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Magnetic Resonance Imaging Findings in the Equine Deep Digital Flexor Tendon and Distal Sesamoid Bone in Advanced Navicular Disease-an Ex Vivo Study

Valeria Busoni, Marianne Heimann, Jacques Trenteseaux, et al.

Veterinary Radiology & Ultrasound, 2005. 46(4): p.279-286.

We describe the abnormal magnetic resonance (MR) imaging findings in the deep digital flexor tendon (DDFT) and distal sesamoid bone in horses with radiographic changes compatible with navicular syndrome. Thirteen postmortem specimens were examined using a 1.5-T magnetic field, with spin echo (SE) T1-weighted, turbo SE (TSE) proton density-weighted (with and without fat saturation), and fat saturation TSE T2-weighted sequences. The limbs were then dissected to compare the MR findings with the gross assessment and histologic examination of the DDFT and distal sesamoid bones. Tendonous abnormalities were detected by MR imaging in 12 DDFTs and confirmed at necropsy. Most tendon lesions were located at the level of the distal sesamoid bone and the proximal recess of the podotrochlear bursa. Tendon lesions were classified based on their MR imaging features as core lesions, dorsal lesions, dorsal abrasions, and parasagittal splits. Areas of increased MR signal in the DDFTs were characterized by tendon fiber disturbance and lack of continuity of the collagen fibers, foci of edema, hemorrhages, and formation of lakes containing eosinophilic plasma-like material or amphophilic material of low density. Bone marrow signal alterations in the distal sesamoid bone were seen in all digits. Two main phenomena were responsible for the abnormal signal, respectively, in T1-weighted (decreased signal) and in T2-weighted fat-suppressed images (increased signal): a decrease in the fat marrow content in the trabecular spaces and an increase in the fluid content. Histologic examination revealed foci of bone marrow edema, hemorrhage, necrosis, and fibrosis. Cyst formation and trabecular abnormalities (disorganization, thinning, remodelling) were also observed in areas of abnormal signal intensity. Increased bone density because of trabecular thickening induced a decrease in signal in all sequences.