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Achilles tendinopathy

87 citationsUpdated Sep 2026

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Overview

Achilles tendinopathy is a degenerative process [4] that primarily affects the watershed area of the tendon, located 2 to 6 cm proximal to its calcaneal insertion [10]. Noninsertional disorders present as peritendinitis without tendinosis, peritendinitis with tendinosis, or isolated tendinosis [10]. While acute peritendinitis causes pain and swelling, chronic tendinosis may be relatively asymptomatic, characterized by bulbous nodularity that moves with passive ankle flexion and extension [10]. Chronic degenerative changes can lead to calcification within the tendon [10]. MRI is helpful in evaluating the extent of these degenerative changes, particularly for preoperative planning and counseling [10]. In athletes, the mechanical properties of the Achilles tendon aponeurosis are altered [44], though repetitive mechanical loading may impart a positive benefit through reduced compliance of the musculotendinous unit [44].

Nonoperative management is the mainstay of treatment for all Achilles tendon diagnoses [1] and is often successful for noninsertional tendinopathy [3, 4, 8]. The majority of patients fully recover symptoms and function with exercise alone [9]. Extracorporeal shock wave therapy (ESWT) improves pain and functional outcomes compared to other nonsurgical treatments [15], with superior subjective clinical outcomes and lower failure rates maintained for over one year in noninsertional cohorts compared to insertional cohorts [25]. However, a wait-and-see strategy is ineffective for chronic recalcitrant tendinopathy of the main tendon body [18]. Platelet-rich plasma (PRP) injections show no proof of enhancing functional or clinical outcomes [31] and are no more effective than placebo [66]; consequently, PRP should not be used until future high-quality randomized controlled trials demonstrate clear clinical benefit [104].

Surgical intervention is indicated for refractory cases [4, 8] or when conservative treatment of at least 6 months has failed [10]. For noninsertional tendinosis, surgical options include ventral paratenon stripping, open tendon debridement, and tendon reconstruction with transfers [10]. In extensive disease involving more than 50% of the tendon volume, reconstruction procedures remain the gold standard but carry significant recovery times and potential complications [10]. Gastrocnemius recession is an alternative with less morbidity [10], and endoscopic debridement of ventral paratenon adhesions yields good results with shortened recovery [10]. Tendon transfer augmentation, typically using the flexor hallucis longus (FHL) or flexor digitorum longus, is supported by literature for extensive disease [10]. Open surgery for midportion tendinopathy is safe and effective in the medium term [29], while multiple percutaneous longitudinal tenotomies are safe, low-cost, and effective in the long term for runners [32]. Secondary reconstruction can be performed safely in obese patients without increasing short-term postoperative complication rates [35]. For insertional tendinopathy, tailored surgical care leads to good functional outcomes and satisfactory return to sports [36], and the Endoscopic SpeedBridge Procedure is an effective minimally invasive option [40]. However, no definite recommendations can be made regarding the best surgical treatment for midportion [41] or insertional [67] Achilles tendinopathy.

Anatomy & Pathophysiology

Anatomy

The Achilles tendon is the largest and most powerful tendon in the ankle [45], formed from the confluence of the gastrocnemius and soleus tendons in the distal calf [110]. It is the only musculotendinous unit that crosses two major joints (knee and ankle, as well as subtalar) in the body [20]. The gastrocnemius muscle attaches above the knee to the posterior aspect of the medial and lateral femoral condyles [45], while the soleus muscle originates from the upper part of the posterior tibia, fibula, and interosseous membrane [45]. Consequently, the gastrocnemius is most effective in plantarflexion of the ankle with the knee extended [45], whereas the soleus is most effective with the knee flexed [45]. The Achilles tendon acts as the major plantar flexor of the ankle joint [20] and a weak knee flexor due to the gastrocnemius insertion on the posterior femoral condyles [20]. It also acts as an inverter of the heel because it runs just medial to the hindfoot axis of rotation [20].

The fibers of the Achilles tendon rotate 90 degrees toward the insertion into the calcaneal tuberosity [45]. At the insertion point, gastrocnemius fibers lie lateral and soleus fibers lie medial [45]. The tendon inserts at the calcaneal tuberosity, separated from the underlying bone by the retrocalcaneal bursa [110]. It is innervated by the tibial nerve [20]. The Achilles tendon is surrounded by a paratenon instead of a true tendon sheath [20], consisting of loose areolar tissue that covers the tendon medially, posteriorly, and laterally [110]. Anteriorly, the tendon is marginated by Kager fat pad [110]. Lubrication is aided by two bursae: one anterior (retrocalcaneal) and one posterior (superficial) to the tendon [20]. The plantaris tendon is variably seen as a thin slip coursing from superolateral to inferomedial along the ventral surface of the Achilles tendon, inserting onto either the distal Achilles tendon or the calcaneal tuberosity [110].

The normal Achilles tendon appears as a cord of uniform caliber, measuring 4 to 7 mm in AP dimension [110]. It can take on a mildly fusiform shape, appearing thicker in the critical zone located midway between the myotendinous junction and the insertion [110]. Vascularity is supplied through the paratenon on the deep surface of the tendon [45], muscular arterial branches within the gastrosoleus complex proximally [45], and small interosseous vessels at the insertion distally [45]. The major blood supply is through the mesotendon, with the richest supply through the anterior mesentery [108]. A zone of relative avascularity exists 2 to 6 cm proximal to the insertion [45], a vascular watershed region resulting from the lack of a true synovial sheath and local anatomy [20]. With increasing age, the anterior mesenteric supply becomes reduced [108]. The sural nerve runs in the midline of the gastrocnemius-soleus muscle to the musculotendinous junction, where it crosses over to the lateral side of the tendon [20].

Pathophysiology

The etiology, pathogenesis, and natural course of Achilles tendinopathy are largely unknown [2]. Histopathological studies have been limited to the chronic phase, and it is not clear whether degenerative features are preceded by an inflammatory phase [2]. Achilles tendinopathy is a degenerative condition related to overuse [21], and the term "tendinitis" is a misnomer [21]. Histopathology typically does not show markers of inflammation within the tendon [21]. In the absence of inflammation in the chronic stage, irritation of mechanoreceptors or triggering of nociceptive receptors may cause pain [2]. Tendon injury is thought to be caused by a failed healing process resulting in altered tendon structure, neovascularization, and nerve ingrowth [16].

