Tendinopathies represent the 45% of the musculoskeletal lesions and they are a big burden in clinics. Indeed, despite the relevant social impact, both the pathogenesis and the development of the tendinopathy are still under-investigated, thus limiting the therapeutic advancement in this field. Indeed, current treatment for tendinopathy are mainly symptomatic, and they present a high rate of pathology re-occurrence. In this contest, the development of an efficient in vivo model of acute tendinopathy, focused on the choice of the most appropriate species and strategy to induce the disease, would allow a better understanding of the pathology progression throughout its phases.

Then, the purpose of this study was to evaluate the dose-dependent and time-related tissue-level changes occurring in a collagenase-induced tendinopathy in rat Achilles tendons, in order to establish a standardized model for future pre-clinical studies.

40 Sprague Dawley rats were randomly divided into two groups, treated by injection of collagenase type I within the Achilles tendon at 1 mg/mL (low dose, LD) or 3 mg/mL (high dose, HD). Tendon explants were histologically evaluated at 3, 7, 15, 30 and 45 days by H&E staining.

Our results showed that both the collagenase doses induced a disorganization of collagen fibers and increased the number of rounded resident cells. In particular, the high dose treatment determined a greater fatty degeneration and neovascularization with respect to the lower dose. These changes are time-dependent, thus resembling the tendinopathy development in humans. Indeed, the acute phase occurred from day 3 to day 15, while from day 15 to 45 it progressed towards the proliferative phase, displaying a degenerative appearance associated with a precocious remodeling process.

The model represents a good balance between feasibility, in terms of reproducibility and costs, and similarity with the human disease. Moreover, the present model contributes to improve the knowledge about tendinopathy development, and then it could be useful to design further pre-clinical studies, in particular in order to test innovative treatments for tendinopathy.

Introduction: The purpose of this work is to create an in vitro model of engineered osteochondral composite by combining a cylinder of calcium phosphate and cartilage tissue produced by isolated swine articular chondrocytes seeded onto fibrin glue.

Methods: Swine articular chondrocytes were enzimatically isolated and seeded onto fibrin glue. Immediately before gel polymerization, the fibrin glue was placed in contact with the cylinders of calcium phosphate. The osteochondral composites were left in standard culture conditions for 1,3,6 weeks. At the end of experimental times the samples were macroscopically analysed and processed for histological evaluation.

Results: Preliminary data showed a macroscopically integrity of the osteochondral samples. Histology showed cartilage like tissue maturing within the fibrin glue scaffold.

Discussion: The results demonstrate that isolated chondrocytes, seeded onto fibrin glue, produce a cartilage-like matrix that integrates with a cylinder of calcium phosphate.

This tissue engineered osteochondral composite could represent a valuable model for further in vivo studies on the repair of osteochondral lesions.