Patellar Tendinopathy

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Description

Patellar tendinopathy is a source of anterior knee pain, characterised by pain localised to the inferior pole of the patella. Pain is aggravated by loading and increased with the demand on the knee extensor musculature, notably in activities that store and release energy in the patellar tendon.

Patellar tendinopathy is primarily a condition of relatively young (15-30 years old) athletes, especially men, who participate in sports such as basketball, volleyball, athletic jump events, tennis, and football, which require repetitive loading of the patellar tendon. The prevalence of this condition in elite volleyball and basketball players has been found to be over 40 percent. While certain intrinsic risk factors for patellar tendinopathy have been identified, such as gender, weight and body mass index, the most significant risk factor appears to be training load (i.e. an extrinsic risk factor).

Clinically Relevant Anatomy

Cross section of a tendon.
Collagen fibres make up the pale
pink background. The fine lines
separate fibre bundles. The black
dots are the tenocyte nuclei.

The quadriceps muscles are connected to the inferior pole of the patella by the common quadriceps tendon through a sesmoid bone, the patella. The patellar ligament then connects the bottom of the patella to the tibial tuberosity. The force generated from the quadriceps muscles acts through the patellar as a pulley, causing the knee to extend

A healthy tendon is composed mostly of parallel collagen fibers closely packed together (86%). Collagen is predominantly type I. Other components of the tendon matrix are elastin (2%), proteoglycans (1–5%), and inorganic components (0.2%). The collagen in tendons are held together with proteoglycan components Decorin and Aggrecan, which bind to the collagen fibrils at specific locations

Tenocytes are a tendon specific fibroblast type cells that produce the collagen molecules, which cluster together to form collagen fibrils. Fibril bundles are organized to form fibres with the elongated tenocytes closely packed between them. The cells communicate with each other through gap junctions, and this signalling gives them the ability to detect and respond to mechanical load.

Blood vessels run parallel to collagen fibres within the tendon with some branching transverse anastomoses. There is thought to be no nerve supply to the internal tendon but adjacent to the tendon are nerve endings and Golgi tendon organs are present at the junction between tendon and muscle.

Pathological Process

Cook &Purdam described a continuum model of tendon pathology with three distinct stages:

1. Reactive tendinopathy
2. Tendon disrepair
3. Degenerative tendinopathy

Load is considered to be the primary stimulus which drives tendon health forward and back along the continuum.

Reactive tendinopathy

A non-inflammatory proliferative response in the cell and matrix, occurs with acute tensile or compressive overload. Tenocytes proliferate and protein production increases in this stage. This causes a short-term adaptation to the tendon and thickening of a portion of the tendon that either allows adaptation to compression or reduces stress by increasing cross-sectional area. This is different from the normal tendon response to load, which generally occurs through tendon stiffening. Clinically, reactive tendinopathies occur with unaccustomed physical activity or acute overload and also after a direct blow (e.g. a direct fall onto the patellar tendon).

Tendon disrepair

The continued attempt of tendon healing following the reactive stage but with greater matrix breakdown. There is an increase in the number of cells present in the matrix, resulting in an increase in protein production (proteoglycan and collagen). The proteoglycan increase causes collagen separation and matrix disorganisation. An increase in vascularity and neuronal ingrowth may also be present. Clinically, this stage of the pathology is seen in chronically overloaded tendons and appears across a spectrum of ages and loading environments.

Degenerative tendinopathy

Degenerative tendinopathy is characterised by areas of cell death due to apoptosis, tenocyte exhaustion or exhaustion. There are large areas of the matrix that are disordered and filled with matrix breakdown products, little collagen and vessels. There is little room for the pathological changes to be reversed at this stage. This stage is primarily seen in the older person.

Clinical Presentation

Patellar tendinopathy, is one of many potential diagnoses for a patient presenting with anterior knee pain. There is considered to be two defining clinical features:

1. Pain localized to the inferior pole of the patella
2. Load-related pain that increases with the demand on the knee extensors, notably in activities that store and release energy in the patellar tendon.

