Version July 2025
INTRODUCTION —
Tendinopathy is a clinical diagnosis characterized by localized tendon pain and loss of function [1]. Most commonly, it is the result of repeated mechanical loading. On occasion, small increases in the loads placed on tendons with low load-bearing capacity can result in a tendon becoming symptomatic for the first time. Tendinopathy is distinct from tendon rupture, where acute pain with disruption of the tendon fibers is the hallmark. Tendinopathy often has an insidious onset and refers to a tendon with abnormal tissue that is structurally intact.
The general epidemiology, risk factors, common clinical findings, terminology, and clinically relevant aspects of the pathophysiology of tendinopathy are reviewed here. The diagnosis and management of tendinopathy generally and in specific tendons are discussed separately, including in the following topics:
●General management (see "Tendinopathy: Overview of management" and "Biologic therapies for tendon and muscle injury")
●Upper extremity tendinopathies (see "Rotator cuff tendinopathy" and "Calcific tendinopathy of the shoulder" and "Biceps tendinopathy and tendon rupture" and "Elbow tendinopathy (tennis and golf elbow)")
●Lower extremity tendinopathies (see "Quadriceps muscle and tendon injuries" and "Patellar tendinopathy" and "Achilles tendinopathy" and "Non-Achilles ankle tendinopathy")
PATHOLOGY AND TERMINOLOGY —
Our knowledge of the pathophysiology of tendinopathy stems mainly from surgical biopsies taken from subjects with chronic tendon pain who have failed conservative treatment and undergone open or arthroscopic tendon debridement.
Historically, tendinopathy was commonly referred to as tendinitis. The suffix "itis" implied that inflammation was central to the pathologic process. During the 1990s, surgical biopsies from symptomatic tendons (ie, in patients who had failed conservative treatment) became available. Numerous histopathology and gene array studies performed on these tissue specimens have revealed that the pathophysiology underlying most cases is a failed healing response within the tendon tissue [2-19]. Histopathology of a wide variety of tendons consistently reveals few inflammatory cells. This is true of the Achilles, posterior tibial, patellar, gluteal [20], adductor [21], extensor carpi radialis brevis and longus, flexor carpi ulnaris, flexor digitorum [22], and rotator cuff tendons [4,9,15,23,24]. Subsequently, the prevailing view became that tendinopathy was essentially a degenerative condition caused by repeated mechanical loading (overuse), not an inflammatory condition. Thus, the term "tendinitis" fell out of favor, and the terms "tendinopathy" and "tendinosis" became more commonly used. The term tendinosis is based on histopathologic characteristics and not clinical findings [25]; the term "tendinopathy" was introduced as a clinical descriptor of the condition [26].
Nevertheless, tissue analyses revealed the presence of iron-containing macrophages in affected tissues, suggesting prior episodes of vascular disruption and the resulting activation of the innate immune response during the development of tendinopathy [16,18]. Furthermore, the widespread presence of neovessels and chemicals such as substance P in longstanding tendinopathy suggests elements of the inflammatory response are indeed present in chronic tendinopathy.
A 2018 systematic review concluded that "prior to 2012, the majority of published reviews did not discuss monocytes, macrophages, or lymphocytes in tendinopathy; rather, they focused on the lack of neutrophils" [27]. This neutrophil-focused definition of inflammation may have contributed to suggestions that the pathophysiology is entirely noninflammatory [28].
A typical inflammatory response does occur in tendons following vascular disruption, whether from microscopic, partial, or complete rupture of the tendon [29-31]. Increased COX-2 or IL-6 expression indicates that there may be a mild low-grade inflammation even in longstanding cases [32]. Indeed, tendon cells from patients with tendinopathy produce more PGE2 than do tendon cells from those with healthy tendons [33].
