Patellar Tendinopathy — Jumper’s Knee

Patellar tendinopathy — commonly termed jumper`s knee — is a chronic overuse condition of the patellar tendon at its proximal attachment at the inferior pole of the patella, characterised by activity-related anterior knee pain and tendon degeneration. It is distinct from an inflammatory tendinitis; the underlying pathology is angiofibroblastic dysplasia (also termed tendinosis) — degenerative disorganised collagen, fibroblast proliferation, and neovascularisation without significant acute inflammatory infiltrate. This distinction is clinically important because anti-inflammatory treatments (NSAIDs, corticosteroids) do not address the underlying pathology and may have deleterious effects on the tendon.

• Epidemiology: affects up to 45% of elite volleyball and basketball players; prevalence of approximately 20% in elite jumping athletes; less commonly affects recreational athletes; male predominance; bilateral in approximately 30% of elite athletes; peak presentation in the 3rd and 4th decade; the dominant leg is more commonly affected
• Site of pathology: the proximal patellar tendon at the inferior patellar pole is the most common location (65% of cases); the distal tendon at the tibial tubercle insertion is less common (25%); mid-substance pathology is rare; the critical zone at the posterior surface of the proximal tendon (adjacent to the inferior pole) is the most vulnerable area — the deep posterior fibres of the proximal tendon are under the greatest compressive and tensile stress during knee loading
• Pathology (Nirschl): identical to lateral epicondylalgia and Achilles tendinopathy — angiofibroblastic hyperplasia; disorganised type III collagen; neovascularity; substance P and glutamate nociceptors accompany the neovessels (explaining pain localisation to the neovascularity on USS Doppler); the Nirschl pain phase classification describes the temporal pattern of symptoms from pain only after activity (Phase 1) to pain during activity (Phases 2–3) to inability to complete activity (Phase 4) to complete tendon rupture (Phase 5)

• History: insidious onset; inferior patellar pain with loading activities (jumping, landing, squatting, running); pain typically at the start of activity that warms up, then returns after activity (Phases 1–2); morning stiffness; prolonged sitting pain (similar to PFPS — distinguish by the point of maximum tenderness)
• Royal London Hospital test (RLHT): the most specific clinical test for patellar tendinopathy; the patient lies supine; the examiner tilts the superior patella anteriorly (applying a dorsal force at the superior patellar pole), which relaxes the proximal patellar tendon; palpation of the inferior patellar pole with the tendon relaxed in this position reproduces less pain than palpation with the tendon under load (knee extended, patella in neutral); pain that is significantly worse with the patella in neutral than when relaxed = positive RLHT; this tests whether the pain source is within the tendon (pain with tendon under load) vs superficial (does not change with patellar tilt)
• Tenderness: maximum tenderness at the inferior patellar pole; point tenderness on direct palpation; pain reproduced by resisted knee extension, single-leg decline squat, or drop-landing
• Single-leg decline squat: the most sensitive functional provocation test; performed on a 25° decline board which loads the patellar tendon maximally (increases the knee flexion moment); the patient performs a single-leg squat while standing on the decline board; pain reproduced at the inferior patellar pole is highly specific for patellar tendinopathy; used for both diagnosis and as a rehabilitation exercise

• Ultrasound: the first-line imaging investigation; demonstrates hypoechoic tendon thickening at the proximal patellar tendon (the degenerate zone); neovascularisation on power Doppler correlates with severity and identifies the site of pathology; allows dynamic assessment and guided injection; operator-dependent; sensitivity approximately 80%, specificity 90% for significant tendinopathy; a normal USS does not exclude tendinopathy in early disease
• MRI: the gold standard for characterising tendon pathology; shows high T2 signal within the tendon at the inferior pole (oedema and degeneration); extent of tendon involvement; associated inferior pole bony changes; distinguishes partial from complete tears; valuable for surgical planning and in athletes where USS is equivocal
• Plain radiographs: often normal; may show an inferior pole ossicle (dystrophic calcification within the degenerate tendon); assess for Osgood-Schlatter changes at the tibial tubercle and Sinding-Larsen changes at the inferior pole in younger patients

• Eccentric loading (decline squat programme): the Alfredson protocol (originally described for Achilles tendinopathy and adapted for the patellar tendon) involves slow-speed heavy-load eccentric exercises on a 25° decline board; the decline position maximises patellar tendon load; the protocol is performed twice daily; it is the best-evidenced non-operative treatment for patellar tendinopathy; response rate approximately 60–70% in good responders; the mechanism is promotion of collagen remodelling and pain desensitisation through mechanical loading
• Heavy slow resistance (HSR) training: an alternative to purely eccentric loading; involves slow-speed (3-second concentric, 4-second eccentric) high-load knee extensions and leg press; evidence from RCTs (Rio et al.) shows HSR is equivalent to eccentric-only protocols and may have higher patient compliance; combines eccentric and concentric phases for more complete tendon loading
• Isometric exercises for in-season athletes: isometric quadriceps contractions (sustained holds of 45–60 seconds at 70% maximum voluntary contraction) have been shown to provide immediate cortical pain inhibition and are particularly useful for in-season management when athletes cannot tolerate the training load required for an eccentric programme; isometric loading reduces pain immediately and facilitates continued competition
• Extracorporeal shockwave therapy (ESWT): high-energy or low-energy shockwaves directed at the degenerate tendon; evidence from multiple RCTs supports ESWT for patellar tendinopathy refractory to exercise; mechanism — stimulates collagen synthesis, disrupts calcification, and modulates pain through neuropeptide release; typically 3–5 sessions; considered after 3 months of failed exercise therapy
• Platelet-rich plasma (PRP) injection: concentrated autologous growth factors (PDGF, TGF-β, IGF-1) injected into the degenerate tendon zone under USS guidance; growing evidence from RCTs and meta-analyses supports PRP superiority over saline and corticosteroid for patellar tendinopathy at medium-term follow-up (6–12 months); leukocyte-rich PRP (LP-PRP) and leukocyte-poor (LR-PRP) formulations have different properties; USS-guided injection into the degenerate zone is standard; typically 1–3 injections
• Corticosteroid injection: should NOT be used in patellar tendinopathy — evidence shows short-term pain relief followed by significantly worse long-term outcomes and increased risk of tendon rupture; the pathology is degeneration not inflammation; corticosteroids are harmful to the degenerate tendon; this is the same evidence as for Achilles tendinopathy and lateral epicondylalgia

