Clinical synthesis based on the most recent meta-analyses and international consensus statements: Cochrane Lopes 2025, the 2025 Dutch guideline, SR/MA Nutarelli 2023, NMAs Challoumas 2021 and 2023, NMA Liu 2026, RCT Breda 2021 (PTLE), the ICON 2019 terminology consensus.

Patellar tendinopathy, commonly called jumper's knee or genou du sauteur (its French name), is a clinical condition of mechanical and overload origin, characterised by pain localised at the inferior pole of the patella (proximal insertion of the patellar tendon), proportional to load.¹,² Long described as "tendinitis", it is now placed in the category of non-inflammatory overload tendinopathies (“tendinoses”): histological studies of tendon biopsies find disorganisation of the collagen fibres, an increase in ground substance and neovascularisation, without a classic inflammatory infiltrate.³ This nuance shapes the therapeutic approach: one does not suppress an inflammation, one guides tendon adaptation to load. 🦵

How is this condition defined, who does it affect and what are the risk factors?

The ICON 2019 terminology consensus (Scott et al., Br J Sports Med 2020) retains the term “tendinopathy” (in English: patellar tendinopathy; in French: tendinopathie rotulienne or patellaire) rather than tendinitis or tendinosis.¹⁶ The classic site of pain is the inferior pole of the patella (proximal insertion, 95 % of cases); distal forms (insertion on the anterior tibial tuberosity) are rare in adults and more frequent in paediatrics (Osgood-Schlatter disease).¹,⁴

The prevalence is particularly high in jumping sports. The Nutarelli 2023 meta-analysis (Orthop J Sports Med, 73 studies, n > 11,000 athletes), the most recent and most comprehensive epidemiological SR/MA to date, establishes an overall prevalence of 18.3 % in athletes, compared with only 0.1 % in the general population.⁵ By sport: volleyball 24.8 %, basketball 20.8 %, football/soccer 6.1 %. Prevalence is 2× higher in adults (21.3 %) than in minors (10.1 %), and higher in men (17 %) than in women (11.2 %). The incidence per season reaches 7 % in athletes practising a jumping sport.⁵ The historical cohort of Lian 2005 (Am J Sports Med, n = 613 elite Norwegian athletes, 9 sports) already found a point prevalence of 14.2 %, reaching 44 % in volleyball and 32 % in basketball, confirming the robustness of the sport-specific gradient.⁶ In male professional footballers, the UEFA cohort of Hägglund 2011 (n = 2,229 players, 7 seasons) documented a point prevalence of 2.4 % and a higher incidence per 1,000 match hours on artificial surfaces.⁷

The risk factors are multifactorial. The Sprague 2018 systematic review (Br J Sports Med) of 31 studies (6 prospective, 25 cross-sectional) failed to identify a modifiable factor with strong evidence, but established significant associations for several modifiable variables.⁸ The synthesis of the 2018-2023 literature brings out the following factors:

• Training load : high weekly jump volume, sudden increase in intensity, high competition frequency. This is the most consistent factor: the condition is load-induced by definition.²,⁸,⁹
• Poor ankle dorsiflexion (< 36.5°): Backman & Danielson 2011 (Am J Sports Med, 1-year prospective cohort, 90 elite junior basketball players) showed that subjects with more limited dorsiflexion developed ~2 times more patellar tendinopathy.¹⁰ Mechanism: limited dorsiflexion is compensated by increased knee flexion and anterior tibial translation on landing.
• Quadriceps and gluteal strength deficit: associated with poor absorption of stresses on landing and excessive loading of the tendon.⁹,¹¹
• Landing mechanics : high peak landing force, landing in dynamic valgus, little hip flexion, poor neuromuscular control (Sprague 2018, Theodorou 2023).⁸,¹²
• Anthropometry : high BMI, larger Q angle, particular tendon dimensions; non-modifiable factors.²
• Male sex : OR ≈ 1.5 in adult men (Nutarelli 2023). Probably linked to jump power and cumulative overload.⁵
• History of tendinopathy or of lower-limb pain: a very strong predictor of recurrence.⁸
• Competition volume : Hägglund 2011, in the UEFA cohort, shows that match frequency increases the risk.⁷

What happens inside the tendon and how does it evolve naturally?

The most widely used conceptual framework remains the Cook & Purdam 2009 continuum (PMID 18812414), revisited and nuanced in 2016. It describes three states of tendon structure that can coexist, move in one direction or the other, and guide load modulation:¹³,¹⁴

1. Reactive tendinopathy : proliferative non-inflammatory response to acute overload (sudden increase in jump volume, return to sport after a break, etc.). The tendon thickens transiently through an increase in proteoglycans to resist stress. A reversible state with a load reduction and analgesic isometrics.
2. Tendon dysrepair (remodelling) : if overload persists, the matrix becomes disorganised, cellularity increases, angiogenic factors appear (new vessels). A partially reversible state: progressive loading (HSR, PTLE, eccentric) stimulates remodelling.
3. Degenerative tendinopathy : areas of focal cell necrosis, severe matrix disorganisation, dense neovascularisation. Often located in the proximal portion of the patellar tendon (enthesis junction) and surrounded by still-healthy tissue. The structural changes are poorly reversible; the therapeutic goal becomes to optimise the function of the remaining healthy tissue to compensate for the degenerated area.¹⁴

The model is conceptual and educational. The three states can coexist within the same tendon (a degenerative area surrounded by reactive tissue), and they cannot be formally distinguished without biopsy. Its clinical value lies in guiding load modulation : a "reactive" tendon (a volleyball player at the start of the season with jump overload for 3 weeks) responds to an immediate load reduction and to isometric work, whereas a "degenerative" tendon (a 30-year-old basketball player with pain for 18 months and marked ultrasound findings) requires prolonged remodelling.¹⁴ The natural history of patellar tendinopathy without adequate intervention is unfavourable. The historical cohort of Kettunen 2002 (Am J Sports Med, 15-year follow-up of male athletes) documented that more than 50 % of athletes with jumper's knee had to give up their sport, and that symptoms can persist for years.¹⁵ Cook & Purdam 2009 stress that the condition rarely resolves spontaneously as long as the athlete continues to be exposed to the triggering activities.¹³ An active and progressive conservative approach, started early, is therefore the rule.

