Generalities of Insertional Tendinopathy 12

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the three-dimensional (3D) shape and position of three fi brocartilages (sesamoid, periosteal, and enthesis) associated with its insertion.¹⁰ A close correspondence between the shape and position of the sesamoid and periosteal fi brocartilages was found. The sesamoid protects the tendon from compression during dorsifl exion of the foot, and the periosteal fi brocartilage protects the superior tuberosity of the calcaneus. The 3D reconstructions of the zone of calcifi ed enthesis, fi brocartilage, and the subchondral bone showed complex interlocking between calcifi ed fi brocartilage and bone at the insertion site.¹⁰

Histopathology

Light and electronic microscopy and enzyme his- tochemistry have been used to study a series of 11 insertional tendinopathy (including two Achilles tendons) specimens.¹¹ The pathological changes of insertional tendinopathy consisted of edema, mucoid degeneration, disruption of collagen bundles, necroses, small hemorrhages, and calci- ﬁ cation. Acid mucopolysaccharides may be present in lake-like accumulations between collagen ﬁ bers, in contrast to neutral collagens seen in aging. Small bony particles lay within the cartilaginous portion of the insertion. Also, there were areas with proliferating blood vessels within tendon tissue with lymphocytes and histiocytes, suggesting a reparative process. There was increased activity of NADP-diaphorase, LDH, β- glucuronidase, and alkaline phosphatase (lower activity of the latter two enzymes) in these tendon Common causes of posterior heel pain are inser-

tional tendinopathy of the Achilles tendon, retrocalcaneal bursitis, Haglund’s deformity, or pretendon bursitis. Insertional tendinopathy of the Achilles tendon, retrocalcaneal bursitis, and Haglund’s deformity, the prominent posterosuperior calcaneal process, constitute the Haglund’s triad. Clain et al.¹ introduced the terms insertional and noninsertional Achilles tendinopathy with a view to better plan management. Insertional tendinopathy had a prevalence of 20% in a surgical and histopathological survey of 163 patients with chronic Achilles tendinopathy.² In a consecutive series of 432 chronic Achilles overuse injury patients in Finland, 107 (24.7%) had insertional Achilles pathology. Of these, 5% (21 patients) had pure insertional tendinopathy, and 20% (86 patients) had calcaneal bursitis alone or in com- bination with insertional tendinopathy.³

The incidence of Achilles insertional tendinopathy is unclear. It is reported as the most common form of Achilles tendinopathy in athletes present- ing to outpatient clinics.⁴ However there are reports that 5% to 20% of Achilles tendinopathy is of the insertional variety.^5,6 Insertional tendinopathy is often diagnosed in older, less athletic, and overweight individuals as well as in older athletes.^7–9

Histology

The osteotendinous junction of the Achilles con- sists of tendon, ﬁ brocartilage, and bone. The dis- tribution of type II collagen in sagittal sections of the Achilles tendon has been used to reconstruct

Generalities of Insertional Tendinopathy

Jonathan S. Young, Murali K. Sayana, and Nicola Maffulli

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samples. Electron microscopy showed marked submicroscopic calciﬁ cation and ﬁ brillar degeneration.

Recent work by Maffulli et al. (unpublished data) has shown increased levels of type II and III collagen and decreased levels of type I collagen present in calciﬁ c insertional tendinopathy. Peri- odic acid Schiff staining showed the constant presence of chondroitin sulphate, suggesting a metaplastic change of the distal portion of the Achilles tendon in calciﬁ c insertional tendinopathy.

Etiopathophysiology

Classically, overuse and poor training habits are considered the main etiological factors of Achilles insertional tendinopathy. Also, a tight Achilles tendon, hyperpronation, pes cavus, and obesity can predispose to degeneration, attrition, mechanical abrasion, and chemical irritation that could lead to chronic inﬂ ammatory response.⁷

The in vitro strain behavior of the anterior portion of the Achilles tendon and how it is affected by the insertional tendinopathy has been investigated.¹² This suggested a role for repetitive tensile loads in the causation of insertional tendinopathy of the Achilles tendon, due to relative strain shielding noticed in this portion of the tendon. The variable response following measures aimed at decreasing tensile loads on the tendon may be explained by these ﬁ ndings.

