Jumpers Knee: Patellar Tendinitis

Malcolm Davies and Fares Haddad give an update on patellar tendinitis or jumpers knee

Patellar tendinitis or jumpers knee as it is more often known is the most common knee disorder found among competitive athletes(1). Those who play high impact sports, involving bursts of intense or repeated stress, tend to be most affected, notably basketball and volleyball players (these sports demand twisting on the spot, deep flexion and sprinting). However, anyone from the casual jogger to contact sport players may develop the condition – all too often with far-reaching consequences. One study has estimated that more than half of athletes diagnosed with this condition were forced to retire from their sporting activity(2).

Classically, patellar tendinitis (jumpers knee) has been explained as chronic inflammation of the tendon connecting the kneecap (patella) to the main shin bone (tibia), at the point of connection to the kneecap. Recent research has, however, effectively revised our understanding of the condition – and with it a change in terminology: it is more correct these days to refer to the condition as tendinosis.

Symptoms start with pain after exercise which can progress to pain during exercise. In extreme circumstances the tendon may weaken and rupture. The pain can be debilitating and prevent athletes from performing at a competitive level or even force them to retire.

Jumpers knee - Risk factors

Ferretti(3) was the first to describe the causes of patellar tendinosis or jumpers knee, dividing them into intrinsic and extrinsic factors. Intrinsic causes were:

* gender

* age

* knee alignment

* Q-angle (longitudinal angle of the quadriceps muscle)

* patella position

* tibial/femoral rotation

* the gross shape and stability of the knee. Extrinsic causes were in essence:

* the nature of the activity (jumping and continuous stress being the major culprits) and

* the consistency of the playing surface (hard surfaces such as concrete being most risky). Ferretti established the school of thought that extrinsic factors were the more significant, causing chronic overload of the extensor mechanism, which inflamed and weakened the patellar tendon.

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In the 1990s a British research team, using MRI scanning, proposed an alternative causation, suggesting that the tendon was being crushed by the patella when it was forced into the sharp angle created by extreme flexion(4), in effect producing an impingement syndrome. A more recent study on the motion of the knee in flexion has shown that the tendon is not being kinked and crushed(5). So Ferretti’s epidemiologically- based causes currently receive greater support.

However, recent research has shifted the bias of significance away from extrinsic factors and towards more intrinsic causations. In an American study of healthy competitive athletes, Witvrouw et al(1) used anthropometric data to try to detect a link between intrinsic risk factors and the development of tendinosis. All 138 subjects in this prospective trial performed the same amount of high intensity, highly competitive activities, across a variety of disciplines, and 19 of them developed tendinosis. The only identifiable common risk factors were poor flexibility of the hamstrings and quadriceps muscle groups. Contrary to Ferretti’s belief, there was no gender difference in risk. This research suggests that an athlete may be able to reduce their tendinosis risk with a good stretching regimen.

Another recent US study supports the findings of Witvrouw et al, and also draws attention to the importance of intrinsic risk factors. This study shows a higher incidence of the condition among subjects whose patellar tilt was at a greater angle during flexion(6). It would seem logical that if the patellar tilt is greater (resulting in increased tension on the top of the patella from the quadriceps tendon), then a quadriceps stretch regime ought to be able to reduce the strain on the tendon.

Likewise, the greater an athlete’s ‘Q’ angle, the more strain is likely on the knee, increasing the risk of knee pain and tendinosis. The Q angle is an estimate of the alignment of the knee in relation to the angle of the thigh and lower leg. Variations in the angle are usually related either to rotation at the hip joint or the shape of the foot on standing. Thus someone with ‘knock knees’ would have a large Q angle. People with flat feet force the outsides of their feet out and push their knees inwards. Studies have shown that some athletes with patellar tendon problems have an increased Q angle(7).

Management

Physiotherapy can enable affected athletes to stabilise their condition, avoiding the need for surgery(8), and even to make good enough progress to return to their previous levels of activity. Eccentric loading of the tendon, as happens when performing a decline squat, seems to give good results, although it is unclear exactly why this should be. Recent research has recommended a protocol for this rehab regime(8), with some variations from that described by Rod Jaques in SIB44 (see Figure 1, above left). In particular, note that the optimum angle of the board on which the athlete stands is recommended to be 25 degrees, not 45 degrees.

The subject should lower slowly from standing upright on one leg to as deep a flexion position as pain allows, performing three sets of 15 reps, twice daily. For best results the athlete should exercise through pain with a gradually increasing load, achieved with hand-held weights(8). The rate of progression depends on the athlete’s level of disability: they may initially need to perform the return to standing using two legs, but ultimately they should aim to be performing the entire manoeuvre using the affected leg only.

Recent developments

The most exciting development has been the introduction of prolotherapy, claimed to be as successful as surgery in treating symptoms (9). This claim is based on observational studies which show an increased formation of blood vessels in the affected tendons, along with nerve growth(10). When these blood vessels are destroyed with a sclerosant (injectable irritant) under ultrasound guidance, pain is relieved. The reduction in symptoms appears to be in proportion to how much of the abnormal blood vessel growth is eradicated(11). The same authors have discovered unusually high levels of pain receptors and stimulators within the affected areas of tendon(10).

What exactly is responsible for creating the pain of patellar tendinosis remains unclear: the tendon itself or aberrant feedback from nocioceptors in surrounding structures(12).

