Rotator cuff tear

1. High-Yield Summary

• Core Pathology: Rotator cuff tears represent a structural failure spectrum extending from partial-thickness articular or bursal-sided laminar fraying to complete full-thickness tendon retraction. Pathology predominantly initiates within the supraspinatus footprint and propagates posteriorly into the infraspinatus or anteriorly across the rotator interval into the subscapularis.
• Primary Diagnostic Benchmark: Plain radiographs (True AP/Grashey, axillary lateral, supraspinatus outlet) rule out glenohumeral osteoarthritis and evaluate acromiohumeral distance (AHD < 7 mm signifies massive cuff failure with superior humeral migration). Non-contrast magnetic resonance imaging (MRI) is the gold standard for defining tear dimensions, tendon retraction (Patte stages 1 to 3), and irreversible muscle fatty degeneration (Goutallier/Fuchs stages 0 to 4). High-resolution dynamic ultrasound provides comparable diagnostic accuracy for full-thickness tears in experienced hands.
• Cardinal Physical Signs: The external rotation lag sign demonstrates 94% specificity for complete posterosuperior cuff detachment (infraspinatus/supraspinatus), while the Jobe (empty can) test provides 84% sensitivity for supraspinatus structural compromise. The bear-hug and belly-press tests reliably isolate subscapularis detachment.
• Management Paradigm: Acute traumatic full-thickness tears in active individuals warrant prompt anatomic surgical repair within 3 to 6 weeks to avoid progressive retraction and irreversible muscle atrophy. Chronic degenerative tears are managed initially with a 6 to 12-week structured physical therapy regimen focusing on anterior deltoid re-education and periscapular stabilization, reserving surgery for failed nonoperative care.
• Irreparability Thresholds: Tendons exhibiting advanced Goutallier Grade 3 or 4 fatty infiltration, profound retraction medial to the glenoid (Patte Stage 3), or static superior humeral escape (AHD = 3) demonstrate high biological re-tear rates after primary repair. These patients require joint-preserving salvage procedures (superior capsular reconstruction, tendon transfers) or reverse total shoulder arthroplasty (rTSA).

2. Anatomy

The rotator cuff consists of four dynamic musculotendinous units originating from the scapula and inserting onto the humeral tuberosities: the supraspinatus, infraspinatus, and teres minor on the greater tuberosity, and the subscapularis on the lesser tuberosity. Dynamically, the cuff provides concavity-compression of the humeral head into the shallow glenoid fossa and restores balanced force couples in both the coronal plane (deltoid vs. inferior cuff musculature) and the transverse plane (anterior subscapularis vs. posterior infraspinatus and teres minor).

The greater tuberosity insertion footprint is divided into three distinct anatomical facets:

• Superior Facet: Receives the anterior portion of the supraspinatus tendon. The supraspinatus footprint measures approximately 12 to 14 mm in medial-to-lateral width and 16 to 18 mm in anterior-to-posterior dimension.
• Middle Facet: Receives the posterior supraspinatus tendon fibers and the superior half of the infraspinatus tendon. The infraspinatus footprint is trapezoidal, measuring approximately 13 mm in medial-to-lateral width and 15 mm in anterior-to-posterior length.
• Inferior Facet: Receives the remaining infraspinatus fibers and the teres minor, which extends distally along the humeral shaft.
• Lesser Tuberosity Footprint: Receives the subscapularis tendon, representing the largest cuff insertion. It is broad and comma-shaped, measuring approximately 18 mm at its superior cranial apex and tapering inferiorly into a muscular insertion.

The microstructural architecture features two functional biomechanical zones described by Burkhart: the rotator cable and the rotator crescent. The rotator cable is a thick, curved transverse fibrous bundle originating from the anterior bicipital groove and coracohumeral ligament, coursing across the deep lamina of the supraspinatus and infraspinatus, and inserting at the posterior border of the infraspinatus. The rotator crescent is a thin, avascular central tissue zone bounded laterally by the greater tuberosity and medially by the cable. Through a suspension bridge mechanism, the rotator cable shields the vulnerable crescent tissue from excessive tensile stress, explaining why crescent tears can maintain reasonable clinical function if the anterior and posterior cable attachments remain structurally intact.

