Turkey leg tendon (TLT) is used as a model system to explore the process of collagen mineralisation. Mineralisation takes place in distinct regions across the length of the tendon and is accompanied by a change in biomechanical properties of collagen. The collagen becomes more aligned and adapted to the mechanical demand of the tendon. This study aimed to: 1) Identify the stages of mineralisation process & associated Raman spectral signatures using the TLT as a model. 2) Determine changes in collagen chemically and mechanically that lead to mineralisation in the maturing TLT. 3) Identify the links between mineralisation in young and old tendons with potential problems which can arise leading to unhealthy ageing of collagenous tissue. These were explored using Raman spectroscopy and in vitro mineralisation with SBF, micro-CT imaging (chemical analysis), and uniaxial tensile loading and video gauge (VG) imaging (mechanical tests). The results showed there were two distinct regions of mineralisation in old tendons compared to the young tendons which had one region or points of immature mineral. The collagen organisation predetermined the maturity of each mineral region therefore regions furthest proximal were always more mature. Turkey tendons mineralise to balance their weight with locomotive activity. The structural integrity of the tendon was compromised during over-mineralisation resulting in high modulus in overall tendon. The occurrence of right leg dominance was revealed by differences in the right tendon’s adaptation for greater mechanical load, the over-mineralisation and the loss of collagen content in remineralisation. The absence of higher signalling components (such as tenocytes in the collagen matrix and proteoglycans present in the ECM) results in a perturbed mineralisation system. Non-mineralised regions of the tendon greatly influenced the mechanical integrity of the collagen. Mineralisation limits the elastic potential of the tendon to provide effective function though predetermined “Never mineralised” regions remained non-mineralised. If tissue that never mineralises can be characterised in a perturbed mineralisation system, it would be possible to control mineralisation thus prolong the longevity of collagenous tissue and open opportunities for new therapeutic agents to target tissues with disrupted mineralisation in a range of metabolic diseases.