The spur formation and calcifi cation at the Achilles tendon insertion is attributed to gradual repetitive traction force. Benjamin et al.¹³ investigated enthesophyte formation in rats, and compared it with human specimens. Bony spurs can develop in the Achilles tendon without the need for preceding microtears or infl ammatory reac- tions, and form by endochondral ossifi cation of enthesis fi brocartilage. The increased surface area at the tendon–bone junction may be an adaptive mechanism to ensure the integrity of the interface in response to increased mechanical loads.¹³

Alternative Biomechanical Theories in Insertional Tendinopathy

The traditional view of a tendon overuse injury as a result of tensile overload appears plausible.

However, although this view is widely accepted, without a prospective design and adequate control groups, any conclusion regarding the etiologic role of factors such as training errors, poor tech- nique, inadequate equipment, inﬂ exibility, and muscle imbalance remains speculative. Only a few studies have attempted to examine these factors in a controlled, prospective manner and these have shown conﬂ icting results.^14–20

Epidemiological studies have also made some interesting observations. For example, overuse injuries, including tendon problems, are signiﬁ - cantly more common in elderly athletes compared with young athletes.^21,22

Biomechanical studies on failure modes of muscle–tendon units have clearly shown that failure will occur within the muscle near the muscle–tendon junction,^23,24 not in the tendon.

Although these load-to-failure studies do not investigate repetitive submaximal loads, they do point out how a healthy tendon is biomechanically

“overengineered” compared with its attached muscle. In insertional tendinopathy, the pathological tendon lesion lies at or very close to the insertion site of the tendon, the enthesis. Insertional Achilles tendinopathy is generally found at the calcaneal side.²⁵ Thus, the pathology is predominantly found at the joint-side of the enthesis.

The enthesis transfers the mechanical tensile loads generated by the muscle–tendon unit onto the bone through a thick tendon, which inserts at a varying oblique angle depending on the position of the joint. The architecture of these tendon insertion sites is complex, with a cartilaginous transition zone most pronounced on the joint side of the tendon.²⁶ Recent work on the increase of proteoglycans within the posterior tibialis tendon indicates that cartilaginous metaplasia can occur as an adaptive response to mechanical compression on the tendon.²⁷ These histological ﬁ ndings question whether the tendon insertion site is uni- formly subjected to tensile loads. This has led to various biomechanical studies on the strains near the tendon insertion sites.

In a study on the Achilles tendon insertion site,²⁸ the tendon was instrumented with strain gauges just proximal to the calcaneus. Again, the lowest strains were found on the calcaneal side, where the pathological changes of Achilles insertional tendinopathy are generally found.

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Although not all biomechanical studies report the same results, a consistent pattern appears to emerge: the strains within the tendons near their insertion site are not uniform. If we assume that the material properties are similar throughout the tendon, this would mean that any muscle force transferred through the insertion site preferen- tially loads the side of the tendon that is usually not affected initially in tendinopathy. In that case, the side affected by tendinopathy is generally

“stress shielded.” Thus, the presence of differen- tial strains opens the possibility of alternative biomechanical explanations for the pathology found in these regions of the tendon. The traditional concept of tensile failure may not be the essential feature of the pathomechanics.

The recent biomechanical data reported above suggest a different biomechanical etiology of insertional tendinopathy. The stress-shielded side of the enthesis shows a distinct tendency to develop cartilage-like and/or atrophic changes in response to the lack of tensile load.^25–27 Over long periods, this process may induce a primary degenerative lesion in that area of the tendon. This may explain why the tendinopathy is not always clearly activity related, but is sometimes more strongly correlated with age. In this manner, tendinopathy would result from stress shielding rather than increased, overuse injury.²⁹

