Chapter 32 Primary Lesions of the Deep Digital Flexor Tendon within the Hoof Capsule
Within the hoof capsule the deep digital flexor tendon (DDFT) is molded to the palmar (plantar) surface of the navicular bone and separated from it by the navicular bursa. Proximally the DDFT is intimately related to the distal digital annular ligament on its palmar aspect. The distal recess of the navicular bursa separates the DDFT and the distal sesamoidean impar ligament (DSIL). The DDFT has a terminal fanlike expansion containing cartilage that occupies the entire space between the medial and lateral palmar processes of the distal phalanx. It inserts on the facies flexoria and semilunar crest of the distal phalanx. The dorsal portion of the DDFT joins with the DSIL immediately before insertion on the facies flexoria of the distal phalanx. There are parallel fibers of dense connective tissue, separated by loose connective tissue, within which are many sensory nerves and numerous blood vessels.1 A prominent line (tidemark) indicates the transition from nonmineralized tendon and ligament to mineralized regions of the DDFT and DSIL before attachment to the distal phalanx.2
Within the digit the DDFT induces axial compression of the articular surfaces of the proximal and distal interphalangeal joints.2,3 It has an important role in stabilizing the distal interphalangeal joint. The anatomical arrangement of the collateral ligaments of the navicular bone facilitates compression of the articular surfaces of the navicular bone into those of the middle and distal phalanges.2 The DDFT has a dorsal fibrocartilaginous pad that supports pressure of the tuberositas flexoria, the transverse prominence on the proximopalmar aspect of the middle phalanx.3
The relationship of the DDFT to the navicular bone varies with the phase of the stride. During the full weight-bearing stance of the stride the DDFT is only in contact with the distal aspect of the bone, whereas in the propulsion phase the DDFT bends over the distal scutum (the fibrocartilaginous insertion of the straight sesamoidean ligament on the middle phalanx) and comes into full contact with the navicular bone. Tension in the DDFT is maximal, and active muscle contraction and the elasticity in the tendon and in its accessory ligament result in extension of the distal interphalangeal joint.3 At the beginning of the swing phase of the stride the tension in the DDFT contributes passively to induce flexion of the interphalangeal joints. During extension of the distal interphalangeal joint, which is maximum at the propulsion phase of the stride, pull on the DDFT creates a shear force between the DDFT and the DSIL.2
Primary lesions of the DDFT have only recently been recognized clinically, and only limited information concerning pathophysiology is available. A progressive increase in proteoglycans with age was seen in the distal aspects of the DDFT and DSIL, which may be an adaptation to stress.2 It was suggested that horses with low, weak heels may be more susceptible to these changes. Similar but more extensive changes were seen in two horses with navicular disease. Lesions within the DDFT within the foot were identified in fewer than 10% of horses with unknown history in a post mortem study of superficial digital flexor tendon and DDFT lesions in the metacarpal region and digit.4
In a post mortem study of 38 horses with suspected navicular disease, one horse had a core lesion of the DDFT with no associated pathological condition of the navicular bone5; four additional horses had histological evidence of focal regions of necrosis within the tendon concurrent with other pathological conditions of the navicular bone. Surface fibrillation was a common finding in horses with navicular disease but not in age-matched controls. No lesions of the DDFT were described in the age-matched controls. Pool et al6 considered lesions in the DDFT to be secondary to navicular disease. Inflammation at the intersection of the DDFT and DSIL was recognized in the Quarter Horse in association with other signs compatible with navicular disease.7 It was considered that these lesions may be involved with the pathogenesis of navicular disease.
A variety of different types of lesions of the DDFT have been identified using magnetic resonance imaging (MRI) and confirmed post mortem.8-11 These include partial or full-thickness sagittal plane splits, dorsal abrasions, fibrillation, and core lesions. Core lesions within the tendon or on the dorsal surface, full-thickness parasagittal splits can be seen alone and are considered primary lesions of the DDFT, whereas fibrillation and small isolated incomplete parasagittal splits are commonly seen in association with other lesions of the podotrochlear apparatus.12-14 Core lesions or full-thickness splits usually occur extending proximally from the proximal aspect of the navicular bursa or distal to the navicular bone. Isolated incomplete parasagittal plane splits, minor dorsal abrasions, and fibrillation are seen most commonly from the proximal level of the navicular bursa distally.
In recent studies comparing MRI and histopathology in groups of horses with chronic foot pain and age-matched control horses, the incidence of DDFT lesions was considerably higher than previously recognized.8-11 Degenerative changes of the DDFT were seen in both groups but were of greater severity in the lame horses. Thickening of septae, with ghosting and occlusion of blood vessels, and fibrocartilaginous and chondroid metaplasia were characteristic findings, which may predispose to fibrillation and dorsal splits of the tendon. Such changes have also been identified in the proximity of necrotic core lesions. The presence of degenerative changes within the DDFT was not age related. With all types of lesions of the DDFT there was a notable absence of acute inflammatory reaction.
Primary deep digital flexor (DDF) tendonitis may be the result of repetitive overstress or an acute-onset traumatic tear, possibly superimposed on preexisting degenerative change. The identification of severe core lesions in young horses that have done relatively little work suggests that some horses may have an inherent predisposition to injury.
Rupture of the DDFT secondary to previous neurectomy of the palmar digital nerves is considered a separate condition; however, it is likely that a preexisting, unrecognized pathological condition of the DDFT predisposes to rupture (see Chapter 70).
Dystrophic or ectopic mineralization within the DDFT was identified radiologically, at the level of the navicular bone and immediately proximal to it, but its clinical significance has been speculative.15 Entheseous new bone at the site of insertion of the DDFT on the facies flexoria and semilunar crest of the distal phalanx was described associated with lameness and unassociated with navicular disease.16 Nuclear scintigraphic examination of horses with palmar foot pain has revealed horses with linear increased radiopharmaceutical uptake (IRU) in the DDFT in pool phase images or focal regions of IRU in the region of insertion of the DDFT on the distal phalanx,17,18 either alone or in association with a region of increased uptake in the navicular bone. This has correlated well with lesions identified using MRI.