Magnetic Resonance Imaging, Computed Tomographic and Radiographic Findings in the Metacarpophalangeal Joints of 31 Warmblood Showjumpers in Full Work and Competing Regularly.

There is a limited description of magnetic resonance imaging (MRI) and no information on computed tomographic (CT) findings in the fetlock of non-lame, non-racing sports horses. This study aimed to document comparative CT, MRI and radiographic findings in the metacarpophalangeal joints of showjumpers in full work. Clinical and gait assessments, low-field MRI, fan-beam CT and radiographic examinations of both metacarpophalangeal joints were performed on 31 showjumpers. Images were analysed descriptively. In most limbs (53/62, 85.5%), there were CT and MRI changes consistent with densification in the sagittal ridge and/or condyles of the third metacarpal bone (McIII). Hypoattenuation (subchondral bone resorption) was seen in CT reconstructions in the metacarpal condyle dorsoproximally (n = 2) and dorsodistally (n = 1), in the sagittal groove (n = 2) and medial fovea (n = 1) of the proximal phalanx. The McIII resorptive lesions were detected on MR images but not the proximal phalanx lesions. None were identified on radiographs. In conclusion, MRI and CT abnormalities previously associated with lameness were seen in the front fetlocks of showjumpers without relevant lameness. Densification in the sagittal ridge and the metacarpal condyles likely reflects an adaptive change to exercise. Subchondral bone resorption may indicate an early stage of disease; follow-up information is needed to establish its clinical significance.

Computed Tomographic Evaluation of the Sagittal Ridge of the Third Metacarpal Bone in Young Thoroughbred Racehorses: A Longitudinal Study.

Metacarpophalangeal joint region pain is a common cause of lameness in racehorses. Radiological abnormalities in the sagittal ridge (SR) of the third metacarpal bone have been associated with joint effusion, lameness and reduced sales prices. The aims were to describe computed tomographic (CT) appearance of the SR in racehorses, and to document the progression of these findings over three assessments. Forty yearlings were enrolled at the first examination (time 0). Re-examinations were performed twice, approximately six months apart on 31 (time 1) and 23 (time 2) horses, respectively. Computed tomographic examinations of both metacarpophalangeal regions were performed with the horses in a standing position. Computed tomographic reconstructions were analysed subjectively and objectively. The mean Hounsfield Unit values (Hus) of eight radial segments and location, size and shape of hypoattenuating lesions were recorded. Mean Hus at time 1 were higher than at time 0. There was no difference between mean HU at times 1 and 2. The mean HU values of the dorsal half were higher in the right forelimbs and in fillies. Hypoattenuation was identified in 33/80 (41.3%) limbs at time 0, in 22/62 (35.5%) limbs at time 1 and in 14/46 (30.4%) limbs at time 2. All hypoattenuations were located in the dorsodistal aspect of the SR. The most common shapes were hypoattenuating lesions elongated proximodistally and those extending towards trabecular bone. An increase in attenuation of the SR occurred in the first six months of training. Hypoattenuating lesions could decrease in size and could resolve during early training. In this population, these lesions were not associated with lameness.

Magnetic Resonance Imaging, Computed Tomographic and Radiographic Findings in the Metacarpophalangeal Joints of 40 Non-Lame Thoroughbred Yearlings.

