In vivo adaptation of tendon material properties in healthy and diseased tendons with application to rotator cuff disease
Keywords: Rotator cuff
tendon
Raman Spectroscopy
Atomic Force Microscopy
tendinopathy
Tissue Engineering

Degenerative disorders of the rotator cuff tendons account for nearly 75% of all shoulder pain, causing considerable pain and morbidity. Given the strong correlation between age and tendinopathy, and unprecedented population aging, these disorders will become increasingly prevalent. Improved understanding of tendon degeneration will guide the development of future diagnostic and treatments, and is therefore urgently needed. However, the aetiology and pathology of rotator cuff tendinopathy remain unclear.
The complicated mechanical environment of the rotator cuff is hypothesised to influence the susceptibility of the tendons to degeneration and tearing. Studies have reported biological adaptations in torn cuff tendons indicative of increased compressive loading within the tendon. The material adaptations of healthy and degenerative cuff tendons are largely unreported but will provide further insight into the role of the mechanical environment in rotator cuff aetiology and pathology. This thesis examined the material adaptations of healthy and diseased tendons to explore the role of mechanical loading in rotator cuff pathology. The material adaptations of healthy animal tendons, and healthy and delaminated human cadaveric rotator cuff tendons, in response to different loading environments were characterised. The effects of age, tears, steroid injection and subacromial decompression surgery on the structural adaptations of human cuff tendons were also studied, as was the effect of tendon cell proliferation on the mechanical properties and degradation behaviour of collagen scaffolds.
Loading environment significantly affected the structural adaptations of healthy tendons. Regions exposed to compressive and shear strains exhibited thinner fibres, shorter crimp lengths and thinner, less aligned fibrils compared with regions exposed to tensile strains alone. In healthy rotator cuff tendons, the inhomogeneous loading environment produced topographically inhomogeneous structural adaptations. The tendons of a delaminated rotator cuff exhibited less topographical variation in properties and thinner, less aligned fibrils compared with healthy cuff tendons. Torn cuff tendons exhibited thinner fibrils and shorter crimp lengths compared with control samples. These adaptations were identifiable early in the disease progression, and neither steroid injection nor subacromial decompression surgery significantly influenced these adaptations at seven weeks post‐treatment. Significant correlations between decreasing dimensions and increasing tear size were found when age was included as a confounding factor, reflecting the importance of age and tear size in determining the material properties of tendons. Tendon cell proliferation influenced the mechanical properties and degradation behaviour of the collagen scaffolds, emphasising the integral role of cells in the functional adaptation of biological materials. These results demonstrate the effect of mechanical environment on the material adaptations of tendons.
They also indicate the importance of the complicated mechanical environment experienced by the rotator cuff tendons in predisposing the tendons to degeneration and tearing. The observed material adaptations of degenerative and torn tendons suggest that rotator cuff pathology is associated with increased levels of compressive and/or shear strains within the tendon. These changes begin early in the disease progression and neither steroid injection nor sub‐acromial decompression surgery are capable of reversing the changes in the timeframe investigated. These findings highlight the urgent clinical need for pre‐rupture diagnostic techniques for the detection of early pathological changes in the rotator cuff. They also emphasize the requirement for new intervention strategies that restore the healthy mechanical environment and reverse early pathological adaptations in order to prevent catastrophic failure of the tendons.