Julie B. Engiles

We performed a retrospective analysis of postmortem reports for racehorses submitted to the Pennsylvania Animal Diagnostic Laboratory System between July 2017 and July 2025. We included 394 (366 Thoroughbred [TB], 28 Standardbred [SB]) racehorses, 2–11-y-old (median = 4-y-old), from the Mid-Atlantic region. Annually, 34–58 TBs and 1–9 SBs were submitted. TB racehorse submissions were highest in July and October; SB racehorse submissions were highest in June and July. Approximately two-thirds of submitted racehorses died or were euthanized within 1 h of racing or training. Catastrophic musculoskeletal (MSK) injury was the highest reported cause of fatality for both TB (272 of 366; 74%) and SB (15 of 28; 54%) cohorts. In TBs, 245 of 272 (90%) of catastrophic MSK injuries were appendicular skeletal fractures, most involving the forelimb fetlock joints. Fractures of the proximal sesamoid bones predominated, occurring alone or as components of polyostotic fetlock fractures. In SBs, 15 of 15 (100%) catastrophic MSK injuries were appendicular skeletal fractures, most commonly involving the proximal phalanx of hindlimb fetlock joints. Undetermined cause of death was the second highest reported cause of fatalities in both TBs (31 of 366; 8%) and SBs (5 of 28; 18%). Fatalities were rarely the result of non-catastrophic MSK disease or diseases involving other organ systems. Our results are similar to those of published reports from other regions and may help inform research initiatives focused on early disease detection or prevention strategies to reduce the risk of racehorse fatalities and improve equine welfare.

Background: Impinging (overriding) spinous processes (ISPs) are commonly identified in horses with back pain. Diagnostic analgesia is widely used as the clinical reference standard for confirming association with clinical signs of back pain, but the specificity of dorsal spinous region diagnostic analgesia remains poorly understood. Objectives: To evaluate the specificity of a midline thoracic interspinous space injection in cadaveric horses using three injectate volumes, assessed by computed tomography (CT) and anatomical dissection. Study Design: Ex vivo experimental study. Methods: The T15–T16 interspinous space of isolated thoracolumbar segments from 10 cadaver horses was injected using a dorsal midline approach with 5, 10, or 20 mL of a 3:1 iohexol:methylene blue solution under radiographic guidance. CT was performed post‐injection to assess contrast distribution, and specimens were serially sectioned to evaluate methylene blue distribution. Bayesian linear regression was used to assess the relationship between injectate volume and spread distance. Results: Injectate was identified in the interspinous space in six specimens. Contrast injectate distribution to ≥1 thoracic articular process joint occurred in nine specimens and ≥1 intervertebral foramen in all specimens. Injectate entered the epidural space in two specimens (10 and 20 mL injectate volumes). Larger injectate volume was associated with greater craniocaudal spread (Bayesian linear regression: +4.094 mm/mL, 95% credible interval [CrI] 0.038–8.399), but not dorsoventral spread. Conclusion: Dorsal midline injection at T15–T16 is a technique with poor specificity for targeting the interspinous ligament and frequently results in periarticular and intervertebral foramen distribution, placing injectate in proximity to adjacent articular and neurovascular structures. This may lead to misinterpretation of clinical results after injection and potential complications. Craniocaudal injectate spread increased with larger injection volume.

Osteoarthritis is a leading cause of chronic pain and disability, which lacks disease-modifying treatment. Given the complex multi-tissue and multifactorial drivers behind disease progression, effective treatments will require simultaneously targeting several mechanisms underlying joint degeneration and pain. Here, we developed and evaluated a combinatorial gene therapy, consisting of a high-capacity adenoviral vector carrying two therapeutic genes to target distinct pathological mechanisms: inflammation (IL-1Ra) and chondrocyte health (PRG4). Intra-articular delivery of this treatment improved functional, structural, and pain outcomes in murine and equine osteoarthritis models. In addition, treatment normalized inflammatory environments in joint tissues, as well as in the dorsal root ganglia (DRG) known to harbor joint-innervating sensory neurons. Moreover, gene therapy reversed OA-induced molecular signatures of neural hyperexcitability, suggesting amelioration of peripheral sensitization. Collectively, these findings support combinatorial gene therapy as a promising treatment for osteoarthritis, while identifying neuroinflammatory signatures for correction of disease progression and pain.

Sudden death (SD) is the second most important syndrome associated with death in racehorses. The cause of SD in a large number of horses remains undetermined, and, in many of these cases, causes are not found by gross or microscopic postmortem examinations. Among the known causes of SD are traumatic injuries, including fractures of skull, neck, and pelvis; intoxications (e.g., anticoagulant rodenticides); and others. For many cases of SD in which no significant lesions are found, heart failure, probably associated with arrhythmias, is suspected. Precise phenotypic characterization of SD in horses is critical for diagnosis and prevention. Standardized gross and microscopic postmortem protocols are needed to discern normal background changes that may be present in healthy horses from significant changes that directly contribute to SD. Here, we review the current knowledge on the pathology of SD in racehorses.