Most catastrophic injuries in Thoroughbred racehorses involve the fetlock. There is no description of comparative imaging in Thoroughbreds entering racehorse training. The aim was to describe MRI, CT and radiographic findings in the metacarpophalangeal joint of non-lame Thoroughbred yearlings. Forty Thoroughbreds underwent low-field MRI, fan-beam CT and radiographic examinations of both metacarpophalangeal joints. Images were assessed subjectively. A hypoattenuating lesion of the sagittal ridge of the third metacarpal bone (McIII) was identified in 33/80 limbs in CT reconstructions. Cone-shaped mineralisation in the sagittal ridge was detected in MR images (n = 17) and in CT images (n = 5). Mild hyperattenuation was common in trabecular bone in the dorsomedial (36/80) and palmarolateral (25/80) metacarpal condyles in CT reconstructions. A focal lesion in the subchondral bone was seen in the proximal phalanx (n = 19) and in McIII (n = 11). Enlarged vascular channels were detected in the metacarpal condyles in 57/80 limbs and in the proximal sesamoid bones in all limbs. Signs of bone modelling are seen in yearling Thoroughbred fetlocks. Sagittal ridge lesions were common and are likely associated with osteochondrosis or other developmental osteochondral defects. Focal lesions in the subchondral bone of McIII and proximal phalanx can indicate developmental abnormalities or subtle subchondral bone injuries.

Magnetic Resonance Imaging Measurements of the Proximal Palmar Cortex of the Third Metacarpal Bone and the Suspensory Ligament in Non-Lame Endurance Horses before and after Six Months of Training.

Proximal metacarpal injury is common in endurance horses, yet exercise-induced changes in this region have not been described. This study aimed to document objective exercise-induced changes in the proximal palmar cortex of the third metacarpal bone (PcMcIII) and the suspensory ligament (SL). Low-field magnetic resonance (MR) images of both proximal metacarpal regions were obtained from six novice and six experienced horses, before and after six months of endurance training. Measurements were acquired in T1-weighted transverse MR images at four levels and included the thickness of the PcMcIII, the mediolateral width, and the dorsopalmar depth of the entire SL and its lobes. We used t-tests or their nonparametric equivalents to compare the measurements from the two examinations and both novice and experienced horses. The medial aspect of PcMcIII was significantly thicker in experienced horses than in novice horses at 2 and 3 cm distal to the carpometacarpal joint. This likely reflects the cumulative effect of long-term exercise and possibly age. The PcMcIII was significantly thicker medially than laterally. There was no significant difference between pre- and post-season measurements. Six months of endurance training were not sufficient to induce changes in the thickness of PcMcIII or the SL that are detectable in low-field MR images.

Complications following diagnostic and therapeutic sacroiliac joint region injections in horses: A study describing clinicians' experiences.

BACKGROUND: There are no detailed data on complications of sacroiliac (SI) joint region injections or on the variability of the methods and circumstances of injections among clinicians. OBJECTIVES: To describe complications following diagnostic, therapeutic and combined SI joint region injections and the details of how these are routinely performed by a large number of clinicians. STUDY DESIGN: Cross-sectional questionnaire survey. METHODS: Clinicians (members of American and European specialist colleges and veterinarians known to the authors), invited by email, who had performed ≥1 SI joint region injection, completed an online questionnaire. Data collected included the clinicians' experience in diagnostic, therapeutic and combined SI joint region injections, details of the injection technique, volume and substance used, and the type of complications seen following SI joint region anaesthesia, medications and combined injections, respectively. Descriptive data analysis was performed and the association between any complications seen and the clinicians' experience, technique, volume and substance used were assessed using binary logistic regression. RESULTS: Of the 212 respondents, 110 had performed diagnostic, 187 therapeutic and 49 combined injections. More clinicians experienced complications after diagnostic (53/110) than after therapeutic (33/187) or combined (6/49) injections (p < 0.01). The most common complications were hindlimb weakness/ataxia after all types of injections (diagnostic: 44/110, 40%, 95% confidence interval [CI]: 30.8-49.8; therapeutic: 15/187, 8.0%, CI: 4.6-12.9; combined: 2/49, 4.1%, CI: 0.5-14.0). Death or horses requiring euthanasia were reported (after therapeutic injections: 5/187; diagnostic injections: 1/110). MAIN LIMITATIONS: No prevalence of complications was established; no detailed descriptions of complications were available. Results may be influenced by selection and recall biases. CONCLUSIONS: Complications were experienced by more clinicians following diagnostic injections than after therapeutic or combined SI joint region injections, but the types and distribution of complications were similar. Results should be interpreted considering the previous reports of low prevalence of complications.

