Pathophysiological Tendinopathy

The purpose of this essay is to describe structure and function of the tendon, present a discussion on the process of pathophysiological Tendinopathy and provide a review of known intervention used to manage or treat both acute and chronic tendinopathies.

Tendons act to serve a connective tissue linking muscle to bony attachment points and in the case of the intermediate tendons that will act to link a muscle belly to another (Benjamin and Kaiser, et al). Tendons are a uniaxial and assist in force transmission thus being able to withstand external forces from multiple planes and angles (Kannus, 2008). Tendons are also responsible for storage of power and changes in the mechanical energy of the body of which in turn reduces muscular work by

Tenoblasts are immature are immature spindle shaped cells that contain cytoplasmic organelles of which reflects their metabolic activity, over time tenoblast elongate and mature becoming tenocyts Minor anorganic components found in the tendon include magnesium, manganese, cadmium, cobalt, copper, zinc, nickel, lithium, lead, fluoride, phosphor, and silico (P Kannus,

The continuum model contain three distinct stages- reactive, disrepair and degenerative tendinopathies. The progression through each stage will inhibit the pathological areas ability to recover. Progression through the stages is dependent on load and internal factors such as genetics and other predisposed pathological illnesses such as including adiposity, cholesterol, insulin resistance, diabetes and menopause (cook and Bass et al 2007).

Reactive tendinopathy is a short term response to acute overload and will lead to a inflammatory response. Proteoglycan contents within the extracellular matrix are increased however collagen will only undergo a small amount of change. The released proteoglycans will bind with water causing thickening in response to tensile and compressive overload (Cook and Purdam 2009).

Tendon disrepair stage attempts to regain organisation within the extracellular matrix sctructiure through increased activation of cells along with the possibility of neuronal and vascular ingrowth (G.Andersson etal 2007). This presents issues from a clinical perspective as tendons become too difficult to distinguish (Cook and Khan, etal,