The risk for developing Achilles tendinopathy is multifactorial, involving an interaction of intrinsic and extrinsic factors that lead to tendon overloading [16]. Lower extremity impairments that produce eccentric overload can result in injury [16]. The body’s response to loading is influenced by health conditions, drugs, and genetic factors [16]. Genes associated with the collagen-production pathway may functionally affect tendon strength and stiffness [16]. Individuals with a family history of tendinopathy have five times the risk of developing Achilles tendinopathy [16]. The multifactorial etiology of noninsertional Achilles tendinopathy includes overuse, mechanical imbalance, poor tissue vascularity, genetic predisposition, and use of fluoroquinolone antibiotics [46]. Noninsertional Achilles tendinopathy accounts for nearly half of all cases and is thought to involve the response to microscopic tearing of the tendon [46].

Tendinitis refers to an acute, reversible inflammatory process with healing potential, whereas tendinosis refers to a chronic, irreversible process characterized by fibrous degeneration without reparative, inflammatory cells [45]. Clinically, these represent differing ends of a continual spectrum [45]. The vascular arrangement is satisfactory for low demand in normal conditions, but increased demand may lead to inadequate vascularity, subsequent degeneration, and fibrosis [45]. Tendinosis is most commonly due to hypoxia, which predisposes the critical zone because of its relative hypovascularity [110]. Myxoid degeneration is the second most frequent etiology, referring to the accumulation of mucoid vacuoles among tendon fibers that may coalesce to form interstitial tears [110]. Less common causes include lipoid degeneration, which describes the accumulation of fat within the tendon and is usually asymptomatic, and ossific degeneration, which describes ossification within the tendon and is often associated with a history of injury [110]. Degenerative ossification occurs proximal to the insertion, while enthesopathy occurs at the insertion [110].

Chronic inflammation is a feature of both mid-portion Achilles tendinopathy and rupture [38]. Pro-inflammatory profiles differ slightly in ruptured tendons, likely due to acute inflammation and increased vascularisation resulting from recent trauma [38]. The Achilles and rotator cuff tendons share common cellular and molecular inflammatory disease mechanisms [38]. Insertional Achilles tendinopathy results from a complex interplay of mechanical loads, vascular impairment, and inflammatory responses [74]. Abnormal vascularization of the ventral mesotenal vessels 2 to 6 cm proximal to the insertion limits blood flow to diseased tissue and decreases capacity for healing [46]. Chronic painful tendons show the ingrowth of sensory and sympathetic nerves from the paratenon with release of nociceptive substances [125]. Up to 34% of asymptomatic tendons show histopathological changes [125].

Age-dependent changes in collagen crosslinking result in increased stiffness and loss of viscoelasticity, predisposing to injury [108]. Repetitive microtrauma to the hypovascular area may make it impossible for the reparative process to keep pace [108]. A degenerative attrition may be responsible for many Achilles tendon ruptures [108]. Another theory is the failure of inhibiting mechanisms at the musculotendinous unit as a result of fatigue, with resultant eccentric overload [108]. The cause of rupture is probably a combination of a relatively hypovascular area and repetitive microtrauma that causes an inflammatory reparative process unable to keep up with stresses due to decreased vascularity [108]. A mechanical overload completes the rupture [108]. Most Achilles tendon ruptures occur as an indirect loading mechanism during eccentric muscle contracture [53]. Seventy-five percent of ruptures occur between 5 and 6 cm proximal to the insertion on the calcaneal tuberosity, a location that correlates to a zone of relative hypovascularity [53]. A subgroup of patients with an acute rupture have antecedent pain at the Achilles, and tendons in these patients frequently show degenerative changes on histopathologic evaluation [53].

The Kager fat pad does not remain static during ankle range of motion, but deforms and its pressure also changes [131]. The plantaris tendon inserting directly into the calcaneus resulted in significantly greater differential motion compared with the Achilles tendon [138]. There was no association between tendon structure and symptoms in nonoperatively treated Achilles tendinopathy [5]. However, measures of tendon morphology and mechanical properties appear to be associated with patient-reported symptoms and calf muscle function [27]. As the factors are uncorrelated, the results of assessment of tendon structure should not be expected to be associated with lower extremity function or biopsychosocial limitations [6]. Participants with insertional Achilles tendinopathy had larger tendon diameter, lower echogenicity indicating degeneration, higher strain, and lower stiffness compared to uninvolved sides and controls [78]. The results of a study on mechanical properties provide a rationale for current clinical approaches to management, whereby repetitive mechanical loading may impart a positive benefit through reduced compliance of the musculotendinous unit [44]. Additional research is required to improve our understanding of the causative factors in Achilles tendinopathy [33].

A lower peak ankle inversion moment is a significant predictor of the onset of Achilles tendinopathy [122]. A lower peak ankle external rotation angle is a significant predictor of the onset of Achilles tendinopathy [122]. A greater running volume is a significant predictor of the onset of Achilles tendinopathy [122]. Compared with healthy controls, runners currently symptomatic with Achilles tendinopathy have a longer duration of eversion [142]. Runners currently symptomatic with Achilles tendinopathy do not have greater excursion or velocity of eversion compared with healthy controls [142]. UTC of tendon structure, Achilles tendon thickness, and foot posture did not significantly contribute to the prediction of Achilles tendinopathy [139].

Classification

Anatomic Location: The most clinically useful classification distinguishes between insertional Achilles tendinopathy at the calcaneal tuberosity and noninsertional Achilles tendinopathy located 2 to 6 cm proximal to the insertion [21]. Noninsertional Achilles tendinopathy is typically located 4 to 6 cm proximal to the insertion [21]. Midportion Achilles tendinopathy is defined as being located 2–7 cm from the insertion onto the calcaneus [96].

