develops OA-associated CP; and (2) to propose strategies that help dyads navigate them more effectively and trigger the rupture point earlier. Deco-construction progressively erodes dyadic self-determination. While the accumulation of CP-related signals may lead the owner to their rupture point, their perceived competence, denial, wait-and-see attitude and apprehension of veterinary cost often delay it. Reco-construction relies on respecting the self-determination of the dog, the owner, and the veterinarian. At home, the adaptation of therapeutic strategies enables the dyad to regain a sense of mutual self-determination. These processes are influenced by biopsychosocial, experiential, environmental, and technical factors specific to the dog, the human, and the disease. A strong co-construction appears to facilitate them. To better capture the dynamics of co-/deco-/reco-construction and anticipate owners’ rupture point, several tools appear promising, but none fully integrate co-construction, bidirectionality, and dyadic attachment. There is an urgent need to develop more integrative conceptual frameworks and tools. This review remains conceptual and narrative in nature (albeit based on an exhaustive literature), and the proposed framework has not yet been clinically validated.

Central sensitization and pain endogenous controls imbalance were reported in humans affected by chronic pain. In cats, nociplastic changes, such as the wind-up phenomenon, ( i.e ., decreased tolerance to repeated stimuli) were described using a validated mechanical device inducing temporal summation of pain (TSP). The study aim was to validate this method in dogs and to describe pro- or anti-nociceptive profiles occurring with canine osteoarthritis (OA). Healthy ( N = 4) and OA ( N = 31) dogs were assessed. Six TSP stimulation protocols were tested for their reliability and specificity, at mid-antebrachium (0.38 Hz at 2–4Newtons [N], 0.25 Hz or 0.50 Hz at 4N) or tail-base (0.25 Hz or 0.50 Hz at 2N). Endogenous facilitatory, or inhibitory, controls were assessed using a pressure pain threshold (PPT) before and after TSP, or conditioning pain modulation (CPM) via an ischemic model, respectively. The PPT pre/post stimuli were used to calculate ratio of facilitation (< 0%) or functional inhibition (> 7%). Statistical analyses included intraclass coefficient of correlation, Spearman’s correlations, Fisher and Mann U tests, with α = 0.05. The response to mechanical TSP scores tended to be moderately reliable, while tail-base stimulation decreased inter-trials variability compared to mid-antebrachium for healthy dogs ( P = 0.029). The response was specific, OA dogs tolerated 50% less stimulations than healthy dogs at 0.5 Hz frequency and 2N ( P = 0.008). This protocol led to spinal hyperexcitability; among facilitated OA dogs, 45% presented functional inhibition versus 73% for the non-facilitated dogs. No correlations were found between radiographic score, orthopedic score, response to mechanical TSP or age with the facilitation or inhibition ratios ( P > 0.173). OA dogs developed central sensitization reflected by the wind-up phenomenon. An imbalance in favor of endogenous facilitatory controls was observed suggesting inhibitory control fatigue and neuroplasticity. Characterizing endogenous pain modulation will enable better management of OA pain by preserving inhibitory control and preventing its fatigue.

Introduction: Feline osteoarthritis (OA) is characterized by somatosensory neuro-sensitization, assessed through quantitative sensory testing. It was hypothesized that somatosensory neuro-sensitization would increase with OA pain severity, as categorized through the validated Montreal Instrument for Cat Arthritis Testing, for Veterinarians (MI-CAT(V)). Methods: Healthy ( n = 10) and cats with naturally occurring OA ( n = 121) were enrolled in this prospective, negatively controlled study. Peripheral and spinal sensitization were respectively assessed by paw withdrawal threshold (PWT) and response to mechanical temporal summation (RMTS). PWT determined allodynia threshold. Derived from MI-CAT(V), cats were sorted into four validated OA severity clusters, from absent to severe OA pain. Outcomes were compared across allodynia status (healthy, non-allodynic and allodynic) and OA clusters, while testing for the influence of demographic data, with alpha set at 5%. Results and discussion: The PWT, RMTS, MI-CAT(V) outcomes and age accurately discerned between healthy and OA animals ( P < 0.002), but not body weight. Non-allodynic cats had similarly altered MI-CAT(V) and RMTS to allodynic cats, but they were younger ( P = 0.010) and had a higher PWT than allodynic ( P < 0.001), and similar PWT ( P = 0.925) but older ( P < 0.001) than healthy cats. Spinal sensitization was similar in the three OA-affected clusters (mild-moderate-severe; P = 1.000), but MI-CAT(V) categorized them sensitively ( P < 0.001). The mild cluster included more non-allodynic cats than the moderate ( P = 0.021) and severe ( P = 0.026) clusters. Interestingly, 32% of mild OA cats were allodynic, when the proportion increased to 61% in pooled moderate/severe OA cats ( P = 0.013). OA cats are sensitized compared to healthy cats, and peripheral sensitization seems to increase with OA severity (or vice-versa ?), which influences pain phenotype.

