Short-term cast immobilisation is effective in reducing lesion propagation in a surgical model of equine superficial digital flexor tendon injury.
ABSTRACT Larger superficial digital flexor tendon (SDFT) injuries have a poorer prognosis than smaller lesions. During the inflammatory phase enlargement of the initial lesion is frequently noted, with biomechanical loading being recently proposed to play an important role.
To evaluate the effect of lower limb cast immobilisation on tendon lesion propagation in an equine model of surgically induced SDFT injury.
Core lesions were surgically induced in both front SDFTs of 6 young mature horses. At the end of surgery, one leg was randomly placed in a lower limb cast and the other leg (control) was bandaged for 10 days. Computerised ultrasonographic tissue characterisation performed at Days 10, 15, 21, 28, 35 and 42 allowed measurement of lesion length (cm) and width (expressed as a percentage of whole tendon cross-section). On Day 42 horses were subjected to euthanasia and both SDFTs were sectioned every centimetre to assess the lesion length macroscopically. Statistics were performed to compare cast vs. control legs with significance set at P<0.05.
When all time points were combined, lesion length was 19% shorter (P<0.0001) and lesion width 57% smaller (P = 0.0002) in the cast legs (6.13 ± 0.12 cm; 6.90 ± 0.64%) than in the control legs (7.30 ± 0.21 cm; 10.85 ± 1.22%). On Day 42 the lesion length on macroscopic evaluation was 19% shorter (P = 0.04) in the cast (7.00 ± 0.36 cm) than in the control legs (8.33 ± 0.33 cm).
Cast immobilisation for 10 days effectively reduced lesion propagation (length and width) compared to bandaging in an in vivo model of artificially-induced tendon lesions.
A short period of cast immobilisation during the early phase of tendon healing may be an easy and cost-effective way to reduce the initial enlargement of lesion size and hence to improve prognosis.
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ABSTRACT: The basic response to injury at the tissue level is well known and consists of acute inflammatory phase, proliferative phase, and maturation and remodeling phase. Knowing these phases, the treatment and rehabilitation program of athletes' acute musculoskeletal injuries should use a short period of immobilization followed by controlled and progressive mobilization. Both experimental and clinical trials have given systematic and convincing evidence that this program is superior to immobilization - a good example where basic science and clinical studies do coincide - and therefore active approach is needed in the treatment of these injuries.Scandinavian Journal of Medicine and Science in Sports 07/2003; 13(3):150-4. · 3.21 Impact Factor
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ABSTRACT: Not much is known about the effects of immobilization and subsequent recovery on tendon connective tissue. In the present study, healthy young men had their nondominant leg immobilized for a 2-wk period, followed by a recovery period of the same length. Immobilization resulted in a mean decrease of 6% (5,413 to 5,077 mm(2)) in cross-sectional area (CSA) of the triceps surae muscles and a mean decrease of 9% (261 to 238 N.m) in strength of the immobilized calf muscles. Two weeks of recovery resulted in a 6% increased in CSA (to 5,367 mm(2)), whereas strength remained suppressed (240 N.m). No difference in Achilles tendon CSA was detected between the two legs at any time point. Local tendon collagen synthesis, measured as the peritendinous concentrations of PINP (NH(2)-terminal propeptide of type I collagen; indirect marker for collagen synthesis), was unchanged after 2 wk of immobilization. However, peritendinous levels of PINP were significantly elevated in the immobilized leg (15 to 139 ng/ml) following 2 wk of remobilization compared with preimmobilization levels. In contradiction hereto, systemic concentrations of PINP remained unchanged throughout the study. Immobilization reduced muscle size and strength, while tendon size and collagen turnover were unchanged. While recovery resulted in an increase in muscle size, strength was unchanged. No significant difference in tendon size could be detected between the two legs after 2 wk of recovery, although collagen synthesis was increased in the previously immobilized leg. Thus 2 wk of immobilization are sufficient to induce significant changes in muscle tissue, whereas tendon tissue seems to be more resistant to short-term immobilization.Journal of Applied Physiology 11/2008; 105(6):1845-51. · 3.48 Impact Factor
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ABSTRACT: Tendons consist of collagen (mostly type I collagen) and elastin embedded in a proteoglycan-water matrix with collagen accounting for 65-80% and elastin approximately 1-2% of the dry mass of the tendon. These elements are produced by tenoblasts and tenocytes, which are the elongated fibroblasts and fibrocytes that lie between the collagen fibers, and are organized in a complex hierarchical scheme to form the tendon proper. Soluble tropocollagen molecules form cross-links to create insoluble collagen molecules which then aggregate progressively into microfibrils and then into electronmicroscopically clearly visible units, the collagen fibrils. A bunch of collagen fibrils forms a collagen fiber, which is the basic unit of a tendon. A fine sheath of connective tissue called endotenon invests each collagen fiber and binds fibers together. A bunch of collagen fibers forms a primary fiber bundle, and a group of primary fiber bundles forms a secondary fiber bundle. A group of secondary fiber bundles, in turn, forms a tertiary bundle, and the tertiary bundles make up the tendon. The entire tendon is surrounded by a fine connective tissue sheath called epitenon. The three-dimensional ultrastructure of tendon fibers and fiber bundles is complex. Within one collagen fiber, the fibrils are oriented not only longitudinally but also transversely and horizontally. The longitudinal fibers do not run only parallel but also cross each other, forming spirals. Some of the individual fibrils and fibril groups form spiral-type plaits. The basic function of the tendon is to transmit the force created by the muscle to the bone, and, in this way, make joint movement possible. The complex macro- and microstructure of tendons and tendon fibers make this possible. During various phases of movements, the tendons are exposed not only to longitudinal but also to transversal and rotational forces. In addition, they must be prepared to withstand direct contusions and pressures. The above-described three-dimensional internal structure of the fibers forms a buffer medium against forces of various directions, thus preventing damage and disconnection of the fibers.Scandinavian Journal of Medicine and Science in Sports 01/2001; 10(6):312-20. · 3.21 Impact Factor