How can patellar tendinopathy be assessed and diagnosed with certainty?

🔗 Copy

The diagnosis of patellar tendinopathy is essentially clinical and rests on three pillars: the precise location of the pain at the tip of the patella, the dose-response relationship with energy storage and release activities, and the reproduction on the decline squat performed on one leg.¹,² The Muaidi 2023 diagnostic review (Knee Surg Sports Traumatol Arthrosc) of clinical tests for patellar tendinopathy confirms that no single test has perfect sensitivity and specificity; the diagnosis results from a cluster of clinical findings.³ Imaging is not recommended as a first-line investigation : the correlation between structural abnormalities on ultrasound/MRI and symptoms is poor; a thickened tendon with neovascularisation can be asymptomatic in a healthy jumper.⁴ Treat the patient, not the image.

Which questions should you ask to understand the patient and their history?

The history opens all the reasoning. 📝 It should characterise the pain, identify actionable risk factors and confirm the typical load-induced pattern.²,⁵

• Precise location of the pain : ask the patient to point with one finger. Typical patellar tendinopathy is almost pinpoint at the inferior pole of the patella (95 % of cases, proximal insertion of the patellar tendon).¹ Diffuse, medial or retropatellar pain should prompt reconsideration of the diagnosis.
• Mode of onset : insidious and progressive over several weeks, typical of an overload tendinopathy. Pain of sudden onset after a jump, with a sensation of a “pop”, should raise suspicion of an avulsion fracture of the inferior pole or a partial patellar tendon rupture : a red flag.
• Load-pain dose-response relationship (pathognomonic): the pain appears and intensifies during jumps, landings, decelerations, sprints, going up/down stairs, deep squats. The “warm-up” pattern is common: initial pain that decreases with warming up, then reappears after exercise and the next morning.²
• Recent changes in training load : return after a break, sudden increase in jump volume or match frequency, change of surface (wooden floor → asphalt), of footwear, of coach or of programme.⁵
• Sporting profile : volleyball, basketball, jumping sports (gymnastics, diving, athletics: long jump, high jump, triple jump), fast running or changes of direction.⁶,⁷
• Personal history of tendinopathy (patellar or other): the strongest risk factor for recurrence.⁹
• Psychosocial profile : fear of movement, catastrophising, beliefs about pain (“my tendon is going to rupture, I have to stop”), level of self-efficacy; these are major predictors of chronicity (Mallows 2017).¹⁰
• Baseline VISA-P score : 8 questions (0-100, 100 = asymptomatic), the reference PROM tool, validated internationally since Visentini 1998.¹¹ It allows severity to be quantified objectively and progress to be tracked.

Which clinical tests should be performed and which other conditions must be ruled out?

The physical examination combines palpation, functional tests and assessment of the kinetic chain. 🩺 No single test is sensitive and specific enough to establish the diagnosis: it is their convergence that confirms it.³

Localised palpation : the most reliable and reproducible test. With the knee in full extension (quadriceps relaxed to expose the inferior pole), direct pressure on the inferior pole of the patella reproduces the familiar pain. The pain disappears when the quadriceps is contracted (the passive flexion sign of Cook). Focal thickening compared with the unaffected side is suggestive.¹

Single-leg decline squat (SLDS) : the most useful functional provocation test. Standing on a board inclined at 25° (decline), the patient performs a single-leg squat to 60° of knee flexion. Reproduction of the familiar pain at the tip of the patella strongly favours patellar tendinopathy.¹,² The specific increase in load on the patellar tendon (vs a standard squat) explains its greater sensitivity.

Kinetic chain assessment :

• Ankle dorsiflexion range (“knee-to-wall” test): a distance < 9-10 cm is a demonstrated risk factor (Backman 2011).¹²
• Quadriceps strength (isometric, Sorensen position or hand-held dynamometry): an asymmetry ≥ 10 % vs the unaffected side is suggestive.²
• Hip abductor and external rotator strength : weakness associated with dynamic valgus on landing.¹³
• Qualitative single-leg squat / drop jump : observation of dynamic knee valgus, hip flexion and neuromuscular control.²,¹³

Place of imaging : the McAuliffe 2016 SR/MA showed that ultrasound abnormalities predict on average a modest increase in the risk of developing tendinopathy in asymptomatic athletes, but with insufficient specificity and predictive value for routine clinical use.¹⁴ Imaging is justified in 4 situations:

1. Suspected patellar tendon rupture or avulsion fracture of the inferior pole (ultrasound or MRI).
2. Failure of at least 12 weeks of well-conducted conservative treatment → reassess the diagnosis.
3. Suspected alternative diagnosis (meniscal lesion, symptomatic plica, stress fracture, tumour process).
4. Surgical request, as a preoperative assessment.