Although chronic pain in feline osteoarthritis involves neuro-sensitization, the associated sensory changes have not been studied. Cats with osteoarthritis ( n = 20) and healthy controls ( n = 6) were assessed for peripheral (paw withdrawal threshold, PWT) and spinal (response to mechanical temporal summation, RMTS) sensitization, with lower values indicating higher neuro-sensitization. Functional impairment was assessed using the Montreal Instrument for Cat Arthritis Testing, for Use by Veterinarians [MI-CAT(V)], with higher scores indicating greater impairment. Cerebral sensory integration was evaluated using cortical somatosensory evoked potential (CSEP), brainstem auditory evoked response (BAER), and visual evoked potential (VEP) under dexmedetomidine sedation. The amplitude and latency of action potentials were recorded. The Mann–Whitney U test and Spearman’s rank correlation (coefficient = ρ ) were applied ( α = 0.05). Cats with pain showed increased CSEP and BAER latency and amplitude ( p < 0.032) but decreased VEP latency and increased amplitude ( p < 0.038) compared to healthy cats. The PWT was negatively correlated with CSEP latency and amplitude ( ρ = −0.51 to −0.43, p < 0.037) and BAER latency ( ρ = −0.80 to −0.60, p < 0.039), while the RMTS was negatively correlated with CSEP latency ( ρ = −0.48, p = 0.017). In contrast, the PWT ( ρ = 0.71 to 0.76, p < 0.010) was positively correlated with VEP latency. The MI-CAT(V) score correlated with CSEP amplitude ( ρ = 0.62, p = 0.006), BAER latency ( ρ = 0.72 to 0.90, p < 0.008), and VEP latency ( ρ = −0.73 to −0.65, p = 0.023). Sensory processing is altered in cats with osteoarthritis-associated chronic pain, suggesting differential inhibitory control mechanisms.

Background: Dogs trained to metabolomics detection can identify pathological changes through their refined smelling sense. During the COVID-19 pandemic, studies worldwide evaluated Detection Dog Signaling Behavior (DDSB) for SARS-CoV-2. However, most statistical approaches failed to account for key sources of bias, potentially distorting performance estimates. This study aimed to estimate DDSB accuracy for SARS-CoV-2 infection in a Canadian population while assessing the impact of selected sources of bias on performance estimates. Methods: Participants attending the COVID-19 assessment clinic at St. Joseph’s Health Centre, Toronto, were recruited between October and December 2021. Each provided a nasopharyngeal swab for reverse transcription-polymerase chain reaction (RT-PCR) testing and three sweat samples for canine detection. Three dogs were trained to detect SARS-CoV-2 in sweat samples. Validation sessions were video recorded and independently reviewed by two blinded observers. DDSB diagnostic accuracy was estimated against RT-PCR, evaluating the impact of ignoring its imperfect accuracy and repeated sniffing of the same samples during validation. Results: Among 2,358 participants (mean age: 34.7 years; 55.7% female), 437 contributed to training. Validation tests included 146 unique participants (25 RT-PCR positive, 121 negative). Assuming RT-PCR was imperfect, DDSB posterior median sensitivity ranged from 67% (95% credible interval [CrI]: 29%–97%) to 78% (95% CrI: 41%–99%), and specificity from 67% (95% CrI: 53%–79%) to 77% (95% CrI: 65%–87%) across the three dogs. Assuming RT-PCR was perfect, sensitivity decreased by 7.9% to 9%, while specificity remained unchanged. Including repeated positive samples without adjustment did not affect specificity estimates but overestimated sensitivity by 7.9% to 13.4% (imperfect RT-PCR) and 11.4% to 18.3% (perfect RT-PCR). Conclusion: DDSB shows potential as a non-invasive screening tool for SARS-CoV-2 infection. Our results highlight the challenges of designing such studies and the need for standardized training and validation procedures to ensure the reliability and validity of DDSB.

