More specifically, it can refer to:
- Tendinitis - tendon injuries that involve larger-scale acute injuries accompanied by inflammation
- Tendinosis - chronic tendon injury with damage to a tendon at a cellular level
Tendon injury arise from a combination of intrinsic and extrinsic factors; acute tendon injuries may be predominantly caused by extrinsic factors, whereas in overuse syndromes as in the case of tendinopathy it may be caused by multifactorial combinations of both intrinsic and extrinsic factors. An example of an intrinsic factor for tendinopathies are: poor biomechanics such as limb malalignments and hyperpronation that may cause increased traction loads acting on the foot and ankle that may increase the incidence of Achilles, flexor hallucis longus muscle, and tibialis posterior muscle tendinopathies.
Tendon injury and resulting tendinopathy are responsible for up to 30% of consultations to sports doctors and other musculoskeletal health providers.  Tendinopathy is most often seen in tendons of athletes either before or after an injury but is becoming more common in non-athletes and sedentary populations. For example, the majority of patients with Achilles tendinopathy in a general population-based study did not associate their condition with a sporting activity.  In another study the population incidence of Achilles tendinopathy increased six fold from 1979-1986 to 1987-1994.
The exact etiology of tendinopathy has not been fully elucidated and different stresses may induce varying responses in different tendons. There are multifactorial theories that could include: tensile overload, tenocyte related collagen synthesis disruption, load-induced ischemia, neural sprouting, thermal damage, and adaptive compressive responses. The intratendinous sliding motion of fascicles and shear force at interfaces of fascicles could be an important mechanical factor for the development of tendinopathy and predispose tendons to rupture. Obesity, or more specifically, adiposity or fatness, has also been linked to an increasing incidence of tendinopathy.
The most commonly accepted cause for this condition however is seen to be an overuse syndrome in combination with intrinsic and extrinsic factors leading to what may be seen as a progressive interference or the failing of the innate healing response.
Tendinopathy can be induced in animal models by a surgical injury to the tendon. In both sheep shoulder (infraspinatus) and horse forelimb (superficial digitor flexor) tendons, a mid-tendon transection caused pathology in the entire tendon after four and six weeks respectively.
Steroid injections are helpful in the short term (first approximately 4 weeks) however, their long term effectiveness is not known, and quality of evidence for its use remains poor and controversial. Other, more conservative and non-surgical, treatment options available for the management and treatment of tendinopathy include: rest, ice, massage therapy, eccentric exercise, NSAIDs, ultrasound therapy, LIPUS, electrotherapy, taping, sclerosing injections, blood injection, glyceryl trinitrate patches, and (ESWT) extracorporeal shockwave therapy. Studies with a rat model of fatigue-damaged tendons suggested that delaying exercise until after the initial inflammatory stage of repair could promote remodelling more rapidly.
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