The characteristics of tendon pathology and its pathogenesis as detected by ultrasound tissue characterisation

Abstract

Tendinopathy is the clinical presentation of pain and dysfunction resulting in prolonged periods of reduced activity. While not directly related, tendon pain is associated with structural pathology. However, the primary histopathological event and the pathogenesis of tendon pathology is not fully understood, with numerous theoretical models proposed. Consistent within all these models is that loading the tendon beyond its capacity (overload) is critical in the development of pathology and possibly pain. Our understanding of how load affects the structural integrity of the tendon and contributes to the pathogenesis is poor due to limitations associated with conventional imaging modalities (ultrasound and magnetic resonance imaging). Ultrasound tissue characterisation (UTC) is a novel imaging modality that captures a three-dimensional ultrasound image, allowing for the quantification of tendon structure based on the stability of pixels brightness over contiguous transverse images. Four echo-types are discriminated that have been validated against histopathological specimens in horses. Quantification of these echo-types have been used to test the efficacy of various treatments in horses and humans, and test the diagnostic accuracy in detecting Achilles tendinopathy in humans. Little research has been performed using UTC to understand how tendons respond to load and the pathogenesis of tendon pathology. The aim of this thesis was to investigate the pathogenesis and features of tendon pathology as characterised by UTC. As load is critical to the development of tendon pathology, the nature and temporal sequence of changes in the normal tendon in response to loading were investigated in both the short- (Chapters three and four) and medium-term (Chapter five). The appearance of normal and pathological tendons determined by UTC were investigated to ascertain whether the pathological tendon lacked sufficient amounts of aligned fibrillar structure and whether tendon dimensions were related to the amount of disorganisation (Chapter six). Finally, tendon structure, as quantified by UTC, was examined in the symptomatic and contralateral asymptomatic tendon in patients suffering from unilateral Achilles tendinopathy compared to normal tendons (Chapter seven). This thesis found evidence that the normal tendon is responsive to load, both in the short- (approximately 48hrs) and medium-term (five months). While definitive statements cannot be made as to whether these observed changes affect the health of the tendon (ie presence of pain and dysfunction), it suggests that the tendon is sensitive to load and that it may affect the structural integrity of the tendon. Furthermore, the pathological tendon exhibited a greater mean cross-sectional area of aligned fibrillar structure than a structurally normal tendon. With a significant relationship observed between tendon dimensions and the amount of disorganisation, tendon thickening may be an adaption to maintain sufficient levels of aligned fibrillar structure in the pathological tendon. The findings of this thesis contributes to our understanding of the responsiveness of the normal tendon to load and provides insight into how the normal tendon transitions towards pathology. Despite the presence of disorganisation, the pathological tendon appears to maintain sufficient structure to tolerate load by increasing tendon dimensions. An improved understanding of the pathogenesis and the tendons response to load will lead to improvements in treatments and outcomes for those with tendinopathy.