The cartilage-like changes in the enthesis in many ways can be considered a physiologic adap- tation to the compressive loads. However, even cartilaginous metaplasia may not allow the tendon to maintain its ability to withstand the high tensile loads in that region. It seems possible that in athletes occasionally certain joint positions will still place high tensile loads on the enthesis. As the stress shielding may have led to tensile weakening over time, an “injury” may occur more easily in this region. In this manner, insertional tendinopathy could be considered an overuse injury, but predisposed by preexisting weakening of the tendon.²⁹

Finally, as the joint changes position, strains in one section of the tendon could be changing in opposite directions. Internal shear forces and heat could be generated, producing injury to the cellular and/or matrix components of the tendon. Accu- mulation of these injuries could lead to the intra- tendinous degeneration seen in tendinopathy.²⁹

Presentation and Diagnosis of Insertional Tendinopathy

The symptoms of insertional Achilles tendinopathy are speciﬁ c, and are related to pain at the bone–tendon junction, frequently worse after exercise, but which ultimately become constant.

Although this is a fairly common ﬁ nding in athletes, other conditions and medications that cause pain in the posterior aspect of the heel should be considered, including the various causes of insertional enthesopathy, seronegative spondyloar- thropathies, gout, systemic corticosteroids, orally administered ﬂ uoroquinolones, familial hyperlip- idemia, sarcoidosis, and diffuse idiopathic skeletal hyperostosis.⁷ Insertional Achilles tendinopathy can be aggravated by running uphill or by activities performed on a hard surface. Frequently, the patient reports a history of poor stretching, of running on the heels or over an excessive distance, or a sudden increase in training intensity.

Examination reveals tenderness at the Achilles tendon insertion, thickening or nodularity of the insertion, and at times limited, painful dorsifl exion of the ankle. Swelling may be present if there is accompanying retrocalcaneal bursitis.³⁰ The tenderness is specifi cally located either directly posterior or posterolateral to the insertion of the Achilles tendon. Dorsifl exion is limited compared with that of the uninvolved ankle because of the relative tightness of the triceps surae. Pain in the heel is the cardinal symptom, and it is increased by prolonged standing, walking, running uphill, or running on a hard surface.⁷

The pain generally emanates from the posterior aspect of the heel and is aggravated by active or passive motion. Haglund’s deformity can lead to a prominent posterosuperior tuberosity of the calcaneum, although Haglund’s triad is more common than isolated insertional tendinopathy of the Achilles tendon. Radiographs help demon- strate Haglund’s deformity. The ossiﬁ cation is in the most proximal extent of the insertion of the tendon or as a spur off the superior portion of the calcaneus.⁷ The size of the osteophyte cannot be accurately determined on radiographs because the structure has a very broad surface that extends across the central half of the insertion of the tendon. Although radiographically the osteophyte

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appears to be located in the tendon that envelops it, the tendon is not actually attached to the spur, and the insertion of the tendon is continu- ous with the posterior wall of the calcaneus. Sec- ondary imaging studies, such as magnetic resonance imaging and ultrasonography, are not necessary to make the diagnosis or to plan treatment. Rarely, magnetic resonance imaging may be helpful if there is extensive degeneration because the extent of the degeneration may have some bearing on the choice of the reconstructive procedure.⁷

Management

Most patients can be successfully managed non- operatively.^1,31,32 The various nonoperative modalities produce an 85% to 95% success rate.^7,33 Even the more active or competitive athletes should persevere with nonoperative management.⁷ Mod- ifi cations in training and the use of ice, nonsteroidal anti-infl ammatory medication, and heel-lifts in conjunction with stretching and strengthening exercises can be effective for athletes. Nonsteroi- dal anti-infl ammatory medications may only provide analgesia.³⁴ Piroxicam showed no benefi t over placebo in a randomized controlled trial when combined with an initial period of rest fol- lowed by stretching and strengthening exercises.³⁵ Diclofenac reduced the accumulation of infl ammatory cells only within the paratenon, but pro- vided no biochemical, mechanical, or functional benefi ts to the rat Achilles tendon following injury when compared with a placebo group.

Also, there was no reduction in the accumulation of neutrophils and macrophages in the core of the tendon.³⁶

Other simple measures, such as widening or deepening the heel-counter of the shoe or distri- bution of pressure with use of a silicone sleeve or pad, may also be effective for active or athletic patients. Various pads should be used to take pressure off the insertion of the Achilles tendon.

