CURRENT CONCEPTS OF ROTATOR CUFF TENDINOPATHY

Abstract

Purpose/Background:

Tendinopathies are a broad topic that can be examined from the lab to their impact upon function. Improved understanding will serve to bring this pathology to the forefront of discussion, whether in the clinic or the classroom. The purpose of this current concepts clinical commentary is to explore intrinsic and extrinsic mechanisms of rotator cuff (RC) tendinopathy in order to improve clinical and research understanding.

Methods:

Pubmed, Medline, Cinahl, PEDro, and Cochrane databases were searched, limiting results to those published in the English language, between the years of 2005 and 2012. The key search terms utilized were intrinsic mechanisms, tendinopathy, stem cells, biologics, platelet‐rich plasma (PRP), healing, rotator cuff tears, full‐thickness tears, tests, impingement, imaging, ultrasound, Magnetic Resonance Imaging (MRI), radiograph, shoulder advances, treatment, diagnoses, tendon disorders, pathogenesis, matrix metalloproteinase, injections, and RC repair. Over 150 abstracts were reviewed and 43 articles were analyzed for quality and relevance using the University of Alberta Evidence Based Medicine Toolkit.

Results/Conclusions:

Current evidence suggests that tendinopathies arise from a multivariate etiology.It is increasingly evident that intrinsic mechanisms play a greater role than extrinsic mechanisms in this process. Emphasis should be placed on patient information (i.e. background information and personal description of symptoms) and imaging/ injection techniques in order to aid in diagnosis. Future treatment technologies such as cell therapy and biological engineering offer the hope of improving patient outcomes and quality of life.

Level of Evidence:

Level 5 – Clinical Commentary Related to a Review of Literature

INTRODUCTION

Shoulder pain is the third most common musculoskeletal complaint.¹ Some commonly diagnosed shoulder problems include impingement of the rotator cuff tendons or subdeltoid bursa, bicipital tendonitis, frozen shoulder, and glenohumeral (GH), and acromioclavicular (AC) arthritis.² With the unknown incidence of partial rotator cuff tears (PRCTs), defined as tears involving less than 50% of the muscle, the clinician needs to fully understand the condition in order to best address the patient's problem.² Authors have shown that full thickness tears are usually due to chronic degeneration.^3,4 Furthermore, most rotator cuff pathologies can be treated with reasonable success using conservative therapy despite the lack of high quality evidence.²

If a diagnosis of tendinopathy has been made, it is important to take the diagnosis a step further and decipher whether the tendinopathy is from extrinsic causes, intrinsic causes, or a combination of the two.When a patient partially tears their rotator cuff (RC), it is common that they present with reduced shoulder function (i.e. dyskinesis, weakness, pain, and stiffness).² They may also have pain at rest, night pain, or a painful arc.² Upon evaluation, the clinician may find weak external rotators, a weak supraspinatus, and signs of impingement.² Signs of impingement may include painful overhead reaching, an inflamed subdeltoid bursa, or positive special tests meant to provoke symptoms. In patients over the age of 60 with two out of three of the aforementioned symptoms (i.e. weak external rotators, weak supraspinatus, impingement signs previously listed), there is a 98% chance of a RC tear.⁵ Patients can also present with pain radiating to the lateral mid‐humerus or anterolateral acromion, pain while lying on the shoulder or sleeping with the arm overhead, and pain that occurs when reaching above the head.⁶ In addition, Fukuda observed that PRCTs are more painful than full thickness tears.⁷

Factors taken into account when considering surgery include the patient's functional needs, age, health, size of the tear, and amount of fatty infiltration into the muscle.^2,8,9 It is estimated that 75,000 RC surgical repairs are performed in the United States each year.¹⁰ Age plays a factor as it is unusual for young patients to have RC tears requiring surgery.¹¹ If a young patient presents with acute, post‐traumatic weakness without any pre‐existing RC problem, then it is generally accepted as an absolute indication for surgery.² In terms of tear size, if the RC tendons are greater than 50% torn, then surgery is commonly recommended.²