• Indicated after failure of at least 3–6 months of structured non-operative treatment (eccentric loading, ESWT, PRP); approximately 10–20% of patients with significant tendinopathy ultimately require surgery
• Open surgical excision (Nirschl procedure adapted for the patellar tendon): the degenerate angiofibroblastic tissue at the proximal patellar tendon and inferior pole is excised; the inferior patellar pole may be trimmed (patellar pole shaving) to remove the compressive bony element; the tendon is débrided back to healthy tissue; the tendon is repaired and the inferior pole is decorticated to stimulate revascularisation; success rates of 70–85% in well-selected cases; the most commonly performed procedure
• Arthroscopic debridement: arthroscopic shaving of the posterior surface of the proximal patellar tendon and the inferior patellar pole; lower morbidity than open debridement; equivalent results in most comparative series; the arthroscopic approach allows concurrent assessment of the patellofemoral joint and intra-articular pathology
• Percutaneous needle tenotomy (dry needling/barbotage): USS-guided multiple needle passes into the degenerate tendon; induces local haemorrhage and healing response; growing evidence; minimally invasive; useful before committing to formal surgery in Blazina Phase 3 disease

• Patellar tendon rupture: acute complete rupture typically in patients with pre-existing tendinopathy or in those on corticosteroid therapy; presentation — acute pain, swelling, inability to straight leg raise (extensor mechanism failure), patella alta (patella migrates superiorly), palpable gap below the patella; X-ray shows patella alta; MRI confirms complete vs partial rupture; management — surgical repair within 2 weeks for complete rupture; end-to-end repair with augmentation (Leeds-Keio ligament augmentation or heavy suture internal brace) through patellar tunnels and tibial tubercle attachment; delayed repair (>6 weeks) requires more complex reconstruction due to retraction and scarring

• Corticosteroid injections cause tendon rupture: multiple retrospective studies and case series have documented spontaneous patellar tendon rupture following corticosteroid injection; the mechanism is inhibition of fibroblast activity and collagen synthesis, leading to further tendon weakening; corticosteroid should never be injected into the patellar tendon substance; it is acceptable to inject the adjacent bursa (pre-patellar or infrapatellar bursa) if bursitis is the diagnosis, but the tendon injection is contraindicated
• The Rio isometric protocol for in-season management: Rio et al. demonstrated that 5 × 45-second isometric wall squats at 70% MVC immediately reduces pain for up to 45 minutes via cortical pain inhibition; this protocol allows athletes to manage symptoms through competition periods when rest is not feasible; it does not replace the long-term eccentric loading programme but serves as an analgesic tool during competition phases
• Vitamin D deficiency and tendinopathy: emerging evidence links vitamin D deficiency to tendinopathy susceptibility and impaired tendon healing; vitamin D receptors are expressed on tenocytes; deficiency impairs collagen synthesis; routine vitamin D screening in athletes with recurrent or refractory tendinopathy is reasonable; supplementation is inexpensive and low-risk

• Patellar tendinopathy: angiofibroblastic dysplasia (tendinosis), NOT tendinitis; proximal patellar tendon at inferior pole; affecting jumping athletes (volleyball, basketball); Blazina Phase 1–4
• Royal London Hospital test: pain reduced when inferior pole palpated with patella tilted anteriorly (tendon relaxed) vs neutral; tests intra-tendon vs superficial pain source
• Single-leg decline squat: most sensitive functional test; 25° decline board; maximises patellar tendon load; also the primary rehabilitation exercise
• Eccentric loading (decline squat programme): best-evidenced non-operative treatment; 60–70% response rate; promotes collagen remodelling
• Isometric exercises: 5 × 45 seconds at 70% MVC; immediate cortical pain inhibition; useful for in-season athletes unable to rest; analgesic effect, not curative
• Corticosteroid injection: CONTRAINDICATED in patellar tendon substance — increases tendon rupture risk; no role in tendinopathy (degeneration, not inflammation)
• PRP injection: superior to corticosteroid and saline at 6–12 months; USS-guided into degenerate zone; 1–3 injections; for phase 3 refractory to exercise
• ESWT: 3–5 sessions; after 3 months failed exercise therapy; stimulates collagen synthesis and modulates pain; good evidence for patellar tendinopathy
• Patellar tendon rupture: patella alta + inability to SLR + palpable gap = complete rupture; urgent repair within 2 weeks; augment with Leeds-Keio or suture internal brace
• Surgical debridement: for Phase 3 failure of ≥3–6 months of structured non-operative treatment; 70–85% success; open or arthroscopic debridement of degenerate tissue + inferior pole shaving