A5-year-old Appaloosa mare was referred to the Veterinary Teaching Hospital at Washington State University for severe left forelimb lameness of 4 months' duration. The horse had become acutely lame on the limb while turned out in an arena. A palmar digital nerve block of the left forelimb eliminated the lameness. Radiographs of the left metacarpophalangeal joint and foot obtained by the referring veterinarian prior to referral had revealed no abnormalities. The mare had been confined to a stall for 4 months since the onset of lameness with no noticeable improvement.
On admission, the horse was bright, alert, and responsive and in good body condition. Vital signs and results of physical examination were considered to be normal. Severe (grade 4/5)1 lameness of the left forelimb was obvious at the walk and trot and was exacerbated when the horse circled to the left. There were no palpable abnormalities in the left forelimb. The mare had a pain response to pressure applied by hoof testers over the frog of the left front foot but no response to hoof testers on the right front foot. A palmar digital nerve block with 2% mepivicaine hydrochloride eliminated the left forelimb lameness. Radiographs of both front feet were obtained, including dorsopalmar, lateromedial, dorsoproximal-palmarodistal, and palmaroproximal-palmarodistal (ie, skyline of the distal sesamoid [navicular] bone) views. No abnormalities were detected on radiographs.
Magnetic resonance imaging of both front feet was performed with a 1.0-T superconducting magnet.a A CBC prior to anesthetic induction revealed no abnormalities. Anesthesia was induced by administration of ketamine hydrochloride (2.2 mg/kg [1 mg/lb], IV) and diazepam (0.05 mg/kg [0.023 mg/lb], IV) and maintained with 2% to 4% isoflurane in oxygen. The horse was positioned in right lateral recumbency on a custom-built transport table for MRI examination. The foot being scanned was placed within a quadrature receiver coil to maximize signal capture. Image sequences were obtained in the sagittal and transverse planes. These included transverse plane (Figure 1) and sagittal plane (Figure 2) PD, T2-weighted, and STIR sequences and transverse 3D-GE sequences centered over the navicular bone. In PD and T2 sequences, healthy cortical bone has low signal intensity (black) and medullary bone has high signal intensity (white). In STIR and 3D-GE sequences, healthy cortical and medullary bone have low signal intensity (black). Magnetic resonance imaging techniques for the front feet of horses by use of superconducting magnets have been reported.2,3
Transverse PD images at the level of the distal sesamoid (navicular) bone in the left (A) and right (B) front feet of a 5-year-old Appaloosa mare. Images were acquired 4 months after acute onset of unilateral forelimb lameness. Notice the low signal intensity in the central portion of the left navicular bone (arrows), compared with that in the right navicular bone (normal). This finding was consistent with the increased trabecular bone density that was identified histologically in this region. Also notice the irregular high signal intensity (arrowhead) over the central area of the flexor cortex of the left navicular bone, compared with that on the right, indicating a defect in the fibrocartilage and subchondral bone.
Citation: Journal of the American Veterinary Medical Association 229, 5; 10.2460/javma.229.5.717
Sagittal PD images of the left (A) and right (B) front feet of the same horse as in Figure 1. Notice the low signal intensity in the left navicular bone, compared with that in the right navicular bone. Irregular high signal intensity can also be seen in the area over the flexor cortex of the left navicular bone (arrow), which is not seen in the right navicular bone.
Citation: Journal of the American Veterinary Medical Association 229, 5; 10.2460/javma.229.5.717
The PD and T2 images revealed a large central area of low signal intensity in the medullary cavity of the left navicular bone on both the transverse and sagittal sections, indicating increased bone density or sclerosis in that area. There was also irregular high signal intensity in the flexor cortex of the navicular bone that communicated with the navicular bursa in the same sections on the PD, T2, STIR, and 3D-GE images. This finding was indicative of a defect in the fibrocartilage and subchondral bone of the flexor cortex. There was no high signal intensity (indicative of inflammatory fluid) in the medullary cavity of the navicular bone on the STIR sequence, as is often seen in horses with navicular bone disease.2 The PD and T2 images of the same region in the right navicular bone revealed the high signal intensity typically seen in the medullary cavity of healthy navicular bones. No abnormalities were observed in the MRI sequences of the right front foot.