Background: There is emerging evidence for the role of the immune system in osteoarthritis (OA) pathophysiology; however, little is known about how immune cells and the synovial transcriptome are altered in naturally occurring equine OA. Objectives: To evaluate synovial fluid (SF) and synovial membrane (SM) immune cell populations and the SM transcriptome in racehorses with fetlock OA. Study Design: Cross‐sectional cadaver study. Methods: Fetlock joints from racehorses euthanised at NY racetracks were considered for inclusion. SF and SM were analysed by flow cytometry using T‐cell (CD3, CD4, CD8) and macrophage (CD14, CD86, CD206) surface markers. OA severity was characterised by gross joint evaluation and SM histology. Bulk RNA‐sequencing of SM was performed to identify differentially expressed genes. Flow cytometry data were analysed with mixed linear modelling, including OA severity as a fixed effect and horse as a random effect. RNA‐sequencing data were evaluated with mixed linear and quadratic modelling using DREAMSeq method to capture differential gene expression over the range of OA severity. Results: Twenty‐four fetlocks from 12 horses met inclusion criteria. CD8+ T‐cells ( R ² = 0.25 for SM, 0.35 for SF) and CD86+ macrophages ( R ² = 0.14 for SM) were positively correlated with OA severity, while CD4+ T‐cells ( R ² = 0.17 for SM, 0.31 for SF) were negatively correlated. Macrophages co‐expressing CD86 and CD206 correlated with OA severity in SM ( R ² = 0.31). Pathways including those associated with TNF‐α signalling, connective tissue development and cell and neuron projection organisation/development were differentially regulated in SM with greater OA scores. Main Limitations: Limited sample size, particularly of horses with severe OA. Conclusions: CD8+ T‐cells, CD86+ macrophages and macrophages co‐expressing CD206 and CD86 are enriched in horses with more advanced OA. Gene set analysis suggests the importance of TNF‐α signalling and disinhibition of neuron and cell projection development in OA pathogenesis.

Summary: Septic arthritis remains a common orthopaedic condition in both human and veterinary medicine which can cause serious morbidity and pose considerable challenges for clinical management. The majority of the published clinical research in humans and veterinary species has been focused on the diagnosis, treatment, prevention and outcome of this condition, with less emphasis on the direct sequelae of this condition, especially regarding its effects on the local bone. Osteomyelitis and osteonecrosis are often discussed as separate entities, but it can be argued that there are numerous similarities between the conditions and they can co‐exist in clinical cases. The coexistence of these conditions has also likely been overlooked historically in part due to the difficulties in diagnosis. The evolution and adaptation of new diagnostic techniques available for the horse have and will continue to enable a more sensitive and specific appreciation of the pathologic lesions affecting tissues within and adjacent to the joint. The detection of these lesions provides new insights into the complex considerations in the management of septic arthritis and its bony sequelae.

OBJECTIVE: To describe the development and maturation of equine proximal sesamoid bones (PSBs) in fetuses and young horses using radiography, microcomputed (micro)-CT, and histology. METHODS: A descriptive study. Forelimb PSBs from 12 equids ranging in age from 105 days of gestation to 540 days postgestation were evaluated. Radiography was used for preliminary assessment of metacarpophalangeal joint and PSB mineralization, and micro-CT imaging was performed to assess mineralized PSBs. Tissue volume, bone volume fraction, height, width, depth, trabecular thickness, and anisotropy were quantified from midplanar micro-CT sections in 3 dimensions. Midsagittal PSB histologic sections stained with H&E and Safranin O/Fast Green were used to determine the ratio of ossification center to cartilage template size and to describe the formation and development of the cartilage template, ossification center, spherical growth plate, articular cartilage, and entheses. RESULTS: Mineralization of equine PSBs is associated with cartilage canals and a spherical growth plate that undergoes endochondral ossification during the late gestation to early postgestational period. The apical, flexor, basilar, and articular ossification fronts demonstrate morphologic variability. Structural organization of the articular cartilage and entheses occurs concurrently with the development of an underlying plate of compact bone. At 540 days postgestation, the fibrocartilaginous entheses of the flexor cortex of the PSB had yet to mature. CONCLUSIONS: Equine PSBs mineralize predominantly by endochondral ossification during the late gestation to early postgestational period. Mineralization precedes maturation of the articular cartilage and fibrocartilaginous entheses. CLINICAL RELEVANCE: The postgestational maturation of the PSB and its surrounding tissues may predispose young horses to developing lesions at these sites, such as apical avulsion fractures, warranting further investigation.