Clinical Features: Achilles tendon disorders are classified by nodularity, location of pain, and the presence or absence of redness and warmth [20]. Acute paratenonitis/tendinitis is characterized by the absence of nodularity, pain throughout the entire tendon that is unaffected by range of motion, and the presence of redness and warmth [20]. Paratenonitis/tendinitis with tendinosis is characterized by the presence of nodularity, pain throughout the entire tendon that is unaffected by range of motion, and the presence of redness and warmth [20]. Tendinosis is characterized by the presence of nodularity, pain that moves with range of motion, and the absence of redness and warmth [20].

Terminology and Pathology: The revised terminology for Achilles tendon-related disorders is based on anatomic location, symptoms, clinical findings, and histopathology [24]. The term “tendinitis” is considered a misnomer because histopathology typically does not show markers of inflammation within the tendon [21]. Achilles tendinopathy is a degenerative condition thought to be related to overuse [21].

Other Considerations: Patients with noninsertional Achilles tendinopathy typically present with fusiform thickening or nodularity of the tendon and associated tenderness to palpation [21]. A contracture of the gastrocnemius-soleus complex is often observed in patients with Achilles tendinopathy [21]. Weight-bearing ankle radiographs may demonstrate intratendinous calcification at the affected level in Achilles tendinopathy [21]. In insertional tendinopathy, radiographs may demonstrate an insertional osteophyte and/or Haglund deformity [21]. Haglund deformity represents a prominence at the superior, posterolateral aspect of the calcaneal tuberosity [21]. MRI or ultrasonography evaluation can detect the degree of tendon degeneration [21]. Midportion Achilles tendinopathy is diagnosed when a spindle-shaped swelling and tenderness at the Achilles tendon 2-7 cm above its calcaneal insertion are present [57]. Retrocalcaneal bursitis is indicated by maximum tenderness localized anterior to the medial and lateral distal Achilles tendon border and posterior to the corresponding posterosuperior calcaneal aspect [57]. Specific findings at the posterosuperior calcaneal tuberosity, such as erosions or cyst formations, indicate chronic retrocalcaneal bursitis [57]. Bone spurs in the Achilles tendon insertion are considered different pathologies from midportion tendinopathy and retrocalcaneal bursitis [57]. The continuum model of tendon pathology has been used to develop ultrasound imaging-based criteria to diagnose tendinopathy [88].

Clinical Presentation

Achilles tendinopathy is a degenerative, not inflammatory, condition that is prevalent and potentially incapacitating in athletes involved in running sports [83]. Histopathology typically does not show markers of inflammation within the tendon, making the term "tendinitis" a misnomer [21]. The risk for developing this condition is likely multifactorial, related to an interaction of intrinsic and extrinsic factors that lead to tendon overloading [16]. The natural history is typically a long protracted course [14]. Beyond pain and symptoms, the condition causes apparent impairments in various aspects of lower leg muscle-tendon function [22].

The most clinically useful classification distinguishes between insertional tendinopathy at the calcaneal tuberosity and noninsertional Achilles tendinopathy located 2 to 6 cm proximal to the insertion [21]. Insertional tendinopathy may be characterized by one or a combination of conditions, including retrocalcaneal bursitis, pretendinous bursitis, or insertional Achilles tendinopathy with or without calcification [37]. A true Haglund deformity refers to a large exostosis off the posterosuperior aspect of the calcaneal tuberosity located anterior to the Achilles tendon [37]. Anatomically, the retrocalcaneal bursa lies between the calcaneal tuberosity and the Achilles tendon just anterior and proximal to the Achilles’ insertional footprint, while a superficial (pretendinous) bursa separates the Achilles tendon from the overlying skin [37].

Patients present with pain at the Achilles tendon that correlates with increased activity [21]. In noninsertional cases, patients often present with pain, swelling, and impaired performance, especially with running [46]. The tender area of fusiform thickening in noninsertional Achilles tendinopathy is localized approximately 2 to 6 cm proximal to the insertion of the tendon [46]. In insertional Achilles tendinopathy, the patient rarely gives a history of acute injury; rather, it is a slow, insidious process of gradual enlargement and pain at the insertion [37]. Progressive difficulty with wearing closed-back shoes and pain after a period of rest, such as when first arising in the morning, are noted in insertional tendinopathy [37]. Pain only when wearing shoes may indicate a pretendinous bursitis, whereas pain when first arising in the morning is more consistent with retrocalcaneal bursitis or Achilles tendinitis [37].

Examination reveals tenderness and swelling at the level of the tendinosis [21]. Patients with noninsertional Achilles tendinopathy typically have fusiform thickening or nodularity of the tendon 4 to 6 cm proximal to the insertion and associated tenderness to palpation [21]. A contracture of the gastrocnemius-soleus complex is often observed in patients with noninsertional Achilles tendinopathy [21]. Examination for insertional Achilles tendinopathy often reveals a significant contracture of the gastrocnemius complex, especially with the knee in extension [37]. In prolonged or severe cases of insertional tendinopathy, retrocalcaneal bursitis, Achilles tendinopathy, and pretendinous bursitis can exist concomitantly [37]. Maximum tenderness localized anterior to the medial and lateral distal Achilles tendon border and posterior to the corresponding posterosuperior calcaneal aspect indicates retrocalcaneal bursitis [57].

Weight-bearing ankle radiographs may demonstrate an insertional osteophyte and/or Haglund deformity in the case of insertional tendinopathy [21]. Calcification within the tendon may ensue from chronic, degenerative tendinosis as seen on radiographs [10]. MRI is helpful in evaluating the extent of the degenerative changes in Achilles tendinopathy, especially in preoperative planning and counseling [10]. MRI or ultrasonography evaluation are useful for presurgical planning and can detect the degree of tendon degeneration [21]. MRI demonstrates thickening of the tendon with intrasubstance intermediate signal intensity consistent with disorganized tissue in noninsertional Achilles tendinopathy [46]. In the setting of a chronic rupture, MRI shows a large gap between the hypoechoic tendon ends [46]. Grey-scale ultrasonography in combination with colour Doppler examination has identified neovascularisation in the area with tendinosis in patients with painful chronic Achilles tendinosis [48]. Ultrasound combined with color Doppler and clinical assessment can detect a close by located plantaris tendon in a high proportion of patients with midportion Achilles tendinopathy [62].