On the basis of MRI findings, a diagnosis of injury to the left front navicular bone resulting in diffusely increased density of the medullary cavity and erosion of the flexor cortex was made. A poor prognosis for return to soundness was given because of the absence of improvement in lameness after stall confinement and the severe changes observed in the medullary cavity and flexor cortex of the navicular bone. As a result of the poor prognosis for soundness, the owner elected to have the horse euthanatized.
Changes associated with navicular bone injury in the acute stages are often observed as high signal intensity on STIR images as a result of fluid (from hemorrhage or inflammation) in the bone. The chronic stages of bone injury are observed as decreased signal intensity on PD and T2 sequences as a result of the bone's remodeling response that results in an increased number and size of trabeculae. It is rare to see horses with navicular bone disease, either acute or chronic, that do not have high signal intensity on STIR sequences, whether or not they also have low signal intensity on PD and T2 sequences. Low signal intensity on PD and T2 sequences is a result of decreased numbers of free hydrogen protons in the tissue and is indicative of increased bone density (sclerosis). This observation in the horse of this report was substantiated by histologic findings in the bone at necropsy and revealed that changes associated with acute unilateral traumatic injury to the navicular bone differ from those typical of navicular disease caused by chronic repetitive injury.
Euthanasia was performed with IV administration of pentobarbital (85 mg/kg [38.6 mg/lb]), and gross and microscopic postmortem examination was performed on tissues of both front feet. The feet were sectioned in the sagittal plane with a high-speed band saw. An adhesion was grossly evident in the left front foot between the dorsal aspect of the deep digital flexor tendon and the flexor cortex defect in the navicular bone (Figure 3). The subchondral bone adjacent to the flexor surface adhesion site was brownish red in color and had increased bone density, compared with the right front navicular bone. Sagittal sections of the left and right front feet were fixed in 10% neutral-buffered formalin and demineralized in hydrochloric acid solution until soft.b Decalcified tissue was processed routinely for paraffin embedding and section-cut at 6 microns and stained with H&E. Microscopically, the medullary area of the left navicular bone had diffusely increased bone density, compared with the right front navicular bone. The increased medullary bone density was characterized by severely narrowed marrow spaces as a result of replacement of trabecular bone with compact lamellar bone composed of thick concentric and interstitial lamellae (Figure 4). The flex-or surface of the left front navicular bone had a 5-mm-diameter fibrocartilage defect that was filled with well-vascularized, dense, fibrous connective tissue extending from the flexor cortex to the adjacent dorsal aspect of the deep digital flexor tendon. At the margins of the fibrocartilage defect, there were 300- × 700-mm invaginations of hypertrophied synovial lining cells forming cystic spaces in the subchondral bone. The cysts communicated with the navicular bursa. The attachments of the distal sesamoidean impar ligament and deep digital flexor tendon to the distal phalanx appeared histologically normal in both limbs. No abnormalities were observed on sagittal sectioning of the right front foot on gross or histologic examination.
Sections through the left (A) and right (B) front feet of the same horse as in Figures 1 and 2. Notice the defect in the flexor cortex of the navicular bone where an adhesion of the deep digital flexor tendon (arrow) was detected in the left foot (A) and the subchondral bone sclerosis surrounding the flexor cortex defect of the navicular bone, compared with the unaffected right navicular bone (B).
Citation: Journal of the American Veterinary Medical Association 229, 5; 10.2460/javma.229.5.717
Photomicrographs of sections of the navicular bones from the left (A, C) and right (B) front feet of the same horse as in Figures 1–3. Notice the diffuse increase in trabecular bone density (dark structures) of the left navicular bone (A), compared with the right navicular bone (B). Dense fibrous adhesions (arrows) have developed between the deep digital flexor tendon (DDFT) and left navicular bone (C).