Codman described a hypovascular “critical zone” located approximately 1 cm proximal to the supraspinatus insertion on the greater tuberosity. This region represents an anastomotic watershed between osseous vessels from the tuberosity and muscular branches of the suprascapular and anterior circumflex humeral arteries. Under active elevation, tensile loading compresses this hypovascular segment, creating intermittent tissue ischemia that accelerates degenerative failure.

Surgical exposure and arthroscopic portal placement require strict adherence to neurovascular danger zones:

• Suprascapular Nerve: Courses under the superior transverse scapular ligament at the suprascapular notch to supply the supraspinatus, then winds around the spinoglenoid notch beneath the inferior transverse scapular ligament into the infraspinatus fossa. The nerve at the spinoglenoid notch lies within 1.5 cm medial to the posterior glenoid rim. Medial dissection, excessive traction, or posterior capsular releases exceeding 1.5 cm medial to the glenoid rim risk direct laceration or traction neuropraxia.
• Axillary Nerve: Traverses the quadrilateral space with the posterior circumflex humeral artery and wraps around the surgical neck of the humerus on the deep surface of the deltoid. The nerve lies 5.0 to 6.5 cm (mean 5.5 cm) distal to the lateral acromial margin, limiting any lateral deltoid-splitting incision to less than 5 cm. Arthroscopically, the nerve lies 2 to 3 mm inferior to the 6 o’clock glenoid rim during inferior capsular releases.
• Internervous Plane: The deltopectoral approach exploits the internervous interval between the pectoralis major (medial and lateral pectoral nerves) and the deltoid (axillary nerve), safely protecting muscular innervation while exposing the anterior cuff and subscapularis.

3. Pathogenesis

Rotator cuff disease develops via a complex, multifactorial pathway combining intrinsic biological tissue degeneration, microstructural failure, and extrinsic mechanical impingement:

• Intrinsic Tendon Degeneration: Tendon aging involves tenocyte senescence, apoptosis, diminished proteoglycan synthesis, and matrix disorganized cross-linking. Microarchitectural analysis demonstrates a pathological shift from normal collagen type I (high tensile stiffness) to disorganized collagen type III, which possesses lower mechanical load capacity and heightened vulnerability to shear stress. The disease typically transitions from an early hypervascular, inflammatory stage with synovitis to a late hypocellular, hypovascular, fibrotic degenerative state incapable of intrinsic repair.
• Extrinsic Mechanical Impingement: Described by Neer, mechanical compression of the bursal surface of the supraspinatus occurs against the anterior third of the acromion, the coracoacromial ligament, and the inferior acromioclavicular joint during forward elevation and internal rotation. Bony enthesophytes and hooked acromial morphology (Bigliani Type III) escalate contact stresses. Internal impingement occurs in overhead athletes when repetitive maximal abduction and external rotation compress the articular surface of the posterosuperior cuff against the posterior-superior glenoid labrum.
• Laminar Shear Stress: Biomechanical studies confirm that the articular surface of the supraspinatus experiences more than double the strain observed on the bursal surface during glenohumeral elevation. The articular layer is less vascularized, contains higher proportions of non-aligned fibers, and has lower ultimate tensile strength. Consequently, partial-thickness tears initiate on the articular surface two to three times more frequently than on the bursal surface. Differential strain between these laminar layers generates interlaminar shear stress, driving delamination and tear propagation.
• Traumatic Failure Mechanism: Acute tears occur when sudden, excessive tensile loads overwhelm tendon structural limits. The classic mechanism is a fall onto an outstretched hand (FOOSH) with the arm in abduction and forward flexion, or an acute glenohumeral dislocation in patients older than 40 years.

