Achilles tendinopathy and its contributing pathologies has been a heavily researched topic throughout multiple professions. Although a unified consensus and classification on the underlying pathology is yet to be reached, a shift from the term tendinitis to tendinosis has slowly been adopted, and is now believed to follow a continuum. Previous incorrect belief of an inflammatory pathophysiology has lead to the development of treatment options that are inappropriate and unsuccessful, leaving the tendon unable to adequately heal or strengthen increasing its risk of repetitive re-injury and the development of chronic Achilles tendinopathy. As a result an understanding of the pathophysiology, its effect on lower limb function and biomechanical risk factors contributing to the development of Achilles tendinopathy need to be considered when developing a rehabilitation program to coincide with new research and to address the underlying degeneration and failed healing of the tendon.
Tendinopathy is a generic description that encompasses many pathologies of clinical conditions arising from chronic overuse in and around the tendon such as ruptures/tendinitis, tendinosis and paratendinitis, which can only be classified post histopathological examination (Maffulli, Sharma, & Luscombe, 2004; Khan, Cook, Bonar, Harcourt, & Astrom, 1999). There has been a shift to replace the pathological term ‘tendinitis’ with ‘tendinosis’ as increasing research fails to detect the presence of prostaglandin mediated inflammatory cell infiltration within the pathological tendon (Khan, Cook, & Kannus, 2002; Khan et al. 1999). Achilles tendinosis pathology is now attributed to a failure of the cell matrix to adapt to repetitive trauma. With fiber disorientation, collagen degeneration, and vascular ingrowth occurring, due to an imbalance between matrix degeneration and synthesis (Cook & Purdam, 2009; Maffulli et al. 2004). Healing and re-injury is believed to follow a continuum, with a chronic overuse tendon classified as being in the disrepair and/or degenerative tendinopathy stages. These two stages will display similar pathophysiology, with the level of damage and disruption being the distinguishing marker (Cook & Purdam, 2009).
The disrepair stage is described as the tendons attempt to heal its self during continual excessive loading. During this stage breakdown of the matrix occurs as increased numbers of chondrocytic and assomemyofibroblast cells appear resulting in increased cartilage and protein production, this can result in separation of collagen fibers further disorganizing the matrix. Tendons in this stage are thick with increasing stiffness. These changes can appear in very localized areas of then tendon and not necessary encompass the whole tendon. Some reversibility from this pathology is possible (Cook & Purdam, 2009).
During the degenerative stage there is greater amounts of ground substance and further destruction to the matrix with disruption of parallel...