Pre‐operative rotator cuff tear size is the main factor in determining long‐term outcome of repair in relation to range of motion (ROM), strength, and need for another surgery.¹² Chronic tears are less likely to heal with surgery than acute tears.¹³ Surgery on chronic RC injuries has a wide ranging failure rate (30‐94%) even with the use of newer techniques (e.g., double‐row repairs), which could point to other variables for surgical failure such as aging, tendon to bone failure, and degeneration.^14‐21 Poor muscle quality, delamination of tendons, and longer post‐operative follow‐up, are all related to lower healing rates and inferior results.^22,23 Even if the structural status of the repair is not ideal, the patient's symptoms after surgery can still improve.^14,24 In addition, better outcomes are associated with proper healing of the greater tuberosity and an intact repair,^14,24 and acromioplasty appears to play a role in successful outcomes after surgery for reducing impingement.^25‐27

Physical therapy can also play a role in the success after a RC surgery, but often varies widely between therapists and typically orthopedic surgeons do not choose their therapist.²⁸ Physical therapists may consider mechanisms involved in the genesis of tendon injury, but the treatment of both tendinopathy and subsequent RC repair is based on the impairments.²⁹ Research supports strengthening the scapular stabilizers and RC muscles, addressing flexibility of the posterior shoulder structures, pectoralis minor muscle, the thoracic spine (with postural education), and activity modifications designed to reduce pain and disability from RC tendinopathy.^30‐32 There is a bias seen with exercise programs to target outlet impingement, which is an extrinsic mechanism.²⁹ Limited evidence exists to support therapeutic exercise and manual therapy for the treatment of RC tendinopathy.²

The purpose of this clinical commentary is to present the findings of a literature review identifying various mechanisms proposed for the development of RC tendinopathy. These mechanisms, or factors associated with RC tendinopathy will then be discussed with emphasis on the supporting evidence.

METHODOLOGY

Pubmed, Medline, Cinahl, PEDro, and Cochrane databases were electronically searched, limiting articles to those published in the English language between the years of 2005 and 2012. Search terms included: intrinsic mechanisms, tendinopathy, stem cells, biologics, platelet‐rich plasma (PRP), healing, RC tears, full‐thickness tears, tests, impingement, imaging, ultrasound, magnetic resonance imaging (MRI), radiograph, shoulder advances, treatment, diagnoses, tendon disorders, pathogenesis, matrix metalloproteinase, injections, and RC repair. Over 150 abstracts were reviewed and 43 articles were analyzed for quality and relevance using the University of Alberta Evidence Based Medicine Toolkit.

DEFINING TENDINOPATHY

It is important that tendinopathy, tendinitis, and tendinosis are systematically defined, in order to ensure that healthcare providers are effectively communicating regarding the condition to be treated. A tendinopathy is an overuse condition that manifests itself as pain in and around tendons²⁸ and happens when the body fails to regenerate properly.³³ This painful condition is associated with tendon disorganization and thickening that reduces its physical properties, which causes the tendon to fatigue, further exacerbating the painful condition with ultimate failure.³³ Tendinitis, which is usually painful, is a generic term that has to do with overuse, irritation, strain, degeneration and poor mechanics.³³ Degenerated and disorganized collagen that has increased vascularity and cellularity without obvious inflammatory cells is termed tendinosis.^33,34 Tendinitis and tendinosis represent tendon pathology and are subsets of tendinopathy.²⁹

Tendons must be able to handle tensile loads and their ability to do so relies on Type 1 collagen.³⁵ However, a key feature of tendinopathy can be seen through collagen structure analysis by showing the disruption of tendon microarchitecture, which helps to understand the response to variable amounts of cyclic loading.^35‐37 The aging process and repetitive use of tendons are thought to be contributors to RC tendinopathy.³⁵ The three general areas of tendinopathy that have been described in the literature are bursal sided, articular sided, and mid‐substance.^38,39

