Although data on the prevalence of chronic Achilles tendinopathy in athletes are limited, the condition is thought to be common. “Tendinopathy” is a newer concept used to describe chronic tendon pathologies that involve tendon degeneration and dysrepair rather than acute inflammation, traditionally referred to simply as “tendinitis” (1). Patients often present with fusiform or nodular tendon enlargement, with varying degrees of localized pain. Tendon thickening may be uniform or focally eccentric when examined under soft-tissue imaging (2). Achilles tendinopathy may be categorized anatomically, as noninsertional (2 cm to 6 cm proximal to the tendon insertion) or insertional (at the tendon's osseous attachment to the calcaneus). This distinction is helpful as optimal treatment may differ, depending on where the pathology lies (1).
Anatomy and Function
The Achilles tendon — also known as the triceps surae or tendo calcaneus — forms from the confluence of the distal gastrocnemius and soleus tendons. The gastrocnemius muscle comprises two heads that originate along the posterior aspect of the medial and lateral femoral condyles (3). The soleus muscle originates from the posterior surface of the proximal fibula and soleal line of the tibia. The three tendons conjoin approximately 12 cm to 15 cm proximal to their calcaneal insertion. The fibers variably spiral about 90° prior to inserting onto the posterior calcaneus (3). The soleus portion inserts medially, and the gastrocnemius portion inserts posterolateral onto the calcaneus (3). The Achilles tendon aids in active ankle plantar flexion. The gastrocnemius and soleus receive innervation from the tibial nerve (3). The Achilles tendon also receives sensory innervation from the sural nerve (3).
The plantaris may variably contribute to the Achilles tendon. The plantaris is a small muscle originating from the lateral femoral condyle and becomes tendinous in the proximal one third of the lower leg (4). This long, thin, slender tendon then courses medially to insert onto the calcaneus. Olewnik et al. (5) delineated five different variations of the plantaris tendon (PT) insertion, with the most common variation being a fan-shaped insertion on the calcaneal tuberosity medial to the Achilles tendon. The plantaris may blend with the Achilles tendon prior to its insertion. It has been estimated to be absent in up to 19% of the population (6). The plantaris is innervated by branches of the tibial nerve (4).
Blood supply to the Achilles tendon is provided by several vessels. The posterior tibial artery supplies the distal 1 cm and a proximal 7 cm to 10 cm segment of the tendon. The much smaller peroneal artery supplies the intervening midportion of the tendon (3). This creates a watershed area with a relative paucity of vascular supply at the midportion, placing the tendon at risk of ischemia. The Achilles tendon does not have a true synovium-lined tendon sheath. Rather, it is enclosed in a paratenon of loose areolar tissue, which is richly vascular and plays an important role in supplying blood to the tendon (3). The distal portion of AT along with the flexor hallucis longus and the calcaneus make up the borders of Kaeger's triangle, which contains the richly innervated Kaeger's fat pad. Pathology in the fat pad is a common mimicker of Achilles tendon pain (7).
The Achilles tendon is comprised mostly of type-1 collagen (90% in a healthy tendon) and a small amount of type 3 collagen (3), organized into microfibrils, fibrils, and tendon fibers. The fibers are colinearly parallel, forming a fascicle, which in turn constitute a primary bundle. The primary bundles are grouped into secondary, and in turn, tertiary bundles. The tertiary bundles are bound together by a layer of fine connective tissue, called the epitenon, to complete the tendon (3). In degenerative tendinopathy, the tendon architecture is disorganized, with disrupted and irregular collagen fibers. Type 1 collagen is replaced by type 3 collagen, leading to fibrotic changes. There also is an increase in glycosaminoglycans and interstitial proteinaceous ground substance (1). The tenocyte concentration is higher in the disease tendon but they are more susceptible to apoptosis (1). These changes alter tendon stiffness and its Young's modulus, leading to lower resistance to stress and strain, which in turn negatively impacts the tendon's ability to transmit force and generate power (8). Focal tendinopathic changes in the tendon also can lead to overloading of the healthy nondegenerative portions of the tendon, predisposing the tendon to further injury.