🎯 The differential diagnosis must be systematic because several conditions can mimic patellar tendinopathy:

• Patellofemoral pain syndrome (PFPS) : diffuse retro/peripatellar pain, aggravated by prolonged sitting (the cinema sign), going up/down stairs, deep squatting. No localised pain at the tip of the patella.¹⁵
• Infrapatellar fat pad syndrome (Hoffa's disease) : pain on either side of the patellar tendon (and not on the tendon), aggravated in hyperextension. Hoffa's test (para-tendinous pressure in extension reproduces the pain, not the squat).
• Symptomatic medial synovial plica : anteromedial pain, clicking sensation, sometimes associated bursitis. The plica snap test. Diagnosis is often delayed in adolescent athletes.
• Meniscal lesion (particularly of the anterior horn of the medial meniscus): pain in deep flexion, locking, positive McMurray. Beware of the reverse trap: the Petrolo 2022 case (PMC9512301) reports a 15-year-old football player labelled with a “lateral meniscal lesion” on MRI, in whom clinical examination found no meniscal signs and whose pain was due to patellar tendinopathy.¹⁶
• Prepatellar bursitis : superficial anterior swelling (over the patella), pain on direct pressure on the bursa.
• Sinding-Larsen-Johansson disease (child aged 10-13): pain at the inferior pole of the patella with radiological fragmentation. Apophysitis of the proximal insertion of the tendon.
• Osgood-Schlatter disease (adolescent aged 11-15): pain at the anterior tibial tuberosity (distal insertion of the tendon). Apophysitis.
• Quadriceps tendinopathy (above the patella): rarer, found in elite jumpers and weightlifters.
• Medial patellofemoral ligament injury / patellar instability : episodes of dislocation/subluxation.

Should patients be classified (VISA-P, clinical stages) and what are the benefits?

Yes, classification is useful for standardising, monitoring and stratifying. Several systems coexist:

1. VISA-P score (Victorian Institute of Sport Assessment-Patella) from Visentini 1998: the internationally recognised PROM tool.¹¹ 8 questions scored from 0 to 100: daily pain, functional capacity, sports participation. Score 100 = asymptomatic. MCID 13-15 points. Recommended for baseline measurement, follow-up and return-to-sport criteria.
2. Blazina clinical staging classification (modified) is useful for teaching how to adapt load management:¹⁷
   • Stage 1 : pain only after activity, without functional limitation. Sport possible with adjustments.
   • Stage 2 : pain at the start of activity (warm-up), during and after, but performance preserved. Training modifications.
   • Stage 3 : pain during and after, limited performance. Significant reduction or temporary cessation of high-load activities.
   • Stage 4 : pain in activities of daily living, increased risk of rupture. Stopping sport, intensive management.
3. Cook-Purdam continuum (reactive/dysrepair/degenerative): guides load modulation (chapter 1).¹⁵

The management of patellar tendinopathy has undergone a conceptual revolution over the last thirty years. The modern approach moves radically away from passive modalities (rest, NSAIDs, corticosteroids, ultrasound) in favour of an active approach centred on progressive loading, supported by patient education and pain monitoring. The Challoumas 2021 network meta-analysis (BMJ Open Sport Exerc Med, 33 RCTs covering 28 modalities) confirms the primacy of progressive loading exercise, HSR and PTLE being common frameworks, with no established superiority of one over the other, whereas PRP as monotherapy is not superior to exercise alone.¹,²

Where do you start? What is the recommended hierarchy of interventions?

The Malliaras 2015 synthesis (JOSPT) and the Theodorou 2023 overview (Arch Orthop Trauma Surg) agree: two essential pillars before any other intervention.³,⁴

1. Patient education and load modulation : explain the non-inflammatory overload nature of the condition, deconstruct the myth of "tendinitis" requiring complete rest, present the pain-monitoring model (Silbernagel 2007), set realistic expectations (recovery = 12 weeks to 6 months, non-linear), make the patient responsible for managing their jumps and load.³,⁵
2. Progressive exercise programme loading the quadriceps and patellar tendon: the cornerstone of treatment, recommended as first line by the 2025 Dutch guideline despite very low to low (Cochrane 2025: seven trials, 211 athletes) and very low (Dutch guideline) certainty of evidence: we start with exercise because the panel recommends it and adjuncts have not done better, not because its effect is solidly quantified. The Breda 2021 PTLE and the Kongsgaard 2009 HSR are possible frameworks.²,⁶,⁷,¹⁹,²⁰,²³

The adjunctive therapies (shockwave, manual therapies, taping) are justified only as a complement to a well-conducted exercise programme, generally after at least 12 weeks of exercise without sufficient improvement. Injections (PRP, sclerosants, corticosteroids) have not shown superiority over placebo or over exercise alone, and some are even contraindicated (corticosteroids: risk of rupture).⁸ Surgery remains exceptional, reserved for documented failures after at least 6 months of structured conservative treatment (Everhart 2017).⁹

What is the role of exercise (PTLE, HSR, isometrics) and is one approach superior?

🏋️ Exercise is the first-line treatment, on evidence of low to very low certainty.¹⁹,²³ Three protocols structure contemporary practice, none of which is established as superior to the others:²,³,⁶