The patient may complain of pain with prolonged sitting, squatting, and stairs, but these complaints are features of other pathologies such as patellofemoral pain. Pain is rarely experienced in a resting state. Pain occurs instantly with loading and usually ceases almost immediately when the load is removed. The pain may improve with repeated loading. An important feature of tendinopathies is that they are dose-dependent, pain increases as the magnitude or rate of application of the load on the tendon increases.The practical application of this is in an examination of pain should increase when progressing from a shallow to a deeper squat, or from a smaller to a greater hop height.

Aggravating activities are predominantly loading activities, such as walking down stairs or when performing a decline squat.

Diagnostic Procedures

Jumper's knee

Knee examination

Dose-dependent pain, see previous section. Deficits in energy-storage activities can be assessed clinically by observing jumping and hopping. Stiff-knee vertical jump-landing strategy may be used by individuals with a past history of patellar tendinopathy.

Examination of the complete lower extremity is necessary to identify relevant deficits at the hip, knee, and ankle/foot regions. Atrophy, reduced strength, malaligned foot posture, quadriceps and hamstring inflexibility, reduced ankle dorsiflexion have been associated with patellar tendinopathy and should also be assessed.

Patellar tendon imaging does not confirm patellar tendon pain, as pathology observed via ultrasound imaging may be present in asymptomatic individuals.

Outcome Measures

• VISA scale (Victorian Institute of Sport Assessment-patella)

Medical Management

Non-steroidal anti-inflammatory drugs

The use of non-steroidal anti-inflammatory drugs (NSAID’s) in the treatment of tendinopathy remains controversial both in the acute stage and in the chronic stage. NSAIDs have been reported to impede soft tissue healing. Although pain may be reduced, they have a negative effect on tendon repair. In reactive tendinopathy, this may be a preferred effect, as this may inhibit proteins responsible for tendon swelling.

Corticosteroid injections

Corticosteroids are used to decrease pain but also decrease cell proliferation and protein production and therefore could be used in the reactive tendinopathies. Repeated peritendinous corticosteroid has been shown to reduce tendon diameter at 7 and 21 days after injection in tendons.

Surgical treatment

Surgery for chronic painful tendons has produced varied outcomes, with 50–80% of athletes able to return to sport at their previous level. Surgery in nonathletic people produced poorer results than in active people. Surgery is considered a reasonable option in those who have failed all conservative interventions.

Physiotherapy Management

Advice regarding selective rest should be provided to allow appropriate tendon healing following a period of acute overloading or unaccustomed exercise (level of evidence: 2a) . There should be a focus on an early return to activities.

Use of patellar strap and sports tape has short term effect on pain.

Pain relief

Isometrics have been suggested as a possible analgesic exercise where isotonic exercises are not possible due to fatigue and high SIN. In a systematic review by Naugle et al. (level of evidence: 2a) isometric exercise has been found to be superior to aerobic and resistance exercises at reducing pain.

Rehabilitation

Exercise is an important component of the management of patellar tendinopathy. A variety of loading programs have been suggested for the treatment of patella tendinopathy with the main types being (level of evidence: 1a) :

1. Eccentric loading
2. Eccentric-concentric loading

Adapted from Malliaras et al. 2013 (level of evidence: 2a)
Programme	Exercise type	Sets & reps	Frequency	Progression	Pain
Alfredson	Eccentric	3x15	Twice daily	Load	Enough load to achieve with moderate pain
Stanish and Curwin/Silbernagel	Eccentric-concentric	3x10-20	Daily	Speed then load, type of exercise	Enough load to be painful in third set
Heavy slow resistance training	Eccentric-concentric	4x6-15	3x/week	6-15RM	Acceptable if was not worse after

Eccentric loading has been the most dominant approach for rehabilitation. Evidence suggests that all loading programs are beneficial in reducing pain and returning function however the eccentric-concentric type has greater patient subjective satisfaction (level of evidence: 1a) . This is perhaps due to time commitment and pain required from eccentric programs. Eccentric-concentric exercises can begin with body weight squats but a significant load is important. Gym machines such as leg press or knee extension provides control to the amount of loading. If suitable for the patient a barbell squat or lunge can be an excellent progression.

