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Home , Achilles tendinitis, Infrapatellar bursitis, Patellar tendinitis, Retrocalcaneal bursitis

9 Insertional in Sports

Per Renström and Thomas Hach

Insertional are common. They are still Insertional tendinopathies are defined as one form very much debated, as their management is still not of overuse injury characterized by pain and optimal and is time consuming. The clinical picture arises discomfort at and around the OTJ [31]. Inser- from degenerative disorders at the osteotendinous junc- tional tendinopathies represent 15% to 25% of all tion. The diagnosis can be straightforward, but a wide tendinopathies [31,41,62], and long-term results after variety of differential diagnoses must be considered. both conventional and surgical treatment are not as sat- Management is based on a progressive controlled exer- isfactory as for other tendon disorders [31,62]. The most cise program, which is the key to stimulate a biological common anatomic sites of insertional tendinopathies are healing response. The main part of this training program the rotator cuff, the lateral epicondyle of the humerus, includes and . Initially, the the lower pole of the , and the program should be supervised, as it is difficult to dose cor- insertion. Since these are the most common sites of rectly. Orthotic devices have clinically some good effect. lesions [31,41,92], and histopathological studies mainly Among modalities, acupuncture has recently been used. refer to these 4 areas, the section on insertional disorders Some authors report good results with extracorporeal in general is followed by clinical examples at these 4 shock-wave therapy, but the scientific evidence is still areas. under scrutiny. Cortisone injections are the last line of treatment, and their effect is usually short lived. These injections should therefore be combined with some rest and gradually increased exercises. Surgery may be indi- Anatomy cated in 5% to 10% of cases and consists of excision of the affected tissue, with a success rate of 60% to 80%. The tendon insertion into bone is a complex anatomical Insertional tendinopathies still continue to be an enigma structure, where collagen fibrils from the tendon insert and may even develop to be a nemesis for both athletes into bone matrix, i.e. viscoelastic tendon tissue is con- and physicians. nected to rigid lamellar bone. There are 2 forms of OTJs: Treatment of tendon disorders has made great ad- fibrous and fibrocartilaginous [11,12], or indirect and vances in the past few years, but there still is confusing direct insertions [111]. Fibrous tendon insertions are terminology concerning tendon injuries. The occurrence typical of that attach to the periosteum of long of tendinitis is rare, and tendinosis should remain a his- bones, whereas fibrocartilaginous insertions are typical tological diagnosis. Accordingly, we refer to problems of tendons that attach to epiphyses [7,8,25,111]. Since of the tendon insertion in general as insertional fibrous tendon insertions are less common and rarely tendinopathies. The term enthesiopathy is a synonym involved in specific pathological conditions, we shall focus usually reserved for rheumatological descriptions. The on fibrocartilaginous tendon insertions. Notably, the tendon insertion into bone—the osteotendinous junc- gradual change from tendon proper to bone tissue occurs tion (OTJ)—has not been widely studied. This chapter within 1mm [68]. reviews basic science, anatomy, and pathophysiology The first scientific description of tendon insertions of tendon insertion to provide the fundamentals to dates back to 1929 [22]. The author divided the OTJ understand the clinical manifestations of insertional into 4 zones: tendon, fibrocartilage, calcified fibrocarti- tendinopathies. Furthermore, we give some details on the lage, and bone [12]. This concept is still valid issues of tendon healing and rehabilitation. [7,20,31,62,96].

70 9. Insertional Tendinopathy in Sports 71

Tendon Zone Tendon cells adopt an elaborate shape to maintain con- tinuous cell contact via gap junctions. Therefore, the The tendon zone of the OTJ consists of dense collagen relatively few interspersed cells are functionally inter- bundles, extracellular matrix—predominantly chon- related, and can sense changes in mechanical load. droitin sulfate, dermatan sulfate and hyaluronic acid In this fashion, the extracellular matrix can be modified [45,68]—and interspersed elongated tenocytes with [12] (see Figure 9-1). ellipsoid nuclei [31,33]. Various different types of collagen are present in tendon tissue: Collagen Type I is the main constituent of Fibrocartilage Zone the tendon zone. Closer to the zone of fibrocartilage, the The fibrocartilage zone of the OTJ shows a gradual tissue amount of collagen Type II continuously increases. Col- change along the collagen fibers (see Figure 9-2). Embry- lagen Type III can also be found in tendons, especially ological studies explain the epiphyseal origin of tendon during the process of tendon healing [31,62]. In addition, and fibrocartilage in OTJs. The gradation of cell pheno- the cartilaginous parts contain collagen Types IX, X, and type between uncalcified fibrocartilage and dense fibrous XI, whereas collagen Type IV is found in the basement tissue seems a logical consequence, taking into account membrane. Collagen, the body’s strongest protein, con- that fibrocartilage cells develop from tenocytes by meta- sists of tropocollagen microfibrils building the smallest plasia [12]. In contrast to tenocytes, fibrocartilage cells are structural units of tendons. These soluble proteins are usually round or oval.They also lack gap junctions, so that right-handed triple helixes 280nm long and 1.5nm wide, fibrocartilage cells act as a barrier to communication formed by 3 left-handed polypeptide chains. Five between osteocytes and tenocytes. In addition, there is tropocollagen microfibrils combine to form insoluble col- also a vascular barrier, as noncalcified fibrocartilage lacks lagen fibrils of 20 to 150nm in diameter. blood vessels. This process is supported by the formation of covalent The fibrocartilage at this location may have the fol- collagen crosslinks. Intermicrofibrillary crosslinks pro- lowing functions: vide collagen fibers with tensile strength and low com- pliance. Crosslinks can be reducible and nonreducible. • Two-layered defense system against excessive shear Moreover, a balance of hydroxylysino-5-keto-norleucin stress [96] and dehydroxy-hydroxylysino-norleucin crosslinks exists. • Dehnungsbremse (stretching brake) [46]. A change in the crosslinking pattern with age is supposed • Device reducing wear and tear at insertion sites [11]. to account for increased mechanical stiffness and de- • Tendon protection of mechanical functional signifi- creased tensile strength values [106]. Collagen fibrils are cance [9]. collected into fibers, which form fiber bundles and finally Collagen fibers pass directly through the zone of fibro- create the tendon itself [31,32,45,92]. cartilage stabilized by the extracellular matrix. Tenascin- Consequently, the tensile strength of tendons relies C content is high in the fibrocartilage layer of the OTJ, on collagen, whereas noncollagenous matrix proteins reflecting good adhesive function when high forces are provide structural support and mediate cell-matrix inter- transmitted [31,34,35]. actions. Furthermore, tenascin-C and fibronectin play a major role in binding tendinous collagen together [9,35]. Calcified Fibrocartilage Zone The calcified fibrocartilage zone of the OTJ is on average 100 to 300mm wide, but varies depending on anatomical Primary Secondary Tertiary Tendon site, tensile forces, and exercise [11,31,46,62]. It is fiber bundle fiber bundle fiber bundle delineated by a basophilic line (tidemark, blue line, or (subfascicle) (fascicle) cement line) clearly visible but not always continuous Collagen fiber under a light microscope [20,31,32]. Scanning electron microscopy does not show a significant tidemark. Colla- Collagen fibril gen fibers within the calcified fibrocartilage are not crimped passing through calcified fibrocartilaginous tissue [20].