The revised terminology for Achilles tendon-related disorders based on anatomic location, symptoms, clinical findings, and histopathology is used by the majority of orthopedic surgeons and is increasingly used in the literature [24]. There is currently no widely supported agreement on diagnostic criteria for Achilles tendinopathy, though ICON meetings could serve as a platform to initiate such an agreement [23]. The literature does not specify sensitivity or specificity of the physical examination findings for distinguishing midportion Achilles tendinopathy from retrocalcaneal bursitis [57].

Investigations

Clinical Examination and Diagnostic Criteria

The physical examination for acute Achilles tendon rupture should include two or more of the following tests: the clinical Thompson test (Simmonds squeeze test), decreased ankle plantar flexion strength, presence of a palpable gap, or increased passive ankle dorsiflexion with gentle manipulation [109]. The Thompson test is highly sensitive (96%) and specific (93%) for a complete acute Achilles rupture [53]. Achilles tendon disorders are clinically classified by nodularity, location of pain, and the presence or absence of redness and warmth [20]. In acute paratenonitis/tendinitis, pain is located in the entire tendon with no effect from range of motion, and redness and warmth are present [20]. In paratenonitis/tendinitis with tendinosis, nodularity is present, pain is located in the entire tendon with no effect from range of motion, and redness and warmth are present [20]. In tendinosis, nodularity is present, pain moves with range of motion, and redness and warmth are absent [20]. Patients with noninsertional Achilles tendinopathy typically present with fusiform thickening or nodularity of the tendon 4 to 6 cm proximal to the insertion and associated tenderness to palpation [21]. Achilles tendinopathy causes apparent impairments in various aspects of lower leg muscle-tendon function as measured with a test battery [22]. There is currently no widely supported agreement on diagnostic criteria for Achilles tendinopathy [23].

Imaging: Radiography

Plain radiography: In insertional tendinopathy, radiographs may demonstrate an insertional osteophyte and/or Haglund deformity, representing a prominence at the superior, posterolateral aspect of the calcaneal tuberosity [21]. Radiographs may also show calcification at the Achilles tendon insertion or a posterosuperior calcaneal prominence in insertional Achilles tendinopathy [55].

Imaging: MRI

MRI: MRI is helpful in evaluating the extent of degenerative changes in Achilles tendinopathy, especially in preoperative planning and counseling [10]. MRI evaluation is useful for presurgical planning and can detect the degree of tendon degeneration in Achilles tendinopathy [21]. MRI is valuable for evaluating the extent of diseased tendon in insertional Achilles tendinopathy and allows the success of nonsurgical treatment to be predicted [55]. MRI revealed the highest overall diagnostic accuracy for the diagnosis of both insertional and midportion Achilles tendinopathy compared to other imaging modalities [87]. However, there was no statistically significant difference in favor of one imaging modality over the others in the diagnosis of Achilles tendinopathy [87]. MRI-derived measures of Achilles tendon fat content may be able to distinguish xanthomas from control and tendinopathic tissue [93]. A computerized 3-D seed-growing technique to monitor and evaluate the volume of the Achilles tendon and mean intratendinous signal using MR imaging shows an overall excellent reliability regarding inter- as well as intra-observer reliability [130]. Achilles tendon thickness of more than 6.1 mm and intratendinous abnormality of over 48.8% were confirmed to be diagnostic cutoff values for insertional Achilles tendinopathy [128]. Interposed tissue between the tendon stumps is suitable for repair of chronic Achilles tendon rupture if preoperative MRI shows a thickened fusiform-shaped Achilles tendon with diffuse intratendinous high-signal alterations throughout [129]. Intra-tendon MRI abnormalities are frequent in chronic Achilles tendon rupture but likely represent non-pathologic cicatricial remodeling [119]. Magnetic resonance imaging techniques can be used as an adjunct to clinical evaluation by monitoring morphologic effects in clinical treatment studies of Achilles tendinopathy [42]. MRI and ultrasonography can both be used to confirm an Achilles tendon rupture in the case of ambiguous physical examination findings but are not routinely necessary [53]. The routine use of magnetic resonance imaging, ultrasound, and radiography to confirm the diagnosis of acute Achilles tendon rupture has inconclusive evidence [109].

Imaging: Ultrasonography

Ultrasonography: Ultrasonographic follow-up of patients with mid-portion painful chronic Achilles tendinosis treated with eccentric calf muscle training showed a localised decrease in tendon thickness and a normalised tendon structure in most patients [127]. Ultrasound plus color Doppler can directly detect a close by located plantaris tendon in a high proportion of patients with midportion Achilles tendinopathy [62]. Clinical assessment can indirectly detect a close by located plantaris tendon in patients with midportion Achilles tendinopathy [62].

Tissue Characteristics and Pathology

Histopathology: Histopathology typically does not show markers of inflammation within the tendon in Achilles tendinopathy, making the term "tendinitis" a misnomer [21]. Histopathological studies of Achilles tendinopathy have been limited to its chronic phase, and it is not clear whether the degenerative features are preceded by an inflammatory phase [2]. The exact aetiology and pathophysiology of non-insertional Achilles tendinopathy are not fully known and warrant further studies [11].

Other Considerations: Participants with insertional Achilles tendinopathy had larger tendon diameter, lower echogenicity (indicating degeneration), higher strain, and lower stiffness compared to uninvolved sides and controls [78]. Bilateral changes in tendon structure are present in patients diagnosed with unilateral insertional or midportion Achilles tendinopathy [51]. The asymptomatic side should not be used as reference in clinical practice for Achilles tendinopathy [51]. The results of assessment of tendon structure should not be expected to be associated with lower extremity function or biopsychosocial limitations because the factors are uncorrelated [6].