Neovascularization is often observed in Achilles tendinopathy because of the proliferation of neovessels, induced by the relative tissue hypoxia. These neovessels are hyperpermeable and fail to adequately perfuse the diseased tendon (9). In contrast to a healthy tendon, which is largely avascular, neovessels may penetrate the tendon and are commonly accompanied by neonerves. These neonerves may play key roles in degenerative processes and the pain experienced by patients (1).
The differential diagnosis of posterior ankle and heel pain often includes pathology of the Achilles tendon. However, several other important etiologies are worth considering (Table).
Differential diagnosis of posterior ankle and heel pain: Selected pathological entities that may present with posterior ankle or heel pain with typical clinical findings.
||Potential Helpful Imaging Findings
|Insertional Achilles tendinopathy
||Chronic pain in the distal third of the tendon to its insertion in the posterior heel.
Early morning stiffness (10).
|Tenderness to palpation at the distal third and insertion site on the calcaneus (10).
||US: presence of hypoechoic area and loss of fibrillar appearance at the distal third of the tendon (11).
MRI: thickening of the tendon distally with intense signal on fat suppressed images (12).
|Noninsertional Achilles tendinopathy
||Chronic pain in the mid and proximal third of the Achilles tendon.
Enlargement of the tendon.
|Tenderness to palpation over the proximal and mid tendon.
Nodules move with the tendon (10).
|US: Focal or diffuse thickening of the proximal and/or midsection of the Achilles tendon, loss of compact linear fibrillar appearance, and presence of hypoechoic areas (11).
MRI: thickening of the tendon with heterogeneous signaling on T1 and T2 weighted images (12).
||Heel pain is not on the Achilles tendon itself but deeper.
Pain on low-load activities, such as heel raises or end-range compression in dorsiflexion (13). Acute onset of pain and swelling.
|Tenderness elicited anterior to Achilles tendon and superior to the Achilles insertion by putting pressure on both sides of the area anterior to the tendon. Swelling and warmth.
||Presence of increased fluid or bursal thickening on US or MRI (13).
|Kager's fat pad inflammation
||Heel pain anterior to the Achilles tendon.
Pain with the first few steps after a long period of immobilization, then improved with ambulation but can worsen with a long period of activities.
|Tenderness elicited anterior to Achilles tendon and superior to the retrocalcaneal bursa by putting pressure on both sides of the area anterior to the tendon.
||MRI: abnormal signals in the fat pad on high intensity sequence. (normal MRI signals in the fat pad include low signal on STIR and high signal on T1-weighted images (12)).
|Achilles tendon rupture
||Acute pain in the posterior heel usually when the person performs a quick change in direction. Audible/tactile snap or pop. Patient reports feeling of getting hit by an object on the posterior heel or ankle.
Immediate swelling and/or bruising (13).
|Possible gap in Achilles tendon on palpation.
Positive calf squeeze test (also known as Thompson's or Simmond's test) (13).
|US: anechoic defect, possibly with edge artifacts at the torn ends of the tendon, as well as a wavy and hypoechoic longitudinal appearance of the tendon (10).
MRI: thickened tendon with heterogeneous signals within the tendon edge (12).
|Haglund's syndrome (May overlap with insertional Achilles tendinopathy)
||Posterior heel pain at the insertion site of AT at the bony prominence. Pain starts with the first few steps after resting (14).
||Bony protrusion on visualization.
Tenderness of palpation at the insertion site. Swelling, warmth, and erythema might be present.
|X-ray: lateral radiograph can show a bony prominence (Haglund’s lesion) at the posterosuperior part of the calcaneal tuberosity (14).
||Diffuse discomfort and swelling in the posterior heel region.
||Diffuse swelling and tenderness on both sides of the tendon that do not move when the ankle is dorsiflexed.
Possibly presents with warmth, erythema, and crepitations (10).
|US: fluid around the tendon, adhesions around the tendon (10).
|Sural nerve pain
||Pain along the posterior or the lateral ankle.
Possible paresthesia along lateral or dorsal foot.
|Positive Tinel sign over the area of the nerve.
||US/MRI: focal enlargement or perineural edema (15).
|Posterior impingement (e.g., Os Trigonum syndrome)
||Chronic deep posterior ankle pain with activities such as running and jumping. Common in ballet dancers, gymnasts, cricket bowlers, and soccer players. Possible recent or remote history of ankle trauma.
Often presents with flexor hallucis longus tendonitis (13).
|Posterior ankle pain with forced plantar flexion or push-off maneuvers (plantar flexion test).
