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Updated: Jun 24, 2026
Murine Flexor Tendon Injury and Repair Surgery
Published on: September 19, 2016
Lesions of the deep digital flexor tendon in the digit: a correlative MRI and post mortem study in control and lame
1Centres for Preventative Medicine, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk CB8 7UU, UK.
Reasons For Performing Study:
Lameness associated with lesions of the deep digital flexor tendon (DDFT) in the digit is now recognised as an important cause of lameness, but there is currently limited information about the pathological nature of the lesions.
Objectives:
To compare: signal intensity changes on magnetic resonance images with histopathology; and histopathological changes in the DDFT from horses with no history of foot-related lameness (Group C) and horses with lesions of the DDFT confirmed using magnetic resonance imaging (MRI) (Group D).
Methods:
Transverse sections of the DDFT were harvested from 3 sites in all horses: (1) immediately proximal to the navicular bursa (E1); (2) at the level of the navicular bone (E2); and (3) close to the tendon's insertion (E3). If lesions were identified at E1 or had been identified further proximally using MRI, additional sections were obtained until, in most cases, the proximal limit of the lesion was identified. All DDFTs were graded histopathologically using predefined criteria. The MR images were reviewed to determine the location and sequences in which increased signal intensity was seen.
Results:
No haemorrhage or inflammatory cell infiltration was seen in any horse. At level E1, septal thickening, ghosting of blood vessels and blood vessel occlusion were common in Group D, but were not seen in Group C. Less commonly, there was core necrosis, only seen in Group D. At level E2, septal and vascular changes were most obvious in Group D. Core necrosis, dorsal splitting, crevicing and fibrillation were seen only in Group D. Septal and vascular changes were present in both Groups C and D at level E3, but fibrocartilaginous metaplasia, splitting, crevicing and fibrillation, or core necrosis or fibroplasia were seen only in Group D. Core lesions in Group D often extended proximal to E1, and ranged in length from 0.5-13 cm. Core necrosis was generally associated with increased signal intensity in fat suppressed images.
Conclusions:
Lesions of the DDFT in the digit appear to be primarily degenerative, and may be a sequel to vascular compromise. Increased signal intensity on fat suppressed MR images is not necessarily associated with frank fluid or evidence of inflammation, but may reflect major matrix changes in the tendon.
Potential Relevance:
Further information about the causes of these lesions is required to develop preventative strategies.