BGP-15 Inhibits Hyperglycemia-Aggravated VSMC Calcification Induced by High Phosphate.

Vascular calcification associated with high plasma phosphate (Pi) level is a frequent complication of hyperglycemia, diabetes mellitus, and chronic kidney disease. BGP-15 is an emerging anti-diabetic drug candidate. This study was aimed to explore whether BGP-15 inhibits high Pi-induced calcification of human vascular smooth muscle cells (VSMCs) under normal glucose (NG) and high glucose (HG) conditions. Exposure of VSMCs to Pi resulted in accumulation of extracellular calcium, elevated cellular Pi uptake and intracellular pyruvate dehydrogenase kinase-4 (PDK-4) level, loss of smooth muscle cell markers (ACTA, TAGLN), and enhanced osteochondrogenic gene expression (KLF-5, Msx-2, Sp7, BMP-2). Increased Annexin A2 and decreased matrix Gla protein (MGP) content were found in extracellular vesicles (EVs). The HG condition markedly aggravated Pi-induced VSMC calcification. BGP-15 inhibited Pi uptake and PDK-4 expression that was accompanied by the decreased nuclear translocation of KLF-5, Msx-2, Sp7, retained VSMC markers (ACTA, TAGLN), and decreased BMP-2 in both NG and HG conditions. EVs exhibited increased MGP content and decreased Annexin A2. Importantly, BGP-15 prevented the deposition of calcium in the extracellular matrix. In conclusion, BGP-15 inhibits Pi-induced osteochondrogenic phenotypic switch and mineralization of VSMCs in vitro that make BGP-15 an ideal candidate to attenuate both diabetic and non-diabetic vascular calcification.

Ferryl Hemoglobin and Heme Induce A1-Microglobulin in Hemorrhaged Atherosclerotic Lesions with Inhibitory Function against Hemoglobin and Lipid Oxidation.

Infiltration of red blood cells into atheromatous plaques and oxidation of hemoglobin (Hb) and lipoproteins are implicated in the pathogenesis of atherosclerosis. α1-microglobulin (A1M) is a radical-scavenging and heme-binding protein. In this work, we examined the origin and role of A1M in human atherosclerotic lesions. Using immunohistochemistry, we observed a significant A1M immunoreactivity in atheromas and hemorrhaged plaques of carotid arteries in smooth muscle cells (SMCs) and macrophages. The most prominent expression was detected in macrophages of organized hemorrhage. To reveal a possible inducer of A1M expression in ruptured lesions, we exposed aortic endothelial cells (ECs), SMCs and macrophages to heme, Oxy- and FerrylHb. Both heme and FerrylHb, but not OxyHb, upregulated A1M mRNA expression in all cell types. Importantly, only FerrylHb induced A1M protein secretion in aortic ECs, SMCs and macrophages. To assess the possible function of A1M in ruptured lesions, we analyzed Hb oxidation and heme-catalyzed lipid peroxidation in the presence of A1M. We showed that recombinant A1M markedly inhibited Hb oxidation and heme-driven oxidative modification of low-density lipoproteins as well plaque lipids derived from atheromas. These results demonstrate the presence of A1M in atherosclerotic plaques and suggest its induction by heme and FerrylHb in the resident cells.

Heme cytotoxicity is the consequence of endoplasmic reticulum stress in atherosclerotic plaque progression.