Possible tenderness over the posterior medial aspect of ankle joint (13).
|X-ray: can demonstrate hypertrophy of os trigonum or prominent posterior process of the talus (13).
|Sever's disease (Calcaneal traction apophysitis)
||Heel pain that is worse during and after activities in adolescents especially with running and jumping (16). Usually in the setting of a new activities or recent growth spurt. Usually improved with rest and absent in the morning (16).
||Possible swelling and tenderness at the Achilles insertion site Positive squeeze test — compression of the posterior calcaneus Positive Sever sign — pain is aggravated with standing on tiptoe (16).
||X-ray: may show fragmentation, sclerosis, or increased
density of the calcaneal apophysis, but these can be seen in normal variants (16).
|Calcaneal stress reaction or stress fracture
||Insidious onset of heel pain with weight bearing activities.
Localized tenderness to palpation on medial and lateral aspect of posterior calcaneus (13).
|Pain is reproduced by squeezing the medial and lateral aspects of the posterior calcaneus (13).
||Xray: sclerotic appearance on lateral radiograph (13).
MRI: high signal within the calcaneus on T2 images (13).
|Flexor hallucis longus (FHL) tendinopathy
||Pain on toe-off or forefoot weight-bearing over the posteromedial aspect of medial malleolus and the calcaneus around the sustentaculum tali (13).
Pain on landing from jumps (13).
|Pain aggravated from resisted flexion or passive stretch into full dorsiflexion. Crepitus in posteromedial aspect of ankle in the sheath of flexor hallucis longus (13).
||MRI: large amount of fluid along the FHL tendon sheath on STIR sequence (13).
|Lumbar (S1) radiculopathy
||Pain is on the lateral posterior ankle with numbness along the lateral plantar foot.
||Decreased sensation over the posterior lateral ankle.
||Normal ankle imaging
|Achilles (superficial calcaneal) bursitis
||Visible and painful solid swelling of the skin. Usually resulted due to friction from heel tabs or tight shoes (13).
||Solid swelling, tenderness, and discoloration most usually found on the posterolateral aspect of the calcaneus (13).
||US/MRI: fluid within the bursa (13).
In addition to clinical history and physical examination, imaging modalities may play an important role in the diagnosis of Achilles pathology. Plain film radiographs (X-rays) may reveal calcification in the tendon, Haglund's deformity, os trigonum, or soft-tissue swelling, but are infrequently diagnostic. Ultrasound (US) and magnetic resonance imaging (MRI) remain the most useful modalities for assessing the AT.
Sonographically, normal tendon morphology appears echogenic and compact-fibrillar in both short axis (bundled-bristled appearance) and long axis (colinearly fibrillar appearance) images, whereas a degenerative tendon may look locally thickened and variably hypoechoic, with an obscuring of the normally crisp and distinct fibrillar appearance at the midsubstance (Fig. 1) or insertional site (Fig. 2) (12). In a nonpathologic AT, the cross-sectional area measures 0.54 cm ± 0.12 cm at the midpoint between the myotendinous junction and the insertion and 0.72 cm ± 0.15 cm at the insertion site (2). The anteroposterior diameter measures 0.44 cm ± 0.06 cm at the midpoint and 0.40 cm ± 0.06 cm at the insertion (2).
Partial and full-thickness tear of the tendon may be ambiguous on physical examination as sometimes plantar flexion is still observed on the Thompson test because of the other ankle plantar flexor tendons remaining intact, but it may be more readily identified using US. Sonographically, a full-thickness tear may be identified as an anechoic defect. Rather than the normal taut, linearly fibrillar echotexture, this defect may have edge artifact at the torn edges of the tendon, as well as a wavy and hypoechoic longitudinal appearance (10). A partial tear can be difficult to distinguish from tendinopathy under US as the tendon may appear thickened with a hypoechoic or anechoic area (11). In complete tendon ruptures, the margins will often widen under dynamic examination. It also is helpful to see how the tendon moves relative to the surrounding tissue, including the paratenon and the more-ventral Kager's fat pad. In addition to gray scale US imaging, sonoelastography, including compression elastography (CE) and shear wave elastography (SWE), may be used to assess the stiffness and homogeneity of the tendon. Pathologic AT exhibits heterogenous and reduced stiffness patterns on CE (17). SWE is useful in evaluating tendon rupture under dynamic examinations. Combining gray scale US and elastography may increase the sensitivity and specificity of sonography for the diagnosis of Achilles tendinopathy (17). Doppler imaging may demonstrate an increased signal in and around the tendon, suggestive of hyperemia or neovascularization (12) (Fig. 3). An important caveat with US assessment is that it is highly user-dependent. The tendon can appear hypoechoic and mimic tendinopathic changes if the US probe is not perpendicular to the tendon, an effect known as anisotropy (17). One advantage of US over MRI is that the tendon can be examined dynamically with ankle dorsiflexion and plantar flexion, and readily be compared with the contralateral Achilles tendon.
