Page 318 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Musculoskeletal system: 1.8 Soft-tissue injuries 293

VetBooks.ir 1.553 1.554

Fig. 1.553 Histological longitudinal section Fig. 1.554 Histological longitudinal section (H&E
(haematoxillin stain) of the SDFT of a young horse stain) of the SDFT of a horse presenting with an old
(×100) showing the parallel organisation of the tendonitis lesion. There is near complete loss of the
collagen fibres and their zig-zag (‘crimp’) pattern. longitudinal, parallel arrangement of the collagen and
Dark nuclei of the tenocytes (tendon fibroblast-like an increase and lack of differentiation of the fibroblastic
cells) are interspersed between fibrils. cells. This image is typical of mature scar tissue.

mainly of longitudinally arranged type I collagen peripheral (palmar or abaxial). This is a different
fibres (Fig. 1.553), the surrounding matrix ensur- condition, but healing patterns are similar to spon-
ing fibre arrangement and biomechanical proper- taneously occurring tendonitis. There is associated
ties. With age and training, there is an increasing paratendonitis (i.e. inflammatory thickening of the
proportion of poorly organised collagens (especially connective tissue wrapping the tendon in unsheathed
type III). Other changes in matrix composition will areas), which further impairs tendon function by
alter the fibre arrangement, but also the capacity of altering vascular supply entering the parenchyma
collagen fibrils to slide in relation to each other. This and physically impairing stretching/elasticity.
leads to decreased elasticity, increased stiffness and Healing initially occurs through removal of the
reduced resistance to cyclic strain. Stretching of the haematoma by white blood cells (WBCs) and fibro-
tendon at fast speed, although within theoretically plasia: fibroblasts produce a temporary, immature
normal tolerance levels, can then cause sudden rup- matrix (lacking any resistance to strain) with hap-
ture or strain of a large proportion of collagen fibres. hazard ingrowth of vascular buds. This will serve
Intralesional haemorrhage subsequently occurs from as a substrate for subsequent scar tissue formation,
endotenon capillary vessels (i.e. intratendinous ves- which gradually replaces the torn tissue (Fig. 1.554).
sels surrounding the fibres). Platelets degranulate, This strong but inelastic matrix may gradually
releasing inflammatory mediators, growth factors undergo maturation and remodelling with a rela-
and collagenases that directly destroy fibres, thus tive increase of more longitudinally arranged type
inducing an influx of inflammatory cells. This will I fibres. The replacement tissue only matures slowly
cause further damage to the tendon and the lesion (over 18 months) and remains less elastic and resis-
may spread or increase in volume over several days tant to cyclic strain than normal tendon. Recurrence
after injury. with worsening of the lesion is therefore very com-
Direct trauma, especially from limb interference mon (40–80% of cases in racehorses in various stud-
(overreach injuries) or hitting jumps or obstacles, ies). Recurring lesions often occur at the extremities
may also cause localised lesions, which tend to be or along the periphery of the former scar, the latter