Treatment

Non-Operative

Achilles tendinosis is a degenerative process that can be treated conservatively with great success [4]. The natural history is typically a long protracted course where management focuses on physiotherapy [14]. Initial nonsurgical treatment consists of a period of rest, activity modification, and the use of heel lifts with or without immobilization in a walking boot [21]. Physical therapy with a focus on eccentric strengthening has shown efficacy for the nonsurgical treatment of insertional and noninsertional Achilles tendinopathy [21]. Heavy-load eccentric strengthening has demonstrated the highest success rate for nonoperative treatment of noninsertional Achilles tendinopathy [46]. Nonoperative treatment is effective in approximately 50% to 70% of cases of noninsertional Achilles tendinopathy [46]. Both traditional eccentric training and heavy slow resistance training yield positive, equally good, lasting clinical results in patients with Achilles tendinopathy [65]. Heavy slow resistance training is associated with greater patient satisfaction after 12 weeks but not after 52 weeks compared to eccentric training [65]. The AOPT clinical practice guidelines recommend clinicians implement a mechanical loading program, which can be either eccentric exercise or a heavy-load, slow-speed (concentric/eccentric) exercise program, to decrease pain and improve function in individuals with Achilles tendinopathy [103]. Eccentric training was found to be effective in reducing pain in male patients but may be significantly less effective in females [115]. Symptomatic females suffering Achilles tendinopathy do not benefit as much as symptomatic males from 12 weeks of eccentric training [43].

Extracorporeal shock wave therapy (ESWT) improves pain and functional outcomes in patients with Achilles tendinopathy compared to other nonsurgical treatments [15]. Shock wave therapy is an effective treatment for chronic noninsertional Achilles tendinopathy [60]. ESWT can improve the symptoms of Achilles tendinopathy, and patients with insertional Achilles tendinopathy who had greater sports activity levels had better therapeutic responses than nonsports-active patients after 5-year follow-up [49]. Superior subjective clinical outcomes together with a lower failure rate were maintained for >1 year in the noninsertional Achilles tendinopathy cohort compared with the insertional cohort, calling into question the long-term benefit of ESWT for patients with insertional Achilles tendinopathy [25]. Current evidence for nonoperative treatment specific for insertional Achilles tendinopathy favors ESWT or the combined treatment of ESWT plus eccentric exercises [86]. Topical glyceryl trinitrate significantly reduced pain with activity and at night, improved functional measures, and improved outcomes in patients with Achilles tendinopathy [90]. There is no proof that platelet-rich plasma (PRP) injections can enhance patient functional and clinical outcomes for Achilles tendinopathy [31]. PRP is no more effective than placebo for treating Achilles tendinopathy and should not be used for this indication until new, large, high-quality RCTs upend current knowledge [66]. Both PRP and autologous adipose-derived stromal vascular fraction (SVF) are safe and effective treatments for Achilles tendinopathy [59]. Both PRP and SVF were safe, effective treatments for recalcitrant Achilles tendinopathy [84]. A randomized clinical trial demonstrates that reducing tendon compression (eg, limiting ankle dorsiflexion) during rehabilitation for insertional Achilles tendinopathy leads to improved clinical outcomes and higher patient satisfaction [63]. Long-term use of an ankle-foot orthosis to neutralize the Achilles tendon can be considered as an alternative to surgery if other nonsurgical treatments have been ineffective [21]. 40% of patients report ongoing pain even after five years of therapy for Achilles tendinopathy [14].

Operative

Indications: Surgical management is indicated for patients in whom conservative treatment of at least 6 months has failed for noninsertional Achilles tendinopathy [10]. Surgical procedures for insertional Achilles tendinopathy are indicated only after failure of conservative treatment [37]. The timing of surgical intervention for Achilles tendinopathy can only be made on a case-by-case basis and is recommended only after exhausting conservative methods of management [97]. Up to 29% of Achilles tendinopathy patients require surgery [97].

Surgical Approach / Technique: There are no level I evidence studies on the use of 1 technique over another in the surgical management of a given tendinopathy [97]. The biologic objective of surgery for Achilles tendinopathy is to modify vascularity and possibly stimulate the remaining viable cells to initiate cell-matrix response and healing [97]. The technical objective of surgery for Achilles tendinopathy classically involves excising fibrotic adhesions, removing degenerated nodules, and making multiple longitudinal incisions in the tendon to detect and excise intratendinous lesions [97]. Less invasive surgical procedures for Achilles tendinopathy focus on the disruption of the neoneurovascularity associated with long-standing symptomatic tendinopathy [97].

For noninsertional Achilles tendinopathy, less invasive operative options include percutaneous longitudinal tenotomies in the area of degeneration and stripping of the anterior aspect of the tendon with a large suture to free adhesions [46]. Isolated gastrocnemius recession has shown good results for noninsertional disease prior to consideration of a tendon débridement in patients with a gastrocnemius contracture [46]. Gastrocnemius release is an effective treatment option in the management of patients with Achilles tendinopathy who have gastrocnemius contracture and have previously failed to respond adequately to non-operative treatment [91]. For moderate to severe noninsertional Achilles tendinopathy, open excision of the degenerated tendon tissue with tubularization has had good results [46]. In extensive noninsertional Achilles disease, reconstruction procedures have excellent results and remain the gold standard but are accompanied by significant recovery times and potential complications [10]. Gastrocnemius recession is becoming more popular as an alternative surgical treatment for noninsertional Achilles tendinopathy with less morbidity and good results [10]. Endoscopic debridement of ventral paratenon adhesions has reported good results and shortened recovery for noninsertional Achilles tendinopathy [10].

For insertional Achilles tendinopathy, the central tendon-splitting approach has gained popularity for insertional Achilles tendinopathy because of its direct approach to the area of pathology [55]. The central tendon-splitting approach has gained favor as a more direct access to the pathology for Achilles tendinosis [115]. Surgical treatment usually is successful for insertional Achilles tendinopathy, although no single method or approach appears to be more beneficial than others [55]. For insertional Achilles tendinopathy, early disease treatment for retrocalcaneal bursitis by removing the Haglund deformity does not necessarily accompany tendon debridement [37]. Recalcitrant retrocalcaneal bursitis without tendinosis can be treated with open or endoscopic calcaneal exostectomy [37]. A dorsal closing wedge calcaneal osteotomy technique has been described to decompress the tuberosity impingement in insertional Achilles tendinopathy [37]. In later stages of insertional Achilles tendinopathy, treatment often requires tendon debridement, calcaneal exostectomy, with or without augmentation with tendon transfers [37]. Open techniques for insertional Achilles tendinopathy require large incisions with significant wound complications and prolonged recovery [37]. Similar success has been reported for insertional Achilles tendinopathy through endoscopic techniques [37]. The endoscopic SpeedBridge procedure can be considered an effective and minimally invasive option in the arsenal of insertional Achilles tendinopathy treatment [40].