Background: Autologous protein solution (APS) has been shown to decrease lameness in horses with osteoarthritis (OA). Synovitis is an early driver of OA, providing an opportunity to intervene in the progression of disease via intra‐articular (IA) therapeutics. Objectives: The objective of this study was to investigate the effects of a single IA APS injection in horses with interleukin‐1β (IL‐1β)‐induced synovitis. We hypothesised that APS would decrease joint swelling and lameness, improve synovial fluid parameters and improve joint pathology scores in horses compared with untreated controls. Study design: Randomised controlled in vivo experiment. Methods: Synovitis was induced with IL‐1β (65 ng) in one randomly selected tarsocrural joint. Twenty‐four hours later, joints were treated with APS (Pro‐Stride®) ( n = 12) or left as untreated controls ( n = 6). Lameness examinations and joint circumference measurements were performed on Days 0 (prior to IL‐1β), 1 (prior to APS), 2, 4, 7 and 14. Synovial fluid, obtained on the same days, was analysed for protein concentration, nucleated cell count, and cytokine (IL‐1β, TNF‐α, IFN‐γ, IL‐6, IL‐10) and prostaglandin E2 (PGE2) concentrations. Gross pathology and synovial membrane histopathology scoring was performed on APS‐treated ( n = 5), untreated control ( n = 4) and normal ( n = 9) tarsocrural joints. Results: APS did not decrease lameness or joint circumference compared with untreated controls. Synovial fluid parameters were not different between treatment groups. APS treatment did significantly decrease gross and histopathology scores. Main limitations: Main limitations included the use of an induced model of the synovitis, inter‐horse variability in the response to IL‐1β and likely variability in the constituents of APS from individual horses. Conclusions: APS treatment of tarsocrural joints with synovitis did not significantly improve lameness or alter synovial fluid parameters. APS did lead to significant improvement in gross joint appearance and synovial membrane histology suggesting that APS may have disease‐modifying effects.

Background: Large colon volvulus is a cause of colic in horses with high morbidity and mortality when not promptly treated. More treatment options are needed to improve the outcome of these cases by protecting against the damage caused by ischaemia and reperfusion injury. Objectives: To determine the effect of preconditioning with dexmedetomidine prior to induction of ischaemia–reperfusion (IR) injury in a large colon volvulus model in the horse. Study design: Randomised blinded in vivo experiments. Methods: Horses received either a dexmedetomidine (DEX) or saline (CON) constant rate infusion (CRI) immediately following induction of anaesthesia. Venous, arterial, and transmural occlusion of a section of the large colon was performed for 3 h, after which the ligatures and clamps were removed to allow for reperfusion for 3 h. Biopsies of the large colon were taken at baseline, 1 and 3 h of ischaemia, and at 1 and 3 h of reperfusion. Results: The severity of crypt epithelial loss (DEX = 2.1 [0.8–2.8], CON = 3.1 [2.5–4], p = 0.03) and mucosal haemorrhage was decreased (DEX = 2.1 [1.3–3], CON = 3.5 [2.5–4], p = 0.03) in group DEX compared to group CON when graded on a scale of 0–4. Crypt length remained longer (DEX = 369.5 ± 91.7 μm, CON = 238.5 ± 72.6 μm, p = 0.02) and interstitium to crypt (I:C) ratio remained lower (DEX = 1.4 (1–1.7), CON = 2.6 [1.8–5.9], p = 0.03) in group DEX compared to group CON during reperfusion. Main limitations: Clinical applicability of pharmacologic preconditioning is limited. Conclusion: Preconditioning with a dexmedetomidine CRI prior to IR injury demonstrated a protective effect histologically on the large colon in the horse. Further investigation into postconditioning with dexmedetomidine is warranted as a possible intervention in colic cases suspected of being large colon volvulus.

Conventional microdiscectomy treatment for intervertebral disc herniation alleviates pain but does not repair the annulus fibrosus, resulting in a high incidence of recurrent herniation and persistent dysfunction. The lack of repair and the acute inflammation that arise after injury can further compromise the disc and result in disc-wide degeneration in the long term. To address this clinical need, we developed tension-activated repair patches (TARPs) for annulus fibrosus repair and local delivery of the anti-inflammatory factor anakinra (a recombinant interleukin-1 receptor antagonist). TARPs transmit physiologic strain to mechanically activated microcapsules embedded within the patch, which release encapsulated bioactive molecules in direct response to spinal loading. Mechanically activated microcapsules carrying anakinra were loaded into TARPs, and the effects of TARP-mediated annular repair and anakinra delivery were evaluated in a goat model of annular injury in the cervical spine. TARPs integrated with native tissue and provided structural reinforcement at the injury site that prevented aberrant disc-wide remodeling resulting from detensioning of the annular fibrosus. The delivery of anakinra by TARP implantation increased matrix deposition and retention at the injury site and improved maintenance of disc extracellular matrix. Anakinra delivery additionally attenuated the inflammatory response associated with TARP implantation, decreasing osteolysis in adjacent vertebrae and preserving disc cellularity and matrix organization throughout the annulus fibrosus. These results demonstrate the therapeutic potential of TARPs for the treatment of intervertebral disc herniation.