MRI remains the most-definitive diagnostic imaging modality for many physicians in the United States. MRI may be pursued if the tendinopathic features remain unclear under US examination or if US is unavailable. Some surgeons prefer having MRI imaging to study the extent of the disease and visualize the surrounding tissues for operative planning (10). Although it is more expensive than US, MRI is sensitive to a number of tendinopathic changes. Common MRI modalities include T1, T2-weighted sequences and short tau inversion recovery (STIR) images. A normal Achilles tendon appears hypointense (dark) on all MRI sequences because of its very low water content. It appears long and thin on sagittal cuts, and round, uniform, and well-defined on coronal images. In Achilles tendinopathy, MRI images demonstrate thickening of the tendon with heterogeneous signaling on T1 and T2 weighted images (12). Peritendinous disease can demonstrate hyperintense signals on STIR and fat-suppressed T2-weighted images surrounding the Achilles tendon (12). The retrocalcaneal bursa is rich in water content and therefore appears hyperintense on high signal intensity T2-weighted or STIR images. On MRI, a large partial rupture or complete rupture of the tendon appears as a thickened tendon with heterogeneous signals within the tendon edge. If the torn ends are retracted, the intervening defect is frequently filled with fluid appearing bright on high signal intensity sequences (12).
The management of AT often starts with a course of rehabilitation therapy and activity modification. Noninvasive adjunctive therapies such as medications, heel lifts, and physical modalities may be added at this time. Shockwave therapy is often used if patients fail to improve with rest and rehabilitation. Most studies involving shockwave therapy selected patients with at least a three-month duration of Achilles tendon pain/dysfunction. If no clinical improvement is achieved, percutaneous procedures can be considered as the next steps. Lastly, surgical procedures can be considered for recalcitrant cases that do not improve with minimally invasive treatments.
Rehabilitation and Noninjectable Physical Modalities
Eccentric strengthening for the treatment of Achilles tendinopathy was first described in the 1980s, gained recognition in subsequent decades with the work of Alfredson and others (18), and remains the mainstay of conservative treatment. A 2018 meta-analysis on exercise, splinting, and orthoses for midportion Achilles tendinopathy concluded that there was a moderate level of evidence to favor eccentric over concentric exercises under similar loads for reducing pain (19). There was moderate-level evidence showing no significant difference between eccentric and heavy slow concentric resistance exercise for pain and function, as well as moderate- to low-level evidence of a significant difference in pain and function between high-dose and low-dose eccentric training (19). There was high- to moderate-level evidence showing no difference in pain or function between orthoses and control (no orthoses or placebo therapy), low-level evidence showing no significant benefit of adding a night splint to an eccentric program for function, and moderate-level evidence showing no reduction in pain (19). Another 2019 meta-analysis concluded that heavy-eccentric calf training may be superior to traditional physical modalities yet inferior to other exercise interventions (18). A randomized controlled trial (RCT) demonstrated that allowing athletes to continue with running and jumping activities (producing up to a 5/10 pain on the visual analog scale [VAS]) during rehabilitation did not negatively affect patients' outcome compared with active rest and rehabilitation for midsubstance Achilles tendinopathy (20). There is a lack of new high-quality studies for insertional Achilles tendinopathy and exercise over the past decade. Eccentric programs adjusted to limit ankle range of motion to neutral remain the standard. Overall, rehabilitation remains the recommended first-line treatment, with no clear superiority of one protocol over another.