1. Progressive Tendon-Loading Exercise (PTLE), Breda 2021 : pivotal RCT (Br J Sports Med, n=76 athletes aged 18-35 with clinically diagnosed PT confirmed on ultrasound, 24-week follow-up). A protocol in 4 progressive phases : (1) analgesic isometric → (2) isotonic with increasing load → (3) energy storage (progressive plyometric jumps) → (4) sport-specific. In this single trial, PTLE achieved a greater VISA-P improvement than decline eccentric exercise at 24 weeks (+28 versus +18 points, adjusted difference 9; 95 % CI 1 to 16); return to sport (43 % versus 27 %) did not differ significantly (p = 0.13).⁶ The Liu 2026 network meta-analysis (17 trials) finds no protocol superior to HSR at 12 weeks, without demonstrating their equivalence; only a few protocols (concentric only, flywheel, eccentric step) do worse.²¹
2. Heavy Slow Resistance (HSR), Kongsgaard 2009 : 3 sets × 6 to 15 RM with slow movement (3 s concentric + 3 s eccentric), 3 times a week, 12 weeks. Exercises: single-leg squat on a machine or with a barbell, heavy leg press, hack squat. External load increased progressively from 15 RM (weeks 1-3) to 6 RM (weeks 9-12). The original RCT (n=39 men, 12 weeks) showed equivalence with decline eccentric exercise at 12 weeks but superiority at 6 months in patient satisfaction and collagen normalisation.⁷ Advantage: only 3 sessions/week (vs 14 with the Alfredson protocol), hence better adherence in practice.
3. Decline eccentric (Young/Purdam protocol) : single-leg squat on a board inclined at 25° of decline (forcing knee flexion with the knee ahead of the toes), 3 × 15 repetitions, twice a day, 12 weeks, progressed with load (weighted backpack). This is the historical protocol for patellar tendinopathy (Visnes & Bahr 2007, critical SR). It has shown positive but inconsistent results as monotherapy; in the Breda 2021 trial, PTLE did better at 24 weeks.¹⁰
4. Analgesic isometrics (Rio 2015) : isometric knee extension 5 × 45 seconds, 70 % MVIC, 1-2 times a day. The Rio 2015 crossover trial (BJSM, six in-season volleyball players) reported an immediate reduction in pain (~7.0 → 0.17 VAS) still present at 45 minutes, the last time point measured, and an increase in MVIC.¹¹ The pre-registered crossover trial by Holden 2020 (21 patients) found a reduction of about 1 point out of 10, not maintained at 45 minutes, with no advantage over dynamic exercise.²² Isometrics remain well tolerated and may relieve pain in the short term, with no duration to promise: an option for the reactive phase, the season, or as the first phase of PTLE. They do not replace a long-term progressive loading programme.

Adjunctive therapies: what is the value of shockwave, PRP and manual therapies?

💡 All adjunctive modalities should be considered as a complement to an exercise programme, never as a substitute.²,³

Extracorporeal shockwave therapy (ESWT) : the Charles 2023 review (Front Immunol) finds a negligible short-term effect of ESWT, alone or added to eccentric exercise, against placebo (low to moderate evidence);¹² Challoumas 2023 finds, with moderate certainty, that adding ESWT to eccentric exercise brings no short-term benefit (two trials);²⁰ the Stania 2022 review does not allow any conclusion (extreme heterogeneity).²⁴ The 2025 Dutch guideline reserves additional treatments, shockwave included, for particular cases after 12 weeks of exercise without change, then prefers the patellar strap and asks that the patient be informed of the absence of evidence.²³ In practice, exercise continues for at least 12 weeks before any adjunct; ESWT tried afterwards is presented as a trial with no evidence of effectiveness.

PRP (Platelet-Rich Plasma) : the data are divergent, and this divergence should be explained to the patient rather than hidden. The Andriolo 2019 SR/MA (Am J Sports Med, 70 studies reviewed, 22 included in the meta-analysis) concludes that multiple injections of PRP achieve the best results beyond 6 months of follow-up (p < 0.05), ahead of shockwave and eccentric exercise, and therefore regards them as a possible option: but it does so by indirect comparison, on trials whose Coleman score indicates generally poor methodological quality.⁸ The Challoumas 2021 NMA, restricted to randomised trials, does not count PRP among the most effective interventions and concludes that progressive loading should remain the first-line treatment.² The Everhart 2017 SR finds a highly scattered improvement with PRP (55 %, 95 % CI 5 to 105 %) and suggests that it might accelerate early recovery, without settling the question.⁹ The Andia 2014 SR/MA (Br Med Bull, 13 controlled studies, various tendons) finds less pain at 3 months and at 1 year after PRP, but judges these results inapplicable to the individual patient, owing to a lack of power and precision.¹³ PRP is not recommended routinely but may be discussed after failure of at least 6 months of structured conservative treatment, as part of shared decision-making.

Intra- or peritendinous corticosteroids : strongly advised against. Documented risk of tendon rupture, high recurrence rate, structural alteration of the collagen.²,³

Manual therapy (deep transverse friction massage, ankle/hip joint mobilisations): limited evidence as monotherapy. May be justified to improve limited ankle mobility (dorsiflexion) or hip mobility (internal rotation, abductors) that maintains deficient landing mechanics, but should not form the core of treatment.² The Acebes-Hueto 2024 SR (Healthcare) on soft-tissue techniques + exercise finds a modest adjunctive effect.¹⁴

Other modalities (low-level laser, therapeutic ultrasound, electrical stimulation, taping, dry needling): insufficient or heterogeneous evidence for a strong recommendation. The 2024 Frontiers SR on dry needling + exercise finds an additional benefit, but the net effect of dry needling as monotherapy remains to be confirmed.

Beyond the physical: how to address psychological factors?

🧠 Psychological factors are a major determinant of chronicity, and are frequently under-treated. The Mallows 2017 systematic review (BJSM) showed that kinesiophobia (fear of movement), catastrophising (negative and amplified interpretation of pain) and low self-efficacy are independent predictors of a poor prognosis at 12 months in tendinopathy in general, including patellar tendinopathy.¹⁵ Patient education must be active and proactive on four points:

• Reframing pain : tolerable pain (≤ 5/10 VAS) during the exercises, which does not worsen during exercise and returns to baseline within 24 h, is acceptable and even productive for adapting the tendon (Silbernagel 2007 model).¹⁶
• Deconstructing myths : “the tendon is not going to rupture because I do heavy squats”, “complete rest makes things worse rather than healing them”, “abnormal imaging does not imply severe, lasting pain”.
• Setting realistic expectations : recovery = 3 to 6 months for a first episode, 6 to 12 months in chronic cases, non-linear, with expected fluctuations. This information prevents discouragement when a bad day comes after a week of improvement.
• Self-efficacy : give the patient concrete tools (logbook, daily VAS, simple criteria for adjusting jump load) so that they become an active agent in their own recovery rather than a passive recipient.¹⁷

For patients with high kinesiophobia, catastrophising and established chronicity, a cognitive-behavioural approach or referral to a psychologist specialising in chronic pain may be needed in addition.