Hemorrhage and hemolysis with subsequent heme release are implicated in many pathologies. Endothelial cells (ECs) encounter large amount of free heme after hemolysis and are at risk of damage from exogenous heme. Here we show that hemorrhage aggravates endoplasmic reticulum (ER) stress in human carotid artery plaques compared to healthy controls or atheromas without hemorrhage as demonstrated by RNA sequencing and immunohistochemistry. In EC cultures, heme also induces ER stress. In contrast, if cultured ECs are pulsed with heme arginate, cells become resistant to heme-induced ER (HIER) stress that is associated with heme oxygenase-1 (HO-1) and ferritin induction. Knocking down HO-1, HO-2, biliverdin reductase, and ferritin show that HO-1 is the ultimate cytoprotectant in acute HIER stress. Carbon monoxide-releasing molecules (CORMs) but not bilirubin protects cultured ECs from HIER stress via HO-1 induction, at least in part. Knocking down HO-1 aggravates heme-induced cell death that cannot be counterbalanced with any known cell death inhibitors. We conclude that endothelium and perhaps other cell types can be protected from HIER stress by induction of HO-1, and heme-induced cell death occurs via HIER stress that is potentially involved in the pathogenesis of diverse pathologies with hemolysis and hemorrhage including atherosclerosis.

Therapeutic Potential of Carbon Monoxide (CO) and Hydrogen Sulfide (H2S) in Hemolytic and Hemorrhagic Vascular Disorders-Interaction between the Heme Oxygenase and H2S-Producing Systems.

Over the past decades, substantial work has established that hemoglobin oxidation and heme release play a pivotal role in hemolytic/hemorrhagic disorders. Recent reports have shown that oxidized hemoglobins, globin-derived peptides, and heme trigger diverse biological responses, such as toll-like receptor 4 activation with inflammatory response, reprogramming of cellular metabolism, differentiation, stress, and even death. Here, we discuss these cellular responses with particular focus on their mechanisms that are linked to the pathological consequences of hemorrhage and hemolysis. In recent years, endogenous gasotransmitters, such as carbon monoxide (CO) and hydrogen sulfide (H2S), have gained a lot of interest in connection with various human pathologies. Thus, many CO and H2S-releasing molecules have been developed and applied in various human disorders, including hemolytic and hemorrhagic diseases. Here, we discuss our current understanding of oxidized hemoglobin and heme-induced cell and tissue damage with particular focus on inflammation, cellular metabolism and differentiation, and endoplasmic reticulum stress in hemolytic/hemorrhagic human diseases, and the potential beneficial role of CO and H2S in these pathologies. More detailed mechanistic insights into the complex pathology of hemolytic/hemorrhagic diseases through heme oxygenase-1/CO as well as H2S pathways would reveal new therapeutic approaches that can be exploited for clinical benefit.

Zinc Inhibits HIF-Prolyl Hydroxylase Inhibitor-Aggravated VSMC Calcification Induced by High Phosphate.

Vascular calcification is a life-threatening clinical condition in chronic kidney disease (CKD) and is associated with reduced zinc serum levels. Anemia is another frequent complication of CKD. Hypoxia-inducible factor (HIF) stabilizers, also known as HIF prolyl hydroxylase inhibitors (PHI), are promising candidates to treat CKD-associated anemia by increasing erythropoietin synthesis. Recent evidence suggests that HIFs play a pivotal role in vascular calcification. Our study explored feasible impacts of HIF PHI on phosphate (Pi)-induced calcification of vascular smooth muscle cells (VSMCs) and tested whether zinc might inhibit this mineralization process. Treatment of VSMCs with PHI aggravated Pi-induced calcium deposition and Pi uptake. PHI promoted Pi-induced loss of smooth muscle cell markers (ACTA-2, MYH11, SM22α) and enhanced osteochondrogenic gene expression (Msx-2, BMP-2, Sp7) triggering osteochondrogenic phenotypic switch of VSMCs. These effects of PHI paralleled with increased pyruvate dehydrogenase kinase 4 (PDK4) expression, decreased Runx2 Ser451 phosphorylation, and reduced cell viability. Zinc inhibited Pi-induced mineralization of VSMCs in a dose-dependent manner and also attenuated the pro-calcification effect of PHI in Pi-induced mineralization. Zinc inhibited osteochondrogenic phenotypic switch of VSMCs reflected by lowering Pi uptake, decreasing the expressions of Msx-2, BMP-2, and Sp7 as well as the loss of smooth muscle cell-specific markers. Zinc preserved phosphorylation state of Runx2 Ser451, decreased PDK4 level, and restored cell viability. PHI alone reduced the expression of smooth muscle markers without inducing mineralization, which was also inhibited by zinc. In addition, we observed a significantly lower serum zinc level in CKD as well as in patients undergoing carotid endarterectomy compared to healthy individuals. Conclusion - PHI promoted the loss of smooth muscle markers and augmented Pi-induced osteochondrogenic phenotypic switch leading to VSMCs calcification. This mineralization process was attenuated by zinc. Enhanced vascular calcification is a potential risk factor during PHI therapy in CKD which necessitates the strict follow up of vascular calcification and zinc supplementation.