RC tendinitis is a term used to described chronic and acute conditions that involve the inflammatory process.²⁹ Histological research shows that there are a minimal number of inflammatory cells present in RC tendons and subacromial bursa.⁴⁰ RC disease has traditionally been thought to be a progressive disorder.⁴¹ Neer believed the process started with tendonitis, then progressed to tendinosis with degeneration and partial thickness tears, and finally resulted in full thickness tears.⁴¹ RC tendinosis is the diagnostic label for tendon pathology that is degenerative with or without inflammation,²⁹ whereas RC tendinopathy is used to signify a combination of pain and impaired performance associated with injury to the RC tendons.^42,43

INTRINSIC MECHANISMS

RC tendinopathy occurs for a multitude of reasons.Intrinsic mechanisms are associated with the tendon itself and can be from aging,^44,45 altered biology,^46‐48 microvascular blood supply,^38,41,49 degeneration, tendon overload, overuse, or trauma.^50‐52 Intrinsic factors that contribute to RC tendon degradation with tensile/shear overload include alterations in biology, mechanical properties, morphology, and vascularity (See Table 1 for a summary of cellular changes associated with intrinsic mechanisms).^{29,46‐48,53,54}

Table 1.

Proposed cellular changes associated with intrinsic mechanisms of rotator cuff tendinopathy

Cellular changes associated with injury, reduced mechanical stimulation, certain medications, etc.: 166‐173 Increased matrix metalloproteinases (MMP); Reduced tissue inhibitors of MMP (TIMPs); Tendon cell apoptosis; Insulin‐like growth factor (IGF‐1); Nitric oxide synthetase (NOS); Chondroid metaplasia of the tendon and matrix changes; Fatty infiltration (following tears); Cytokines; Caspases

NOTE: All of these changes negatively affect the turnover rate of collagen, adversely affecting collagen proliferation, and likely lead to tendon changes such as degeneration and apoptosis.

As the human body ages, the properties of tendons are negatively impacted by processes such as calcification, fibrovascular proliferation, degeneration, decreased tensile loading, decreased toe‐region on the stress strain curve, and decreased elasticity.^55,46

Vascularization may be another intrinsic factor to consider.Codman described a critical zone where there was deficient blood supply within supraspinatus tendons.⁵⁶ But the research of some authors refutes this thought process and describes the lack of this region of hypovascularity, or that the hypovascularity is only limited to the articular side and not the bursal side of the tendon.^49,57 In RC tendinopathy, neovascularization occurs in regions that have sustained smaller tendon tears and degenerative changes.^{38,39,46,58‐60} Levy et al showed that subjects with acute RC tendinopathy had hypovascularity in the supraspinatus tendon that compared to subjects without RC disease.⁵⁸ In chronic tendinopathy, the tears showed hypervascularity near the degenerative changes.⁵⁸ Thus, the literature is not clear on whether hypovascularity directly causes tendinopathy per se, but there is conjecture that the presence of blood vessels in the tendon matrix crowds out necessary collagen, which may further weaken the tendon prior to failure.⁶¹

EXTRINSIC MECHANISMS

Extrinsic mechanisms for RC tendinopathy include anatomic variables that set up conditions for impingement (usually occurring at the anterior aspect of the acromion).^62‐64 It is currently thought that between 44‐64% of all shoulder pain is from subacromial impingement syndrome (SAIS), the most common shoulder disorder.⁶⁵ Seitz et al showed that anatomical variants (acromial shape, subacromial joint spurs, and AC joint spurs) can lead to RC tendinopathy²⁹ and have proposed that these variables, along with overuse, could predispose an individual to the pathology.⁶⁶ Also, the angle and shape of the acromion could be a possible cause of the pathology.^29,67 The acromial shape has been broken down in to three types flat (Type 1), curved (Type 2), and hooked (Type 3).⁶⁸ It is still unclear if the shape changes with age or if its shape is determined congenitally or if both may contribute to the occurrence of tendinopathy.^51,69,70 Prior RC damage could cause increased stress to the coracoacromial arch and cause a hooked acromion to develop.⁵¹ Wang et al found that as age progressed so did the shape of the acromion from flat to curved or hooked.⁷¹ Shah et al found that this was possibly due to traction forces on the acromion,⁷² which could offer some explanation as to why there is a higher incidence of RC tears with age but still suggests an initiating intrinsic reason.⁵¹ It is believed that acromial shape and the severity of RC pathology are related.^73,74