Chronic osteoarthritis (OA) pain is a complex nociplastic condition that affects humans, as well as cats and dogs. This review summarizes the physiology of pain in healthy individuals, the physiopathology of OA pain, and the use of quantitative sensory testing (QST) to objectively assess somatosensory sensitization associated with chronic OA pain. It discusses the translation of human OA pain phenotype profiles to animals, the management of neuro-sensitization with currently prescribed treatments, and complementary methods for evaluating neuro-sensitization, such as electrodiagnostic testing. Additionally, this review serves as a practical guide for standardizing QST in rats, cats, and dogs, with explanatory appendices. It was hypothesized that in translational comparison with the human condition, OA-induced rat models and naturally occurring OA in cats and dogs would exhibit similar somatosensory sensitization profiles. As observed in human OA, an imbalance between facilitatory and inhibitory endogenous controls is also evident in animal OA. This dysregulation can be characterized using QST and underlies the distinct nociceptive phenotypes. Confirming and validating OA pain profiles will promote a patient-tailored approach to effectively alleviate neuro-sensitization in humans and animals.

Osteoarthritis (OA) is a complex and increasingly prevalent condition, affecting an estimated 600 million people worldwide and significantly reducing quality of life. Understanding OA as both an inflammatory and neurological disease presents challenges for diagnosis and treatment, as no curative therapy is currently available. The neuroactive effects of OA pain on neuropeptide systems, particularly within the spinal cord, remain underexplored, impeding therapeutic advances. Mass spectrometry (MS) was employed to characterize the spinal cord peptidome in a validated rat model of OA pain. The peptidome was analyzed longitudinally over 84 days using the Montreal Induction of Rat Arthritis Testing (MI-RAT©; n = 20) model, compared to arthrotomic (Sham; n = 4) and healthy (Naive; n = 9) groups. Label-free peptidome profiling using liquid chromatography coupled with tandem MS (LC-MS/MS) revealed dynamic changes in endogenous spinal peptides during OA progression, leading to the identification of 624 peptides derived from 29 prohormone precursors. The findings reveal substantial changes in peptide levels in the spinal cord, particularly involving neuropeptide substance P and peptides derived from proenkephalin, calcitonin gene-related peptide, and somatostatin. These results provide novel insights into the molecular mechanisms underlying OA-associated pain and identify potential targets for new therapeutic interventions in neurological pain conditions.

Dyadic co-construction, the mutual adaptation that occurs between dogs and their owners, is often discussed in terms of cooperation and participation, yet it remains poorly defined and under-conceptualized in the literature. This review proposed that self-determination theory (SDT), with its three core psychological needs—autonomy, competence, and relatedness (attachment)—offers a valuable framework for understanding this phenomenon within a dyadic context. The objectives of this review were twofold: (1) to conceptualize co-construction in owner–dog interactions through the lens of SDT, and (2) to propose methodological approaches for studying this process, while acknowledging their current limitations. Dyadic co-construction emerges as a dynamic, evolving process of mutual influence, shaped by biopsychosocial factors, individual and shared experiences, and the physical and social environments of both human and dog, as well as the dyad as a unit. Depending on the nature of the interaction, co-construction can be beneficial or detrimental. Positive training practices and secure attachment patterns in both humans and dogs tend to foster more harmonious co-construction, whereas aversive methods and insecure attachment may hinder it. Although existing methodologies offer promising insights into this process, they often lack standardization, statistical robustness, and true bidirectionality. This review underscores the need for more integrative, longitudinal, and empirically grounded approaches to fully capture the complexity and clinical relevance of owner–dog dyadic co-construction.