Critique and controversy

The exercise protocol war is evolving: although decline eccentric exercise was long regarded as the reference, the Breda 2021 RCT and the Challoumas 2021 NMA have called this supremacy into question. The Breda PTLE, incorporating the 4 progressive phases (isometric → isotonic → plyometric → sport-specific), did better than isolated decline eccentric exercise in one trial; the 2026 NMA shows no protocol to be superior to HSR.²,⁶,²¹ Kongsgaard's HSR remains an excellent adherence/effect compromise, particularly useful in patients for whom adherence is an issue.⁷

More problematic: the injection industry (PRP, sclerosants, stem cells, polidocanol) continues to grow even though the evidence supporting it remains of low methodological quality and divergent.²,⁸ Clinicians must take care not to give in to commercial pressure or to patients' expectations of non-validated “modern treatments”. Finally, the imaging-pain paradox remains a major clinical trap: tendons that look “healed” on ultrasound can remain painful, and vice versa.¹⁸ Return-to-sport decisions should not be based on follow-up imaging, but on functional criteria and the VISA-P (chapter 4).

The lasting recovery and the prevention of recurrence are the major challenge in patellar tendinopathy: the historical Kettunen 2002 cohort (Am J Sports Med, 15-year follow-up) documented that more than 50 % of athletes had to give up their sport because of persistent symptoms.¹ Beyond resolving the acute episode, the patient must be prepared for a structured return to jumping activities, and for years of self-monitoring of sporting load.

How can the patient become an active participant through the pain-monitoring model?

🎯 The Silbernagel 2007 pain-monitoring model transformed management by demonstrating, in a randomised trial (n = 38), that continuing sport during rehabilitation is not only safe but also effective, provided a simple rule is followed:²

• Pain kept tolerable (≤ 5/10 VAS) during exercise.
• Pain that does not worsen from session to session.
• Pain that returns to baseline within 24 h after exercise.
• Morning stiffness that does not worsen from week to week.

If any of these criteria is not met → reduce the load (speed, distance, intensity, frequency) by 20-30 % and reassess. If the criteria are met → increase progressively (the +10 %/week rule is a benchmark, with no demonstrated predictive value).

Concrete tools to give the patient:

• Logbook kept weekly: jump volume (number, intensity), morning and post-exercise pain VAS, morning stiffness. It makes trends objective and allows decisions to be taken without emotional bias.³
• Monthly VISA-P : 0-100 score to objectify progress. An improvement of 13-15 points is clinically significant (MCID).⁴
• Maintaining the strengthening programme in the long term: at least 2-3 sessions of HSR or loaded squats per week, even after complete resolution of symptoms, to maintain tendon capacity.⁵
• Regulating external load : progression of jump volume adjusted to the tendon's response the next day, a season plan including 1 deload week every 3-4 weeks. The 10 % per week rule and the acute:chronic workload ratio are benchmarks drawn from team sports, contested and not validated as prevention tools.⁶ ¹² ¹³

When and how should a safe return to sport be planned?

🏃 Return to sport (RTS) should never be based on elapsed time alone or on the absence of pain. The Breda 2021 PTLE protocol now structures RTS into 4 progressive phases with objective functional criteria.⁷

Minimum criteria to meet before resuming jumping / sport-specific activity :

1. No pain on the single-leg decline squat (SLDS) repeated 5 times consecutively.
2. Quadriceps strength symmetry ≥ 90 % vs the unaffected side (hand-held dynamometry or isokinetic measurement).⁸
3. Hop tests (single-leg hop, triple hop, side hop) with asymmetry < 10 % vs the unaffected side.
4. VISA-P > 80/100 or a clinically significant improvement ≥ 15 points from baseline.
5. Tolerance of bilateral then unilateral jumping, drop-jump landing with good neuromuscular control (no dynamic valgus).
6. Hip abductor and external rotator strength that is symmetrical, an often-neglected point (Mendonça 2018).⁹

Progression of return to sport in 4 phases (Breda PTLE) :

1. Phase 1: pain management (weeks 0-4): analgesic isometrics (Rio 2015), modulation of sporting load, education about tolerable pain. No jumping. Low-impact activities may continue if tolerated (cycling, swimming, pull-ups).
2. Phase 2: slow isotonic strength (weeks 4-12): HSR or slow squats with progressive load, 3 sessions/week. Concurrent work on the kinetic chain (ankle, hip). No plyometrics.
3. Phase 3: energy storage (progressive plyometrics) (weeks 8-16): graded introduction of jumps (bilateral static → bilateral dynamic → unilateral static → unilateral dynamic). Monitor pain at 24 h.
4. Phase 4: sport-specific (weeks 12-24): reintegration of specific movements (spike, dunk, running, decelerations, changes of direction), progressive increase in competition volume, maintenance of the strengthening programme.