The AC joint could be another contributing factor.Over time, this joint degenerates and osteophytes can form on the inferior aspect of the distal clavicle.^69,75 These arthritic signs have been correlated with the presence of RC pathology.⁷⁵ Whether bone spurs cause RC tears continues to be debated.⁵¹ The spurs are termed an enthesopathy and are thought to form from a coracoacromial ligament sprain.⁵¹ These spurs may also be a secondary formation after sustaining a bursal‐side RC tear.^76,77 Utilizing conservative treatment with a patient with the Type 1‐acromion has a better outcome than conservative care in those with other types of acromion.^78,79 The majority of patients with SAIS can be treated nonsurgically, however, many authors have demonstrated the success of a variety of surgical procedures.⁶ Further high‐quality research is needed on the treatment and diagnosis of SAIS.⁶

Shoulder impingement is the main extrinsic cause of RC tendinopathy. It occurs with mechanical compression of the external portion (bursal side) of the tendon, which leads to inflammation and degeneration.⁴¹ Upon repeated occurrence, the coracoacromial ligament may thicken, decreasing the subacromial space.⁶ Overuse activity coupled with coracoacromial arch changes have a significant effect on tendon injury.⁶ Significant relationships have been demonstrated between acromion morphology, the patient's self reported shoulder function, and the severity of the RC pathology.⁵⁰

Decreased microvascular blood supply has been discussed as a possible cause of intrinsic pathology but it can also be from an extrinsic cause.⁵¹ For example, when the arm is in full abduction, and the supraspinatus is compressed by the humeral head, the reduction in perfusion may be significant.⁵¹

A tight posterior capsule may cause changes in GH movement which could set up the patient for the development of impingement.⁶ Harryman et al showed that when posterior capsule tightness was surgically induced in cadaveric specimens, there was an increase in anterior superior humeral head translation during passive GH flexion, leading to a narrowing of the subacromial space (SAS).⁸⁰ Stretching should be used to address impairments in posterior shoulder tightness.⁸¹ Due to this relationship between posterior shoulder tightness and those with RC tendinopathy,⁸² horizontal adduction and internal rotation ROM should be examined.^81,83‐85

Newer models of impingement have been proposed with limited supporting evidence.⁵¹ Internal impingement (also known as posterior superior impingement or superior impingement) accounts for the majority of articular sided tears because the humeral tuberosity compresses the RC on the glenoid fossa.⁸⁶ Internal impingement (extrinsic mechanism for tendinopathy) is unique and occurs in overhead throwing athletes.^87‐89 This is due to the extreme external rotation, abduction and extension of the arm, which can, in turn, cause the humerus to pinch the RC tendons on the superior glenoid rim.^90,86 The articular side of the tendons, not the bursal side, compresses between the humerus and the upper rim of the glenoid fossa when the arm is in extension, abduction and full external rotation.⁶ In this case, the clinician will not usually see a narrowing of the SAS.²⁹ Most PRCTs are articular sided as opposed to bursal‐sided, are degenerative in nature, and occur before the acromion degenerates.^91‐93

Aberrant scapular muscle activity has been identified in patients with SAIS and has been directly linked to abnormal scapular motion.^6,94‐96 The serratus anterior and trapezius stabilize the scapula and induce scapular upward rotation, ER (external rotation), and/or posterior tilt, allowing the humeral head the appropriate amount of space for clearance during elevation motions.⁹⁴ Individuals can have reduced muscle performance or balance, latency in activation, and EMG (electromyography) activity of these muscles.^94‐96