Bone Zone Bone at the OTJs has the least tensile strength of this Endotenon Epitenon complex. Collagen fibers enter the bone matrix directly Figure 9-1. Organization of tendon structure. without merging to bony lamellae. The mechanism of 72 P. Renström and T. Hach

amplify neural activity on blood vessels and tenocytes, and may have a role in tendon healing [1].

CT Juxta Insertion Site The juxta insertion site is specific for every tendon. Often UF adjacent bursae and paratenon tissue are also affected by CF degenerative processes or associated inflammation. At AC B many tendon attachment sites, the juxta insertion struc- tures act as protective devices for the OTJs. Small syn- TM ovial bursae allow the tendon to move freely relative to the bone. Periosteal cartilage on the bone protects tendons from friction. Examples of juxta insertion dis- Figure 9-2. Osteotendinous junction. The 4 zones of tissue at orders are paratendinopathy, retrocalcaneal , and the tendon insertion to bone: Dense fibrous connective tissue [41,46]. (CT), uncalcified fibrocartilage (UF), calcified fibrocartilage (CF), and bone (B). The calcified and uncalcified fibrocartilage are separated by a tidemark (TM) that is straight and continu- Summary ous with a similar tidemark in the adjacent articular cartilage (AC). Overall, the OTJ is a durable bond between tendon and bone. Because of its complex and differentiated structure (Table 9-1), it provides protection for the insertion site adhesion is not yet fully understood. Also, the develop- and functionality of the muscle attachment [9,11,62,84]. ment of bone at the OTJs is from different origin than Tendon ruptures usually do not involve the OTJ [20,28]. other bone structures: possibly, the bony insertion devel- However, when degenerated, OTJs are the weakest link ops from tendon fibrocartilage [20,70]. of the musculotendinous unit [94]. Hypovascularity can act as a contributing factor to insertional tendinopathies [4,31,37,42]. Furthermore, minimal pliability, a perpen- Blood Supply dicular architectural arrangement against the direction of Tendons have a poor blood supply. The blood flow of muscle force, and a relatively small insertion zone com- tendons is only about one-third of the blood flow of pared to muscle size supposedly predispose the OTJ to muscle [11]. In tendon regions where hypovascularity is injury [73]. associated with friction, torsion, or compression, there seems to be an increased risk for tearing, calcification, and degenerative changes [31,41,54,84,108]. Blood supply General Aspects of Insertional reaches the OTJ from paratenon and periosteum. Tendinopathies Approximately the lower third of a tendon is perfused in this fashion. There is clear distinction between vessels in Functional and structural disorders of the OTJ can be calcified and noncalcified fibrocartilage, because the cal- due to rheumatological disorders, sports activities, or cification of fibrocartilage acts as an impenetrable border degenerative changes [52]. for anastomoses, and fibrocartilage itself is almost com- Rheumatological conditions such as rheumatoid pletely avascular [11,31–33,41,46,62]. Blood supply to arthritis, spondylarthropathy, calcium pyrophosphate the OTJ increases during exercise and healing [36,47]. deposition, and diffuse skeletal hyperostosis play a major Histopathological findings suggest a vascular prolifera- role concerning insertional tendinopathies [99]. Since tion in tendinosis [31,33,41,47,63,72]. enthesopathies—in rheumatological terms—belong to a different clinical entity, they are not discussed here. Nerve Supply During the diagnostic workup, a rheumatological contri- bution to insertional tendinopathies must not be over- Nerve supply to the OTJ is mainly afferent. Most nerve looked [102]. Insertional tendinopathies can manifest at endings in tendons are found at the myotendinous junc- the insertion of every tendon of the human body. tion. Free nerve endings near the OTJ act as pain recep- The most common anatomic sites are rotator cuff, tors, and are predominantly found in the connective lateral humeral epicondyle, patella, and Achilles tendon. tissue of the attachment site [22,31,46,62]. Localized pain Insertional tendinopathies in the groin are also not at the OTJ is mediated by free nerve endings. Nerve uncommon, and are most difficult problems [83]. The fibers accompanying small blood vessels have an impor- tendons of the foot, wrist, and fingers can also be affected tant role in tissue vasoregulation. Various neuropeptides [31]. 9. Insertional Tendinopathy in Sports 73