Implant Selection: For more than 50% degenerative involvement of the Achilles tendon, débridement with an flexor hallucis longus (FHL) tendon transfer is recommended [46]. MRI evidence of significant involvement (diffuse thickening of the tendon without a focal area of disease) indicates the need for FHL transfer in noninsertional Achilles tendinopathy [46]. If the tendon gap is under 2 cm, an end-to-end repair can be completed along with FHL transfer; if 2 to 5 cm, V-Y advancement is considered; if greater than 5 cm, a turndown procedure or allograft is used to bridge the gap [46]. Most literature supports the use of flexor hallucis longus tendon transfers for surgically treated patients with extensive disease (>50% of the tendon volume), but similar outcomes have been reported with flexor digitorum longus transfers [10]. The flexor hallucis longus can be harvested through a single- or double-incision technique [10].

Other Considerations: In a level I study of 39 patients randomized to débridement and decompression alone or débridement and decompression with FHL transfer, no difference was found between groups at 1 year in terms of visual analog scale pain scores, American Orthopaedic Foot & Ankle Society ankle/hindfoot score, and FHL plantar flexion strength [115]. FHL transfer may be best reserved for revision cases based on the lack of difference in outcomes compared to débridement alone in a level I study [115]. In a retrospective review, FHL transfer led to significant improvement in Achilles tendon function, physical function, and pain in patients who were older than 44 years and relatively inactive at 2-year follow-up [115]. Postoperative care for FHL tendon transfer involves protecting the reconstruction with a boot with heel wedges that are slowly removed so that the patient begins shoe wear around 8 weeks and gradual return to activities 3 to 4 months from surgery [113]. In a small series of runners treated with open procedures for insertional Achilles tendinopathy, 67% were able to return to the same level of sport at 8 months after an exostectomy [37]. In a small series of runners treated with open procedures for insertional Achilles tendinopathy, 78% were able to return to the same level of sport at an average of 10 months after reconstruction procedures [37]. Isolated gastrocnemius lengthening in insertional and noninsertional tendinopathy has reported success, but patients exhibit continued plantarflexion weakness 18 months after this procedure when compared with controls [37].

Complications

Wound complications: Open surgical techniques for insertional Achilles tendinopathy require large incisions, resulting in significant wound complications and prolonged recovery [37]. Minimally invasive techniques for chronic Achilles tendon ruptures may result in a lower wound complication incidence than the conventional open procedure [116].

Tendon rupture: Achilles tendon rupture following surgical exploration for tendinopathy has been reported to occur at five weeks post-operatively during isometric loading [50].

Thromboembolism: Repair of chronic Achilles ruptures has a high incidence of venous thromboembolism [39].

Functional deficits: Patients treated with isolated gastrocnemius lengthening for insertional and noninsertional tendinopathy exhibit continued plantarflexion weakness 18 months after the procedure [37]. Richardson et al. demonstrated decreased hallux pressure and FHL weakness after a single incision FHL transfer [10].

Heterotopic ossification: Heterotopic ossification occurs relatively frequently after Achilles tendon ruptures but appears to have no adverse effects on functional outcomes [101].

Other Considerations: Superior subjective clinical outcomes together with a lower failure rate were maintained for >1 year in the noninsertional Achilles tendinopathy cohort compared with the insertional cohort following ESWT [25].

Recovery

Non-Operative Recovery

Functional Outcomes: Exercises improve function in the majority of patients with Achilles tendinopathy [14]. However, 40% of patients report ongoing pain even after five years of therapy [14]. Symptom duration did not influence baseline measures of tendon health in patients with Achilles tendinopathy [133].

Structural and Symptom Association: The tendon structure returns to asymptomatic values in nonoperatively treated Achilles tendinopathy [5]. The results of assessment of tendon structure should not be expected to be associated with lower extremity function or biopsychosocial limitations [6].

Modalities and Predictors: Heavy slow resistance training tends to be associated with greater patient satisfaction after 12 weeks but not after 52 weeks compared to eccentric training [65]. ESWT can improve the symptoms of insertional Achilles tendinopathy [49]. Patients with insertional Achilles tendinopathy who had greater sports activity levels had better therapeutic responses than nonsports-active patients after 5-year follow-up with ESWT [49].

Operative Recovery

Rehabilitation Protocol: Differences in rehabilitation loading pattern in the initial 8 weeks after the repair of an Achilles tendon rupture did not measurably alter the outcome [52]. The ruptured Achilles tendon elongates for 6 months after surgical repair regardless of early or late weightbearing in combination with ankle mobilization [52].

Complications: Achilles tendon rupture following surgical exploration for tendinopathy occurred at five weeks post-operatively during isometric loading [50].

