Jumper's knee (JK) is a clinical diagnosis that almost always refers to symptomatic proximal patellar tendinopathy (some authors on occasion may use the term to refer to injury of the quadriceps and distal patellar tendon in jumping athletes). Patellar tendinosis suggests structural tendon damage, with or without symptoms, while patellar tendinopathy implies both structural changes and symptoms.
Jumping athletes repetitively load the extensor tendon apparatus, during both takeoff and landing, and functional overload is believed to be a cause of patellar tendinopathy. Elite volleyball athletes have a very high prevalence of JK,between 40% and 50% (1). The morbidity associated with JK can be significant, with perhaps as many as 33% of athletes unable to participate in sport for more than 6 months (2). Some data also suggest that perhaps as many as 50% of athletes with JK may retire prematurely from their sport as a result of their knee impairment (3).
Much attention has been given to making the distinction between patellar tendinosis versus patellar tendonitis. The concept of patellar tendonitis (also spelled "tendinitis") has come under scrutiny because of a relative dearth of histopathologic evidence that inflammatory mediators are present in symptomatic tendons. In fact, contemporary research, with a focus on unfolding the microscopic biochemical, hormonal, and neuronal milieu present in patellar tendon pathology, does suggest that inflammatory mediators may be present and at work (4). Of course, this may have profound implications for clinicians and their treatment approaches.
Diagnosis and treatment approaches for patellar tendon problems are evolving. Recent research does support more use of diagnostic ultrasound (US) as opposed to magnetic resonance imaging (MRI), and conservative treatment, including eccentric exercise protocols and sclerosing injections, appears largely as successful as surgical intervention in terms of returning athletes to sport.
The remainder of this article will attempt to update the reader on the most current literature concerning the diagnosis and treatment of JK.
EVALUATION OF THE ATHLETE WITH JUMPER'S KNEE
Athletes will complain of anterior knee pain, most often localized to the infrapatellar region, although the pain may be suprapatellar involving the quadriceps tendon or in the region of the distal patellar tendon at its insertion onto the tibial tuberosity. The quality of the pain may be achy, sharp, or both. Most often, there is no history of a trauma or inciting event. The pain usually is worse during sports participation, and it may be exacerbated by any activity that increases tendon loading. In the earlier stages, the pain improves with relative rest. Patients may be unable to participate in training or competitive sport. The athlete may complain of weakness or giving way due to pain-related muscle inhibition. The clinician should understand and document the duration of symptoms, the intensity of training and number of sessions, and any recent changes to the athlete's training regimen.
Of note, it would be atypical for the athlete to complain of significant swelling or mechanical symptoms such as catching and locking, and such symptoms should elicit a more broad differential diagnosis and consideration of intra-articular injury. Complaints of numbness or tingling may suggest neuromuscular impairment and also are uncharacteristic for isolated tendon injury. When such a history is elicited, additional diagnostic work-up should be considered.
Physical examination usually reveals tenderness at the inferior patellar pole with otherwise normal neuromusculoskeletal testing. A functional strength examination, however, in which for example the athlete is asked to perform a set of squats or lunges, may elicit subtle weakness or early muscle fatigue. Functional testing also has the potential added benefit of discovering other deficits, such as faulty motor patterns or weakness elsewhere along the kinetic chain (5).
Intrinsic Risk Factors
One prospective study in an athletic cohort over a 2-yr period identifies inflexibility of the hamstrings and quadriceps as intrinsic risk factors for developing patellar tendon pain (6). Other researchers found that, in addition to reduced thigh flexibility, several other factors increased susceptibility to patellar tendinopathy, including reduced ankle dorsiflexion, an increased volume of weight training, higher body weight, increased waist girth over 83 cm in men, and better jumping performance (7-10).
Previous authors suggest that increased height, male sex, knee varus and valgus, patella alta and patella baja, increased Q angle, and limb-length inequality may be other intrinsic risk factors, although none have been confirmed in prospective trials (11). A recent cohort study by Lorbach (12) demonstrates that a longer lower patellar pole might be associated with chronic patellar tendinopathy.
Dynamic Biochemical Factors
Altered lower limb biomechanics and improper jumping and landing technique may be risk factors. Bisseling et al. recently compared ankle and knee joint dynamics between healthy volleyball players and those previously treated for patellar tendinopathy (13). The authors conclude that decreased ankle and knee flexion during the first part of a spike jump landing, a higher rate of force development during the eccentric phases of the spike jump-landing sequence, and higher knee angular velocity might increase the risk of developing patellar tendinopathy. The asymptomatic volleyball players with previous tendinopathy show less ankle and knee flexion than the healthy group. This is consistent with a stiffer landing strategy for athletes with previous JK, which is believed to place a higher strain upon the patellar tendon.
