An overview of structure, mechanical properties, and treatment for age-related tendinopathy

Abstract

Tendons transfer tensile loads from muscle to bone, which enable joint motions and stabilize joints. Tendons sustain large mechanical loads in vivo and as a result, tendons were frequently injured. Aging has been confirmed as a predisposing factor of tendinopathy and bad recovery quality following tendon repair. Current treatment methods are generally not effective and involve either symptomatic relief with non-steroidal antiinflammatory drugs and physical therapy or surgery when conservative treatments failed. The limitation in treatment options is due to our incomplete knowledge of age-related tendinopathy. Studies over the past decades have uncovered a number of important mechanical and cellular changes of aging tendon. However, the basis of aging as a major risk factor for tendon injury and impaired tendon healing remained poorly understood. The objectives of this review are to provide an overview of the current knowledge about the aging-associated changes of structure, mechanical properties and treatment in tendon and highlight causes and therapies for age-related tendinopathy.

Incidence and prevalence of lower extremity tendinopathy in a Dutch general practice population: a cross sectional study

“…One theory attributes the effect to the accumulation of chronic repetitive damage over time [ 23 ]. Another hypothesis is that age-related changes in tendon structure and biomechanics could decrease the loading capacity and regenerative capacity of the tendons [ 24 ].…”

Tendon development and musculoskeletal assembly: emerging roles for the extracellular matrix

“…Hallmarks of tendinopathies include COL1A1, COL1A2, COL4A1 and COL4A2 overexpression, fibril disorganization, increased collagen crosslinking, reduced tissue inhibition of MMPs (i.e. TIMP activity), and elevated expression of MMP2, MMP14 and MMP19 as well as of versican, biglycan and Dcn (Jelinsky et al, 2011;Parkinson et al, 2011;Dunkman et al, 2013;Zhou et al, 2014). Recent studies have also identified COL6A1/2/3 and COL12A1 as genes underlying one form of human 'myotendinopathy', which affects both myomatrix structure and tendon matrix structure (Bönnemann, 2011;Pan et al, 2013).…”

Donor age affects proteome composition of tenocyte-derived engineered tendon

“…Ageing is associated with an increasing incidence of tendinopathies and impaired tendon repair following injury [ 1 – 3 ]. These events are thought to result from age-related modifications in tendon structure, especially extracellular matrix (ECM) content, accumulation of mechanically induced micro-trauma and decreased regenerative potential of tendon tissue [ 1 , 4 – 7 ]. Tendon adaptability to loading conditions and its healing capacity depend predominantly on the cellular component, represented by tenocytes and tendon-derived stem cells (TDSCs) [ 8 – 11 ].…”