Key Evidence

• [L5] The mainstay of treatment for all Achilles tendon diagnoses is nonoperative. [1] (10.2106/jbjs.o.00002)
• [L5] [2] (10.2106/00004623-200211000-00024)
• [L5] Non-insertional Achilles tendinopathy is often managed conservatively with excellent clinical results, while insertional Achilles tendinopathy management is improved by recognizing coexisting pathologies and evolving surgical approaches. [3] (10.1302/0301-620x.95b10.31881)
• [Paper] Achilles tendinosis is a degenerative process that can be treated conservatively with great success or surgically for refractory cases, though there is currently a lack of consensus regarding the best treatment options. [4] (10.1016/j.csm.2020.05.001)
• [L2] There was no association between the tendon structure and symptoms. [5] (10.1177/0363546515605077)
• [L4] As the factors are uncorrelated, the results of assessment of, for example, tendon structure should not be expected to be associated with lower extremity function or biopsychosocial limitations. [6] (10.1186/s12891-022-05702-1)
• [L4] Surgical intervention gave superior patient reported outcome compared with non-surgical treatment for patients affected by a chronic Achilles tendon rupture. [7] (10.1186/s12891-026-09890-y)
• [L5] Most cases of Achilles tendon disorders are successfully treated nonoperatively, while a small subgroup of recalcitrant cases may benefit from surgical intervention. [8] (10.1177/03635465020300022501)
• [L4] The majority of patients with Achilles tendinopathy fully recovered in regard to both symptoms and function when treated with exercise alone. [9] (10.1177/0363546510384789)
• [L5] The exact aetiology and pathophysiology of non-insertional Achilles tendinopathy are not fully known and warrant further studies. [11] (10.1136/jisakos-2017-000164)
• [L2] ESWT improves pain and functional outcomes in patients with Achilles tendinopathy compared to other nonsurgical treatments. [15] (10.1177/2325967120903430)
• [L1] The wait-and-see strategy was ineffective for the management of chronic recalcitrant tendinopathy of the main body of the Achilles tendon. [18] (10.1177/0363546506295940)
• [L4] Achilles tendinopathy causes not only pain and symptoms in patients but also apparent impairments in various aspects of lower leg muscle-tendon function as measured with the test battery. [22] (10.1007/s00167-006-0150-6)
• [L5] The ICON meetings could be an appropriate platform to initiate a new widely supported agreement on diagnostic criteria for Achilles tendinopathy. [23] (10.1136/bjsports-2020-102863)
• [L4] The revised terminology for Achilles tendon-related disorders based on anatomic location, symptoms, clinical findings and histopathology is used by the majority of orthopedic surgeons and is increasingly used in the literature. [24] (10.1007/s00167-021-06566-z)
• [L3] Superior subjective clinical outcomes together with a lower failure rate were maintained for >1 year in the noninsertional Achilles tendinopathy cohort compared with the insertional cohort, calling into question the long-term benefit of ESWT for patients with insertional Achilles tendinopathy. [25] (10.1177/23259671241265330)
• [L2] Measures of tendon morphology and mechanical properties appear to be associated with patient-reported symptoms and calf muscle function for patients with Achilles tendinopathy. [27] (10.1177/2325967120917271)
• [L2] Open surgery for midportion Achilles tendinopathy is safe and effective in medium term. [29] (10.1007/s00167-014-3232-x)
• [L1] There is no proof that PRP injections can enhance patient functional and clinical outcomes for Achilles tendinopathy. [31] (10.3390/jcm12030995)
• [L4] This approach to the management of midportion Achilles tendinopathy is safe, has a low cost, and is effective in the long term. [32] (10.1177/0363546513494356)
• [L3] Additional research is required to improve our understanding of the causative factors in Achilles tendinopathy. [33] (10.1177/0363546509332250)
• [L3] Our findings suggest that secondary reconstruction for Achilles tendinopathy can be done safely in obese patients without increasing short-term postoperative complication rates. [35] (10.5435/jaaos-d-25-00746)
• [Paper] Surgery for insertional Achilles tendinopathy led to good functional outcomes and satisfactory return to sports when the surgical care was tailored to the degree of tendon involvement. [36] (10.1016/j.otsr.2018.05.003)
• [L4] [38] (10.1136/bjsports-2017-098161)
• [L5] This procedure can be considered an effective and minimally invasive option in the arsenal of insertional Achilles tendinopathy treatment. [40] (10.1016/j.eats.2021.05.014)
• [L4] In terms of the surgical treatment of midportion Achilles tendinopathy, no definite recommendations can be made. [41] (10.1007/s00167-014-3407-5)
• [L4] Magnetic resonance imaging techniques can be used as an adjunct to clinical evaluation by monitoring morphologic effects in clinical treatment studies of Achilles tendinopathy. [42] (10.1177/0363546504263148)
• [L3] Symptomatic females suffering Achilles tendinopathy do not benefit as much as symptomatic males from 12 weeks of eccentric training. [43] (10.1007/s00167-009-1006-7)
• [L3] The results of this study provide a rationale for current clinical approaches to management of Achilles tendinopathy, whereby repetitive mechanical loading may impart a positive benefit through reduced compliance of the musculotendinous unit. [44] (10.1177/0363546510366234)
• [L4] Grey-scale ultrasonography in combination with colour Doppler examination has identified neovascularisation in the area with tendinosis in patients with painful chronic Achilles tendinosis. [48] (10.1007/s001670000189)
• [L3] ESWT can improve the symptoms of Achilles tendinopathy, and patients with IAT who had greater sports activity levels had better therapeutic responses than nonsports-active patients after 5-year follow-up. [49] (10.1177/2325967119898118)
• [Case_report] Achilles tendon rupture following surgical exploration for tendinopathy has not been previously reported; the rupture occurred at five weeks post-operatively during isometric loading, though the exact cause remains unexplained. [50] (10.1186/1471-2474-8-19)
• [L3] These results stress the importance of monitoring both symptomatic and asymptomatic tendon structures and in addition highlight that the asymptomatic side should not be used as reference in clinical practice. [51] (10.1007/s00167-019-05495-2)
• [L1] Differences in rehabilitation loading pattern in the initial 8 weeks after the repair of an Achilles tendon rupture did not measurably alter the outcome. [52] (10.1177/0363546518781826)
• [L4] The use of a free gastrocnemius aponeurosis flap to treat chronic ruptures and reruptures of the Achilles tendon rendered a good overall subjective and objective outcome in the majority of patients. [54] (10.1007/s00167-008-0492-3)
• [L3] [57] (10.1007/s00402-014-2030-8)
• [L1] Both PRP and SVF are safe and effective treatments for Achilles tendinopathy. [59] (10.1177/2325967116s00128)
• [L3] Shock wave therapy is an effective treatment for chronic noninsertional Achilles tendinopathy. [60] (10.1177/0363546507309674)
