Patellar Tendinitis

Patellar tendinopathy, commonly known as jumper's knee, is an overuse injury that causes pain at the inferior pole of the patella. It is characterised by focal degeneration of the proximal patellar tendon. The old name, "tendinitis", implies an acute inflammation that the histology does not show, so use tendinopathy (or tendinosis) in the exam.

Who gets it. Prevalence is high in jumping sports: in a study of elite athletes (Lian) it was 44.6% in volleyball and 31.9% in basketball. Patients are typically aged 15-30, and men are affected more often than women, about 2:1.

Risk factors. Extrinsic factors are hard playing surfaces and increased training volume. The intrinsic ones are poor quadriceps flexibility, ankle dorsiflexion stiffness and vertical jump height.

The tendon. The patellar tendon connects the patella to the tibial tubercle. Pathology is most common at the inferior pole, in the proximal posterior aspect of the tendon, and that posterior proximal insertion is a relatively hypovascular zone, the "watershed area".

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Tendinosis, not tendinitis. The condition was historically called tendinitis, but it is a degenerative process. Histology shows four features:

1. Angiofibroblastic hyperplasia - neovascularisation with nerve ingrowth
2. Mucoid degeneration - increased ground substance
3. Collagen disorganisation - loss of the parallel type I collagen bundles
4. Absence of inflammatory cells - no neutrophils or macrophages

The continuum model (Cook and Purdam). Rather than a binary "inflamed versus degenerate" view, tendon pathology is best understood as a continuum, which guides load-based rehabilitation.

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"Jumper's knee" is an umbrella term. The same overload disorder can strike anywhere along the extensor mechanism, and the examiner will expect you to localise it by the site of maximal tenderness.

The pathology (degenerative tendinosis), the imaging (ultrasound and MRI) and the loading-based rehabilitation are the same wherever it sits. The practical point is to palpate the superior pole, inferior pole and tubercle separately, so that you label the correct tendon and watch the right spot on imaging.

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History. Anterior knee pain localised to the inferior patellar pole, aggravated by jumping, landing and deceleration, which are the eccentric loads. Ask about a recent increase in training volume. Pain with prolonged sitting (the "movie sign") can overlap with patellofemoral pain syndrome.

Bassett's sign. In full extension the patellar tendon is lax and the inferior (distal) pole can be palpated. At 90 degrees of flexion the tendon tightens like a trampoline, and the tension makes the posterior aspect of the proximal tendon impalpable. Tenderness in extension that disappears in flexion is a positive sign, and it distinguishes patellar tendinitis from other anterior knee pain.

Differential diagnosis. Rule out Sinding-Larsen-Johansson apophysitis in adolescents, patellofemoral pain syndrome and Hoffa's fat pad impingement. Location and patient age are the key discriminators.

Radiographs are usually normal and miss soft-tissue pathology, but they rule out bony causes. They may show:

• An elongated inferior patellar pole (impingement theory)
• Intratendinous calcification (chronic)
• Osgood-Schlatter or Sinding-Larsen-Johansson sequelae

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Ultrasound is the first-line imaging modality. Assess thickness, echotexture, calcification, cortical change and Doppler flow systematically. The typical findings are tendon thickening and a hypoechoic area of focal degeneration. It is dynamic, cheap and allows bilateral comparison, but it is operator dependent.

Doppler flow shows neovascularisation. It is the key marker of active neo-neurovascularisation and correlates with pain.

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MRI has high sensitivity (95%), showing increased signal on T2/STIR in the proximal posterior tendon. It defines the anatomy and rules out other pathology (meniscus, cartilage, bone oedema), but it is expensive and static, with a high false-positive rate. Signal abnormalities can be present in asymptomatic athletes, the "imaging-clinical mismatch": treat the patient, not the scan.

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Progressive loading is the treatment. Injections are adjuncts, and surgery is the last resort after failed eccentric rehabilitation.

Algorithm

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ConservativeInterventionalSurgical

First steps (stages 1-2). Relative rest from aggravating activities such as jumping, ice for symptom control, and a short course of NSAIDs for analgesia rather than healing. Correct the biomechanics with orthotics or technique modification.

The rehabilitation protocol. This is the gold standard, and eccentric loading is the key to remodelling. Educate the patient about the long recovery timeframe, 3-6 months. The progression runs:

1. Isometric loading (e.g. Spanish squat hold) - analgesic effect
2. Isotonic loading - slow heavy resistance
3. Eccentric loading - decline board squats
4. Functional and plyometric work - return-to-sport progression

The decline board. Single-leg squats on a 25-degree board, 3 sets of 15, twice daily, for a minimum of 12 weeks. The protocol is "pain allowed": mild pain during the exercise is acceptable. Adherence to the eccentric programme is the single most important factor in conservative success.