Table 9-1. Characteristics of the different zones of the OTJ cause microscopic tendon fiber rupture. These repetitive Collagen Nerve microtraumata lead to overuse injury [31]. Partial or com- type Vascularity supply Cellularity Strain plete tendon ruptures result from strains of greater than Tendon I + ++ + +++ 8% of original length. Fibrocartilage II -+ +++Recently, investigations on the strain patterns of the Calcified suggested that stress shielding rather fibrocartilage II -+ ++than excessive tensile loads may be a causative factor Bone I +++ +++ ++ + in patellar tendinopathy [123]. This goes hand in hand with the description of compressive loads causing degen- erative changes in tendons and tendon insertions re- Sports activities and degenerative changes are closely spectively [124–126]. These findings warrant further interwoven reasons for insertional tendinopathies. In ath- investigation of biomechanical aspects in insertional letes, overuse-related microtrauma can induce premature tendinosis, and aggravate degenerative changes. Overuse injuries account for 30% to 50% of all sports injuries. Tendon overuse injuries in particular are the most com- mon reason for breaks in training and competition [38]. Insertional tendinopathies account for 15% to 25% of sports-related tendon disorders. The etiology of inser- tional tendinopathies still needs further elucidation. Overuse is a well-established etiologic factor for these injuries [31,33,38,41]. To effectively prevent insertional tendinopathies, it is important to understand, identify, and affect predisposing risk factors. Intrinsic and extrin- sic risk factors can be differentiated. The most important intrinsic risk factors are: malalignments, decreased flexi- bility, muscle weakness and imbalance, , and predisposing conditions, such as inflammatory arthritides, Haglund deformity, etc. Crucial extrinsic—and conse- quently more easily affectable—risk factors are: exces- sive load, training errors, and poor equipment [31,92]. Predisposing risk factors will be discussed in the treat- A ment section.

