Chondroitin sulphate glycosaminoglycans contribute to widespread inferior biomechanics in tendon after focal injury. Issue 13 (6th September 2016)

• Record Type: Journal Article
• Authors: Choi, Rachel K.; Smith, Margaret M.; Martin, Joshua H.; Clarke, Jillian L.; Dart, Andrew J.; Little, Christopher B.; Clarke, Elizabeth C.
• Is Part Of: Journal of biomechanics. Volume 49:Issue 13(2016)
• Page Start: 2694
• Page End: 2701
• Publication Date: 2016-09-06
• Subjects: Tendon -- Glycosaminoglycan -- Tendinopathy -- Biomechanics -- Chondroitinase; Animal mechanics -- Periodicals; Biomechanics -- Periodicals; Biomechanics -- Periodicals; Mécanique animale -- Périodiques; Biomécanique -- Périodiques; Electronic journals; 571.4305
• DOI: 10.1016/j.jbiomech.2016.06.006
• Languages: English
• ISSNs: 0021-9290

Abstract

Abstract: Both mechanical and structural properties of tendon change after injury however the causal relationship between these properties is presently unclear. This study aimed to determine the extent of biomechanical change in post-injury tendon pathology and whether the sulphated glycosaminoglycans (glycosaminoglycans) present are a causal factor in these changes. Equine superficial digital flexor tendons (SDF tendons) were surgically-injured in vivo ( n =6 injured, n =6 control). Six weeks later they were harvested and regionally dissected into twelve regions around the lesion (equal medial/lateral, proximal/distal). Glycosaminoglycans were removed by enzymatic (chondroitinase) treatment. Elastic modulus (modulus) and ultimate tensile strength (UTS) were measured under uniaxial tension to failure, and tendon glycosaminoglycan content was measured by spectrophotometry. Compared to healthy tendons, pathology induced by the injury decreased modulus (−38%; 95%CI −49% to −28%; P <0.001) and UTS (−38%; 95%CI −48% to −28%; P <0.001) and increased glycosaminoglycan content (+52%; 95%CI 39% – 64%; P <0.001) throughout the tendon. Chondroitinase-mediated glycosaminoglycan removal (50%; 95%CI 21–79%; P <0.001) in surgically-injured pathological tendons caused a significant increase in modulus (5.6 MPa/µg removed; 95%CI 0.31–11; P =0.038) and UTS (1.0 MPa per µg removed; 95%CI 0.043–2; P =0.041). These results demonstrate that the chondroitin/dermatan sulphate glycosaminoglycans that accumulate in pathological tendon post-injury are partly responsible for the altered biomechanical properties.