A quarter-inch to half-inch (0.64- to 1.3-centime- ter) felt heel-lift can be incorporated inside the shoe, although this tends to lift the heel out of the shoe. When this happens, a heel-wedge is added to the sole of the running shoe. A horseshoe- shaped felt pad is most effective and may be

applied to either the shoe or the posterior aspect of the heel. If these modalities are not effective, more intensive stretching of the Achilles tendon should be performed with use of a night splint to hold the foot in maximum dorsifl exion. However, eccentric calf muscle training helped only 32% of patients with insertional tendinopathy, compared with 89% of patients with noninsertional tendinopathy of Achilles tendon.³⁷ If the condition is refractory, some authors suggest immobilizing the leg in a below-knee weight-bearing walking cast or a walker boot for six weeks.^7,38 This can be counterproductive; tendon loading stimulates collagen fi ber repair and remodeling. Therefore, complete rest of the injured tendon is not advis- able.³⁰ After a short period of rest from formal exercise, activities are gradually resumed with incorporation of a good fl exibility program that includes correction of any biomechanical abnor- malities. Cross-training may be useful after the acute phase subsides. The introduction of non- loading-type activities, such as swimming, bicy- cling, and aqua jogging, or open-chain kinetic-type weight-lifting exercises to the management program permits the athlete to stay conditioned.

An added advantage is better compliance on the part of the athlete because he or she has a training alternative.⁷ Ice, compression, and elevation, as well as nonsteroidal anti-infl ammatory medication for a short period, may be helpful in the early phases of the condition. Physical therapy focuses on fl exibility of the hamstrings and the gastrocne- mius-soleus complex as well as the use of modalities such as ultrasound and contrast baths to help to control pain and infl ammation at the site of the insertion. Ultimately, when activity (particularly running) is resumed, the distance should be decreased compared with that before the injury, and the running surface should be soft. Occasion- ally, a biomechanical abnormality, such as hyperpronation, is identifi ed. A semirigid orthosis can help to control such a problem. Slight undercor- rection of a pronated foot with use of an orthosis is better tolerated by runners than is complete correction and overcorrection is frequently intol- erable. Again, the injection of corticosteroids is contraindicated.⁷ In a pilot study,³⁹ polidocanol (a sclerosing agent) was injected into local neoves- sels localized by ultrasound and color Doppler.

Eight of 11 patients experienced good pain relief,

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and seven of them had no neovascularization at a mean follow-up of eight months. Two of the three patients who had poor results had bony spurs.

Therefore, it appears that patients with severe bone pathology and mechanical problems are less suitable for sclerosing therapy.⁴⁰

Surgery

Only when conservative management is exhausted is surgery undertaken. The principles of surgery include debridement of the calciﬁ c or diseased portion of the Achilles insertion, excision of the retrocalcaneal bursa, and resection of the Haglund’s deformity. Sayana and Maffulli³⁰ prefer to reattach the Achilles tendon using bone anchors if one-third or more of the insertion is disinserted.

Augmentation using tendon transfer is also described.

Anderson et al.⁴¹ studied the surgical management of chronic Achilles tendinopathy in 48 patients. Twenty-eight patients (58%) underwent surgery for Achilles insertional tendinopathy with tenolysis, excision of the bursa and/or excision of the posterosuperior portion of the calcaneum through a 10-cm medial incision. The recovery in these patients was longer (31 weeks) when compared with patients with tendinopathy of the main body of the Achilles tendon who underwent tenolysis only (22 weeks). The success rate was 93%.

Calder et al.⁴² reported the results in patients who had less than 50% of the tendon excised (49 heels), and whose ankles had been immediately mobilized free of a cast. There were two failures using this regimen: one patient with psoriatic arthropathy and another who underwent bilateral simultaneous procedures.

Kolodziej et al.⁴³ reported a biomechanical study that concluded that superior-to-inferior resection offers the greatest margin of safety when performing partial resections of the Achilles insertion, and as much as 50% of the tendon may be resected safely.

