Tendinopathy refers to a disease of a tendon. The clinical presentation includes tenderness on palpation and pain, often when exercising or with movement.
Three terms have evolved in the medical terminology to refer to injuries that cause tendon pain:
- Tendinitis - acute tendon injury accompanied by inflammation
- Tendinosis - chronic tendon injury with degeneration at the cellular level and no inflammation
- Paratenonitis - Inflammation of the outer layer of the tendon (paratenon) alone, whether or not the paratenon is lined by synovium
- Paratenonitis with tendinosis - Paratenonitis associated with intratendinous degeneration
- Tendinopathy - chronic tendon injury with no implication about etiology
Tendon injuries 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.
Video Tendinopathy
Cause
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 involves cellular apoptosis, matrix disorganization and neovascularization.
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.
Quinolone antibiotics are associated with increased risk of tendinitis and tendon rupture. A 2013 review found the incidence of tendon injury among those taking fluoroquinolones to be between 0.08 and 0.2%. Fluoroquinolones most frequently affect large load-bearing tendons in the lower limb, especially the Achilles tendon which ruptures in approximately 30 to 40% of cases.
Maps Tendinopathy
Common sites of overuse tendon injuries
Achilles tendon - Achilles tendinopathy; Patella tendon - Patellar tendinopathy; Supraspinatus tendon - Supraspinatus syndrome; Other rotator cuff tendons (infraspinatus, subscapularis, teres minor) - Rotator cuff tendinopathy; Common wrist extensors - Lateral epicondylitis (tennis elbow); Common wrist flexors - Medial epicondylitis (thrower's elbow, golfer's elbow, little league elbow)
Pathophysiology
As of 2016 the pathophysiology is poorly understood; while inflammation appears to be a play a role, the relationships among changes to the structure of tissue, the function of tendons, and pain are not understood and there are several competing models, none of which had been fully validated or falsified. Molecular mechanisms involved in inflammation includes release of inflammatory cytokines like IL-1? which reduces the expression of type I collagen mRNA in human tenocytes and causes extracellular matrix degradation in tendon.
Treatment
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. There is insufficient evidence on the routine use of injection therapies (Autologous blood, Platelet-rich plasma, Deproteinised haemodialysate, Aprotinin, Polysulphated glycosaminoglycan, Corticosteroid, Skin derived fibroblasts etc.) for treating Achilles tendinopathy. As of 2014 there was insufficient evidence to support the use of platelet-rich therapies for treating musculoskeletal soft tissue injuries such as ligament, muscle and tendon tears and tendinopathies.
Epidemiology
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 sixfold from 1979-1986 to 1987-1994. The incidence of rotator cuff tendinopathy ranges from 0.3% to 5.5% and annual prevalence from 0.5% to 7.4%.
References
External links
- http://www.webmd.com/a-to-z-guides/tendon-injury-tendinopathy-topic-overview
Source of article : Wikipedia
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