Heel lifts and physical modalities, including acupuncture, massage, low-level laser therapy, and US, are frequently used in combination with exercise rehabilitation. A 2021 parallel group randomized superiority trial compared a 12-mm heel lift to an eccentric exercise program and found heel lifts to be superior for pain and function at 12 wk. However, the difference in The Victorian Institute of Sports Assessment — Achilles Questionnaire (VISA-A) score between the groups was not considered clinically significant (21). Regarding acupuncture, evidence from one RCT with both insertional and midsubstance tendinopathy comparing acupuncture with eccentric exercise found a significant improvement in VISA-A score, but the study was limited by a small sample size as well as no comparison of acupuncture and exercise combined (22). Evidence on massage showed that it is a reasonable option in patients who cannot complete exercise protocols. However, research is limited especially for insertional AT, and there is no evidence of additive effect when combined with exercise (23). A 2020 systematic review and meta-analysis concluded that low-level laser therapy had low to very low certainty of evidence and insufficient to support its regular use for Achilles tendinopathy (24). Therapeutic US is commonly used by physical therapists. In theory, it is used to increase blood supply, leading to an increase in oxygenation which improves resistance to ischemia and promotes healing. However, the most recent studies lack patient-oriented outcomes. It has unclear efficacy to treat midsubstance tendinopathy but is low risk and seems reasonable to implement in a rehabilitation plan (25). Overall, these treatments have limited evidence of efficacy but are generally low risk and can be considered as adjuncts.
Medical management, most commonly topical nitroglycerin or non-steroidal anti-inflammatory drugs (NSAIDs), is often considered for the treatment of Achilles tendinopathy. Evidence for the efficacy of topical nitroglycerin has been conflicting for noninsertional AT, and very limited for insertional AT (13,26,27). It is a form of nitric oxide therapy, and therefore, it is important to understand the current literature on nitric oxide. Most recent research related to nitric oxide has focused on genetics. Specifically, the inducible nitric oxide synthase is responsible for nitric oxide generation, and a 2020 study demonstrated a genotype variant was protective, reducing the risk of Achilles tendinopathy (28). It is possible that different phenotypes of AT may respond differently to nitric oxide therapy, and more research is needed to identify its clinical applications. The limited data suggest improvements are unlikely prior to 12 wk (27,28). It is a reasonable noninterventional adjunct, as long as patients are counseled.
NSAIDs are frequently recommended by clinicians. However, a 2021 RCT found Naproxen 500 mg twice daily for 1 wk in the early stage of AT did not augment clinical improvement compared with placebo (29). In this study, both groups received an identical 12-wk rehabilitation protocol. Another study found that in vivo Achilles tendinopathic cells are largely unresponsive to ibuprofen treatment (1800 mg·d−1) (30). NSAIDs may be a consideration if pain responds with a brief trial, but the authors recommend the lowest dose and duration, with cessation if no improvement.
Topical capsaicin is frequently used as an adjunct treatment for pain, but there is a lack of studies to evaluate its efficacy for treatment of pain and dysfunction in Achilles tendinopathy.
Extracorporeal Shockwave Therapy
The mechanism of action of extracorporeal shockwave therapy (ESWT) in tendinopathy is still not fully understood. A recently proposed hypothesis states shockwaves may promote proinflammatory and catabolic processes leading to removal of damaged matrix, with concurrent promotion of anabolic repair processes (31). A 2019 systematic review reported results trended toward favorability for shockwave therapy for both midsubstance and insertional Achilles tendinopathy, but there was heterogeneity in study outcomes due to the complexity of Achilles dysfunction, differences in shockwave application, and objective outcome measures (32). Most studies used a 3-month duration of symptoms for inclusion cutoff. Both radial (energy dissipated over larger area) and focused (maximal energy at focal point) shock wave therapy studies were included. Three sessions spaced 1 wk apart was the most common protocol. ESWT performed better than control or sham therapies in the majority of studies. Combining an eccentric exercise program with ESWT seems more effective than exercise alone based on several RCTs, with one study's “completely recovered or much improved” rate increasing from 52% to 82% (32). ESWT was not found to be superior to other treatment modalities, including platelet-rich plasma (PRP), peritendinous hyaluronan injection, or high-volume image-guided injection (32). A 2020 double-blind randomized sham-controlled trial for insertional AT concluded a significant difference in VAS scoring at weeks 4 and 12 but not at week 24 (33). Overall, ESWT is safe with enough evidence to offer it as a minimally invasive second-line treatment option for both insertional and noninsertional Achilles tendinopathy.