Regardless of where the pain is coming from, what is clear is that the pain and collagen damage are not a result of inflammation (13). None of the usual chemicals or cells associated with inflammation are present in patellar tendinosis. This would cast doubt on the rationale for treating this condition with steroids or NSAIDS.

In another development, animal studies of blood injections have shown some promising results for tendon strengthening (14). Blood carries many cells that signal the need for repair. Initial studies have shown that tendons injected with blood are stronger and, at a cellular level, have correctly arranged collagen fibres, which would suggest that the blood constituents organise appropriate, normal healing. Tendons are notoriously slow to heal and have high rates of re-rupture because of their poor blood supply. This study only assessed short-term strengthening, but, if it gets past the hypothetical stage, it could have broad implications for the treatment of damaged or ruptured tendons.

Surgery

Where surgery is necessary, the inflamed fat pad surrounding the tendon is removed; the visibly abnormal areas of tendon are excised and any abnormal blood vessels are cauterised. Any abnormal tissues on the patella at the site of tendon attachment will also be removed. This can be done either as open surgery or a keyhole procedure (under local, or more usually, general anaesthetic). Overall outcomes are comparable, but on average the arthroscopy patient will enjoy a four-month advantage in recovery time and return to full sporting activities, because of the less invasive approach.

Conclusion

Patellar tendinosis (Jumpers Knee) can be a disastrous condition for an athlete if not dealt with promptly. Yet potential sufferers could probably be identified with simple screening and given prophylactic stretching and physiotherapy exercises. A simple pro forma could be used to assess those most at risk of developing symptoms (see box). Further research is needed to decide how useful other rehab aids such as orthotics and knee braces might be in treatment or prevention of patellar tendinosis. It may be impossible to eradicate the condition from sports that carry the highest risk, but prolotherapy and autologous blood injection could one day substantially reduce the need for surgery.

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References

1.Witvrouw E, Bellemans J, Lysens R, Daniels C, Cambier D, ‘Intrinsic Risk Factors for the Development of Patellar Tendinitis’,Am J Sports Med, 29 (2001) (2 (mar-apr)), 190-195.

2. Kettanen M, Kvist E, Alnen UM, Kujala, ‘Long term Prognosis for Jumpers Knee in Male Athletes. A Prospective Follow-up’, Am J Sports Med, 30 (2002) (5 (sep-oct)), 689-692.

3.Ferretti A, ‘Epidemiology of Jumpers Knee’, Sports Med 3 (1986) (4 (jul-aug)), 289-295.

4.Johnson DP, Wakely J, Watt I, ‘Magnetic Resonance Imaging of Patellar Tendinitis’, J Bone Joint Surg Br, 78 (1996) (6 (may)), 452-457.

5.Schmid MR, Hodle J, Cathrein P, Duewell S, Jacob HA, Romero J, ‘Is Impingement the Cause of Jumper’s Knee’, Am J Sports Med, 30 (2002) (3 (may-jun)), 388-395.

6.Tyler TF, Hershman EB, Nicholas ST, McHugh MP, ‘Evidence of Abnormal AP Patellar Tilt in Patients with Patellar Tendinitis with use of a New Radiographic Measurement’, Am J Sports Med, 30 (2002) (3 (may-jun)), 396-401.

7.BaileyMP, Maillerdet FT, Messenger N, ‘Kinematics of Cycling in Relation to Anterior Knee Pain and Patellar Tendinitis’, J Sports Sci, 21 (2003) (8 (aug)), 659-657.

8.Young MA, Cash JL, Purdam CR, Kiss ZS, Alfredson H, ‘Eccentric Decline Squat Protocol for Patellar Tendinitis in Volleyball Players’, Br J Sports Med, 39 (2005) (2 (feb)), 102-105.

9. Alfredson H, Ohlberg L, ‘Neovascularization in Chronic Patellar Tendonosis. Promising Results After Sclerosing Neovessels Outside Tendon, Challenges Need for Surgery’, Knee Surg Sports Traumatol Arthrosc, 13 (2005) (2 (mar)), 74-80.

10. Alfredson H, Forsgren S, Thorsen K, Lorentzon R, ‘Tendon Tissue Demonstrated High Amounts of Free Glutamate and Glutamate NMDAR-1 Receptors but no Signs of Inflammation in Jumper’s Knee’, J Orthop Res, 19 (2001) (5 (sep)) 881-886.

11. Alfredson H, Ohlberg L, ‘Neovascularization in Chronic Patellar Tendonosis. Promising Results After Sclerosing Neovessels Outside Tendon, Challenges Need For Surgery’, Knee Surg Sports Traumatol Arthrosc, 13 (2005) (2 (mar)), 74-80.

12.Koen HC, Roeland JJ et al, Patellar ‘Tendinopathy in Athletes; Current Diagnostic and Therapeutic Recommendations’, Sports Med, 35 (2005) (1), 71-87.

13.Khan KM, Cook JL, Bonar F, Harcourt P, Astrom M, ‘Histopathology of Common Tendinopathies. Update and Implications for Clinical Management’, Sports Med, 27 (1999) (6(jun)), pp. 393-408.

14.Taylor MA, Normal TL, Clovis NB, Blake JD, ‘Response of Rabbit Patella Tendon After Autologous Blood Injection’, Med Sci Sports Ex, 34 (2002) (1 (jan)), 70-73.