Protocol

Protocol as described by Malliaris et al. (2015) (level of evidence: 2a)
Stage	Indication	Dosage
1. Isometric loading	More than minimal pain during isometric exercise	5 repetitions of 45 seconds, 2 to 3 times per day; progress to 70% maximal voluntary contraction as pain allows
2. Isotonic loading	Minimal pain during isotonic exercise	3 to 4 sets at a load of 15RM, progressing to a load of 6RM, every second day; fatiguing load
3. Energy-storing loading	Adequate strength and consistent with other side and load tolerance with initial-level energy storage exercise (ie, minimal pain during exercise and pain on load tests returning to baseline within 24 hours)	Progressively develop volume and then intensity of relevant energy-storage exercise to replicate demands of sport
4. Return to sport	Load tolerance to energy-storage exercise progression that replicates demands of training	Progressively add training drills, then competition, when tolerant to full training

Malliaris and colleagues report common management pitfalls, which are worth considering when planning treatment:

• Unrealistic rehabilitation time frames
• Inaccurate beliefs and expectations about pain
• Failure to identify central sensitization
• Over-reliance on passive treatments
• Not addressing isolated muscle deficits
• Failure to address kinetic-chain deficits
• Not adequately addressing biomechanics

Tendon neuroplastic training

Rio et al found that current rehabilitation uses self-paced strength training (for e.g. a patient does 3x10 contractions lifting a weight - without any external cues/advice on timing). This type of training may lead to recurrence of tendinopathy, as it does not address motor control sufficiently and thus does not change the corticospinal drive to the muscle.

Externally paced training would be when the patient contract the muscle, concentrically and eccentrically on auditory (like using a metronome) or on visual cues. Externally paced strength training was shown to alter tendon pain and corticospinal control of the muscle.

Tendon neuroplastic training uses strength-based training with external cues as a strategy to optimise neuroplasticity. This was shown effective with patellar tendinopathy and further research is required into other tendinopathies.

Other forms of therapy

Alternative therapies like administering shockwaves were also investigated. It has been shown that shockwave therapy is a safe method for patients who are unresponsive to coventional therapy, and it should always be used in combination with other methods. (level of evidence:1a) Recording to F. Abat et al. USGET (Guided-Galvanic Electrolysis Technique) provides better results than shockwave therapy, but also combined with eccentric exercise therapy. (level of evidence: 1b)

Differential Diagnosis

• Infrapatellar bursitis
• Fat pad impingement
• Patellofemoral pain
• Plica injuries
• Osgood-Schlatter syndrome
• Sinding-Larsen-Johansson syndrome

Key Evidence

• Isometric exercise induces analgesia and reduces inhibition in patellar tendinopathy. (Rio 2015) (Level of evidence 1b)
• Patellar Tendinopathy: Clinical Diagnosis, Load Management, and Advice for Challenging Case Presentations. (Malliaris 2015) (Level of evidence 1a)
• Physiotherapy management of patellar tendinopathy (jumper's knee). (Rudavsky 2014) (Level of evidence 1a)
• Achilles and patellar tendinopathy loading programmes. (Malliaris 2013) (Level of evidence 1a)
• Abat, F. et al. “Randomized Controlled Trial Comparing the Effectiveness of the Ultrasound-Guided Galvanic Electrolysis Technique (USGET) versus Conventional Electro-Physiotherapeutic Treatment on Patellar Tendinopathy.” Journal of Experimental Orthopaedics 3 (2016): 34. PMC. Web. 19 Dec. 2017. (Level of evidence 1b)

Resources

Click on Patellar Tendinopathy YouTube Playlist for more videos

Case Studies

• High jumper