Why does Supraspinatus Tendinopathy Occur?
There are a few mechanisms that may cause a tendinopathy. When a tendon undergoes maximal tensile load, ischemia (lack of blood flow) may result. When the load is removed blood is redistributed to the tendon and there is an influx of tendon damaging substances called oxygen free radicals which may result in a tendinopathy (Sharma &Marffulli, 2005).
Microtears in the connective tissue leads to an increase in tendon repair cells which may decrease the tensile strength of the tendon, increasing the chance of tendon rupture (Wikipedia, 2009). During the healing process tendon repair cells cause the tendon to change from its tightly bundled glistening white appearance, to a disorganized, soft, thickened yellow-brown tendon (Simons & Kruse, 2008). The damaged fibers are initially replaced with type III collagen which is a weaker type of substance than the normal tendon that is type I collagen. The healing process is also a very slow one due to the low level of vascularisation (blood supply) and slow collagen turnover of tendons; therefore tendons rarely regain their original strength and there is an increased susceptibility of re-injury (Wikipedia, 2009).
In a study by Millar, Wei, Molloy, Bonar and Murrell (2008), it was hypothesised that an increase in the amount and duration of load on a tendon leads to the activation of stress activated protein kinases, oxygen free radicals and apoptic (programmed cell death) mediators. The persistent activation of these substances may cause the tendon to undergo excessive apoptosis, leading to a weakened tendon structure; therefore increasing the amount of tendon degeneration and the tendon becomes more vulnerable to rupture.