The authors suggest that players with such stiff patterns be taught to soften their landings by increasing awareness of the need for appropriate ankle and knee joint flexion, and that athletic trainers be cautious with players ramping up their training regimen by helping these players avoid too many jump-landing sequences (14) (Fig. 1).
Future research could examine other intrinsic factors, such as nerve and muscle fiber density, and the association with the development of JK. For instance, one might postulate that those with better jumping ability may have an increased density of type II muscle fibers. Perhaps the balance or imbalance of muscle fiber types could predispose an athlete to a tendinopathy like JK.
Extrinsic Risk Factors
Hard court surfaces and excessive training volume are both extrinsic risk factors that relate to JK (15,16). Beach volleyball athletes who jump and land in soft sand, thereby delivering less tendon load, have a 9% prevalence of JK as compared with a prevalence of up to 45% for indoor elite volleyball players (17).
US and MRI are both accurate in detecting structural tendon changes. US has certain clear advantages, however, including its high resolution for delineating focal changes in tendon architecture, the availability of color doppler (CD) and/or power doppler (PD) to detect subtle changes in tendon vascularity, the relative ease of access to the technology, which also is becoming more and more portable, the increased comfort for the patient, and its lower cost. Both CD and PD measure blood flow, although PD may be preferable to CD when measuring tendon vascularity because of improvements in sensitivity to flow and less artifact.
Warden et al. (18) compared MRI and US with and without color doppler in individuals with clinically diagnosed patellar tendinopathy to asymptomatic controls. They conclude that US is more accurate than MRI in confirming clinically diagnosed patellar tendinopathy, and positive findings using US with CD indicate a strong likelihood that an individual is symptomatic. As has been noted previously, this study demonstrates several symptomatic tendons with a normal appearance, and some asymptomatic tendons that are morphologically abnormal. This underscores the value of the history and examination, because imaging findings, both positive and negative, do not always correlate with symptoms.
The patellar tendons of volleyball players assessed using US and PD, as compared with asymptomatic controls, have a significantly higher prevalence of combined structural abnormalities and neovascularization. Structural abnormalities without neovascularization occur at a similar rate between those with JK and controls (19). This suggests the importance of increased tendon vascularity in clinically significant symptomatic patellar tendinosis, although it does not clarify whether this increase represents a cause or an effect.
US assessment may have a role in the risk assessment of which volleyball athletes are likely to develop JK. It is of interest that one study describes a small number of asymptomatic tendons with structural changes and neovascularization, raising the question as to whether these findings predict future development of JK (20). Subsequent research, however, shows that one third of asymptomatic tendons with US structural abnormalities will develop clinical JK (21). On the other hand, normal US combined with a normal clinical examination has been shown to carry a very low risk for the development of JK in elite volleyball players. Only 2 of 25 clinically normal and US normal tendons (approximately 2%) developed JK in 3 yr time in a study of Swedish elite junior volleyball athletes (21).
The present body of research substantiates the notion that US (particularly with CD and/or PD) is the diagnostic imaging modality of choice for patellar tendon abnormalities given its availability, portability, comfort to the patient, and the favorable cost profile.
HISTOPATHOLOGIC FINDINGS IN JUMPER'S KNEE
Tendon tissue samples from those with symptomatic patellar tendinosis, asymptomatic patellar tendinosis, and from control tendons harvested during unrelated knee surgery have been examined and compared using immunohistochemical and flow cytometry techniques. This research reveals several interesting findings with potential implications for the treatment of JK.
The recent scientific literature does suggest the presence of inflammatory mediators such as prostaglandins, interleukins, and COX-2. This is in contrast to the present prevailing mantra, which argues that diseased tendons are devoid of inflammatory markers and therefore without true "tendinitis" (4).
The histopathology of diseased tendons appears to have degenerative, regenerative, and inflammatory properties. Disorganized and discontinuous collagen fibers are seen with light microscopy. Histologic examination reveals a variety of findings consistent with degeneration (i.e., mucoid or myxoid degeneration, fatty infiltration, fibrinoid necrosis, and tenocyte necrosis) and regeneration (i.e., neovascularization, tenocyte infiltration, and chronic and acute inflammation) (4).