Individuals who have some sort of impingement are thought to develop compensational movement patterns that relieve the compression and increase the subacromial space (SAS).⁹⁷ Published evidence does not currently support scapular dyskinesis as a major finding and does not describe it as a prime extrinsic mechanism for individuals with RC tendinopathy.²⁹ Scapular dyskinesis in subjects with RC tendinopathy has been theorized to include aberrant scapular and RC neuromuscular activation and muscle performance, thoracic kyphosis, pectoralis minor shortening, and posterior shoulder tightness.²⁹ A shortened pectoralis minor muscle at rest has been indirectly correlated with RC tendinopathy, functional deficits, and pain.^29,98‐100 This is again thought to be attributed to abnormal scapular kinematics.²⁹ In subjects with RC tendinopathy, it was found that the serratus anterior and lower trapezius muscles demonstrate reduced muscle force and performance.^95,101

Muscle deficits, soft tissue tightness and abnormal posture directly influence shoulder kinematics.²⁹ Weakness or dysfunction of the rotator cuff muscles can set up a situation that leads to SAIS due to a narrow SAS.^6,102 Authors have shown that there is superior humeral head translation and decreased abduction torque when there is reduced force of RC muscles, especially infraspinatus.^103,104 RC tendinopathy is seen in individuals with significant decreases in muscle peak isometric, eccentric and concentric torque when compared to those without these deficits.^105,106Decreased muscle co‐activation ratios between subscapularis, infraspinatus, and supraspinatus during the first 30 degrees of arm elevation and an increase at above 90 degrees was seen in patients exhibiting impingement as compared to the control group with no impingement.^29,107

HEALING

After a tendon injury, the tendon normally heals through scar tissue formation which can take up to 24 months to fully mature.¹⁰⁸ The types and characteristics of collagen in scar tissue are different from that which comprises normal tissue.³³ A greater ratio of Type 1 and Type 3 collagen is present in scar tissue (20‐30%, instead of 1%).¹⁰⁹ Type 3 collagen, although possessing excellent elastic properties, demonstrates inferior strength properties because the diameter of Type 3 fibers is smaller than Type 1 fibers.³³ As the scar matures, it becomes much stronger because of improved interdigitation of collagen fibers and increased fiber diameter.³³ However, the properties are still inferior to native tendon because of the structural organization and poor matrix formation.¹¹⁰ Therefore scar tissue must thicken to make up for its mechanical insufficiency, resulting in a stiffer tendon.³³

Subjects who use tobacco products (e.g., cigarettes) are at greater risk for RC disease and poorer surgical outcomes.^111,112 This relationship becomes stronger as the dose and length of exposure increases.⁵¹ Nicotine induces vasconstriction, which decreases oxygen delivery, and carbon monoxide reduces cellular oxygen levels.^113,114 Nicotine also contributes to a decrease in collagen concentrations, mechanical properties, deposition and repair after surgical intervention, while also causing unrelenting inflammation.^115,116 Postoperative outcomes of smokers are poorer than nonsmokers in terms of pain levels, postoperative satisfaction and overall function.¹¹²

Metabolic diseases can also negatively impact tendon healing and have a higher rate of complications, including infections (10%) and failures (7%).^51,117 Gharaibeh et al stated “In vitro experiments showed that a Cox‐2‐ specific inhibitor (NS‐398) slows the proliferation and maturation of differentiated myogenic precursor cells and thus delays the regenerative myogenesis process.”¹¹⁸ This may impair skeletal muscle healing.¹¹⁸ Similar results have been seen using the Cox‐2 selective inhibitor SC‐236.¹¹⁹ Even in highly vascularized skeletal muscle, NSAIDs seem to impair the healing process and may affect the recovery of other soft tissues.¹¹⁸

HEALING: QUANTIFYING LEVELS OF MATRIX METALLOPROTEINASE – 13 (MMP‐13)

