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Sports Medicine & Orthopedics & Family Medicine

Tendinitis and tendinopathy

The term tendinitis - which implies acute inflammation of the tendon - has been largely supplanted in modern medical literature by the more precise and histopathologically accurate term tendinopathy, because electron microscopy and histology studies have demonstrated that chronically painful tendons actually show little or no cellular inflammatory infiltration (few neutrophils + few prostaglandins) but rather structural degenerative changes - disorganization and fragmentation of collagen fibers + abnormal neovascularization (vascular ingrowth) + increased amorphous intercellular matrix + and apoptosis of tenocytes (tendon cells) - a process referred to as tendinosis. This distinction is not purely academic: it has direct therapeutic implications, as anti-inflammatories (NSAIDs + corticoids) targeting inflammation have a limited and potentially deleterious long-term beneficial effect on chronic tendinopathies (corticoids injected repeatedly weaken collagen and increase the risk of tendon rupture), whereas mechanical and biological therapies targeting collagen regeneration (eccentric exercises + progressive loading + PRP) are the most effective long-term approaches. Tendinopathies are extremely common in clinical practice - accounting for 30 to 50 % of all sports injuries - and affect both competitive athletes and the active general population, particularly in tendons subjected to high repetitive loads: Achilles tendon (runners) + patellar tendon (jumpers - jumper's knee) + rotator cuff tendons (shoulder) + epicondylial tendons (tennis elbow - lateral epicondylitis) + gluteus medius tendon + hamstring tendons.

Main tendinopathies by location

Location Clinical name At-risk population Clinical trial
Achilles tendon Achilles tendinopathy (mid-body or insertional) Runners + triathletes + masters + rapid increase in training volume Painful palpation of the tendon + arc of pain on palpation during mobilization + chair test (arc sign) + Royal London Hospital test
Patellar tendon Patellar tendinopathy (jumper's knee) Jumping sports (volleyball + basketball + track and field) + adolescents + Osgood-Schlatter in children Pain at the lower pole of the patella on palpation + VISA-P test + decline single-leg squat
Lateral epicondyle (elbow) Lateral epicondylitis (tennis elbow) Tennis + badminton + repetitive manual labor (plumbers + painters + butchers) Pain on palpation of the lateral epicondyle + Cozen's test (resisted wrist extension) + Mill's test (passive wrist flexion with elbow extended)
Medial epicondyle (elbow) Medial epicondylitis (golfer's elbow) Golf + tennis + throwing sports + strength training Medial epicondyle pain + painful wrist flexion against resistance
Rotator cuff (shoulder) Supraspinatus, infraspinatus, and subscapularis tendinopathy Throwing sports + swimming + overhead work + 40-60 years old Neer Test + Hawkins-Kennedy Test + Jobe Test (painful arc) + Speed Test + Resisted external rotation of rotator cuff
Gluteus medius (hip) Gluteal tendinopathy Perimenopausal women ++ runners + sedentary people Greater trochanter pain + worsened by standing with crossed legs + FABER + single-leg stance > 30 sec → pain
Hamstrings (hip) Proximal hamstring tendinopathy Long-distance runners + cyclists + master athletes Ischial tuberosity pain on palpation + aggravated by prolonged sitting + Puranen-Orava test

Pathophysiology – Tendon Continuum Model

  • Stage 1 - Reactive Tendinopathy: Rapid adaptive response (non-inflammatory) to acute overload → nodular thickening of the tendon + increased matrix → reversible if load is reduced quickly → do not stop activity completely (tendon atrophy) → manage load
  • Stage 2 - Dysrepair (early tendinosis): disorganized repair attempt + vascular ingrowth + abnormal cell proliferation → partially reversible → essential progressive rehabilitation
  • Stage 3 - Degenerative tendinosis major collagen disorganization + acellular areas + calcifications + abundant neovascularization → little to no structural reversibility + but can become asymptomatic with rehabilitation + high risk of rupture
  • Intrinsic risk factors: Age (> 35 years) + Female sex (estrogen effect on collagen) + Diabetes (collagen glycosylation) + Hypercholesterolemia (intratendinous lipid deposits) + Fluoroquinolones (direct toxicity on tenocytes → risk of tendon rupture — particularly Achilles tendon) + Systemic corticosteroids
  • Extrinsic risk factors: Too rapid increase in training volume or intensity (10% rule % per week) + poor running or movement technique + unsuitable equipment (shoes) + playing surface