Pathogenesis An overuse injury is defined as a recurring orthopedic problem and pain in the musculoskeletal system, which begins during exertion because of repetitive microtrauma [31]. The OTJ adapts to increasing mechanical demands by changes in collagen cross-sectional area [36], extra- cellular matrix [34,35], and fibrocartilage distribution [10] within physiological limits. When repair and adaptation capabilities are exceeded, degenerative changes result (Figure 9-3). At histopathology, a dull, gray, and friable appearance is typical of the degenerative process in con- trast to a shiny, white, and firm normal tendon [31,47,63]. Microscopically, the specimens show thinning, disruption of collagen fibers, increased vascularity and cellularity, B tenocyte dedifferentiation/alteration (rounded nuclei Figure 9-3. (A) Normal tendon. Photomicrograph showing and blastlike morphology), granulation tissue, increased parallel collagen fiber distribution and uniform-appearing ground substance, fibrocartilaginous metaplasia, and collagen structure oriented along the axis of the tendon microtears. Inflammatory cells are not normally seen (Hematoxylin/Eosin). (B) Tendinosis. Photomicrograph show- in insertional tendinopathies [4,31,33,41,55,89,93]. ing hypercellularity, wavy collagen structure, and hypervascu- Repeated tendon strains to 4% to 8% of original length larity (Hematoxylin/Eosin). 74 P. Renström and T. Hach tendinopathies, especially for athletes and rehabilitative fractures can be ruled out using routine and exercises. radiographs. Tendon avulsions or bone fragments at the Insufficient blood supply is also regarded as a patho- insertion (e.g. Osgood-Schlatter disease) can also be genetic factor contributing to tendon failure, insertional easily detected on plain radiographs [31,92]. Special disorders and overuse injury in general, respectively radiographic views can facilitate the diagnosis of inser- [31,37]. The vascular elements of a tendon can also be tional tendinopathies at certain anatomic sites, e.g. shoul- damaged by microtrauma. Therefore, degenerative pro- der, , etc. cesses are perpetuated. Finally, both overuse injury and Diagnostic ultrasonography is a quick, safe, noninva- impaired circulation interfere with collagen crosslink- sive, easily obtainable, and inexpensive method of tendon ing patterns. As a consequence, the above mentioned evaluation. In Europe, it is much more commonly used pathology develops, and microtears expand in the tendon than in North America. Since the possible shortcomings and the fibrocartilage zone of the OTJ [31]. The tendon of diagnostic ultrasonography, such as limited field of insertion is thus weakened, eventually leading to view, limited soft tissue contrast, and reduced sensitivity microtears and the clinical findings of pain, crepitus, and are continuously improved upon, its reliability and field tenderness. of application are continuously enhanced. Apart from Insertional tendinopathies are degenerative disorders that, operator dependency is an important feature of that do not arise from chronic inflammation. Although diagnostic ultrasonography that warrants educational misnomers such as lateral epicondylitis and chronic patel- and training programs for soft tissue evaluation. In the lar tendinitis persist, inflammatory processes are rarely field of tendon disorders, diagnostic ultrasonography is involved in insertional disorders [6,31,33,40–42,55,89, particularly useful for the detection of tears at the tendon 110]. Sometimes associated structures can become insertion or attachment, and associated degenerative or inflamed (paratenonitis, bursitis, etc.), but tendon inser- inflammatory changes [5,31,56,92]. Furthermore, diag- tion tissue damage is caused by exceeded repair capabil- nostic ultrasonography is a practical method for follow- ities. A tendon probably never reaches its original up examinations [43]. strength after healing [31,42], and for this reason tendon MRI is considered by some as the standard for soft healing probably cannot be considered to confer restitu- tissue imaging [105] and visualization of tendon pathol- tio ad integrum. ogy [92]. High intrinsic tissue contrast and high spatial resolution are the striking features that allow detailed Diagnosis analysis of tendon pathology [81]. Since MRI offers excellent diagnostic results, but is expensive, it should A detailed history is essential. As tendinosis per se can be confined to evaluations when only MRI results can be asymptomatic, clinical history related to sports activi- propose therapeutic consequences [92]. The possibility of ties or manual work can provide valuable information. detecting even slight pathological changes by MRI [81] Insidious onset of symptoms is characteristic of degener- allows the identification of the early stages of insertional ative disorders. If certain activities or movements are pathology, so that successful secondary preventive mea- associated with pain, the location of the lesion can be sures can be implemented. pinpointed. CT has limited value in tendon pathology, since its The classic orthopedic examination scheme of “look, limited contrast makes differentiation of normal and feel, and move” is undertaken. Inspection may reveal pathological conditions difficult [81]. In principle, it is a muscle atrophy, compensatory postures, and swelling useful aid, and insertional disorders, if they involve the because of associated bursitis or paratenonitis. bone, can be detected [31]. Nevertheless, a CT scan is may detect definite points of tenderness rarely indicated in insertional tendinopathy. (typical for insertional tendinopathies), bony promi- Bone scanning is a sensitive method for assessing nences (e.g. Haglund deformity), crepitus (e.g. Achilles pathologic activity in insertional tendinopathies. Since paratenonitis or calcific tendinopathy), and nodules or its specificity is low, and the soft tissues are not gaps in the tendon [31,92]. demonstrated [31], bone scanning should be limited Active and passive motion usually show characteristic to evaluations of insertional tendinopathies associated deficits corresponding to the affected tendons. Early after with other diseases that cause bone alterations, e.g. the onset of symptoms, the range of motion is frequently , spondylarthropathies, osteoporosis, unaffected, but it decreases during the course of etc. deterioration. Diagnostic studies of insertional tendinopathies in- Management clude plain radiography, , magnetic resonance imaging (MRI), computed tomography (CT), and bone Even though the outcomes of nonoperative and opera- scanning. Bony abnormalities can be detected and tive management are improving, the methods are still 9. Insertional Tendinopathy in Sports 75 mostly empirically based and often lack scientific evi- other overuse injuries [31,92], especially in runners. In dence [31,92]. When it comes to establishing a manage- general, the most important training errors are too long ment plan for insertional tendinopathies, the patient’s distance, too high intensity, and too fast progression. state of health must be identified, and management goals Therefore, failure to allow for physical adaptation should be discussed. The management principles for results in degenerative changes. Excessive, monoto- acute and chronic insertional tendon injuries are outlined nous, asymmetric training, sudden changes in training hereinafter. program or training ground, insufficient warm-up, Acute insertional tendinopathies are rare. Often, inadequate general conditioning, as well as poor tech- associated inflammation causes acute pain. In case of nique and fatigue training all jeopardize the athlete’s acute symptoms, e.g. avulsions, partial or full-thickness tendons. Evaluation and modification of the training tears, bursitis, or paratenonitis, the management follows program and correction of poor technique, e.g. faulty the well-known rules of managing acute sports injuries. backhand technique in , or modified Protection, rest, ice, compression, elevation, support landing in basketball or volleyball in jumper’s knee (PRICES), and NSAIDs are widely used [31,59]. may markedly improve if not resolve the patient’s Avulsions should be repaired surgically, and surgery symptoms [31,42,92]. for tendon tears must be considered on the basis • Poor equipment of anatomical site, loss of function, and goals of Poor equipment is also a major risk factor. rehabilitation. Both operative and nonoperative ap- shoes are important to stabilize the foot and reduce proaches produce a high percentage of good results impact forces.The replacement of unfitted or worn-out [31,42,54,92,99]. shoes with appropriate ones is a valuable first step in Chronic insertional tendinopathies are often recalci- successful management. Tennis racquets that are too trant to conservative management [44,92]. The ultimate stiff or strung too tightly may initiate symptoms of goal of any form of management is to restore the integrity tennis elbow. Hand paddles in swimming may induce of the tendon-bone unit. Therefore, further injury must rotator cuff tendinopathy. Inadequate adjustment of be avoided, and the healing process must be supported. bicycle seats can lead to problems of the knee exten- In addition, symptomatic management can be added. sor apparatus [31]. Once identified, these conditions Nonoperative methods are the primary methods of can be tackled more easily. choice. Operative management should be limited to • Malalignments patients who have failed conservative management for at Malalignments are a serious intrinsic predisposing least 6 to 9 months, or are restricted in their daily life risk factor for insertional tendinopathies. Hyperprona- activities. Correction of predisposing risk factors, func- tion of the foot is both the most common and best tional rest, stretching, strengthening, and described malalignment that can result in Achilles are important management methods. Recently, extracor- tendon insertion disorders, patellofemoral stress poreal shock-wave therapy (ESWT) has been used on syndrome, runner’s knee, etc. A high-riding patella and tennis elbow,Achilles tendinopathy, and tendinoses asso- patellar are associated with jumper’s ciated with tendon calcification. Preliminary results are knee, even though the cause-and-effect relationship is promising, but some studies also show inconsistent results unclear [23,27,31,42,79,87]. As the correction of [13,29,88]. malalignments can be simple, they must not be overlooked. • Decreased flexibility—Muscle weakness and Correction of Predisposing Risk Factors imbalance • Excessive load on the body Low flexibility and interference of muscle function pre- Repeated overload is the main risk factor for inser- dispose to and perpetuate chronic tendon disorders. tional tendinopathies in athletes and manual workers Especially for insertional tendinopathies, optimal [19,31,33,44,82]. Counter-force braces for jumper’s muscle and tendon function is essential. Stretching and knee and tennis elbow are the most popular manage- strengthening are a mainstay of management and ment options, acting directly on muscle force to the prevention. tendon insertion. They constitute an additional option • Overweight of nonoperative management. The detrimental effects of overweight on the muscu- The following extrinsic and intrinsic factors con- loskeletal system are well known, recognized, and tribute to and aggravate the problem. scientifically proven. Sedentary lifestyle is associated • Training errors with degenerative tendon disorders [31,33,37,41,106]. Training errors are considered the most important Moreover, overweight, sedentary lifestyle and inactiv- extrinsic risk factor for overuse sports injuries, and ity impair adaptive capabilities and the healing process probably contribute to 60% to 80% of tendon and of tendons. 76 P. Renström and T. Hach