Tendinopathy is characterized by disorganized tendon structure with some deterioration [34,35]. Changes can occur in different regions of a tendon, such as the insertional region (portion of tendon that inserts onto bone, often called the enthesis) or the midportion (free tendon) [36]. The attached figure presents examples of normal tendon appearance and some common changes observed in pathologic tissue (picture 1). These features include areas of tendon fibroblast proliferation, the presence of smaller and less organized collagen fibers, and neovascularization/angiogenesis. This pathology may be summarized as "angiofibroblastic hyperplasia" [19].
Paratendinopathy is a diagnosis where the typical history involves the onset of swelling around the tendon associated with crackling sensations (crepitus) [37]. The role of inflammation in acute paratendinopathy (eg, de Quervain tenosynovitis) may be more prominent [14]. However, in the chronic stage, de Quervain tenosynovitis is also characterized by minimal inflammation and widespread degenerative and fibrotic changes affecting the sheath and the tendon itself.
EPIDEMIOLOGY AND RISK FACTORS —
Tendinopathy is common [38,39]. Increased participation in recreational sporting activity, particularly among middle-aged adults, has led to an increasing incidence of tendinopathies [39]. However, tendinopathy may be unrelated to activity and can develop in older adults. As an example, it is estimated that two-thirds of Achilles tendinopathy cases occur in nonathletes [40]. This suggests that insufficient load-bearing capacity of the tendon may be as important as excessive external loading in the development of tendinopathy.
Risk factors for tendinopathy are often divided into intrinsic factors (pertaining to the properties of an individual's tendon or healing capacity) and extrinsic factors (pertaining to the load placed on the tendon; ie, the volume of exercise) (table 1). Among these many factors, advancing age (intrinsic) and increased overall volume of tendon load (extrinsic) pose the greatest risk for developing tendinopathy.
Intrinsic risk factors — Intrinsic risk factors for developing tendinopathy may include the following:
●Prior history of tendinopathy
●Increased age
●Sex
●Muscle weakness
●Genetics
●Metabolic disease (eg, diabetes)
The strongest risk factor for developing tendinopathy is a prior history of tendinopathy [41-44]. This fact suggests that certain individuals have a combination of unfavorable genetic, biomechanical, and behavioral characteristics that predispose them to tendinopathy.
Age over 35 years is associated with an increased incidence of many tendinopathies, including Achilles tendinopathy in runners and rotator cuff tendinopathy in throwing athletes or manual laborers [39]. As tendons age, they lose their energy-storing capacity (in particular the Achilles tendon), which may predispose to injury [45-47]. In addition, the capacity to adapt to tendon-loading activities appears to diminish with age [48].
The influence of sex on tendinopathy is incompletely understood but a combination of biomechanical variables (eg, hip-to-knee angles), hormonal influences (eg, estrogen levels and menopausal status), and different sporting or occupational behaviors may account for differences [49]. Sex appears to exert a strong effect on developing certain tendinopathies but not all. As examples, while patellar tendinopathy is five times more common in male compared with female jumping athletes [50], gluteal tendinopathy is three times more likely to develop in females in the general population [51], and females may have a slightly higher risk of developing lateral elbow tendinopathy [52].
While evidence is limited, biomechanical abnormalities and muscle weakness may be associated with an increased risk of tendinopathy, particularly in the lower extremities. If poor postures or flawed movement patterns are noted in patients with chronic tendon pain, biomechanical assessment is warranted.
Muscle weakness may increase the risk of developing certain tendinopathies. Stronger muscles absorb and distribute loads more efficiently during physical activities. This reduces the amount of force transmitted directly to tendons, thereby decreasing tendon strain. Decreased calf muscle strength has been identified as a risk factor for Achilles tendinopathy [41], and decreased hip abductor muscle strength is associated with gluteal tendinopathy [53].
Structural tendon abnormalities represent a significant risk factor for developing tendinopathy. In high-risk groups, such as athletes participating in jumping sports with a high prevalence of patellar or Achilles tendinopathy, asymptomatic structural abnormalities identified on ultrasound at the start of an athletic season are associated with an increased risk of developing symptomatic tendinopathy during the season [54,55].
