You are in: eMedicine Specialties > Orthopedic Surgery > FOOT AND ANKLE Achilles Tendon PathologyArticle Last Updated: Aug 10, 2005AUTHOR AND EDITOR INFORMATIONSection 1 of 9
  Author: Richard Hargrove, MBBS, FRCS(Ire), Orthopedic Specialist Registrar, Department of Trauma, St Georges University Teaching Hospital, London, UK Richard Hargrove is a member of the following medical societies: Royal College of Surgeons of England and Royal Society of Medicine Coauthor(s): Chris McLean, MBBS, MRCS(Glasg), AFRCS(Ire), Specialist Registrar, Departments of Orthopedic and Trauma Surgery, Frimley Park Hospital, UK; Edward Behn, MBBS, MRCS Editors: James K DeOrio, MD, Director of Foot and Ankle Fellowship Program, Assistant Professor of Orthopedic Surgery, Orthopedic Surgery, St. Luke's Hospital, Jacksonville, Florida; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Shepard R Hurwitz, MD, Executive Director Designate, American Board of Orthopaedic Surgery; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of Orthopedic Surgery, University of Missouri Author and Editor Disclosure Synonyms and related keywords: Achilles' tendon, Achilles tendinosis, peritenonitis, peritendinitis, tendinitis, tendinosis, tendinopathy, paratendinopathy, pantendinopathy, intratendinous inflammation, paratenon inflammation ACHILLES TENDON PATHOLOGYSection 2 of 9
  The Achilles tendon is the largest tendon in the body. It must withstand great forces, especially during sporting exercises and pivoting. Pathology of the Achilles tendon is not well understood. Treatments can vary widely and are occasionally controversial, especially in relation to tendon rupture. Choices include a conservative approach versus open, mini-open, or percutaneous repair. This article highlights some of the basic aspects of tendon pathology, especially in regard to tendinosis and tendon failure. Part of the problem in defining Achilles tendon pathology is the confusing nomenclature, with authors using different words to describe the same pathology or using the same words to describe different aspects of the problem. The terms peritenonitis, peritendinitis, tendinitis, tendinosis, and tendinopathy are all interlinked in the literature. Most experts in the field now use the terminology suggested by Puddu et al (Puddu, 1976; Maffulli, 1998 Nov-Dec). Those authors believe that tendonitis is a misleading term that should no longer be used because signs of true inflammation are almost never present on histologic examination. Instead, the term tendinosis should be used to describe tendon degeneration without clinical or histologic signs of intratendinous inflammation. They also describe the use of the terms tendinopathy, paratendinopathy, and pantendinopathy. For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center. Also, see eMedicine's patient education articles Tendinitis, Ruptured Tendon, and Achilles Tendon Rupture. MACROSCOPIC ANATOMY AND BLOOD SUPPLYSection 3 of 9
The two muscle bellies of the gastrocnemius muscle join the deeper soleus muscle in an aponeurosis roughly 12-15 cm from the insertion of the tendon into the os calcis, although the soleus can remain independent until insertion. The length of the tendon is variable, and the tendon spirals about 90° prior to its insertion, with most of the rotation occurring in the last 5-6 cm (Schepsis, 2002). The rotation is thought to aid in elastic recoil of the tendon (Palalastanga, 1989). The tendon inserts into the posterior-superior aspect of the calcaneal tuberosity with the bursa lying anteriorly. Running concurrently with the tendon is the plantaris, which crosses the soleus to run medial to the Achilles tendon and which also inserts into the calcaneus. Like the palmaris longus in the forearm, it is absent in about 7-10% of individuals. The tendon is covered by a paratenon. This is a double-layered sheath of synovial cells. The inner layer is in contact with the tendon itself, and the outer layer is continuous with the subcutaneous tissue and ventral mesotendon and its rich blood supply. The paratenon can become inflamed and enlarged, usually in runners, with acute crepitus felt over the fusiform swelling, which can originate from the paratenon or the tendon itself. Just anterior to the Achilles tendon lies the retrocalcaneal bursa. This can become inflamed, leading to pain anterior to the tendon, especially on dorsiflexion of the foot. It is important to differentiate this type of pain from paratenon inflammation or tendinosis. An enlarged bony prominence at the posterosuperolateral aspect of the calcaneus, called the Haglund process, may be associated with retrocalcaneal bursitis but also with insertional tendinitis as well. This is a reason why plain radiography still has value in diagnosis and management. The blood supply to the Achilles tendon is derived mainly from vessels traversing the mesotendon. The main blood supply is derived from the vincula, both long and short, via the paratenon and especially from the ventral mesotendon. Small