Realistic trajectory to share with the patient : clinically perceptible improvement expected at 4-8 weeks, peak improvement around 12-24 weeks, full recovery and return to competitive sport between 3 and 6 months for a first episode, 6 to 12 months in chronic cases (Breda 2021).⁷ More than 50 % of athletes saw their careers cut short in the historical Kettunen 2002 cohort, hence the importance of maintaining the programme and monitoring load in the long term.¹

Critique and controversy

The “5/10 VAS” threshold of the Silbernagel model is a clinical heuristic that is widely adopted, but its exact threshold has never been formally validated on a large scale in patellar tendinopathy (the original Silbernagel 2007 trial concerned the Achilles tendon). It may be too permissive for some patients (catastrophisers, kinesiophobic patients) and too restrictive for others (high-level athletes used to tolerating pain). Personalisation remains necessary according to psychological profile and activity level. The return-to-sport criteria (symmetry ≥ 90 %, VISA-P > 80) are logical, but their predictive value for non-recurrence in the long term remains only moderately established. Most studies measure the rate of return to sport, not the recurrence rate at 2-3 years in patellar tendinopathy. Finally, in routine practice, these criteria require time, equipment (hand-held dynamometer, inclined board) and specific training: the risk is that they remain theoretical and that the clinician allows return to sport on looser criteria (absence of pain at rest), which is very insufficient and increases the risk of recurrence.

Patellar tendinopathy that is recalcitrant (not responding to 12 weeks of well-conducted progressive exercise) calls for the framework to be reconsidered: tendon pain is rarely an isolated problem. The kinetic chain of the lower limb works as a coupled ankle-knee-hip system, in which a distal or proximal limitation imposes mechanical overload on the patellar tendon.¹,² The Mendonça 2018 cross-sectional study (J Orthop Sports Phys Ther, 192 volleyball and basketball players) shows that a combination of hip and foot factors (passive hip internal rotation, shank-forefoot alignment, hip external rotator and abductor strength) distinguishes athletes with and without patellar tendinopathy.²

Ankle and hip: screening for the deficits that sustain overload

🔄 Three areas should be systematically assessed in the jumping athlete with patellar tendinopathy:

1. Ankle dorsiflexion (knee-to-wall) : Backman & Danielson 2011 (Am J Sports Med, 1-year prospective cohort, 90 elite junior basketball players) demonstrated that athletes with limited dorsiflexion range (< 36.5°) developed ~2× more patellar tendinopathy over the season.³ Mechanism: reduced dorsiflexion is compensated by increased anterior tibial translation and knee flexion on landing, increasing the knee extensor moment and therefore the load on the patellar tendon. Clinical test: knee-to-wall (KTW); target > 10 cm bilaterally or symmetry < 1 cm. Treatment: talocrural mobilisations, specific stretching of the triceps surae (gastrocnemius + soleus), self-mobilisation at home.

2. Strength and activation of the hip stabilisers : abductors (gluteus medius), external rotators (piriformis, gemelli). A documented weakness is associated with dynamic knee valgus on landing and with mechanical overload of the patellar tendon.²,⁴ Tests: single-leg squat (observation of valgus), Trendelenburg, hand-held dynamometry of hip abduction. If the deficit is ≥ 15 % vs the unaffected side → targeted strengthening (clamshells, single-leg deadlift, hip thrust, side plank with abduction).

3. Landing mechanics (drop jump) : Bisseling 2008 (Br J Sports Med) showed in a cohort of 24 volleyball players that patients with patellar tendinopathy have a “stiffer” landing strategy : higher peak landing force, less hip flexion, “stiff-legged” landing.⁵ Rehabilitation: drop jumps with qualitative coaching (“land softly, bend hip + knee + ankle at the same time”), work on shock-absorbing reflexes, video feedback.

Stratifying a recalcitrant tendinopathy: red flags and referral

🚩 Before concluding that a tendinopathy is “recalcitrant”, it is essential to systematically reconsider the diagnosis and rule out:

• Subclinical avulsion fracture of the inferior pole of the patella : especially if onset followed a powerful jump. Lateral radiograph + ultrasound.
• Meniscal or plica lesion : especially in adolescents or if there is joint locking. MRI if suspected, bearing in mind that up to 63 % of asymptomatic knees in adolescent footballers show a meniscal tear on MRI (Petrolo 2022).
• Inflammatory disease : spondyloarthritis (chronic enthesitis), early rheumatoid arthritis. If there is night pain, morning stiffness > 1 h or involvement of other entheses: blood tests (FBC, CRP, HLA-B27, RF, anti-CCP).
• Poorly controlled diabetes : a factor of poor response to exercise, possibly through altered collagen quality.

Patellar tendinopathy illustrates the permanent tension between aggregated evidence (NMA, SR/MA) and heterogeneous clinical reality. Clinical cases shed valuable light on atypical presentations, on treatment failures and on differential diagnoses of critical importance that randomised trials do not capture. 🧐 Clinicians must nevertheless interpret these cases rigorously: they illustrate but do not demonstrate efficacy.

A "classic" case: adolescent footballer, the diagnostic error reported by Petrolo 2022

The case reported by Petrolo A. 2022 (J Can Chiropr Assoc, PMID 36275082) illustrates a common diagnostic error.¹ A 15-year-old adolescent football player consults for anterior left knee pain that has been developing for 10 weeks. His general practitioner requests an MRI, which shows a lesion of the left lateral meniscus : the diagnosis of a meniscal lesion is accepted and a surgical opinion is scheduled. The patient seeks a second opinion before this consultation. The second-opinion examination found:

• No clinical signs of meniscal involvement : it was this finding that led to the case being reopened.
• An anterior knee pain compatible with involvement of the patellar tendon.
• A history and an injury mechanism that did not fit with a meniscal tear.

The diagnosis retained was left patellar tendinopathy, and progressive rehabilitation was proposed rather than surgery. After a complete rehabilitation programme of 6 weeks, the patient had fully recovered.¹

⚠️ Methodological limitations: this is a single case (n = 1), level of evidence 5 (Oxford CEBM). It illustrates a clinical reasoning process, but does not demonstrate a general rule.