MMPs, aka zinc dependent proteases, are important for tendon repair and are associated with tenocyte cellular changes (see Table 1). Elevated levels of MMP‐13, determined through equalized protein extracts in an enzyme‐linked immunosorbent assay, could be an indicator of an impending tear because they play a critical role in the degradation process of RC tissue. Appropriate pharmacological management is important, as ibuprofen appears to be associated with upregulation of MMP‐13 and other enzymes associated with collagen‐degradation.¹²⁰ If MMP‐13 activity is unchecked, then tears can occur.^121‐123 Furthermore, MMP‐13 levels show a significant relationship with patients' pain ratings,¹²¹ and it has been observed that MMP‐13 contributes to the inflammation found in OA (Osteoarthritis), RA (Rheumatoid arthritis), and periodontal disease and is found at increased levels in full thickness RC tears.^35,123‐125

EVIDENCE IN IMAGING

The function of the upper limb is critical in deciding the treatment approach and determining the patient's prognosis.¹²⁶ Clinical evaluation of the shoulder correlates well with magnetic resonance imaging (MRI) findings.¹²⁶ MRI and ultrasound have comparably high accuracy for finding RC tears and biceps pathologies,^126‐130 clinical tests have moderate accuracy for both conditions.¹²⁶

Patients with RC tendinopathy will not always show significant narrowing in SAS with the arm at rest.^131‐133Clinicians should look at the active range of motion biomechanics and then examine the SAS.¹³⁴ Glenohumeral internal and external rotation have opposing effects on subacromial pressure with external rotation decreasing the pressure in this space.^135,136 Some MRI studies show that active arm elevation reduces the acromial humeral distance (AHD) in those with RC tendinopathy but more research is necessary.^134,137 AHD is the shortest distance between the acromion and the humerus and the term can be used interchangeably with acromial humeral interval.Ardic et al found that the basic office clinic exam (not radiography or ultrasound) has 78.3% sensitivity for patients with subacromial impingement syndrome.¹²⁶ Advanced imaging plays an essential role when conservative therapy approaches fail after three weeks.¹²⁶ Clinical exam impingement tests have 71.2% accuracy, far better than the 40.7% accuracy of Speed's test for an injured biceps tendon.¹²⁶ Musculoskeletal ultrasound had 93.2% accuracy in finding RC tears and was 100% accurate in displaying biceps pathology.¹²⁶ MRI has been shown to be superior to ultrasonography for the detection of overall pathologies, except when there is damage to the biceps tendon.¹²⁶ Some studies found that ultrasonography and MRI had no significant difference when comparing their sensitivity and specificity ratings.^127,128,130 Ultrasongraphy, however, is poorly correlated with surgery or arthrography for diagnosing RC tears.^{126,138‐140}

When measuring the coracoacromial arch in relation to the humerus and the AHD both have a similar measurements and can vary from 1.0 to 1.5 cm as seen on radiographs.⁶ Some studies place the AHD for healthy shoulders between 0.7 cm and 1.4 cm when viewed with ultrasonography, radiography, and MRI.⁶ When the AHD is less than 0.7 cm with the arm resting, a less favorable surgical outcome can be predicted.¹⁴¹ Mayerhoefer et al. stated that AHD and measurements of the acromial shape do not correlate using radiography or MRI and that the acromial shape does not actually mean that the subacromial space is smaller.¹⁴² This means that just because an acromion has a particular shape that it does not mean that the subacromial space is smaller or the acromial humeral distance is reduced.

The lateral acromial angle (LAA) is the relationship between the scapular glenoid plane and the slope of the inferior surface of the acromion. The LAA and acromial humeral interval (AHI) are reliable techniques when measured objectively on X‐ray and MRI and their reliability increases with experienced observers.¹⁴³ LAA measurements have shown that a downsloping acromion correlates to an increased incidence of RC tears.^143‐145 The significance of the AHI needs more research in examining its connection to impingement syndrome.¹⁴³