longitudinal supplies from the muscle bellies and the distal insertion are also present. However, blood supply is also directly derived from the muscle bellies themselves and distally from bone where the tendon inserts into the calcaneus. Microvascular Doppler flow studies have shown that flow is evenly distributed throughout the tendon, but it is less at the insertion (Astrom, 1994). Studies have also demonstrated that individuals with tendinosis have higher resting blood flow rates than in healthy control subjects (Astrom, 1994 Mar). Cadaveric studies have shown a relative decrease in both the frequency and the total area of vessels in the mid portion of the Achilles tendon (Carr, 1989). More recent dynamic studies have refuted the once-popular historical theory that the pathology is mainly related to a hypovascular zone at the mid tendon. However, the relative lack of blood vessels in the area that usually ruptures has led to the term watershed area, which is still used today. As discussed below, the blood supply is a factor in Achilles tendinosis, but whether it is causative or reactive is still under debate. ETIOLOGY OF ACHILLES TENDINOPATHYSection 4 of 9
The incidence of Achilles tendinopathy is rising, both in terms of tendinosis and acute ruptures. An estimated 10% of Americans are involved in some form of recreational running or other jumping or pivoting activities and often for longer periods than in previous generations. No data describe the incidence or prevalence of Achilles tendinopathy, but it is known to affect 7-18% of club runners. Excessive repetitive strain of the tendon is thought to be a major influence in the etiology of tendinopathy (Kvist, 1994). Komi has recorded forces of up to 4000 N passing through the Achilles tendon when a person is running on his or her toes (Komi, 1987). The tendon can be subjected to 8-10 times a person's body weight during strenuous exercise. Traditionally, tendinosis is thought to occur with overuse, causing microtrauma at a degree and frequency at which the tendon can no longer heal itself. This situation leads to mechanical breakdown of the tendon (Almekinders, 2003). Several authors have studied factors that may influence the development of tendinosis, such as training mileage, rest periods for military recruits between runs, anatomic alignments of the lower limb, and mechanical factors related to shoes and inserts. As yet, no clear-cut evidence has been found. Further confusion arises because tendinopathy also can occur in relatively inactive individuals (Astrom, 1998). Evidence suggests that tendon problems are more common in the older sportsman than in the younger sports participant (Kannus, 1989). Those who have had an Achilles rupture are also more likely than others to have tendinopathy and repeat rupture on the contralateral side (Aroen, 2004). Although a link between smoking and biceps tendon rupture has been proven, no association between smoking and Achilles tendinosis or rupture is reported in the literature. At this time, the exact etiology of Achilles tendinopathy seems multifactorial, complicated, and incompletely understood. PATHOLOGYSection 5 of 9
Microscopic pathology Adult tendons are composed of large-diameter type I collagen fibrils. These are 150 nm in diameter, tightly packed with type III collagen, and dispersed in an aqueous gel containing proteoglycan and elastic fibers (Harries, 1998). The actin and myosin bundles are arranged helically. In healthy tendons, 95% of the collagen is type I (Maffulli, 2000 Jul-Aug). Degenerate tendons have less type I collagen and significantly more type III collagen. The same changes are also seen during the natural aging process, although to a lesser extent. This may be why the tendon is less elastic in older individuals and more prone to rupture (Jozsa, 1984). Type III collagen seems to be the major collagen synthesized in the healing tendon after injury. This observation again suggests that the tendon degeneration in tendinosis is an incomplete repair process. Animal testing has shown that tendons can stretch by 4% of their original length before damage occurs. If stretched more than 8%, rupture is likely (Whittaker, 1991). Systemic pathology affecting the Achilles tendon A number of systemic or external factors appear to be linked to tendon degeneration and rupture. As has been mentioned, age is a factor. Other factors that affect the Achilles tendon include the following:
Intrinsic pathology of tendinosis Histologic changes in the Achilles tendon include changes to the extracellular and intracellular matrices. These include collagen degeneration, fiber disorientation, and increased mucoid ground substance, but no increase in inflammatory cells occurs. Focal hypercellularity and vascular proliferation are usually present. The number and morphologic variations of tenocytes increases (Kannus, 1991). Also increased is the number of apoptotic (dead) cells, both in the degenerate and in the ruptured tendon (Yuan, 2003). The proportion of type III collagen is also increased in the degenerate tendon. Pathologically, Achilles degeneration has been described as lipoid or mucoid (Jozsa, 1997). In mucoid degeneration, the tendon becomes more brown or gray, with mucoid patches and vacuoles. Lipoid degeneration involves increased lipid content in the tendon tissue (Maffulli, 2000 Nov-Dec). Other studies have shown an increase of type I and type III collagen mRNA. Also, glutamate concentrations increase in the painful degenerate tendon (Kader, 2002). Neovascularization is often a feature of the degenerate tendon. It is associated with painful tendinosis (Zanetti, 2003). Eccentric training leading to good clinical results is associated with a reduction and/or absence of neovascularization, and conversely, poor results are associated with continuing neovascularization (Ohberg, 2004 Apr; Alfredson, 2003). Tendon rupture is almost always the terminal event in the ongoing degenerative process of the tendon, as confirmed in histologic studies of ruptured tendons (Cetti, 2003). IMAGINGSection 6 of 9
The medical world relies increasingly on imaging. It is good practice to examine the entire lower extremity prior to further investigative studies. A good history and examination enables correct diagnosis in most cases, and imaging can be used to confirm the diagnosis. The choice of image is really between MRI and ultrasonography to look at the tendon. Also recommended is plain radiography in cases of tendinosis to look for a Haglund process. However, remember that, in some cases, a patient can have severe symptoms and signs of tendinosis with normal or near-normal findings sonographically. CONSERVATIVE TREATMENT OPTIONS FOR TENDINOSISSection 7 of 9
Many techniques have been used to treat Achilles tendinosis nonoperatively, but the scientific evidence for most of these approaches is limited. The Cochrane review for Achilles tendinitis (McLaughian, 2004) sampled all reports in 1966-2000 and found only 9 trials (which included 697 patients) that satisfied their criteria. The conclusion was that some evidence supported a role for oral nonsteroidal anti-inflammatory drugs (NSAIDs). Evidence for the role of heel pads, heparin injection, and peritendinous steroid injections was weak, and data on the role of glycosaminoglycan sulfate versus NSAIDs were insufficient. Further research is needed. Ultrasonographic therapy Results of laboratory studies in rats suggest that ultrasonography increases the healing rate in ruptured tendon (Ng, 2003). However, little evidence of this effect in humans in the clinical setting exists. Yet ultrasonography does appear to have a short-term pain-relieving effect on the tendon. Eccentric training Eccentrically loading the Achilles tendon has been a mainstay of treatment in the past. It probably stimulates collagen growth by means of physiologic feedback loading (Niesen-Vertommen, 1992; Curwin, 1984). More recently, eccentric training has been associated with reduction in tendon thickness, decreased pain, and restoration of normal tendon architecture (Ohberg, 2004 Feb). Heavy-load eccentric training has had excellent results in acute phase tendinosis, but trials included only small numbers of patients (Alfredson, 1998). Investigators have evaluated the close correlation between good clinical results with eccentric training and a marked reduction in neovascularization of the tendon (Ohberg, 2004 Apr). Steroid injections Steroid injections are still controversial. They can certainly provide short-term relief of painful symptoms; however, whether steroids should still be used as part of the tendinosis treatment regimen is open to debate (Shrier, 1996). Astrom found that corticosteroid injection was the only predictor of partial tendon tears in a large series of chronic Achilles tendinoses that eventually required surgery (Astrom, 1998). A comparative review of NSAIDs and corticosteroids showed little evidence that either were effective in tendinopathy (Almekinders, 1998). NSAID therapy Logic dictates that anti-inflammatories should not help because tendinosis is not an inflammatory process. Indeed, studies have shown no clinical benefit of NSAIDs (Astrom, 1992). However, they do appear to have some effect, and most physicians use NSAIDs in nonoperative treatment regimens. This practice persists because NSAIDs enable the patient to ignore mild symptoms (Almekinders, 1993). Results of laboratory studies have suggested alternate roles for the NSAID effect, wherein tendon healing is improved (Forslund, 2003). Findings from other studies have suggested a reduction in the neutrophil and macrophage count within the tendon; however, these counts are known to be limited in true tendinosis anyway (Marsolais, 2003). Sclerosis of vessels A small study has shown improvement in symptoms after the injection of a sclerosing agent (polidocanol) in painful Achilles tendinosis. The assumption is that the sclerosant reduces neovascularization and, therefore, pain. In this study of only 