Tendinopathies often develop bilaterally or at multiple locations in the same individual, suggesting a genetic role [56]. Tendinopathies have a multifactorial etiology likely involving multiple, complex interactions among various genes. Multiple genetic loci controlling structural pathways have been implicated in the susceptibility for tendinopathy [57]. Associations have been found for genetic loci involved in collagen synthesis, glycoprotein production, tendon homeostasis, inflammation, apoptosis, and angiogenesis [58].
More recently, researchers have come to appreciate the role of metabolic diseases in tendinopathy. The most common example is diabetes mellitus [59,60]. Patients with diabetes are more likely to develop tendinopathy at a variety of sites (eg, rotator cuff, hand flexor tendons). An association has also been found between lower extremity tendinopathies and obesity, heterozygous familial hypercholesterolemia, and systemic lupus erythematosus [61]. An increase in waist circumference is associated with an increased risk for patellar tendinopathy [62]. Other metabolic disorders thought to increase the risk for tendinopathy include hypertriglyceridemia, inflammatory bowel disease, and hyperuricemia.
Extrinsic risk factors — Extrinsic risk factors associated with tendinopathy include the following:
●Training errors (eg, large, abrupt increase in tendon-loading activity; inadequate rest)
●Poor environmental conditions (eg, cambered road surfaces, hard gym floors, frozen turf, low temperatures [63,64])
●Poor ergonomics
●Inadequate equipment (eg, old or inappropriate footwear)
●Premature return to sport following injury [39,65-69]
Based primarily on clinical experience, sudden substantial increases in training load without adequate time for the tendon to adjust (eg, doubling of cumulative running distances from one week to the next) incur the greatest risk. As an example, the incidence of Achilles tendinopathy increases in runners preparing for long-distance running events [44].
Suboptimal ergonomics contribute to the development of many upper extremity tendinopathies [65]. Excessive movement or awkward postures involving the hand, wrist, or shoulder during daily or occupational activities can lead to tendon overuse [70].
Certain medications increase the risk for tendinopathy. These include fluoroquinolones, glucocorticoids, statins, and aromatase inhibitors [71]. Because hypercholesterolemia is also a potential risk factor for tendinopathy, it can be difficult to distinguish between the effects of the condition (hypercholesterolemia) and the treatment (statins). However, in an observational cohort study, an increased risk for tendinopathy was found only among current statin users and not former users, supporting the assertion that statin use contributes to tendinopathy [72]. (See "Fluoroquinolones", section on 'Tendinopathy' and "Statin muscle-related adverse events".)
MAJOR CLINICAL FINDINGS
History — A careful history and physical examination can help to confirm whether an injury involves a tendon and why the injury occurred now. Important questions to ask include:
●Did the pain develop suddenly or gradually?
●Is the pain localized to a specific location (ie, tendon)?
●Has there been any recent increase in training volume or any new activities?
●Has there been any change in equipment (eg, new racquet) or training programming (eg, running on a different surface, hill running)?
●Have you recently returned from time away from training or regular activities (tendons lose strength and conditioning quickly)?
●Is there any history of an inflammatory condition, such as inflammatory joint or spinal disease, uveitis, psoriasis, or inflammatory bowel disease, in the patient or their family?
●Is there a history of metabolic diseases, such as diabetes or hypercholesterolemia?
●Has there been any recent use of tendinopathic medications (eg, quinolone antibiotics, glucocorticoids, statins, or aromatase inhibitors)?
Physical examination — The major features of tendinopathy on physical examination are tenderness at the affected part of the tendon and pain with tendon loading (resistance or stretch tests) [73]. Load can be introduced by having the tendon work against resistance or by stretching the tendon. Many people experience some discomfort when their tendons are palpated, and thus tenderness may be present in the absence of tendinopathy. Comparison with the tendon of the unaffected extremity may be helpful. Absence of tenderness is rare for Achilles tendinopathy and, depending on the circumstances, should prompt the clinician to consider other diagnoses. However, palpation of some deeper tendons, such as the proximal hamstrings and rotator cuff, may not elicit pain.