Corneal Manifestations of Systemic Sclerosis.

Purpose: Corneal involvement in systemic sclerosis (SSc) is rare, but due to rich collagen composition cornea is especially vulnerable to connective tissue diseases. Therefore, our aim was to evaluate corneal parameters of SSc patients. Methods: The study included 32 SSc patients and 39 control subjects with no ocular symptoms or ocular surface disorders. All study participants underwent Pentacam evaluation and objective signs of dry eye disease (DED), and clinical parameters were evaluated. Results: All pachymetric values, most of the corneal front surface, corneal volume, as well as anterior chamber depth measurements were significantly lower in the SSc group than in the control group (p < 0.05). Significant negative correlation was found between corneal parameters and age on the one hand, and disease duration on the other. Conclusions: Early recognition of corneal impairment, a possible extraintestinal manifestation of SSc, should be included in the check-up of the disease in order to reduce sight-threatening complications.

Heme Induces Endoplasmic Reticulum Stress (HIER Stress) in Human Aortic Smooth Muscle Cells.

Accumulation of damaged or misfolded proteins resulted from oxidative protein modification induces endoplasmic reticulum (ER) stress by activating the pathways of unfolded protein response. In pathologic hemolytic conditions, extracellular free hemoglobin is submitted to rapid oxidation causing heme release. Resident cells of atherosclerotic lesions, after intraplaque hemorrhage, are exposed to heme leading to oxidative injury. Therefore, we raised the question whether heme can also provoke ER stress. Smooth muscle cells are one of the key players of atherogenesis; thus, human aortic smooth muscle cells (HAoSMCs) were selected as a model cell to reveal the possible link between heme and ER stress. Using immunoblotting, quantitative polymerase chain reaction and immunocytochemistry, we quantitated the markers of ER stress. These were: phosphorylated eIF2α, Activating transcription factor-4 (ATF4), DNA-damage-inducible transcript 3 (also known as C/EBP homology protein, termed CHOP), X-box binding protein-1 (XBP1), Activating transcription factor-6 (ATF6), GRP78 (glucose-regulated protein, 78kDa) and heme responsive genes heme oxygenase-1 and ferritin. In addition, immunohistochemistry was performed on human carotid artery specimens from patients who had undergone carotid endarterectomy. We demonstrate that heme increases the phosphorylation of eiF2α in HAoSMCs and the expression of ATF4. Heme also enhances the splicing of XBP1 and the proteolytic cleavage of ATF6. Consequently, there is up-regulation of target genes increasing both mRNA and protein levels of CHOP and GRP78. However, TGFß and collagen type I decreased. When the heme binding proteins, alpha-1-microglobulin (A1M) and hemopexin (Hpx) are present in cell media, the ER stress provoked by heme is inhibited. ER stress pathways are also retarded by the antioxidant N-acetyl cysteine (NAC) indicating that reactive oxygen species are involved in heme-induced ER stress. Consistent with these findings, elevated expression of the ER stress marker GRP78 and CHOP were observed in smooth muscle cells of complicated lesions with hemorrhage compared to either atheromas or healthy arteries. In conclusion, heme triggers ER stress in a time- and dose-dependent manner in HAoSMCs. A1M and Hpx as well as NAC effectively hamper heme-induced ER stress, supporting their use as a potential therapeutic approach to reverse such a deleterious effects of heme toxicity.

