Investigating tendon mineralisation in the avian hindlimb: a model for tendon ageing, injury and disease.

Mineralisation of the tendon tissue has been described in various models of injury, ageing and disease. Often resulting in painful and debilitating conditions, the processes underlying this mechanism are poorly understood. To elucidate the progression from healthy tendon to mineralised tendon, an appropriate model is required. In this study, we describe the spontaneous and non-pathological ossification and calcification of tendons of the hindlimb of the domestic chicken (Gallus gallus domesticus). The appearance of the ossified avian tendon has been described previously, although there have been no studies investigating the developmental processes and underlying mechanisms leading to the ossified avian tendon. The tissue and cells from three tendons - the ossifying extensor and flexor digitorum longus tendons and the non-ossifying Achilles tendon - were analysed for markers of ageing and mineralisation using histology, immunohistochemistry, cytochemistry and molecular analysis. Histologically, the adult tissue showed a loss of healthy tendon crimp morphology as well as markers of calcium deposits and mineralisation. The tissue showed a lowered expression of collagens inherent to the tendon extracellular matrix and presented proteins expressed by bone. The cells from the ossified tendons showed a chondrogenic and osteogenic phenotype as well as tenogenic phenotype and expressed the same markers of ossification and calcification as the tissue. A molecular analysis of the gene expression of the cells confirmed these results. Tendon ossification within the ossified avian tendon seems to be the result of an endochondral process driven by its cells, although the roles of the different cell populations have yet to be elucidated. Understanding the role of the tenocyte within this tissue and the process behind tendon ossification may help us prevent or treat ossification that occurs in injured, ageing or diseased tendon.