Functional Rest tric strengthening program should consist of warm-up and stretching, eccentric exercises, postexercise stretch- As in the acute phase, rest and immobilization are also ing, and icing or cold in case of swelling or pain [24,31,92]. commonly prescribed to relieve pain in chronic degener- Finally, it is important to evaluate and encourage the ative tendon disorders. Initially, rest protects from further patient’s improvements in strength and flexibility. Tradi- injury and allows the patient to better tolerate a physical tionally, return to limited sports activity is possible with therapy program [92]. Since pain at the insertion site is full range of movement and 80% to 90% of the strength very common and may persist over a longer period of of the uninjured extremity, which can be objectively mea- time [25,62], protracted immobilization should be sured by functional testing [67]. Before returning to full avoided to prevent its adverse effects [31,92]. Therefore, activity, sports-specific activities must be tested. In this early mobilization should be implemented. The term way, premature return to sports, a common cause for the “functional rest” emphasizes treating the injured body recurrence of symptoms, can be avoided. parts with care while still maintaining general body conditioning. Physical Therapy Stretching Physical therapy is frequently employed together with stretching and strengthening. Heat, cold, therapeutic Stretching is considered an important element of an ultrasound, and electrical stimulation are the physical integrated management protocol for tendon injuries therapy modalities most commonly used. There is still [23,83,98,110]. As the musculotendinous units in inser- little scientific evidence on the effectiveness of physical tional tendinopathies are frequently tight due to disuse therapy, but patients generally describe physical therapy or protective , stretching is advisable as comfortable and helpful. It can be generally recom- to restore function by stress relaxation and reduction of mended to use heat to prepare for stretching and stiffness [92]. Furthermore, mechanical stimulation leads strengthening exercises and cold to support the allevia- to adaptive changes in the tendon [11,35,106]. Therefore, tion after strenuous exercise.A more detailed description controlled stretching is likely to result in acceleration of the effects of physical therapy is given in Figure 9-4. of collagen synthesis, fibril neoformation, and proper Extracorporeal shock-wave therapy (ESWT) may be fiber alignment, and thus increase the tensile strength of effective in some patients not responding to nonopera- the tendon [36]. The recommended stretching technique tive management. The success rates for management of is contract, relax, antagonist contract (CRAC). Jerky insertional tendinopathies such as tennis elbow, Achilles motion, rapid movements, and ballistic stretching should insertion disorders, and shoulder tendinoses are esti- be avoided during rehabilitation. Stretching can be used mated at 50% to 80% [29,88]. Since the prognosis for for both management and prevention of insertional recalcitrant tendinopathies is good, and ESWT does not tendinopathies [92]. show major adverse effects, it is an option before surgery is planned. However, the excellent results reported in Strengthening Strengthening of the affected muscle-tendon unit is another mainstay of nonoperative management of inser- COLD HEAT tional tendinopathies. The strengthening program should Cellular metabolism Permeability begin as soon as possible after the diagnosis or after the Oxygen requirements Vascularity acute associated inflammation phase. The primary goal Amount of lissue damage Cellular metabolism is to restore complete function of the damaged tissue. Edema Pain Spasm Pain is a useful guide for progression in a strengthen- Viscoslty Pain-spasm-ischemia cycle ing program. Exercises should be carried out until the Viscoslty patients feels pain, and possibly slightly beyond that limit Tissue extensibility [75,92]. Further strain will result in recurrent micro- ELECTRICAL STIMULATION ULTRASOUND trauma, and should be avoided. In this way, strengthen- Vascular permeability Thermal effects of heat ing can progress from light resistance exercises to Edema Mechanical effects: Pain Tendon tensile strength eccentric exercises. Maximum stress is placed upon a Tendon strength Collagen production tendon during eccentric exercises, and only if one can Muscle atrophy Microvascular rebuilding strengthen the tendon to withstand these stresses will the Myolibroblasts Wound contraction tendon be able to cope and be protected against reinjury Viscosity Tissue extensibility [24]. Since mechanical loading and adaptive processes are closely interrelated [34,35], the aim of maximal load Figure 9-4. Effects of physical therapy modalities on tissue without microtraumatization is appropriate. The eccen- response to injury, adapted from Houglum PA (1992). 9. Insertional Tendinopathy in Sports 77 some studies have not been universally replicated enitor cells as a pluripotent cell source into the heal- [13,109]. ing environment. The combination of cell therapy with growth factor application via gene transfer offers new avenues to improve ligament and tendon healing Medication [14,112,155]. Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the drugs most commonly used by athletes Surgery [4,31,42,67,92]. The effectiveness of NSAIDs in chronic tendon disorders remains questionable [42]. Their most Surgery has become an accepted therapeutic option for important effect is presumably not anti-inflammatory but failed nonoperative care of insertional tendinopathies analgesic [4,31,92]. In addition, the role of NSAIDs con- [50], but should be considered a last resort [44], especially cerning wound healing remains questionable [42]. In when one appreciates the confirmed degenerative origin patients with insertional tendinopathies, NSAIDs may be of insertional tendinopathies, and the fact that improve- used to facilitate rehabilitation and to treat associated ment of nonoperative results over a long period of time inflammatory processes like bursitis or paratenonitis. is not uncommon [54]. Topical diclofenac has recently been shown to be effec- Leadbetter et al. itemized 7 goals for surgery in tive in tennis elbow [16]. In this way, oral administration tendon overuse injuries. These apply to insertional and adverse effects may simultaneously be decreased. tendinopathies [50]: “As much as needed but as little as possible” should be 1) To improve tissue structure and strength by inducing the guiding principle. scar tissue. The use of injections should remain a 2) To remove aberrant tissue, i.e. granulation tissue, cal- form of adjunctive therapy. Almekinders and Temple cific deposits, and degenerative or necrotic tissue. state the early pain relief with steroids but remind of the 3) To encourage revascularization of injured tissue. uncertain final outcome, since recurrences are common 4) To relieve extrinsic pressure, e.g. bony spurs. [4]. Overall, corticosteroid injections have lost favor 5) To relieve tensile overload. because of their inhibition of collagen synthesis and their 6) To discover and repair relevant tears. potential deleterious effect when injected into the tendon 7) To replace or augment injured tendon structure. [42]. In case of persistent pain and inability to perform a rehabilitation program, corticosteroid injections may be The surgical techniques available to achieve these indicated. In any case, the guidelines for steroid adminis- goals include the following: Intratendinous or paratendi- tration must be respected. should not be nous excision, decompression, synovectomy or bursec- injected into tendons, no more than 2 injections spaced tomy, longitudinal tenotomy, tensile release, repair, and several weeks apart should be given, repeat injections tendon transfer or graft [92]. The end result of surgical should be used only after at least partial relief, and they procedures is not restitutio ad integrum. Both patient and should not be used after an acute injury, before a com- physician must take into account that a scarred, repaired petition, or in the presence of infection [92]. The effect of tendon is probably prone to reinjury lifelong. Conse- corticosteroid injections is usually short lived, i.e. less quently, the importance of rehabilitation cannot be than 6 weeks. Furthermore, corticosteroid injections overemphasized. Overall, a success rate of 75% to 85% should be accompanied by a few days of rest and gradu- of surgery for insertional tendinopathies has been ally increased exercise afterwards. reported [44,50,92]. New research dealing with neuropeptide activity and The enormous variety of surgical procedures for gene therapy in tendon ailments provides a better under- specific insertional tendinopathies exemplifies the lack standing of the underlying pathology and innovative of generally accepted management regimens. Operative management approaches [1,112]. New techniques, such as procedures for insertional tendinopathies require repeat tissue engineering, offer the potential to improve tendon surgery in 10% to 15% of patients, showing the delicate healing.These concepts are based on the manipulation of balance between success and failure [92]. cellular and biochemical mediators to affect protein syn- In general, most insertional tendinpathies are degen- thesis and improve tissue remodeling. Recently, applica- erative disorders often due to overuse. Despite thorough tion of growth factors and gene transfer techniques have histopathological investigations of OTJs, little is known shown promising results, and may become effective ther- of the biomechanical properties and functional behavior apies. Gene-activated matrix (GAM) was the first gene of the OTJ under various loading conditions in vivo. Bio- therapy designed specifically for tissue engineering appli- chemical investigations of overuse-related tissue degen- cations. GAM could serve as a platform technology for eration, studies of tendon avulsions, and biomechanical local gene delivery to enhance soft tissue healing. Cell investigations of overuse effects on OTJs will foster a therapy involves the introduction of mesenchymal prog- better understanding of insertional tendinopathies. 78 P. Renström and T. Hach