10 patients monitored for 6 months, 8 had a reduction of symptoms (Ohberg, 2002). Platelet injections Laboratory studies have shown that the injection of platelets in rats improves tendon healing (Aspenberg, 2004). Friction massage Sparse clinical evidence supports the use of deep friction massage. A Cochrane review in 2002 showed no obvious benefit, although the reviewers were not evaluating Achilles tendons in particular (Brosseau, 2002). In laboratory experiments, friction massage was associated with increased cellular growth in rat tendons (Davidson, 1997). Actovigen therapy In 1994, Pforringer compared subcutaneous injections of actovigen (an enzyme) and compared it placebo. The treatment significantly reduced pain, but the patients were monitored for only 3 weeks (McLaughian, 2004). Other treatments Other treatments include the use of heat, cold, and heel risers. All of these anecdotally improve symptoms of Achilles tendinosis and are commonly used in the clinical setting. However, good quality evidence of their benefit from randomized prospective trials is sparse. Future treatments As research on the efficacy of current treatments continues, newer approaches are being developed. Examples include gene therapy with the direct or indirect transfer of genes for platelet-derived growth factor (PDGF) and/or other growth factors that modulate responses to healing and promote type I collagen growth in the tendon (Maffulli, 2002). TREATMENTSection 8 of 9
Treatment for Achilles rupture Little scientific evidence from prospective randomized controlled trials is available for a comparison of the different treatments. Basic variations include conservative treatment such as cast application, use of a range-of-motion [ROM] walker, relatively early mobilization, and late mobilization, among others. Surgical options include open repair, mini-open techniques, and percutaneous repairs; some of these are done with local anesthesia. Methods of rehabilitation also vary. Surgical treatment for tendinosis The long-term outcome of tendinosis is not understood. General orthopedic clinics do not serve a population predominantly of 60-year-old patients with long histories of tendinosis. Conversely, most individuals with Achilles tendon ruptures have had some degree of pain, and probably tendinopathy, prior to the rupture. Therefore, the natural history remains unclear. Paavola et al monitored more than 83 patients who were treated with conservative therapies initially. They found that 29% underwent surgery during the 8- to 10-year follow-up period (Paavola, 2000 Sep-Oct). Once all of the nonoperative treatment modalities have failed, surgical options must be considered. Leading authors have offered various recommendations. For example, Maffulli recommends an open procedure with up to 5 longitudinal tenotomies and the removal of the abnormal tissue (Maffulli, 1998 Mar-Apr). He has also advocated a purely percutaneous approach to create a 3- to 4-cm area of tenolysis to aid repair (Maffulli, 1997; Testa, 2002). Most authors advocate sharply dissecting the area to the paratenon, freeing any adhesions, exploring the tendon, and excising any necrotic areas. The reported surgical success rates in surgery are 75-100% (Paavola, 2002). However, in an excellent critical review of papers that reported outcomes in chronic tendinopathy, Tallon et al (Tallon, 2001) found a direct inverse correlation between poor study method and the reported success rates. That is, the use of less-stringent guidelines and definitions led to better results. They also found a potential correlation between the year of publication and any improvement in the surgical results. More complex surgical problems, such as concurrent partial rupture of the tendon, may require the use of synthetic allografts or autografts from the flexor hallucis longus, semitendinosus, or gracilis muscle. In a study of more than 430 patients treated surgically, the complication rate was 11%, and one half of the complications were wound-healing problems (Paavola, 2000 Jan-Feb). Rates of surgical rehabilitation also vary greatly, with immobilization times ranging from only 2 weeks to longer than 8 weeks; approaches also ranged from the use of ROM boots or braces to full casting. To the authors' knowledge, no prospective randomized trial has been conducted to compare conservative management versus surgical treatment. Summary The etiology and pathology of Achilles tendinosis is significantly better understood today than even a decade ago. Increasing awareness of the problem, along with new approaches and surgical techniques, hopefully will improve diagnosis and treatment. Because of the relatively poor outcome of the chronic condition, the sports medicine community must standardize outcome measures used to evaluate Achilles pathology so that the success of all the excellent work being done on this painful condition can be clarified. REFERENCESSection 9 of 9
Achilles Tendon Pathology excerpt Article Last Updated: Aug 10, 2005 |