Association between objective signs and subjective symptoms of dry eye disease in patients with systemic sclerosis.

The aim of this study was to evaluate the association between clinical signs and symptoms of dry eye disease (DED) in patients with systemic sclerosis (SSc). This cross-sectional observational study included 19 SSc patients and 19 normal subjects with no ocular symptoms or ocular surface disorders. Clinical parameters included tear film break-up time (tBUT), Schirmer I, lissamine green (LG) dye, and tear film osmolarity tests, tear production, and tear secretion flow. For assessment of the dry eye symptoms, the Ocular Surface Disease Index (OSDI) questionnaire was administered to all patients. The following mean values were found in SSc patients: OSDI 33.6 ± 19.86; osmolarity of the tear fluid 310.8 mOsmol/l ± 14.47; tBUT time 5.158 ± 2.328 s; Schirmer I test 5.395 mm/5 min; LG grading score 2.026 ± 0.8893; collected tear fluid volume 6.397 ± 2.761 µl. The calculated average tear velocity was 4.654 ± 1.963 µl/min. A significant correlation was found between the OSDI as a subjective parameter and disease duration. Early recognition of dry eye symptoms, a possible extra-intestinal manifestation of SSc, should be included in the check up of the disease to reduce ocular complications. The objective tear functional tests were strongly influenced by individual factors like age and disease duration.

Early Corneal Cellular and Nerve Fiber Pathology in Young Patients With Type 1 Diabetes Mellitus Identified Using Corneal Confocal Microscopy.

PURPOSE: The aim of this study was to quantify epithelial, stromal, and endothelial cell density, and subbasal nerve morphology in young patients with type 1 diabetes mellitus with and without diabetic retinopathy. METHODS: A total of 28 young patients (mean age, 22.86 ± 9.05 years) with type 1 diabetes, with (n = 18) and without (n = 10) retinopathy, and 17 age-matched healthy control subjects (mean age, 26.53 ± 2.43 years) underwent corneal confocal microscopy (CCM). RESULTS: We found significantly lower epithelial (P < 0.0001) and endothelial (P = 0.001) cell densities and higher keratocyte cell density (P = 0.024) in patients with type 1 diabetes compared to controls. Significantly lower corneal nerve fiber density (P = 0.004), nerve branch density (P = 0.004), total nerve branch density (P = 0.04), and nerve fiber length (P = 0.001), and greater nerve fiber width (P = 0.04) were observed in patients with type 1 diabetes compared to control subjects. Significantly lower epithelial (P < 0.001) and endothelial (P = 0.02) cell densities, nerve branch density (P = 0.02), and nerve fiber length (P = 0.04), and significantly higher keratocyte cell density (P = 0.02) were found in patients with type 1 diabetes without retinopathy compared to control subjects. CONCLUSIONS: Corneal confocal microscopy identifies corneal cellular and small nerve fiber pathology in young patients with type 1 diabetes without retinopathy, which increases in severity in those with retinopathy. Corneal confocal microscopy appears to have considerable use as an imaging biomarker for early subclinical pathology in young patients with type 1 diabetes mellitus.

A veterinary review of endurance riding as an international competitive sport.

The popularity of competitive endurance riding is growing worldwide and this has led to considerable changes in the discipline (e.g., fitter and faster horses and different types of injuries), which create challenges to all involved in the sport, including veterinarians. During endurance competitions, horses are closely monitored by veterinarians throughout the ride, with the aim of removing from the competition animals whose welfare appears to be endangered. This close monitoring provides veterinarians with an insight into problems during competitions. However, there is a relatively small amount of clinically relevant, evidence-based data published on endurance horses, and this article reviews the evolution of the discipline, the published information on epidemiological data on endurance rides, the problems veterinarians face at competitions, and highlights those areas where research is warranted.