Treatment Algorithm for Insertional Tendinopathies articular cartilage and supraspinatus tendon insertion as a useful indicator for the integrity and tensile strength of Onset of Abusive Overuse/Overload activity – “Overtraining” the supraspinatus tendon. Accordingly, an evaluation of Subclinical Injury – Cumulative Microtrauma the sulcus width, either arthroscopically or by MRI, can have prognostic significance as it correlates with the Clinical Injury (Patient presents in office “injured”) severity of degenerative changes [50]. PRICES Aging, diminished vascularity, overuse, microtraumata, subacromial pathologies, impingement, and calcification Control of Abuse – Rehabilitation (Eccentric Exercises as soon as possible) are various reasons for the multicausal pathology in Unimproved – Persistent Pain rotator cuff tendinopathy [31]. Tendon tears are found in the so-called critical zone of the supraspinatus tendon Cryotherapy, Iontophoresis, and at the OTJ.Tendon degeneration has been suggested Ultrasound, Acupuncture as a main pathogenetic factor of rotator cuff tears Unimproved [69,76,94]. Since degenerative changes are more common disorders in patients older than 50 years, and rotator cuff Improved Corticcosteroids, ESWT tears in cadaveric studies increase with age [58], trau- matic rotator cuff tears in athletes must be distinguished. Unimproved Finally, both disorders demonstrate underlying degener- Surgery ation, but the mechanisms of injury are different. Degen- erative rotator cuff tears can occur during daily activities Careful Attention to Transition and Retraining and are often asymptomatic [31,54], whereas traumatic tears in athletes result from tendon failure due to over- Safe Return to Sports strain [45]. The most noteworthy clinical findings are stiffness, Figure 9-5. Algorithm for the management of insertional weakness, crepitus on passive glenohumeral motion, and tendinopathies. pain during movement or at rest [76,85,110]. Functional muscle tests help to locate the rotator cuff insertional tendinopathy. As this entity infrequently exhibits unequivocal symptoms, imaging techniques are helpful for diagnosis. Ultrasonography and MRI help to detect rotator cuff More aggressive postoperative rehabilitation has insertional disorders [31,85,92]. MRI arthrography is very become a mainstay of management in an attempt to sensitive for the identification of even very small partial return patients faster to a high level of sports activities. tears. The question is whether nearly asymptomatic cuff Figure 9-5 summarizes the description of management pathology should be detected at all, because the point for modalities for insertional tendinopathies. therapeutic implications has not yet been convincingly made. Initial management of partial or full-thickness rotator Rotator Cuff Insertional Tendinopathy cuff tears—if symptomatic—should follow the manage- ment regimen described above, so that edema formation The most common cause of shoulder pain is soft tissue can be decreased and further injury is reduced [31]. dysfunction. Rotator cuff tendinopathy and microtears Depending on the patient’s symptoms and activity level, are therefore regarded as the primary component of sub- a nonoperative or operative approach is to be considered. acromial pain syndrome [56,108]. The supraspinatus Operative management for rotator cuff tears offers a tendon is the most commonly affected by wear and tear great variety of procedures, both arthroscopic and open. of all rotator cuff tendons. Consequently, insertional Excellent and satisfactory results range between 70% tendinopathies of the supraspinatus are most common. and 90% [85]. The supraspinatus tendon has a relatively hypovascular zone close to its insertion.This “critical zone” is subjected to great tensile stresses and friction [54,56]. In addition, Tennis Elbow the OTJ is also a weak link in the bone-tendon complex [94]. Tennis elbow is one of the most common clinical Codman already suggested in 1934 that chronic shoul- problems in , already described in 1873 der problems are of degenerative origin [21]. Sano et al. [91]. In 1883, the term lawn tennis elbow was coined have described the width of the sulcus between humeral [60]. 9. Insertional Tendinopathy in Sports 79