Tendinopathy generally causes tendon thickening, but this may be difficult to appreciate by palpation depending on the depth of the tendon involved. As examples, thickening of the Achilles, may readily be appreciated, while thickening of a rotator cuff or gluteal tendon cannot.
Tendons are often exposed to high tensile forces, but compression forces may also provoke symptoms [74]. As an example, in patients with insertional Achilles tendinopathy, full ankle dorsiflexion may cause compression of the Achilles against the calcaneus. Similar patterns may be seen with hamstring tendon origin on the ischial tuberosity with full hip flexion and with the gluteal tendon insertion on the greater trochanter with full hip adduction.
A characteristic of many tendinopathies is the delayed appearance of more severe pain, termed "latency." This phenomenon is sometimes referred to as the "warm-up effect." Latency is seen characteristically in Achilles and patellar tendinopathy but is found with other tendons. During loading of the tendon (eg, when running), there may be a short-lived increase in tendon pain initially that subsides as exercise continues. The tendon may feel fine for the remainder of the exercise. However, subsequently (ie, a few hours after exercise or the next day), more severe pain, worse than baseline, develops. Recognizing latency can help with diagnosis.
Although pathology may exist within the tendon or its associated structures, clinical experience may suggest that the cause of pain lies elsewhere. Careful assessment performed by a clinician knowledgeable about musculoskeletal evaluation often reveals changes elsewhere in the kinetic chain, including muscle weakness, abnormal movement patterns, or joint stiffness. In addition, tendinopathy, like other pain syndromes, may involve referred pain, muscle spasm or tenderness, or other regional (or even contralateral) motor abnormalities [75].
DIAGNOSTIC IMAGING —
Characteristic changes in tendon appearance on ultrasound or magnetic resonance imaging (MRI) studies can be used to confirm the likelihood of tendinopathy as a source of load-related tendon pain, identify macroscopic tears (which may be amenable to surgical repair), and determine the extent of involvement of associated structures (eg, presence of bony spurs or fragments, labral lesions, bursal pathology).
Greyscale or color power Doppler ultrasound are particularly useful for detecting tendon pathology and may reveal tendon thickening, hypoechoic areas, and increased microvascular blood flow in the deep portions of the tendon. There is conflicting evidence about the association between the extent of Doppler signal and patients' symptoms [76-78]. Doppler signal is of limited use for prognosis [79].
Improvements in ultrasound technology have enabled trained musculoskeletal ultrasonographers to better distinguish the pathologic conditions underlying tendinopathy, including tendon dislocations, paratendon involvement, and partial tendon tears. While evidence that these features help with diagnosis or prognosis is limited, they can assist management. As an example, a patient with Achilles tendinopathy where the pathology appears predominantly paratendinous on ultrasound may be able to tolerate high levels of exercise more quickly than a patient with a partial tendon tear.
MRI reveals increased signal in abnormal tendons, corresponding to the increased water content associated with excessive proteoglycans and increased blood flow, and for some tendons is more effective than ultrasound at distinguishing partial tears [80]. However, in a small observational study, the signal intensity of MRI was not useful for determining the alleviation of symptoms in patients with Achilles tendinopathy [81].
Follow-up imaging is not typically recommended for patients who are treated with physical rehabilitation, particularly when symptoms and function are improving. There is conflicting evidence from clinical trials about the association between ultrasound findings during rehabilitation and improvement of symptoms [82-85]. As improvements in ultrasound and MRI are made and emerging technologies develop (eg, ultrasound tissue characterization, elastography), diagnostic imaging may be used to assess tendon healing in select cases [86,87].