Citation: Journal of the American Veterinary Medical Association 229, 5; 10.2460/javma.229.5.717
Discussion
Findings in this horse revealed that injury to the navicular bone can occur in horses without fracture of the bone. The difference between the densities of the 2 navicular bones was not a result of differential weight bearing because the horse had been placing less weight on the affected limb for the 4 months prior to evaluation. The relationships expressed in Wolff's law indicate that bone will be removed from areas of lesser stress and added to areas receiving more stress.4 Therefore, the most likely explanation is that the navicular bone in the affected limb was injured by blunt trauma, resulting in bone proliferation in the medullary cavity. Although it is theoretically possible that the horse fractured the navicular bone, it was considered highly unlikely because navicular bone fractures rarely heal5 and no findings on MRI, gross inspection, or histologic examination indicated that a fracture had occurred. The increased bone density appeared to be a response to injury similar to changes observed around microfractures or subchondral bone damage in other appendicular structures in horses.6–9 Bone contusion or microfractures in the trabecular bone may have been the initiating cause of the marked bone response observed in this horse's navicular bone medullary cavity, but evidence of trabecular bone fractures was not observed histologically.
Antemortem evidence obtained by use of MRI of the feet in this horse enabled accurate diagnosis of the cause of lameness. Magnetic resonance imaging revealed pathologic changes in the navicular bone that were not detected on radiographs and supported earlier observations10–12 that MRI can reveal changes in the equine foot that cannot be observed on radiographs. The MRI findings were confirmed on gross and histologic evaluation of the horse's feet at necropsy.
The navicular bone is a common site for pathologic change in the foot of the horse. A mild decrease in signal intensity (low signal) in the navicular bone on PD and T2 sequences has been observed in horses with clinical signs of navicular disease.2,10,11,13,14 However, those horses had histories of chronic lameness and changes affecting the navicular bone and supporting soft tissue structures in both forefeet. Many also had inflammatory fluid in the medullary cavity of the navicular bone, even with chronic disease, in contrast to the horse of this report. Attributing the present horse's lameness to a variation of navicular disease is difficult because of the history of severe acute lameness and pathologic changes that were detected in only 1 navicular bone. The most likely explanation for the changes in the navicular bone medulla and flexor cortex is that the palmar aspect of the navicular bone was injured by means of blunt traumatic injury to the frog region and underwent subsequent reparative responses.
Navicular disease has been described as chronic progressive degeneration of the bone in response to chronic inflammation from repetitive loading.15–19 Sclerosis of the navicular bone has been reported in horses with clinical signs of navicular disease that underwent MRI examination.10,11 However, the horse of this report had clinical signs of severe unilateral forelimb lameness that were different from those in horses with navicular disease. Unilateral navicular bone injury resulting in diffuse, severe medullary sclerosis and flexor cortex erosion has not been reported, to the authors' knowledge. In a postmortem study20 of 38 horses with navicular disease, no horses had unilateral medullary sclerosis and horses that had partial bilateral medullary sclerosis had surrounding areas of trabecular lysis, histologic findings that were different from those in the horse of this report. The erosion of the flexor cortex in the present horse was similar in location and size to those noted in the previous study,20 although changes were seen in both limbs of horses in that study. Most of the horses in the previous study were from 7 to 14 years in age, which is a more typical age range for horses with navicular disease, whereas the horse in the present report was 5 years old.
Findings in the horse of this report indicate that navicular bone injury can occur without a fracture. Magnetic resonance imaging was important in making an accurate diagnosis and yielded evidence that navicular bone injury, even in the absence of radiographic evidence of a fracture, should be considered as a differential diagnosis for horses with an acute onset of severe unilateral forelimb lameness originating from the heel portion of the foot.
ABBREVIATIONS
| MRI | Magnetic resonance imaging |
| PD | Proton density |
| STIR | Short tau inversion recovery |
| 3D-GE | Three-dimensional gradient echo |
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