There is an increased concentration of nerve fibers, neurotransmitters, and neurotransmitter receptors in peritendinous and tendon tissue proper, and this may have a role in the development of tendinopathy, pain mediation, and tendon recovery (4,22).
Sympathetic innervation is increased in the perivascular paratendinous tissues of those with JK, and some postulate that what we believe are "neovessels" in diseased tendons merely represent vessels already present with increased flow caused by sympathetic nervous system input. Such vessels might be imperceptible with color or power doppler under normal circumstances (23).
Other studies have found that tenocytes themselves may produce neurotransmitters (i.e., glutamate or acetylcholine) (24,25). These substances may have modulating effects on pain, cell proliferation, and apoptosis.
Biopsy specimens from a cohort with patellar tendinosis compared with normal controls show an increased number of apoptotic cells per unit area, while at the same time showing an increase in the overall number of tenocytes. This suggests that cell death and proliferation may occur simultaneously in response to repetitive loading (26).
Scott et al. found an increased number of mast cells, and this correlates with both symptom duration and vascular hyperplasia (27). The large extracellular matrix proteoglycan, Versican, was increased in another study by Scott et al. that examines the molecular changes in pathologic tendon samples compared with controls without JK. Versican functions as both a structural and regulatory molecule. Versican deposition is believed to be a prominent feature of normal and pathological fibrocartilaginous tissues, but Versican production is up-regulated with excessive mechanical loading. The authors hypothesize that this increased Versican content may weaken the tendon by transforming tensile tendon regions to more vulnerable fibrocartilage that is less resistant to mechanical loads. Additionally, increased Versican deposition may provide the framework for angiogenesis and neovessels. It is not yet clear whether these molecular changes represent positive or pathological adaptation (28).
All of these recent findings represent small pieces of a larger histopathologic puzzle and raise questions as to potential future treatment directions. For instance, these findings imply a continued role for the use of corticosteroids in addressing inflammatory mediators, and they suggest that sympathetic blockade and pharmacologic modulation of neurotransmitters may have a role in the treatment of JK.
TREATMENT APPROACHES TO THE ATHLETE WITH JUMPER'S KNEE
Before the development of a treatment plan for JK, a thorough clinical evaluation is warranted to identify additional areas of biomechanical impairment along the kinetic chain. For instance, if during single leg stance or a hop assessment, the athlete demonstrates excessive pelvic motion, then there may be comorbid weakness of hip or lumbopelvic stabilizers affecting jumping mechanics and deserving of attention during the athlete's rehabilitation. While it may not be possible to determine whether these other impairments represent the cause or an effect of JK, a successful rehabilitation plan still hinges on restoring any deficiencies that may limit an athlete's performance (29).
Choice of conservative treatment for JK often will depend on the clinical stage. An acute or sub-acute situation will follow the usual sports medicine paradigm of treatment, including relative rest and cryotherapy, and perhaps compression with a patellar tendon strap or other unencumbering knee orthosis. Taping, massage, non-steroidal anti-inflammatory drugs, and other modalities such as therapeutic US and iontophoresis may also be used. If the athlete's performance is hampered, or when symptoms persist beyond the acute timeframe (6-12 wk), then the problem is at a more advanced stage, warranting more intensive treatment.
To measure treatment stage and effect, one may wish to use a validated outcome tool, such as the Victorian Institute of Sport Assessment (VISA), a 100-point scale that assesses symptoms, simple tests of function, and ability to play one's sport (30). The modified Blazina scale may also be useful to grade clinical status and monitor response to treatment (15,16) (Table).
Physical therapy can be very effective. Current research evidence supports eccentric exercise protocols as the standard. A recent review of studies testing eccentric exercise protocols by Visnes and Bahr (31) show a positive effect in each of seven studies evaluated. Because of significant variation in study methodology, the authors do not recommend one specific protocol. They surmise that an effective eccentric protocol should use a decline board, permit the athlete to perform the exercise with some discomfort, and involve a break from sports participation during the treatment. They estimate that eccentric training provides a 50%-70% chance of improving knee function and pain and a return to pre-injury level of sports activity.
Zwerver et al. recently performed a biomechanical evaluation of the single-leg decline squat often used both as a clinical assessment tool and as a rehabilitation exercise. They found that squats at decline angles of greater than 15° results in 40% increase in patellar tendon forces, while at decline angles of greater than 60°, patellofemoral forces increase more than patellar tendon forces. The authors conclude that decline angles between 15° and 30° can be used to increase the patellar tendon load, while knee flexion greater than 60° should be avoided to prevent excessive patellofemoral forces (32) (Fig. 2).
