Tendinosis

Etiology

The etiology of tendinosis is not well understood. Because it was previously thought to be the result of chronic tendinitis, it was hypothesized that chronic inflammation leads to structural tissue changes and tendon calcification. That description entirely mischaracterizes the types of tissue changes occurring in each process. Study results have shown elevated lactate levels within tendinitis sites, suggesting tissues experience hypoxia. Another model suggests the tendon cells fail to maintain homeostasis with exposure to pressure and thermal and ischemic changes.[8] Multiple factors, including age, genetic predisposition, and comorbidities, can contribute to healing failure, increasing the risk of tendinosis.[5][6]

Epidemiology

Limited data exist on the demographics and incidence of tendinosis in the United States or worldwide. Many cases go unreported, and the reported cases are poorly monitored and described. Data on tendon injuries vary by tendon and activity.

• Achilles tendon injuries may account for 20% of all tendon injuries, with ruptures occurring in up to 1% of men aged 30 to 50, 52% of former elite runners, 5.9% of sedentary people, 24% of competitive athletes, and 18% of athletes under 45.[2]
• Patellar tendinopathy affects 45% of volleyball and 32% of basketball players.
• Lateral epicondylitis affects as many as 4 to 7 per thousand people over a lifetime.
• Rotator cuff pathology is present in 9.7% of people younger than 20, 50% of 60-year-olds, and 62% of people 80 and older.[4] 

Many of these studies lump together all tendinopathies, including ruptures, overuse injuries, and anatomical diagnoses of tendinopathy. 

Pathophysiology

Clinicians theorize that tendinosis results from impaired tendon healing. While tendon healing is often described in 3 stages for simplicity, it occurs as a continuous, dynamic process:

Stage 1 begins with the tendon’s initial insult, stress, or injury, often caused by acute overload, repetitive strain, or chemical irritation. Agents like fluoroquinolones have been associated with tenocyte death, potentially contributing to tendon damage.

Stage 2 is defined by failed tendon healing, though the exact cause remains unclear. A common theory suggests that an altered tendon environment disrupts proper cell recruitment and the healing cascade. Medications like steroids and nonsteroidal anti-inflammatory drugs may further impact this process, offering short-term relief but potentially contributing to long-term pathology.

Stage 3 is characterized by cellular apoptosis, matrix disorganization, and neovascularization. Many patients seek evaluation at this stage due to mechanical weakness, increased pain, or tendon tears. Neovascularization is believed to introduce neonerves, contributing to pain through neurogenic inflammation. Studies show that disrupting these neovessels can significantly reduce pain.[4][9]

Various systemic and lifestyle factors contribute to tendon injury risk, including body mass index, nutrition, body mechanics, muscle imbalances, and flexibility, all of which influence tendon loading and stress. Smoking reduces oxygen delivery to tendons, while diabetes mellitus alters collagen structure and ischemic tolerance. Dyslipidemia can also cause collagen fibril disorganization and weaken tendons by fat deposition. Genetic factors and treatment with fluoroquinolone and corticosteroids can decrease tending strength and healing.[2] Finally, several sources suggest that hemodialysis also contributes to risk factors for tendon rupture.[10] 

Toxicokinetics

Corticosteroids affect tendon cell metabolism by decreasing cell viability, changing matrix synthesis, and promoting apoptosis. Nonsteroidal anti-inflammatory drugs (NSAIDs), which are often the first-line treatment for sports injuries, may decrease tendon cell growth, inhibit the production of extracellular lattice components, and promote the presence of damaging enzymes. NSAIDs are now thought to increase the risk of tendinopathy when used for overuse injuries.[10] 

Fluoroquinolone antibiotics have been associated with tendinopathy and tendon rupture. Results from a study of chronic levofloxacin use in patients treated for tuberculosis saw 18.5% of users develop tendinopathy while being treated, and many improved once treatment was completed. Ciprofloxacin, another fluoroquinolone, has been linked to tendinopathy, particularly in patients with chronic renal impairment, which increases phenylacetic and quinolinic acid levels.[10] Other factors that increase the risk of developing tendinopathy include being older than 60 years, undergoing corticosteroid therapy, having renal failure or diabetes mellitus, and having a history of tendon rupture.[11] Tendon ruptures have a 46-fold occurrence when concurrently exposed to fluoroquinolones and corticosteroids.[12] 

Local anesthetics have been found to cause tenocyte injury in 3 ways:

1. Restricting mitochondrial energy metabolism
2. Increasing caspase production
3. Suppressing the signaling pathways that inhibit autophagy

In general, the detrimental effects of local anesthetics are increased with concentration and more prolonged time exposure. Results from in vitro studies suggested that bupivacaine and lidocaine were found to be more toxic than mepivacaine and ropivacaine, and ropivacaine was not found to be harmful to tenocytes when used alone.[13]

History and Physical

When taking a patient history, it is essential to identify the mechanism of injury to differentiate between degenerative and overuse conditions causing tendinosis and inflammatory tendinitis. Tendinosis often involves a history of increased mechanical stress on the affected tendon. Additionally, it is important to ask about how daily activities are affected, if taking any new medications (including antibiotics), or if the patient has had any recent procedures involving local anesthetics. These details help guide treatment. A thorough physical exam should include musculoskeletal evaluation and tendon palpation, with special tests as needed based on the tendon involved. Tendinosis is typically diagnosed following the history and physical exam, with further testing considered depending on the clinical situation.[14]

Evaluation

If the etiology of tendinosis remains unclear after the history and physical exam, laboratory tests can help differentiate it from tendinitis. While C-reactive protein and erythrocyte sedimentation rate lack specificity, they can indicate an underlying inflammatory process, such as spondyloarthritis. If bone injury is suspected, x-rays should be performed.

Ultrasound is increasingly used due to its dynamic imaging capabilities and role in guiding tendinosis treatments. However, sensitivity and specificity vary based on operator experience and tendon location, with different frequencies optimizing visualization. Common ultrasound findings include increased spacing of hyperechoic fibrillar lines, reduced echogenicity, tendon thickening, and neovascularization seen on color Doppler. Magnetic resonance imaging is also useful but is often less preferred due to higher costs and lower spatial resolution.

Treatment / Management

Initial treatment for tendinosis, like other musculoskeletal disorders, is typically conservative. Rest, cryotherapy, and eccentric exercises guided by a physical or occupational therapist should be prescribed. The role of oral and topical nonsteroidal anti-inflammatory drugs remains debated, with some study results suggesting potential harm. Previously, steroid injections were a common treatment, but they are no longer first-line due to their association with worse long-term outcomes despite providing short-term pain relief. Most patients with overuse tendinopathies recover within 3 to 6 months. Conservative management often includes biomechanics correction and tendon-specific muscle loading, such as isotonic and eccentric exercises. Extracorporeal shockwave therapy may serve as an adjunct for certain tendons.[14](B3)

For patients who do not respond to conservative treatment, additional options focus on disrupting neovascularization. These include high-volume guided injections, percutaneous needle tenotomy, sclerosis, and percutaneous needle scraping. Other potential treatments include glyceryl trinitrate patches, percutaneous ultrasonic tenotomy, and orthobiologics such as platelet-rich plasma and stem cells. Percutaneous tendon release or surgical intervention may be considered when all other treatment options have been exhausted.[15][16][17][18](A1)

Differential Diagnosis

The differential diagnoses for tendinosis 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.[19][20]

Complications

Complications with tendinosis can include the following:

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