McGarvey et al.⁴⁴ reported on 22 heels that had surgery using a midline-posterior skin incision combined with a central tendon splitting approach for debridement, retrocalcaneal bursectomy, and

removal of the calcaneal bursa projection as necessary. Twenty of 22 patients were able to return to work or routine activities by three months.

Only 13 of 22 were completely pain free and were able to return to unlimited activities. Overall, there was an 82% (18 of 22) satisfaction rate with surgery.

Watson et al.⁴⁵ reported that retrocalcaneal decompression in patients with insertional Achil- les tendinopathy with calciﬁ c spur was less satisfactory when compared with retrocalcaneal decompression in patients with retrocalcaneal bursitis.

Den Hartog et al.⁴⁶ reported successful use of fl exor hallucis longus transfer for severe calcifi c Achilles tendinopathy in 26 patients (29 tendons) in whom conservative treatment failed and who also had failed tendon debridement and/or Haglund’s resection. These patients were seden- tary, overweight, and had chronic symptoms. The AOFAS ankle-hindfoot scale improved from 41.7 to 90.1. The time to maximum recovery was approximately 6 months. All patients lost fl exor strength at the interphalangeal joint of the great toe.

Leitze et al.⁴⁷ recently reported decompression of the retrocalcaneal space using minimally inva- sive techniques. Patients with retrocalcaneal bursitis, mechanical impingement, and/or Achilles insertional tendinopathy who failed to respond to conservative management had an endoscopic decompression performed. However, major cal- ciﬁ c insertional tendinopathy of Achilles tendon was considered a contraindication for endoscopic decompression. The advantages of the endoscopic procedure included quicker surgery and fewer complications, although the recovery time was similar to open decompression.

Maffulli et al.⁴⁸ reported a series of 21 patients with recalcitrant calcifi c insertional Achilles tendinopathy who underwent bursectomy, excision of the distal paratenon, disinsertion of the tendon, removal of the calcifi c deposit, and reinsertion of the Achilles tendon with bone anchors. The outcome of surgical management was rated according to Testa et al., using the 4-point functional scale validated for evaluation of long-term results following surgery for tendinopathy. Eleven patients reported an excellent result and fi ve a good result. The remaining fi ve patients could not

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return to their normal levels of sporting activity and kept ﬁ t by alternative means.⁴⁸

Conclusions

Much progress has occurred in our understand- ing of Achilles insertional tendinopathy since Clain and Baxter classifi ed Achilles tendon disorders into noninsertional and insertional tendinopathy in 1992.¹ Insertional tendinopathy of the Achilles tendon is a degenerative rather than an infl ammatory condition, although the accompanying bursitis may paint an infl ammatory picture.

The etiology of tendinopathy is likely to be mul- tifactorial, with factors including some of the traditional ones such as overuse, inﬂ exibility, and equipment problems. However, other factors need to be considered as well, such as age-related tendon degeneration and biomechanical consid- erations as outlined in this chapter. Recent in vivo and in vitro studies have shed some light on the biomechanics of the main body of tendon, but more research is needed to determine the signiﬁ - cance of tensional loads, stress shielding, and compression in tendinopathy. The current biomechanical studies indicate that certain joint positions are more likely to stress the area of the tendon commonly affected by tendinopathy.

These joint positions seem to be different from the traditional positions advocated in stretching exercises used for prevention and rehabilitation of tendinopathies. Incorporating different joint position exercises may exert more controlled stresses on these affected areas of the tendon, pos- sibly allowing better maintenance of the mechanical strength of that region of the tendon, and therefore prevent injury. Alternatively, it could stress a healing area of the tendon in a controlled manner, and thus stimulate healing once an injury has occurred. Newer management measures will be introduced as the etiology of insertional tendinopathy of the Achilles tendon becomes clearer.

Various surgical techniques are aimed at debrid- ing the degenerate area of the Achilles tendon, accompanied by excision of the retrocalcaneal bursa and resection of the superior prominence.

Endoscopic procedures shorten the operating time, and may decrease the complications and morbidity associated with open procedures.

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