Decline Board Mechanism

The 25-degree decline board increases the knee extension moment and isolates the patellar tendon by minimising calf/ankle-dorsiflexion and hip contribution. In Purdam's pilot, decline-board eccentrics dropped mean VAS from 74 to 29 over 12 weeks while flat-foot squats barely changed - the slope, not the eccentric mode alone, drives the benefit.

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How much pain is allowed. Loading is governed by a pain-monitoring model, not pain avoidance. Pain during the exercise is acceptable up to about 5 out of 10 on a VAS, provided it settles back to baseline by the next morning and morning stiffness is not creeping up week to week. If pain exceeds that ceiling or lingers beyond 24 hours, step the load down a level.

Monitoring. Day to day, follow the single-leg decline-squat pain score and the trend in morning symptoms; the VISA-P tracks progress over weeks. Complete rest is the wrong advice: it de-loads and weakens the tendon, which needs progressive, tolerable load to remodel.

Injection relief is temporary, and patients should always be cautioned that it is not the same as true healing.

Platelet-rich plasma (PRP) is used on the theory that introducing growth factors stimulates healing. The evidence is conflicting, some studies showing benefit over saline and others no difference, and it is generally accepted as a second-line option.

Sclerosing injection (polidocanol) targets the neovessels seen on Doppler ultrasound; the theory is that it destroys them and the nerve endings that accompany them. It gives good short-term pain relief.

High-volume image-guided injection (HVIGI) uses saline with hydrocortisone, peritendinous only. It strips neovessels and nerves from the tendon surface ("chemical adhesiolysis").

Extracorporeal shockwave therapy (ESWT) works through mechanotransduction and neovascular and neural modulation, stimulating a healing response. A systematic review of RCTs found only limited evidence: results are inconsistent, and it is best viewed as an adjunct, not a proven stand-alone cure.

NO Corticosteroids

Intratendinous corticosteroid injection is strictly contraindicated and is an immediate fail point in a viva. It inhibits collagen synthesis, causes collagen necrosis and significantly increases the risk of acute tendon rupture. The hydrocortisone in HVIGI is peritendinous only.

Indications. The criteria for surgery are:

• Failure of a minimum of 6 months of supervised conservative care (eccentrics)
• Blazina Stage 3 - performance limiting, unable to compete at the desired level
• MRI (or ultrasound) confirmation of focal pathology
• Pain localised to the inferior pole

Timing and the evidence. The evidence below sets a lower floor than six months. Bahr's trial found open tenotomy no better than eccentric training at 12 months and supports trialling eccentric training for at least 12 weeks first; the guidance reserves surgery for failure of at least 3 to 6 months of structured loading.

Options. Arthroscopic and open debridement are described under Surgical Technique. Tenotomy makes longitudinal incisions in the tendon to stimulate bleeding and healing. None is a quick fix: rehabilitation is still required after surgery.

Tendon rupture is the most devastating complication. It is rare in virgin cases, and the risk increases with multiple steroid injections. Reconstruction is complex and often needs augmentation because of poor tissue quality.

The infrapatellar branch of the saphenous nerve runs transversely across the proximal tibia and tendon. A transverse incision risks it and leaves lateral numbness, so longitudinal incisions are safer.

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Conservative treatment succeeds in 60-80% with a proper eccentric programme. After surgery, 70-80% return to their pre-injury level, and 70-90% have good or excellent results.

Return to play. 50-60% return to their previous level of sport. Many return to sport, but at a lower level or with residual symptoms.

Refractory cases. Consider other diagnoses (Hoffa's fat pad, plica) and look for biomechanical contributors at the hip and ankle.

Practice Variation:

• There is no joint-registry equivalent for tendinopathy (registries cover arthroplasty/implants), so the evidence base is trial- and consensus-driven rather than registry-driven.
• Practice differs mainly in the interventional middle ground: PRP, sclerosing/high-volume injection and extracorporeal shockwave are used more readily in some sports-medicine systems (often physician-led, before any surgical referral), whereas other systems move from supervised loading straight toward surgical opinion. The high-level evidence for these adjuncts remains limited, so their use reflects local resources and clinician preference rather than strong guideline mandate.
• The one near-universal agreement across all guidance is that structured progressive loading is first line and intratendinous corticosteroid is avoided because of rupture risk and inferior long-term outcomes.