• [L4] US + CD directly, and clinical assessment indirectly, can detect a close by located plantaris tendon in a high proportion of patients with midportion Achilles tendinopathy. [62] (10.1186/s12891-016-0955-5)
• [L1] This randomised clinical trial demonstrates that reducing tendon compression (eg, limiting ankle dorsiflexion) during rehabilitation for insertional Achilles tendinopathy leads to improved clinical outcomes and higher patient satisfaction. [63] (10.1136/bjsports-2024-109138)
• [L1] Both traditional eccentric training and heavy slow resistance training yield positive, equally good, lasting clinical results in patients with Achilles tendinopathy, with the latter tending to be associated with greater patient satisfaction after 12 weeks but not after 52 weeks. [65] (10.1177/0363546515584760)
• [L1] PRP is no more effective than placebo for treating Achilles tendinopathy and should not be used for this indication until new, large, high-quality RCTs upend current knowledge. [66] (10.1097/corr.0000000000003478)
• [L2] It is not possible to draw conclusions regarding the best surgical treatment for insertional Achilles tendinopathy. [67] (10.1007/s00167-012-2219-8)
• [L5] Insertional Achilles tendinopathy results from a complex interplay of mechanical loads, vascular impairment, and inflammatory responses, where understanding these mechanisms is essential to optimizing conservative treatments, refining surgical approaches, and developing novel therapeutic strategies. [74] (10.1016/j.jisako.2025.100867)
• [L3] Participants with insertional achilles tendinopathy had larger tendon diameter, lower echogenicity (indicating degeneration), higher strain, and lower stiffness compared to uninvolved sides and controls. [78] (10.2519/jospt.2014.5369)
• [L4] Achilles tendinopathy is a degenerative, not an inflammatory, condition that is prevalent and potentially incapacitating in athletes involved in running sports. [83] (10.1136/bjsm.36.4.239)
• [L1] Both PRP and SVF were safe, effective treatments for recalcitrant Achilles tendinopathy. [84] (10.1007/s00167-017-4479-9)
• [L2] Current evidence for nonoperative treatment specific for insertional Achilles tendinopathy favors ESWT or the combined treatment of ESWT plus eccentric exercises. [86] (10.1186/s13018-021-02370-0)
• [L2] There was no statistically significant difference in favor of one imaging modality over the others, but MRI revealed the highest overall diagnostic accuracy for the diagnosis of both insertional and midportion Achilles tendinopathy. [87] (10.1177/23259671211006826)
• [L4] This is the first study to use the continuum model of tendon pathology to develop an USI- based criteria to diagnose tendinopathy. [88] (10.1136/bmjsem-2019-000699)
• [L1] Topical glyceryl trinitrate significantly reduced pain with activity and at night, improved functional measures, and improved outcomes in patients with Achilles tendinopathy. [90] (10.2106/00004623-200405000-00005)
• [L4] The results of this review suggest gastrocnemius release to be an effective treatment option in the management of patients with Achilles tendinopathy, who have gastrocnemius contracture and have previously failed to respond adequately to non-operative treatment. [91] (10.1007/s00167-022-07039-7)
• [L4] MRI-derived measures of Achilles tendon fat content may be able to distinguish xanthomas from control and tendinopathic tissue. [93] (10.1186/s12891-021-04494-0)
• [L3] [96] (10.1007/s00167-012-2203-3)
• [Paper] [97] (10.1177/0363546508324283)
• [L3] Heterotopic ossification occurs relatively frequently after Achilles tendon ruptures but appears to have no adverse effects on functional outcomes. [101] (10.1097/corr.0000000000001085)
• [L1] Until future high-quality RCTs show a clear clinical benefit, PRP should not be used to treat Achilles tendinopathy. [104] (10.1097/corr.0000000000003349)
• [L3] Minimally invasive technique may result in a lower wound complication incidence and provide better early functional recovery and return to moderate-intensity exercise time than the conventional open procedure in treating chronic Achilles tendon ruptures. [116] (10.1007/s00167-022-07167-0)
• [L4] Complications correlate with age, and intra-tendon MRI abnormalities are frequent but likely represent non-pathologic cicatricial remodeling. [119] (10.1016/j.otsr.2013.03.021)
• [L2] We identified a lower peak ankle inversion moment, a lower peak ankle external rotation angle and a greater running volume as significant predictors of the onset of Achilles tendinopathy. [122] (10.1136/bjsports-2025-110260)
• [L5] [125] (10.1007/s00167-011-1535-8)
• [L4] Ultrasonographic follow up of patients with mid-portion painful chronic Achilles tendinosis treated with eccentric calf muscle training showed a localised decrease in tendon thickness and a normalised tendon structure in most patients. [127] (10.1136/bjsm.2001.000284)
• [L3] Achilles tendon thickness of more than 6.1 mm and intratendinous abnormality of over 48.8% were confirmed to be diagnostic cutoff values for IAT. [128] (10.1186/s13018-025-06036-z)
• [L4] Interposed tissue between the tendon stumps is suitable for repair of chronic Achilles tendon rupture if preoperative MRI shows a thickened fusiform-shaped Achilles tendon with diffuse intratendinous high-signal alterations throughout. [129] (10.1177/0363546506295939)
• [L4] A computerized 3-D seed-growing technique to monitor and evaluate the volume of the Achilles tendon and mean intratendinous signal using MR imaging shows an overall excellent reliability regarding inter- as well as intra-observer reliability. [130] (10.1007/s00167-004-0546-0)
• [L5] The Kager fat pad does not remain static during ankle range of motion, but deforms and its pressure also changes. [131] (10.1007/s00167-019-05585-1)
• [L3] Symptom duration did not influence baseline measures of tendon health. [133] (10.1177/23259671231164956)
• [L5] The plantaris tendon inserting directly into the calcaneus resulted in significantly greater differential motion compared with the Achilles tendon. [138] (10.1177/0363546517745291)
• [L2] UTC of tendon structure, Achilles tendon thickness, and foot posture did not significantly contribute to the prediction of Achilles tendinopathy. [139] (10.1177/0363546517750854)
• [L3] Compared with healthy controls, runners currently symptomatic with AT or MTSS have a longer duration of eversion but not greater excursion or velocity of eversion. [142] (10.1177/0363546517708193)

See Also

• Achilles tendon rupture

References

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[91] Gastrocnemius release is an effective management option for Achilles tendinopathy: a systematic review. Knee Surgery, Sports Traumatology, Arthroscopy. 2022. DOI: 10.1007/s00167-022-07039-7

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[122] Biomechanical insights into Achilles tendinopathy risk and protection in runners: a large prospective study 4HAIE. British Journal of Sports Medicine. 2025. DOI: 10.1136/bjsports-2025-110260

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