4. Natural History

The prevalence of rotator cuff tears increases markedly with advancing age. Asymptomatic full-thickness tears are present in approximately 10% of adults under 50 years, 20% to 25% of individuals aged 60 to 69 years, and exceed 50% in patients aged 80 years and older.

Longitudinal imaging cohorts demonstrate that asymptomatic rotator cuff tears do not remain dormant. Between 35% and 50% of asymptomatic tears become symptomatic within a 2 to 5-year observation period. Furthermore, approximately 50% of full-thickness tears exhibit measurable structural propagation over 2 to 5 years, with an average tear expansion rate of 2 to 4 mm per year. Partial-thickness tears involving more than 50% of the tendon thickness carry a high risk of progressing to full-thickness disruption.

Chronic tendon detachment produces progressive, irreversible alterations in the associated muscle belly. Loss of mechanical tension triggers volumetric muscle atrophy, best quantified on sagittal MRI using the Thomazeau tangent sign. Simultaneously, muscle fibers undergo intramyocellular fatty degeneration (Goutallier and Fuchs stages 0 to 4). Histological and clinical studies confirm that muscle fatty infiltration is biologically irreversible, persisting even after successful structural tendon repair. When fatty infiltration progresses to Goutallier Stage 3 or 4, structural healing rates drop precipitously.

In massive, chronic tears involving two or more tendons, uncoupling of the coronal force couple allows the unopposed deltoid to pull the humeral head superiorly. Persistent proximal migration leads to abnormal contact against the acromial vault, resulting in acetabularization of the acromion, femoralization of the humeral head, secondary cartilage loss, and end-stage rotator cuff tear arthropathy (Hamada classification).

5. Clinical Presentation

History

Patients typically present with dull, aching anterolateral shoulder pain that radiates along the lateral deltoid to its insertion. Symptoms are characteristically exacerbated by overhead reaching, lifting, or internal rotation behind the back. A hallmark historical feature is severe nocturnal sleep disturbance, particularly when rolling onto the affected shoulder or resting with the arm overhead. Clinicians must distinguish an acute traumatic presentation (a sudden tearing sensation or pop during a fall or high-energy event followed by immediate functional deficit) from chronic degenerative progression (insidious onset of aching over months or years with gradual loss of active elevation). Additional historical clues include mechanical catching, crepitus, and subjective weakness during abduction or external rotation.

Physical Examination

Physical examination begins with visual inspection from the anterior, lateral, and posterior perspectives to assess muscle wasting in the supraspinatus and infraspinatus fossae. Active and passive range of motion are systematically measured in forward elevation, external rotation at the side, and internal rotation behind the back. A critical clinical distinction must be made: full passive range of motion with a loss of active elevation indicates a structural tendon defect or nerve palsy (pseudoparalysis), whereas a concordant loss of both active and passive motion points toward adhesive capsulitis or glenohumeral osteoarthritis.

Methodical provocative testing isolates individual musculotendinous units with validated diagnostic accuracy:

6. Imaging and Diagnostic Studies

Radiographs

The standard radiographic evaluation consists of a dedicated four-view shoulder series: True AP (Grashey view in neutral, internal, and external rotation), Axillary lateral, and Scapular Y outlet view. Radiographs assess bony anatomy, rule out glenohumeral osteoarthritis, and evaluate indirect signs of rotator cuff deficiency:

• Acromiohumeral Distance (AHD): Measured on the true AP view between the dense inferior acromial cortex and the superior articular cortex of the humeral head. The normal interval measures 7 to 14 mm. An AHD < 7 mm signifies a massive, chronic rotator cuff tear with superior humeral head migration. An AHD < 5 mm indicates severe cuff deficiency with complete superior escape and subacromial contact.
• Bigliani Acromial Morphology: Evaluated on the scapular Y outlet view. Type I is flat (low risk of impingement); Type II is curved parallel to the humeral head; Type III is hooked anteriorly, demonstrating a strong association with subacromial impingement and full-thickness tears.
• Hamada Classification of Cuff Tear Arthropathy: Stage 1: AHD > 6 mm, normal joint; Stage 2: AHD <= 5 mm, superior humeral head migration; Stage 3: AHD <= 5 mm with acetabularization of the acromion; Stage 4: Glenohumeral joint space narrowing (4A without acetabularization, 4B with acetabularization); Stage 5: Humeral head collapse (osteonecrosis-like articular destruction).