The problem generally arises from tendinopathy of the attachment of the tendon to the extensor carpi radialis brevis muscle at the lateral epicondyle. The diagnosis can be straightforward, although there are some other differ- ential diagnostic options, such as cervical radiculopathy, referred shoulder pathology, radial tunnel syndrome, or posterior interosseous nerve entrapment. The most char- acteristic symptoms of tennis elbow are pain and tender- ness at the lateral epicondyle of the humerus. The pain may radiate distally and, more rarely, proximally. The range of motion of the elbow is usually full except in chronic, severe cases [19]. Functional and provocative tests are of great diagnostic value. The “coffee cup test,” i.e. picking up a full cup of coffee, is almost pathogno- monic for tennis elbow. Pain from resisted wrist or middle finger dorsiflexion with the elbow fully extended is Figure 9-6. Partial interstitial tear of extensor carpi radialis brevis tendon in the area of tendinosis; the lateral epicondyle typical. The area of tenderness pinpoints the affected elbow. extensor muscle [19,63,72,82]. Grip limited by pain is another useful index, and dynamometry can quantify these functional strength deficiencies objectively [66]. [129,130]. Therefore, activities such as basketball, volley- Management is based on a progressive, controlled ball, American or European football, tennis, or track and exercise program, which is the key to stimulate the bio- field (long jump, high jump, hurdles) are most commonly logical healing response. The main part of this training affected [42,44,119,129]. Table 9-2 shows a comparison of program includes eccentric action and some stretching. the tendinosis classification from Nirschl [63] and the Initially this exercise program needs supervision, as it is jumper’s knee classification from Blazina [119]. Despite difficult to dose correctly. Counterforce bracing has some the different dates of publication and purpose, the simi- good effect clinically. Among modalities, acupuncture larities are striking. Another useful instrument for evalu- seems to be a possibility.Some studies report good results ation of patellar tendinopathy is the more differentiated with ESWT [13,29,88], but the scientific evidence is still VISA (Victorian Institute for Sports Assessment) score not fully convincing. Cortisone injections are the last line [131]. of conservative management. Their effect is usually short It is important to correctly diagnose patellar lived.These injections should therefore be combined with tendinopathy as early as possible (Stage 1), so that pro- some rest and gradually increased exercises. Surgery may gression and chronic disease may be prevented. Patients be indicated in 5% to 10% of patients, and consists of often report an insidious onset of symptoms and a dull excision of the pathology in the extensor carpi radialis anterior . Tenderness at the inferior patellar brevis. This can be completed by decortication of the pole is the key finding. It is most distinct in full knee anterior lateral condyle for vascular enhancement [46,63, extension, and may be decreased in knee flexion [42]. In 72,92]. Figure 9-6 shows the intraoperative appearance of tennis elbow. The success rate for surgery is usually higher than 80% [19,25,47,63,64,72,148]. Table 9-2. Comparison of tendinosis and jumper’s knee classi- fications, adapted and modified by permission Tendinosis classification Jumper’s knee classification Jumper’s Knee (Nirschl, 1992) (Blazina, 1973) Stage 1 Temporary irritation Pain after activity, no Jumper’s knee is a classic overuse disorder [23] with functional impairment microtearing of the patellar tendon along the knee exten- Stage 2 Permanent tendinosis— Pain at beginning of activity, sor mechanism between the upper patellar pole and the less than 50% tendon disappearing after warm-up, tibial tubercle. The lower pole of the patella is affected in cross section reappearing after activity 65% of cases, with the upper pole (25%) and the tibial Stage 3 Permanent tendinosis— Pain during and after insertion (10%) less commonly involved [23,31]. Inter- greater than 50% tendon activity with functional estingly, the outcome of management for insertional cross section impairment 3a: able to train tendinopathy is not as good as for disorders of the main and play 3b unable to train and play body of the patellar tendon [42]. Jumper’s knee is more frequent in athletes with vigor- Stage 4 Partial or total rupture Complete tendon rupture of tendon ous and repeated exertion of the quadriceps muscle 80 P. Renström and T. Hach more severe stages, clinical examination may reveal pain runners of about 10% [62]. Training errors are very com- during resisted knee extension. mon for athletes with Achilles tendinopathy.A change in Many ultrasonographic studies have been performed surface, a sudden increase in mileage, hill running, and [132–142], and MRI can also be a useful diagnostic tool. improper stretching techniques often exacerbate the pain However, ultrasonograms and MRI scans do not always [27,62,118]. There is a high association of insertional correlate with pathologic appearance and clinical findings tendinopathy with , and up to 60% [55,115]. Therefore, clinical examination and imaging of patients also have Haglund’s deformity [62,118]. must support each other to establish the diagnosis of Tenderness directly at the Achilles tendon insertion is patellar tendinopathy. typical. Pain may be aggravated by passive dorsiflexion, The biomechanical analysis of patellar tendinopathy and a loss of passive dorsiflexion is not uncommon [117]. needs further investigation. The etiology of insertional Sometimes even a palpable defect in the tendon may be patellar tendinopathy is widely discussed, and it remains noted [62]. Hyperpronation and forefoot varus are com- to be elucidated whether tensile strains [23,31,147] or monly associated with insertional Achilles disorders [148]. compressive loads and impingement [123,146] are the Therefore, gait analysis is a useful tool in diagnostics. major causative factors of disease. Radiographs frequently demonstrate calcification or There is a surprising lack of scientifically proven man- ossification of the Achilles tendon insertion. Ultrasonog- agement options [42,92,114,115,121,123]. In the early raphy and MRI are useful to evaluate Achilles tendon stages, the management modalities described above are pathology [27,39]. However, both methods are of limited generally effective, and local corticosteroid injection use regarding surgical decision-making, since the pathol- should be avoided [115,143]. Careful eccentric exercises ogy is easily detected clinically. However, imaging may be should be included as soon as possible in the rehabilita- used as prognostic indicator as it shows the severity of tion program [24,42,44,137,144]. High eccentric loads tissue alterations [5]. Figure 9-7 shows typical changes in during training (e.g. squatting) should be avoided until the MRI at the Achilles tendon insertion. recovery [115]. Stretching exercises should accompany the strengthening program to encourage flexibility and adaptation of muscle-tendon units. For basketball and volleyball players, landing from a jump on two feet can be a simple and effective step to reduce wear and tear of the patellar tendon. Surgery for patellar tendinopathy includes stripping of the paratenon, removal of pathological tissue, longitudi- nal tenotomies, and drilling of the bone-tendon junction [23,42,115,147]. Recently, arthroscopic procedures have been described as an alternative surgical approach, but the effectiveness of arthroscopic over open surgery has not been proven [87,145,149]. Recommendations for surgery range from 6 to 12 months of unsuccessful con- servative management, and suggest recalcitrant Stage 2, Stage 3, or only Stage 4 for surgical management [23, 50,115,147]. Therefore, despite relatively high surgical success rates, the mainstay of management remains con- servative management, and the sports physician must decide with the patient whether surgery is indicated.