Studies of ultrasound and MRI for the diagnosis of tendon pathology report relatively high sensitivity and specificity for full-thickness tendon tears but limited test characteristics for partial tears and other rotator cuff conditions [88-90]. Estimates of the sensitivity and specificity for the detection of tendinopathy are likely to change as studies involving more advanced equipment are published. Available systematic reviews of diagnostic accuracy are difficult to interpret, as many compare imaging with physical examination findings rather than more definitive standards [91,92].
NATURAL HISTORY AND TREATMENT —
The majority of patients with tendinopathy present to health professionals in the chronic stage (over three months of symptoms). Once present, tendinopathies may be refractory to treatment, and some become career-limiting for professional athletes. However, tendinopathy may also be transient, causing minor irritation that resolves over a period of days or weeks [93].
The recalcitrant nature of many cases of untreated tendinopathy is well documented. In a randomized trial of 75 patients with chronic Achilles tendinopathy, patients in the control group ("wait and see") experienced a gradual improvement in the average load-induced pain score from 8/10 to 6/10 over the course of four months [94]. However, beyond four months, only one-quarter reported resolution of symptoms or significant improvement. In a network meta-analysis of 29 studies of Achilles tendinopathy, any treatment intervention was found to be superior to a wait-and-see approach [95]. In a randomized trial of 185 patients with lateral elbow tendinopathy of at least six weeks duration, improvement rates were slightly better, with 42 percent of patients in the control group ("wait and see") reporting significant improvement in day-time pain after three months [96]. Another randomized trial of 204 patients with gluteal tendinopathy reported that 33 percent of patients in the control group experienced significant clinical improvement at 12 weeks, which increased to 52 percent at one year [97].
Patients treated with physiotherapy emphasizing active exercise experience significantly higher improvement rates than those treated with alternative approaches [98,99]. (See "Tendinopathy: Overview of management".)
Debate continues about the extent to which the tissue changes underlying tendinopathy are reversible as determined by histology or imaging. Longitudinal studies have reported a reduction in ultrasound abnormalities in successfully treated tendons, including normalization of tendon thickness and reduction of hypoechoic areas [100]. However, considerable symptomatic improvement and successful return to activity are seen in some patients with persistent, macroscopically apparent pathology who follow a proper rehabilitation program [85]. (See "Tendinopathy: Overview of management".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General issues in muscle and tendon injury diagnosis and management" and "Society guideline links: Muscle and tendon injuries of the upper extremity (excluding shoulder)" and "Society guideline links: Muscle and tendon injuries of the lower extremity (excluding Achilles)".)
SUMMARY AND RECOMMENDATIONS
●Pathology and terminology – Tendinopathy is a clinical diagnosis characterized by localized tendon pain that is exacerbated by mechanical loading. Tendon overuse is a leading cause, and metabolic factors may contribute. (See 'Pathology and terminology' above.)
Tendinopathy is primarily characterized by disorganized tendon structure, cellular hyperplasia, increased vascularization, and low-grade inflammation (picture 1).
A classic cellular inflammatory reaction is present only minimally in most cases of chronic tendinopathy, but elements of inflammation are involved in every stage of the condition.
●Epidemiology and risk factors – Risk factors for tendinopathy are often divided into intrinsic factors (pertaining to the properties of an individual's tendon or healing capacity) and extrinsic factors (pertaining to the load placed on the tendon) (table 1). Among many risk factors, prior tendinopathy, advancing age, and increased overall volume or intensity of tendon load pose the greatest risk for developing tendinopathy. (See 'Epidemiology and risk factors' above.)
●Clinical findings – The major clinical features associated with tendinopathy are pain with palpation of the affected part of the tendon and pain with tendon loading. (See 'Major clinical findings' above.)
●Diagnostic imaging – Tendinopathy manifests characteristic findings on imaging with ultrasound or MRI. Findings include tendon thickening, abnormal tendon appearance, and increased Doppler flow. (See 'Diagnostic imaging' above.)
ACKNOWLEDGMENTS —
The UpToDate editorial staff acknowledges Alexander Scott, PhD, RPT, and Karim Khan, MD, who contributed to earlier versions of this topic review.