INJECTIONS

Various injections can and have been used to aid in the diagnosis or treatment of RC tendinopathy. Andres et al found that corticosteroid injections relieve pain in cases of tendinitis for up to six Proposed cellular changes associated with intrinsic mechanisms of rotator cuff tendinopathy weeks, but there is no evidence for benefit beyond six months.^28,146‐148 Arroll et al observed that corticosteroid injections into the SAS for RC tendinitis can be effective for up to nine months.¹⁴⁹ It is thought that higher doses may be more effective than lower doses and that the injections are most likely more effective than NSAIDs.¹⁴⁹ Additionally, accuracy can be improved when using ultrasound guidance to ensure effective injection placement, which could help to improve outcomes.^150,151

Bursal‐sided PRCTs should receive a subacromial injection whereas intra‐articular injections provide greater pain relief for articular sided PRCTs or in patients with PRCTs along with other conditions such as capsulitis.² An indirect suprascapular nerve block may improve pain levels, allowing greater compliance with a rehabilitation program and improving comfort when sleeping.²

PLATELET‐RICH PLASMA

Platelet‐rich plasma (PRP) is developed from autologous blood injections¹⁵² with the aim of improving tendon healing.¹⁵² Evidence points to specific growth factors within the blood that promote the healing process, but evidence refutes the effects of using whole blood injections.^152,153 When using PRP, the platelets add more growth factors to the injection site for seven to ten days.¹⁵² These growth factors are transforming growth factor b1 (TBFb), platelet‐derived growth factor, vascular endothelial growth factor, hepatocyte growth factor, and insulin‐like growth factor 1.¹⁵² These factors are biologically active and stimulate angiogenesis, epithelialization, cell differentiation, proliferation, and the formation of extracellular matrix and fibrovascular callus.^154‐156

Previous studies examining tenocyte cultures showed that cell proliferation and total collagen production was enhanced with platelet‐rich plasma‐clot releasate (PRCR).^157,158 Recent studies provide evidence that PRP treatment in vivo may enhance tendon healing by increasing tenocyte number and production of collagen (types 1 and 3), which makes up a major portion of the tendon.^110,159

PRP can be used to enhance extracellular matrix organization in the short term.¹⁵² Injections given one week post‐op showed increased tendon strength after four weeks when combined with early therapy.¹⁶⁰ There are have been no adverse effects reported after treatment.¹⁵² Some low level evidence exists of improved healing times and increased strength, and in some cases subjects have avoided surgery.¹⁵² It has also been used as a safe adjunct to surgery to improve healing.¹⁵² No studies exist proving that the use of NSAIDS affect the efficacy of PRP but it is currently recommended that NSAIDS should not be taken 2 days before or 14 days after the injections.¹⁵² At this point, there is only limited clinical support for PRP when used for RC repair and cartilage healing, although it is safe for clinical use.¹³

STEM CELLS AND BIOLOGIC AIDS

Stem cell research is rapidly evolving and the literature is uncovering evidence that could greatly improve the treatment of tendinopathy through cell therapy.³³ The evidence is currently limited in humans and not many clinical trials exist,³³ thus, discussion of this area will be limited.

Surgical repair failure rates range from 20 to 70%, which can be attributed to a host of factors.^22,161,162 Biologically engineered scaffolds, exogenous growth factors, and stem cells may show potential when used to encourage RC repair and tendon healing.^163‐165The best way to improve tendon healing is probably through a mixture of different growth factors, but the precise combination is unknown.¹⁶⁵ The optimal proportion of catabolic and anabolic factors will create conditions for a superior repair and encourage the redevelopment of glenohumeral cartilage and tendon to bone insertion.^13,165 Greater research is still needed encompassing animal and human trials.

CONCLUSION

The common belief is that tendinopathy is generated from multivariate etiology. It is increasingly evident that intrinsic mechanisms play a greater role than extrinsic mechanisms in this process. Emphasis should be given on the evidence from patient information and imaging/injection techniques in order to aid in diagnosis of RC tendinopathy. It is the belief of the authors of this commentary that increased effort and research should be placed into future treatment technologies such as cell therapy and biological engineering in order to attempt to improve patient outcomes and quality of life.