Objectives. The present study describes a novel technique for revitalising allogenic intrasynovial tendons by combining cell-based therapy and mechanical stimulation in an ex vivo canine model. Methods. Specifically, canine flexor digitorum profundus tendons were used for this study and were divided into the following groups: (1) untreated, unprocessed normal tendon; (2) decellularised tendon; (3) bone marrow stromal cell (BMSC)-seeded tendon; and (4) BMSC-seeded and cyclically stretched tendon. Lateral slits were introduced on the tendon to facilitate cell seeding. Tendons from all four study groups were distracted by a servohydraulic testing machine. Tensile force and displacement data were continuously recorded at a sample rate of 20 Hz until 200 Newton of force was reached. Before testing, the cross-sectional dimensions of each tendon were measured with a digital caliper. Young’s modulus was calculated from the slope of the linear region of the stress-strain curve. The BMSCs were labeled for histological and cell viability evaluation on the decellularized tendon scaffold under a confocal microscope. Gene expression levels of selected extracellular matrix tendon growth factor genes were measured. Results were reported as mean ± SD and data was analyzed with one-way ANOVAs followed by Tukey’s post hoc multiple-comparison test. Results. We observed no significant difference in cross-sectional area or in Young’s modulus among the four study groups. In addition, histological sections showed that the BMSCs were aligned well and viable on the
All cells exist within a 3D microenvironment where they are exposed to a multitude of mechanobiological cues, from nano-level cell/matrix interactions, to tissue-level mechanical strain. These cues are fundamental to maintaining tissue homeostasis, but when disrupted during disease, can promote pathological outcomes and impair healing. This is particularly true in tendons; 3D load bearing connective tissue structures composed of a complex arrangement of matrix proteins, organised in a highly aligned manner and maintained by tendon cells (tenocytes). When diseased or injured (termed tendinopathy), the tendon begins a journey of poor healing, characterised by mechanically inferior disorganised scar tissue which ultimately results in compromised or total loss of function. In both health and disease, the mechanobiological stimuli experienced by tenocytes will directly affect their behaviour, yet this is a poorly studied area of research. We have used decellularised