Clinical and diagnostic imaging findings in horses with subchondral bone trauma of the sagittal groove of the proximal phalanx.

Eight sports horses with unilateral (4) or bilateral (3) forelimb or unilateral hindlimb (1) lameness had subtle radiologic abnormalities of the subchondral bone of the sagittal groove of the proximal phalanx associated with moderate or intense increased radiopharmaceutical uptake. High-field or low-field magnetic resonance (MR) imaging confirmed the presence of a fissure fracture or subchondral and trabecular bone trauma. Seven of eight lesions were located approximately midway between the dorsal and palmar cortices of the proximal phalanx; the eighth was sited more dorsally. Two horses underwent follow-up MR imaging and abnormal signal intensity persisted, with little change.

Magnetic resonance anatomy of the carpus of the horse described from images acquired from low-field and high-field magnets.

Cadaver carpi of 30 mature horses with no history of carpal or proximal metacarpal pain were examined using low-field (0.27 T) and high-field (1.5 T) magnetic resonance imaging (MRI). Normal MRI anatomy in transverse, sagittal, and dorsal plane images was determined by comparison with anatomical specimens and standard texts. Subchondral bone and cortical bone thickness measurements were obtained from standardised sites. There was variable subchondral bone thickness in the radius and carpal bones; subchondral bone thickness was consistently larger at dorsal compared with palmar sites in the proximal row of carpal bones. The endosteal surface of the subchondral bone was smooth. The shape of the ulnar carpal bone was variable and one or more small osseous fragments were identified palmar to the bone in 5/30 limbs. There was no evidence to suggest that these were pathological fractures or avulsions of the lateral palmar intercarpal ligament. The amount of muscle tissue in the superficial and deep digital flexor tendons in the proximal aspect of the carpus varied, but none was present at the level of the middle carpal joint and distally. Several structures could be evaluated that cannot be imaged using radiography, ultrasonography, or arthroscopy, including the transverse intercarpal ligaments, the radiocarpal ligament, the short palmar carpal ligaments, and the carpometacarpal ligaments. Anatomical variations not previously described were identified, including the layers of the medial aspect of the carpal fascia. Knowledge of the variation in MRI appearance of the carpus of nonlame horses is helpful for interpretation of MR images of lame horses.

Ultrasonographic findings in the lumbosacral joint of 43 horses with no clinical signs of back pain or hindlimb lameness.

The transrectal ultrasonographic appearance of the lumbosacral joint was assessed in 43 horses with no history or clinical evidence of back pain or hindlimb lameness. In the majority of horses (34/43, 79.1%) the lumbosacral disc had uniform or mildly heterogeneous echogenicity. However, variation in the ultrasonographic appearance of the lumbosacral joint was also identified, including hyperechogenic regions within the lumbosacral disc with or without an acoustic shadow, and mild or moderate irregularity of the opposing surfaces of the last lumbar and the first sacral vertebral bodies. Marked irregularity of the bony surfaces or marked disruption of the lumbosacral disc was not seen in any horse. The mean distance between the ventral aspects of the last lumbar and first sacral vertebrae was 14.2 mm (range: 7.1-26.5 mm, median: 14.4 mm). The degree of protrusion of the ventral aspect of the lumbosacral disc ranged from 0 to 5 mm (mean: 1.32 mm, median: 1.2 mm). The mean angle between the ventral surfaces of the last lumbar and first sacral vertebrae was 147 degrees (range: 118-165 degrees, median: 150 degrees). There was no significant effect of age, breed, gender, or the size of the horses on either subjective findings in the lumbosacral joint or objective measurements.