While consensus is lacking, interventional procedures may be considered in cases that fail to achieve clinical goals after 3 to 6 months of conservative therapy. A number of these interventional options are discussed below.
Sclerosing treatments under US guidance for chronic tendinopathy have seen use for decades, with polidocanol being a more commonly selected agent. RCTs by Alredson and colleagues in the mid-2000s demonstrated that neovascularization-targeted polidocanol injections improved VAS scores at 3 months compared with lidocaine control and similar clinical outcome compared with surgically treated midsubstance Achilles tendinopathy (34,35). A small pilot study in 2003 included 11 patients with insertional tendinopathy who underwent sclerosing therapy with polidocanol showed improvement in VAS score at 8 months follow-up (36). A later study found no difference between 5 and 10 mg·mL−1 treatments (37). In a 2018 RCT, 48 patients with Achilles tendinopathy who failed 3 months of eccentric exercise were randomized to polidocanol or lidocaine injection (38). While no differences in walking VAS and VISA-A between the groups were found at 3 and 6 months, this study did not distinguish between insertional and midsubstance tendinopathy. While most trials showing benefit of sclerotherapy were performed in midsubstance Achilles tendinopathy, optimal patient selection for this procedure has not yet been clearly elucidated.
Hydrodissection Brisement, Mechanical Stripping, and Tendon Scraping
These are extratendinous procedures that aim to disrupt neovascularization and neoinnervation associated with tendinopathy. One such procedure is high-volume injection (HVI) or hydrodissection brisement. A 2017 RCT compared eccentric training with either HVI (50 mL mixture of bupivacaine, methylprednisolone, and normal saline), four PRP injections, or placebo injections (“a few drops” of subcutaneous saline away from the Achilles tendon). VISA-A score, VAS, tendon thickness, and neovascularity were found to be better in PRP and HVI groups than placebo at 6 wk, 12 wk, and 24 wk, with HVI performing better than PRP at 6 wk (39). A 2019 study comparing HVI plus eccentric therapy with and without steroid injection determined that the steroid group performed better at 6 wk and 12 wk, with no difference seen at 24 wk (40). However, a 2020 RCT compared a 50-mL HVI to 2-mL placebo injection and found no difference between the groups at any point from 2 wk to 24 wk (41). Maffulli and colleagues (42) used a minimally invasive tendon stripping technique to manage noninsertional Achilles tendinopathy and found significant improvements in the VISA-A scores. Afredson compared percutaneous needle with mini-open tendon scraping with a scalpel and showed improvement in VAS score in both groups without a significant difference in the two techniques (43). Ruergård et al. (44) retrospectively evaluated 136 midsubstance Achilles tendons after US and color Doppler-guided minimally invasive tendon scraping with and without plantaris tendon removal and found improved VAS scores, with 92% of patients reporting satisfaction and being back to full loading activities at follow-up. The authors pointed out that patients were able to load the tendon immediately posttreatment and participate in aggressive rehabilitation postprocedure compared with tenotomy or other surgical methods. While tendon brisement and scraping to treat midportion Achilles tendinopathy has been shown to be safe with promising results in decreasing pain and allowing patients to return to desired activities, there is a lack of studies for its use in treating insertional Achilles tendinopathy.
There are several studies assessing the efficacy of hyaluronic acid (HA) injection to treat midsubstance Achilles tendinopathy. A 2020 pilot study on a single, peritendinous HA injection for Achilles tendinopathy showed significant improvement in VAS at 2 wk and 12 wk (45). Another randomized controlled observer-blinded study compared two peritendinous HA injections spaced a week apart, to three shockwave therapy treatments, and found HA to be superior at 4 wk, 3 months, and 6 months using VISA-A scores (46). Another study used three peritendinous HA injections and found significant improvement in VAS as well as tendon thickness and tendinopathic site at 3 months (47). While high-quality evidence is lacking because of protocol variability, lack of control groups, and lack of blinding, HA is safe, and there is low-quality evidence to support its use.