Major clinical lesson : in adolescent athletes, a meniscal abnormality seen on MRI is not enough to explain anterior knee pain. The author points out that up to 63 % of asymptomatic knees of adolescent footballers show a horizontal or oblique meniscal tear on MRI: the image must be compared with the history, the injury mechanism and the physical examination before making a diagnosis and, a fortiori, before indicating surgery. The corollary also applies the other way round: in the absence of a response after 6-8 weeks of well-conducted progressive exercise, systematically reconsider the diagnosis and explore intra-articular pathology (meniscal and chondral lesions, plica, ACL injury).

The diagnostic challenge: when anteromedial knee pain hides something else

Anteromedial knee pain in a jumping athlete is not always patellar tendinopathy. ⚠️ Several conditions can mimic this diagnosis, sometimes with serious consequences if the diagnosis is delayed:

• 🔍 Anterior meniscal lesion (anterior horn of the medial meniscus): pain in deep flexion, positive McMurray, occasional locking. MRI for confirmation, but Petrolo 2022 points out that up to 63 % of asymptomatic knees of adolescent footballers show a meniscal tear on MRI.¹
• 🔍 Patellofemoral pain syndrome (PFPS) : diffuse retro/peripatellar pain, aggravated by prolonged sitting (cinema sign). Compression-extension test. No localised pain at the tip of the patella.²
• 🔍 Symptomatic medial synovial plica : anteromedial pain, clicking sensation in flexion-extension. Positive plica snap test. Diagnosis often delayed.
• 🔍 Fat pad syndrome (Hoffa's disease) : pain on either side of the patellar tendon, aggravated in hyperextension. Hoffa's test: para-tendinous pressure in extension reproduces the pain, the squat less so.
• 🔍 Sinding-Larsen-Johansson disease in children aged 10-13: pain at the inferior pole of the patella with radiological fragmentation. Apophysitis of the proximal insertion of the tendon.
• 🔍 Osgood-Schlatter disease in adolescents aged 11-15: pain over the anterior tibial tuberosity (distal insertion): a different patient profile and location.
• 🔍 Avulsion fracture of the inferior pole of the patella : after a powerful jump with a “pop” and weakness of extension. X-ray + ultrasound.
• 🔍 Partial ACL injury or micro-instability: especially in young women, jumping athletes, abrupt decelerations. Lachman and pivot shift tests.
• 🔍 Prepatellar bursitis : superficial anterior swelling (over the patella), distinguished by its location.

Study of a complex case: patellar pain resolving with lumbar treatment (Serres 2025)

The Serres and Van Cant 2025 case (Int J Sports Phys Ther, PMC12129631) illustrates the complexity of the extended kinetic chain.³ A 45-year-old man, a fire safety officer and volunteer firefighter, was referred by his sports physician for patellar tendinopathy of the right knee. He was preparing for a marathon, running 60 km a week, and described pain at the inferior pole of the patella, with recurrent episodes of anterior knee pain for about ten years and a current episode lasting one year. He had received no treatment for this knee. Knee MRI and arthrography were unremarkable; lumbar MRI showed L5-S1 disc disease. The initial VISA-P was 57/100, the NRS 4/10 at rest after sport and 7/10 during activity. The examination reproduced the knee pain on the single-leg decline squat, on three single-leg hops and five step-downs, whereas resisted knee extension remained pain-free with full range. As the patient reported a history of low back pain, a full lumbar examination was carried out: minimal loss of flexion and extension, low back pain on overpressure in flexion, right straight leg raise reproducing the low back pain at 60°. Assessment using Mechanical Diagnosis and Therapy (MDT, McKenzie method) showed that repeated lumbar extensions in prone lying immediately improved the decline squat, single-leg hops and step-down, whereas repeated flexions brought all signs back to their baseline state. The presentation was classified as a lumbar derangement with a directional preference for extension. The treatment consisted solely of repeated lumbar movements:

• Repeated lumbar extension in prone lying (McKenzie protocol): 10 repetitions, 4 to 5 times a day, and before runs.
• Progression of forces over the sessions: self-overpressure at end of range, then overpressure applied by the clinician, reproduced at home with a towel.
• Postural correction: maintaining lumbar lordosis when sitting.

At the fourth session, about three weeks after the initial assessment, the patient reported no pain at all over the previous seven days, in long runs as in interval sessions; knee and spine tests were pain-free and the VISA-P reached 99/100, the NRS 0/10 at rest after sport and during activity. He completed his marathon without knee pain. At six months he was running without pain, continuing his lumbar extensions, and reported a VISA-P of 100/100. His Achilles tendon pain, however, remained unchanged and was managed separately. ⚠️ Limitations: case report (n=1), level of evidence 5, result not generalisable and causality not demonstrable, final follow-up conducted by telephone. The authors put forward three hypotheses, without deciding between them, for knee pain of lumbar origin: altered dynamic alignment of the spine, contribution of the L4 root and of the anterior innervation of the knee, or a hypoalgesic effect of spinal loading.

Clinical lessons :

1. Chronic or recurrent patellar pain calls for assessment of the extended kinetic chain (ankle, hip, but also the lumbopelvic spine), all the more so in a patient who reports a history of lumbar problems.
2. The MDT/McKenzie approach was enough here, in four sessions, to reveal a directional preference for extension that redirected the entire therapeutic strategy.
3. The psychosocial components (kinesiophobia, catastrophising) must remain present in the background (Mallows 2017).⁴

Critique and controversy: where do clinical cases sit in the hierarchy of evidence?

🧠 Clinical cases are fundamental for generating hypotheses and reporting rare presentations, but their level of evidence is the lowest in the entire scientific hierarchy. A single case illustrates a possibility, not a general rule. It cannot control for placebo, regression to the mean or spontaneous evolution.⁹ Publication bias is massive (failures are rarely published).