Insertional Achilles Tendinopathy

The Achilles tendon is the largest tendon in the human body. Insertional tendinopathies comprise about 10% to 25% of Achilles complaints [27,100,150]. Insertional Achilles tendinopathy is caused by chronic degeneration within the tendon insertion onto the , com- Figure 9-7. Sagittal STIR image shows increased signal inten- monly presenting as an overuse syndrome [120]. It is most sity (arrow) in calcaneal bone marrow as sign of reactive edema. common in middle- and long-distance running, dancing, Also, retrocalcaneal bursae and adjacent Kager’s fat pad show soccer, and tennis [27,118,151], with an incidence in increased signal intensity. 9. Insertional Tendinopathy in Sports 81

The management scheme for the insertional thy: a comparison of ultrasonography, magnetic resonance tendinopathies described above applies very well to the imaging and surgical findings in 27 histologically verified Achilles tendon. A sleeve or heel pad can provide a cases. Skeletal Radiol. 25(7):615–620. simple and inexpensive alleviation of pain [62,148]. 6. Astrom M, Rausing A. (1995) Chronic Achilles tendinopa- Finally, the choice of appropriate footwear, possibly thy. a survey of surgical and histopathologic findings. Clin Orthop. 316:151–164. antipronation shoes, is essential to treat the condition and 7. Becker W. (1971) Electronmicroscopic studies of tendon prevent recurrence. insertion into bones. Arch Orthop Unfallchir. 69(4): There are many surgical approaches to deal with inser- 315–329. tional Achilles disorders, and evaluation of these goes 8. Belling Sorensen AK, Jorgensen U. (2000) Secondary beyond the scope of this chapter. Regardless of the sur- impingement in the shoulder. an improved terminology in gical approach, it is important to debride tissue abnor- impingement. Scand J Med Sci Sports. 10(5):266–278. malities, resect a potentially inflamed retrocalcaneal 9. Benjamin M, Evans EJ, Copp L. (1986) The histology of bursa, and to remove Haglund exostoses or other calcifi- tendon attachments to bone in man. J Anat. 149:89–100. cations [62]. Combined with current techniques of surgi- 10. Benjamin M, Ralphs JR. (1998) Fibrocartilage in tendons cal repair and rehabilitation programs, innovations like and ligaments—an adaptation to compressive load. J Anat. growth factor therapy [153] or low-energy photostimula- 193(Pt 4):481–494. 11. Benjamin M, Ralphs JR. (1997) Tendons and ligaments— tion [154] could improve the outcome of athletes with an overview. Histol Histopathol. 12:1135–1144. Achilles tendon injuries. 12. Benjamin M, Ralphs JR. (2000) The cell and develop- mental biology of tendons and ligaments. Int Rev Cytol. 196:85–130. Conclusions 13. Boddeker I, Haake M. (2000) Extracorporeal shockwave therapy in treatment of epicondylitis humeri radialis. A Despite—or possibly because of—so much disagreement current overview. Orthopade. 29(5):463–469. about the etiology and management of insertional ten- 14. Bonadio J. (1999) Tissue engineering via local gene deliv- dinopathies, this field needs much more research [121]. ery. J Mol Med 2000;78(6):303–311. A well-planned rehabilitation program with stretching 15. Boyer MI, Hastings H 2nd. (1999) Lateral tennis elbow: and strengthening exercises is the mainstay of manage- “Is there any science out there?” J Shoulder Elbow Surg. 8(5):481–491. ment to promote healing and prevent further injury. An 16. Burnham R, Gregg R, Healy P, Steadward R. (1998) The injured tendon does not regenerate, but heals by forma- effectiveness of topical diclofenac for lateral epicondylitis. tion of inferior scar tissue. 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