Sclerosing injections of hypervascular areas in patellar tendinopathy using US and CD guidance shows promise as a treatment for those with chronic JK. Hoksrud et al. performed a randomized placebo-controlled crossover trial that found an overall 84% success rate for the treatment as defined by an athlete's return to training with little or no pain. Participants required between two and five injections over 8 months. The control group showed a clear improvement after crossing over to active treatment (33).
Dry-needling the site of tendinosis under US guidance followed by autologous blood injection has recently been tested in a prospective cohort of athletes (non-volleyball players) with a marked improvement in the VISA score and a return to sports participation. The authors performed dry-needling of the affected area for 1 min, followed by autologous blood injection. The procedure was repeated once after one month. The authors suggest that all participants returned to sporting activity, and follow-up US examination at 6-22 months demonstrates a reduction in tendon thickness and a decrease in the size of the hypoechoic region of tendinosis (34).
Two very recent trials demonstrate promising results for treating JK with extracorporeal shock wave therapy (ECSWT). Vulpiani et al. treated 73 athletes with imaging-confirmed JK lasting at least 3 months, and after three to five ECSWT sessions and over a follow-up period of 24 months, satisfactory results with return to sports participation were obtained in 73.5% of tendons treated (as measured by Blazina's clinical classification) (35).
Wang et al. (36) compared ECSWT to conservative treatment (with NSAIDs, physical therapy modalities, and primarily eccentric exercise), prospectively randomizing a group of 50 patients with chronic patellar tendinopathy (symptoms at least 6 months; none were volleyball athletes). At 2-3 yr follow-up, 90% of the intervention group showed an excellent or good outcome compared with 50% in the control group (excellent = no pain in all activities; good = mild pain and overall 75% improvement). Return to sport was permitted in 4-6 wk.
It recently has been demonstrated that low-intensity pulsed US (LIPUS) is not effective for treating chronic patellar tendinopathy. The authors performed a randomized and placebo controlled trial, using both active and sham LIPUS, and both groups were given standardized eccentric exercises. After 12 wk of treatment, there was no between-group difference in the visual analog scale score (37).
There has been one randomized, controlled trial comparing open patellar tenotomy to eccentric exercise training in a group with severe patellar tendinopathy (no volleyball players included). The participants had disabling exercise-related symptoms for at least 3 months, MRI findings of tendon thickening and increased signal changes, and a willingness to undergo surgery. After 12 months of follow-up, no significant differences were noted in VISA scores, functional testing, overall treatment satisfaction, or return to sports (38). Previous retrospective evidence of open tenotomy showed good to excellent results in jumping athletes, although volleyball players in particular seemed to have more unsatisfactory results (39).
Other authors recently have studied arthroscopic surgical procedures for recalcitrant patellar tendinopathy. All of these trials were uncontrolled, and all showed positive results. Lorbach et al. described an arthroscopic resection of the lower patellar pole in MRI-confirmed patellar tendinopathy with excellent or good outcomes as early as 6 wk post-operatively through the 2-yr follow-up (40).
Willberg et al. described a novel method of arthroscopic shaving of the dorsal proximal patellar tendon with good results in 13 of 15 tendons. Athletes were permitted to return to sport fully at 2 wk, and elite athletes returned to competition as soon as 2 months postoperatively. The authors boast that while their results compare favorably to studies of polidocanol sclerosing injections, the injection therapy requires a mean of three treatments, 6-8 wk apart, adding up to 4-6 months of total treatment. They suggest that an athlete facing an important competition may wishto consider this new arthroscopic approach given the rapid return to competitive sport demonstrated in this pilot study (41).
The same authors also report upon a method of arthroscopic shaving and simultaneous examination under US and CD, thereby improving the accuracy of the procedure and avoiding trauma to adjacent normal tissues (42).
Recent research findings support the use of diagnostic US with and without CD or PD, rehabilitation protocols involving eccentric decline squats, and several interventional treatment techniques including sclerosing polidocanol injections, ECSWT, and arthroscopic shaving of the lower dorsal patellar pole. Future studies likely will evaluate further the neuronal, vascular, and cellular architecture of patellar tendinosis, and treatment approaches may attempt to modulate neurotransmitters or inflammatory mediators and regulate cellular processes of tenocyte apoptosis and reproduction.
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