Tendinosis

Etiology

The etiology of tendinosis is not fully understood. Practitioners theorize that an insult causing damage and acute inflammation sets the process in motion. The insult can be mechanical stressors, repetitive overloading, or toxic chemicals. Multifactorial confounding variables, including age, genetic predisposition, or comorbidities, make one more prone to healing failure that causes tendinosis.[5][6]

Epidemiology

Data are more prevalent for specific anatomical diagnoses of tendinosis. Overall, epidemiology studies on tendinosis are scarce. It is likely underreported due to self-treatment and improper coding or classification.

Pathophysiology

Practitioners theorize that tendinosis is a result of impaired tendon healing. For simplicity, it has been described as occurring in three stages when, in reality, it occurs on a continuum. Stage one begins when the tendon experiences the initial insult, stress, or injury. This could result from acute overload, repetitive stress, or chemical irritation by agents such as fluoroquinolones, which have been linked to the death of tenocytes. The failed healing of the tendon characterizes stage two. It is unclear what this is caused by, but a common belief is that an altered tendon environment causes improper cell recruitment and a cascade of healing. Theoretically, medications such as steroids and nonsteroidal anti-inflammatories (NSAIDs) could also alter the natural healing cascade, providing short-term relief but leading to further pathology. The third stage is highlighted by apoptosis of cells, disorganization of the matrix, and neovascularization. It is at this stage that many patients present for evaluation. They may experience mechanical weakness, resulting in tears or increased pain. Neovascularization has been theorized to supply neonerves, which are part of the genesis of pain in tendinosis. In the literature, this has been termed neurogenic inflammation. It has been proven that when these neovessels are sclerosed, disrupted, or destroyed, pain improves.

Toxicokinetics

Fluoroquinolones have been associated with tendinopathy/tendon rupture. Ciprofloxacin is the most commonly reported fluoroquinolone associated with tendinopathy. Other risk factors are age older than 60 years, corticosteroid therapy, renal failure, diabetes mellitus, and history of tendon rupture. It is noted that there is a 46-fold increase in the incidence of tendon rupture with fluoroquinolone use and concurrent corticosteroid exposure. Certain anesthetics have been found to cause injury to tenocytes. Bupivacaine is most toxic to tenocytes and fibroblasts when compared to ropivacaine. When ropivacaine and lidocaine were compared, lidocaine was found to be significantly toxic to tenocytes in a dose-dependent manner. Ropivacaine was not found to be toxic to tenocytes when used alone. This should be considered when doing interventional tendon procedures.

History and Physical

When acquiring a history, it is important to identify if an acute stressor is the culprit of injury. For example, if the patient recently changed their workout routine or has any new occupational responsibilities that increase mechanical stress on the injured tendon. It is also important to ask the patient about the impact the injury has on their activities of daily living (ADLs) and if the patient is on any new medications (including antibiotics), as these answers will help guide treatment. A physical exam should include a basic musculoskeletal evaluation and palpation of the tendon. Special tests can be used to evaluate further depending on the tendon involved. Tendinosis is often diagnosed after the history has been gathered and a physical exam is performed. Further testing can be obtained to better characterize the injury, depending on the clinical scenario.

Evaluation

If, after the history and physical, it is unclear what the etiology of tendinosis is, labs can be done to evaluate for tendinitis. C-reactive protein (CRP) and ESR are not very specific tests, but they can help the physician determine if an inflammatory process occurs, like that seen in spondyloarthritis. Given the history and physical exam findings, X-rays should be performed if there is a question of potential bone injury. Given the dynamic nature of the study, ultrasound machines are being used more frequently. Several interventions used to treat tendinosis are also done under sonographic guidance. Specificity and sensitivity vary between sonographic operators as well as when examining different tendons in the body. Different frequencies are recommended for optimal visualization depending on which part of the body the examiner is investigating. Common ultrasound findings in tendinosis include increased spacing of the hyperechoic fibrillar lines, reduced echogenicity, thickening of the tendon, and neovascularization (via color Doppler). The MRI is also a valuable tool that can be used when evaluating tendinosis.

Treatment / Management

Initial treatment for tendinosis, like other musculoskeletal disorders, is initially conservative. Initially, rest, cryotherapy, and eccentric exercises with a physical or occupational therapist should be prescribed. There is debate over the role of both oral and topical NSAIDs in the treatment of tendinopathy, with some studies even showing harm associated with their use. This issue is still being debated, and recommendations are unclear. Previously, steroid injections were a common form of treatment, but this is no longer a first-line treatment. Short-term reduction in pain has been seen with steroid injections; however, long-term follow-up has linked steroid injections to worse clinical outcomes. Most patients with overuse tendinopathies fully recover within 3 to 6 months. For those patients who are refractory to conservative treatment, other options are available—many of the treatments used for refractory tendinosis target the associated neovascularization. High-volume guided injections, percutaneous needle tenotomy, sclerosis, and percutaneous needle scrapings theorized mechanisms of action involve disrupting these neovessels. Other treatments include glyceryl trinitrate patches, percutaneous ultrasonic tenotomy, and orthobiologics (platelet-rich plasma, stem cells). Last-line treatment includes percutaneous tendon release or surgical intervention.[7][8][9][10](A1)

Differential Diagnosis

The differential diagnoses for tendonitis include the following:

• Acute compartment syndrome
• Ankle injury
• Bursitis
• Carpal tunnel syndrome (in emergency medicine)
• Gout and pseudogout
• Hand infections
• Reactive arthritis
• Rheumatoid arthritis
• Rotator cuff injuries
• Soft tissue knee injury

Prognosis

Tendons are slow to heal because they have a limited vascular supply. Tendinosis healing can last 3 to 6 months, but therapy, rest, and medication can improve the outlook. If left untreated tendinosis can result in tendon rupture.[11][12]

Complications

Complications with tendinosis can include the following:

• Contractures of the tendon, with reduced tendon liability
• Tendon adhesions
• Atrophy of muscles
• Loss of functionality, even up to and including disability