Treatment — Phased Approach

  • Fundamental Principle – Load Management: The tendon needs mechanical load to regenerate (load stimulates tenocytes + collagen synthesis) but overload damages it → the objective is not complete rest (deleterious) but optimized and progressive loading → maintain activity within pain limits (pain ≤ 4/10 during and return to normal within 24 hours)
  • Acute phase — reduction of irritating load: Identify and reduce (but not eliminate) aggravating activities → substitute with low-impact activities for the tendon (cycling + swimming + unloaded exercises) + ice after activity (pain-relieving effect) + paracetamol or short-term NSAIDs (symptomatic relief) + brace or splint if necessary
  • Eccentric exercises (cornerstone of chronic tendinopathy treatment): muscular contraction during tendon lengthening → Alfredson's program for the Achilles tendon (200 repetitions/day × 3 sets of calf raises → slow descent over 3 counts) + Stanish's program + pain reduction from 60–90 % to 3 months in Achilles and patellar tendinopathies + mechanism: stimulation of collagen synthesis + fiber reorganization + reduction of neovascularization
  • Isometric exercises (acute phase + reactive tendinopathies): Intense static contraction (70–80 % of maximal force) × 5 repetitions × 45 seconds → immediate pain reduction (cortical analogue effect) + no dynamic load on tendon → useful in the initial painful phase
  • Isotonic and plyometric exercises (progressive loading phase): Progression: Isometric → Slow Isotonic → Fast Isotonic → Plyometric → Sport-Specific Activity → Return to Sport. Progression must respect the absence of residual pain (> 24 hours) before moving to the next stage.
  • Corticosteroid injections short-term analgesic effect (4–8 weeks) + but does not alter long-term progression + repeated infiltrations (≥ 3) weaken collagen + increase rupture risk → limit to a maximum of 1–2 infiltrations over time + do not infiltrate the body of the Achilles tendon (rupture risk) + associated bursitis may benefit from targeted infiltration
  • Platelet-rich plasma (PRP): Platelet-rich plasma (PRP) injection (growth factors + PDGF + TGF-β + VEGF + IGF) → stimulation of tendon regeneration + randomized studies: mixed results but positive trend for chronic refractory tendinopathies (epicondylitis + Achilles) + less risk than corticosteroids
  • Extracorporeal Shockwave Therapy (ESWT) Acoustic microtrauma → stimulation of vascularization + collagen synthesis + desensitization of nociceptors → proven efficacy in calcific tendinopathies of the shoulder + epicondylitis + plantar fasciitis + 3–5 sessions weekly
ℙ️ Fluoroquinolones (ciprofloxacin + levofloxacin + moxifloxacin) are associated with a significant risk of tendinopathy and tendon rupture—particularly of the Achilles tendon—up to several months after treatment discontinuation. The risk is multiplied by 2 to 6 in patients over 60 years old + on corticosteroids + kidney transplant recipients + or with a history of tendinopathy. Any patient on fluoroquinolone who develops tendon pain should stop the antibiotic and be evaluated → a painful Achilles tendon while on fluoroquinolones should prompt exclusion of a partial or impending rupture.
Urgent medical consultation

Consult the emergency room immediately if sudden, intense pain accompanied by a «popping» sensation in the calf or heel occurs during exertion—especially in individuals over 40, or those taking fluoroquinolones or corticosteroids—as these signs can indicate a complete Achilles tendon rupture (positive Thompson's sign = absence of plantar flexion when the calf is squeezed → orthopedic surgical emergency). For the assessment and management of chronic tendinopathy, Clinique Omicron offers medical consultations at its service points in Quebec and via telemedicine. To make an appointment, visit cliniqueomicron.ca.

Consult at Clinique Omicron

Clinique Omicron's physicians and nurse practitioners (NPs) diagnose tendinopathies through clinical examination (specific tests depending on location), prescribe appropriate imaging assessments (ultrasound + MRI if rupture is suspected), initiate load management, and refer to physiotherapy for eccentric exercise and progressive loading programs, prescribe short-term NSAIDs for symptomatic relief, assess the indication for corticosteroid injections or PRP based on the clinical presentation, and screen for systemic contributing factors (diabetes + dyslipidemia + fluoroquinolones). Consultations are available at several service points in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.

The content on this page is for informational purposes only and does not replace the advice of a doctor, physical therapist, or sports physician. A complete tendon rupture (particularly of the Achilles tendon) is an orthopedic emergency. Repeated corticosteroid injections into a tendon weaken collagen and increase the risk of rupture — limit to a maximum of 1-2 injections over the course of tendinopathy.

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