There remains only one RCT in the literature looking at prolotherapy in Achilles tendinopathy. A 2011 BMJ study concluded that peritendinous hypertonic dextrose prolotherapy combined with eccentric exercise for midsubstance Achilles tendinopathy led to faster reduction in stiffness and activity restrictions, but the VISA-A scores at 12 months were not different (48). A 2018 meta-analysis, which did not separate midsubstance from insertional Achilles tendinopathy, concluded that prolotherapy is safe, well-tolerated and promising, but more research is needed to recommend it (49).
A 2020 meta-analysis of six studies reported promising findings for PRP injections, with 4 of 6 showing significant improvements in VISA-A of midsubstance Achilles tendinopathy (50). However, one included RCT did not show a difference between PRP and saline group at 3 months (50). A 2017 RCT compared eccentric training with injections of PRP, HVI, or placebo, and found that both HVI and PRP groups reduced pain significantly at 6 wk, 12 wk, and 24 wk (40,51). A 2020 study found factors such as age <40, males, less than 12 months of symptoms, body mass index <25, and adherence to eccentric training to be predictors of positive PRP outcomes in cases of midsubstance Achilles tendinopathy (52). A case series found no difference in VISA-A scores between groups treated with leukocyte-rich versus leukocyte-poor PRP for midsubstance Achilles tendinopathy (53). Insertional Achilles tendinopathy research is limited, however, with one retrospective study assessing two PRP injections showing a significant improvement in VISA-A at 2 months, 4 months, and 6 months (54). While the PRP literature still lacks an abundance of high-quality evidence, it has been found to be safe and is an appropriate consideration in cases that fail to improve with conservative management.
Adipose-Derived Mesenchymal Stem Cells
Adipose-derived mesenchymal stem cells (ADMSCs) are a multipotent subset of mesenchymal cells with several proposed mechanisms of action including cell differentiation, paracrine effects of secreted growth factors and cytokines, and immunomodulation leading to decreased inflammation (55). One study compared injection of PRP with adipose-derived stromal vascular fraction for midsubstance Achilles tendinopathy and found, after 6 months, that both groups improved VAS scores over baseline (56). Another similar RCT found the stromal vascular fraction within adipose tissue, compared with PRP, led to significant improvement in VISA-A scores at 15 d and 30 d for midsubstance Achilles tendinopathy (57). While studies on ADMSCs have shown promise, more research is needed to elucidate these therapies' optimal place in the clinician's therapeutic armamentarium.
Tenotomy with or without debridement may be done under US guidance percutaneously. Its rationale is to elicit a healing response in the degenerative tendon via microtrauma. Percutaneous tenotomy lends itself well to the outpatient setting and has seen increasing use because of its low complication rate and favorable tolerability. Chimenti and colleagues (58) retrospectively evaluated ultrasonic tenotomy with debridement of insertional Achilles tendinopathy in 34 patients (40 procedures), reporting decreased pain, improved quality of life, and low complication rates. However, the study was limited by incomplete baseline data and limited long-term follow-up in more than a third of the patients (58). While tenotomy is safe, well-tolerated, and promising, more research is needed to elucidate optimal methods and whether or not tenotomy with debridement has better outcomes than without debridement.
Operative treatment may be considered for refractory cases of Achilles tendinopathy that have failed to improve after 6 months of conservative management. Common techniques include open, mini-open, endoscopically assisted tenotomy and debridement, tendon scraping, percutaneous tendon stripping, peritenolysis, partial gastrocnemius resection, flexor hallucis longus tendon transfer, flexor digitorum tendon transfer, and soleus fibers transfer. These operative techniques are beyond the scope of this article and discussed in further detail elsewhere.
Achilles tendinopathy is a complex and common ailment that may present with pain, swelling, and impaired function. Primary management goals are to alleviate pain, improve strength, and regain range of motion to resume daily activities or performance in a high-functioning athlete. There is no single, definitively effective treatment at this time, but expert consensus favors a trial of conservative treatment for most cases of chronic Achilles tendinopathy, including stretching, strengthening, and medications. Minimally invasive procedures have been used more frequently in recent years and show promising results. These include sclerotherapy, percutaneous tendon hydrodissection brisement and scraping, and tenotomy. New advancements in biologic therapies, including PRP and ADMSC bring in exciting adjuvant therapies for recalcitrant cases, but evidence on their effectiveness is lacking, with PRP having the most promising results in select patients.
The authors declare no conflict of interest and do not have any financial disclosures.
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