A persistent controversy in patellar tendinopathy is the exact place of imaging. The poor correlation between symptoms and structural abnormalities (thick asymptomatic tendons) argues for sparing use, but routine practice remains very “image-dependent”: over-prescription of ultrasound, therapeutic decisions based on the image rather than on the clinical picture. McAuliffe 2016 (SR/MA) showed that the predictive value of imaging for the development of symptoms is insufficient in practice.⁵ Treat the patient, not the image. Another controversy concerns the publication bias of experimental protocols (multiple PRP injections, prolotherapy, polidocanol, embolisation). Successes are published, failures stay in the drawer. Clinicians must be particularly wary of “miracle new techniques” without solid aggregated data. On PRP, the Challoumas 2021 NMA keeps progressive exercise as first line while the Andriolo 2019 SR/MA judges multiple injections worth considering: two opposite readings of a low-quality literature.⁶,⁷ Finally, the heterogeneity of patients makes generalisation hazardous. A PTLE protocol that is effective in a motivated 22-year-old volleyball player may be unsuitable for an adolescent in a growth spurt, a recreational athlete who has become sedentary or a female patient with a dominant psychological component. A clinical stratification (sporting intensity, age, psychosocial profile, comorbidities) remains to be developed, but already guides decision-making.

Applying the recommendations in routine practice remains the weak link in the evidence-based chain. Knowing what to do (Breda 2021, Challoumas 2021 NMA, Malliaras 2015) is not the same as knowing how to apply it with each patient, given their time constraints, preferences and comorbidities. 🧑‍⚕️

When and to which other healthcare professionals should you refer?

The first, non-negotiable step of triage is screening for red flags. Clinicians should have a low threshold for referral: sensitivity takes precedence over specificity when serious conditions are at stake.

Beyond emergencies, yellow flags (psychosocial factors of failure) justify a broader approach. The Mallows 2017 review (BJSM) identifies high kinesiophobia, catastrophising and low self-efficacy as major predictors of chronicity.² In these cases, consider collaborating with a psychologist specialising in chronic pain, and integrate a cognitive-behavioural approach into the rehabilitation programme. Interprofessional collaboration is required for complex profiles:

• Sports physician / general practitioner : full work-up, management of comorbidities, overall follow-up.
• Orthopaedic surgeon / knee surgeon : failure ≥ 6 months of structured conservative treatment, suspected complex intratendinous lesion, avulsion fracture, meniscal lesion (Everhart 2017).³
• Interventional radiologist : for the rare refractory cases in which ultrasound-guided injections (PRP) are considered through shared decision-making, despite the limited evidence.
• Podiatrist / pedorthist : biomechanical analysis of jumping and landing, insoles if necessary (rare), footwear advice.
• Coach / strength and conditioning coach / club staff : review and restructuring of the training programme (jump volume, periodisation, recovery) to manage load in the long term.
• Psychologist specialising in pain : persistent kinesiophobia, catastrophising, context of widespread chronic pain.

How do you measure outcomes and overcome barriers to implementation?

📊 Measuring outcomes is the sine qua non of quality practice. The VISA-P score (Visentini 1998) remains the reference PROM tool for patellar tendinopathy, validated internationally.⁴ Although there is not yet a Core Outcome Set specific to patellar tendinopathy (unlike the 2024 COS-AT for the Achilles tendon), there is consensus on the essential outcomes:

Essential outcomes in patellar tendinopathy :

• Pain : numeric rating scale (NRS) 0-10, measured at rest, on the SLDS and during activities.
• Function and severity : VISA-P, 8 questions, score 0-100. MCID ≈ 13-15 points.⁴
• Participation : return to sporting activities, level of practice vs before the injury.
• Quality of life : EQ-5D or similar.
• Global rating of change by the patient (PGIC).
• Quadriceps strength and symmetry: hand-held or isokinetic dynamometry.

Integrating these PROMs into routine practice comes up against documented barriers: lack of time (the most common), lack of suitable IT tools, lack of training in interpretation, the perception that it is “administrative” rather than clinically useful.

Implementation strategies to overcome these barriers:

• Digital tools : a tablet or smartphone app that the patient fills in in the waiting room, automatic calculation of the VISA-P score, graphical display of progress.
• Continuing education : practical workshops on using PROMs and on shared decision-making.
• Integration into routine : VISA-P at every follow-up visit (every 4-6 weeks), not only at the start and end of care.
• Shared decision-making : present the options to the patient (PTLE vs HSR vs isolated ECC), discuss the pros and cons (weekly volume, equipment, sporting calendar), decide together. This significantly increases adherence and satisfaction.

Critique and controversies: beyond the guidelines

The red flag paradox still holds: no single sign taken in isolation has a high positive predictive value. It is the cluster of findings + probabilistic clinical reasoning that guide referral, not a checklist. The risk is twofold: over-diagnosing (sending every pain for an MRI) or under-diagnosing (missing an avulsion fracture or a meniscal lesion by attributing the pain to a simple tendinopathy). The Petrolo 2022 case is a reminder of the mirror-image risk: over-interpreting an image and considering meniscal surgery for pain that came from the tendon.¹ The “knowing-doing” gap is particularly striking in patellar tendinopathy: the Challoumas 2021 NMA confirmed the lack of superiority of PRP as monotherapy and the primacy of progressive exercise, the Breda 2021 RCT found, in a single trial, PTLE better than isolated decline eccentric exercise, and yet routine practice sometimes still imposes a single eccentric protocol or prescribes costly PRP injections without indication.⁵,⁶ Moving to genuine EBP requires more than disseminating information: it requires an overhaul of economic incentives and of continuing education. Finally, the tension between standardisation and personalisation is central. The VISA-P and functional criteria are essential for comparability, but the clinician must know how to adapt the programme to the patient's profile (high-level athlete, recreational athlete who has become sedentary, growing adolescent, patient with a dominant psychological component).