Advanced Imaging

Cross-sectional imaging provides definitive structural assessment of tendon integrity, retraction, and muscle architecture:

• Magnetic Resonance Imaging (MRI): Non-contrast 1.5T or 3.0T MRI is the established gold standard. Diagnostic criteria for full-thickness tears include fluid-equivalent hyperintensity on T2-weighted or proton density fat-suppressed (PDFS) sequences extending completely through the tendon substance from the articular to the bursal surface. Coronal oblique images define medial-to-lateral tear width, footprint detachment, and tendon retraction (Patte stage). Sagittal oblique images assess anterior-to-posterior tear dimensions, Goutallier fatty muscle infiltration, and the Thomazeau tangent sign (a line drawn from the superior border of the coracoid to the scapular spine; atrophy is present when the supraspinatus muscle belly falls below this line). Axial images evaluate subscapularis detachment and long head of the biceps stability.
• High-Resolution Dynamic Ultrasound: Demonstrates high sensitivity (>90%) and specificity (>90%) for full-thickness tears in experienced hands. Advantages include dynamic real-time evaluation during impingement maneuvers, point-of-care availability, and safety in patients with MRI contraindications (pacemakers, claustrophobia). Limitations include high operator dependency and inferior visualization of medial retraction and muscle fatty infiltration.

7. Classification

Validated classification systems define rotator cuff tear depth, dimension, retraction, muscle fatty degeneration, and functional pattern, directly guiding operative decision-making:

8. Treatment

Nonoperative Management

Nonoperative treatment represents the established first-line intervention for chronic degenerative partial- and full-thickness rotator cuff tears in elderly or low-demand individuals, as well as asymptomatic tears discovered incidentally. The therapeutic cornerstone is a 6 to 12-week structured physical therapy protocol emphasizing anterior deltoid re-education and hypertrophy to compensate for superior cuff deficiency, periscapular stabilizer strengthening (serratus anterior, rhomboids, lower trapezius), and posterior capsular stretching to correct glenohumeral internal rotation deficits. Oral nonsteroidal anti-inflammatory drugs (NSAIDs) assist in pain control during rehabilitation.

Judicious subacromial corticosteroid injections provide short-term analgesic relief (up to 6 to 12 weeks) to facilitate physical therapy participation. Injections should be limited to a maximum of 2 to 3 applications spaced over several months, as repeated corticosteroid exposure causes local collagen matrix degradation and microvascular compromise. Subacromial corticosteroid injections within 3 to 6 months prior to surgery significantly increase postoperative infection rates and structural re-tear risk. Objective failure thresholds include persistent refractory night pain, progressive loss of active elevation, or documented tear propagation on serial imaging despite 3 to 6 months of supervised rehabilitation.

Operative Management

The primary objectives of operative repair are to achieve an anatomic, watertight footprint restoration onto bleeding decorticated bone under low tension, re-establish balanced transverse and coronal force couples, and eliminate mechanical subacromial abrasion:

• Single-Row vs. Double-Row Transosseous-Equivalent (TOE / SutureBridge): Single-row repair utilizes suture anchors placed along the lateral footprint or medial articular margin; it is biomechanically appropriate for small tears (< 1 to 2 cm). Double-row TOE constructs combine medial-row anchors at the articular cartilage margin with knotless lateral-row anchors on the greater tuberosity, creating a compression bridge across the entire footprint. Double-row constructs significantly increase footprint contact area, maximize contact pressure, and reduce structural re-tear rates in tears larger than 2 to 3 cm.
• Margin Convergence and Tendon Mobilization: Retracted U-shaped or L-shaped tears should not be pulled directly to the lateral tuberosity under excessive tension. Sequential 360-degree releases of the coracohumeral ligament, superior capsule, and posterosuperior adhesions medial to the glenoid advance the tendon. Side-to-side margin convergence sutures close the longitudinal split, advancing the tendon edge laterally and converting a large defect into a smaller crescent tear that reduces footprint strain.
• Biceps Management: Pathological changes in the long head of the biceps tendon (fraying, subluxation, partial tears) represent a primary anterior pain generator. Concomitant arthroscopic biceps tenotomy or subpectoral tenodesis provides reliable pain relief. Tenotomy is preferred in elderly, lower-demand patients (with counseling regarding cosmetic Popeye deformity), whereas tenodesis is preferred in younger, active patients and manual laborers to preserve supination strength and muscle contour.
• Irreparable Tear Salvage: For tears with advanced fatty infiltration or retraction refractory to mobilization, salvage modalities include: Superior Capsular Reconstruction (SCR) utilizing fascia lata autograft or acellular dermal allograft to act as a static spacer depressing the humeral head in young patients with intact cartilage; Tendon Transfers (lower trapezius with Achilles tendon allograft or latissimus dorsi) restoring active external rotation in young active patients; and Reverse Total Shoulder Arthroplasty (rTSA) as the definitive solution for patients older than 65 to 70 years presenting with pseudoparalysis, anterior-superior escape, or cuff tear arthropathy (Hamada >= 3).

Indications & Contraindications

Indications for Surgical Repair:

• Acute traumatic full-thickness rotator cuff tears in active patients, ideally repaired within 3 to 6 weeks to prevent rapid retraction and fatty infiltration.
• Symptomatic full-thickness tears failing a 3 to 6-month trial of structured nonoperative therapy with reparable muscle morphology (Goutallier <= 2, Patte <= 2).
• Partial-thickness tears exceeding 50% of the tendon thickness (Ellman Grade 3, > 6 mm depth) refractory to nonoperative management.
• Progressive loss of active elevation or documented structural tear propagation on serial MRI in active individuals.

Contraindications to Primary Surgical Repair:

• Severe muscle fatty degeneration (Goutallier Grade 3 or 4) or severe tendon retraction (Patte Stage 3) where primary repair fails biologically; salvage reconstruction or rTSA is indicated.
• Advanced rotator cuff tear arthropathy with glenohumeral joint destruction (Hamada Stage >= 3); primary tendon repair fails and rTSA is the procedure of choice.
• Asymptomatic rotator cuff tears in elderly, low-demand patients.
• Active local or systemic infection.
• Deltoid muscle denervation or axillary nerve palsy (absolute contraindication to both primary repair and rTSA).
• Severe medical comorbidity or cognitive impairment precluding adherence to postoperative sling immobilization.

9. Outcome

Operative repair of rotator cuff tears delivers reliable pain relief, functional restoration, and high patient satisfaction across validated patient-reported outcome measures (PROMs), including the American Shoulder and Elbow Surgeons (ASES) score, Constant-Murley score, Penn Shoulder Score, and Simple Shoulder Test (SST). Overall patient satisfaction rates consistently exceed 85% to 90% following successful anatomical repair.

Structural tendon healing rates depend directly on preoperative tear size, patient age, tissue quality, and the degree of muscular fatty degeneration. Small and medium full-thickness tears (< 3 cm) achieve complete anatomical healing in 80% to 90% of cases. Conversely, large and massive tears (> 3 to 5 cm or involving multiple tendons) experience structural re-tear rates of 40% to 60% on postoperative imaging.

A notable clinical-radiographic dissociation frequently occurs: patients with structural re-tears or partial nonhealing often report substantial pain relief and meaningful functional improvement compared to their preoperative status, provided that transverse force couples remain restored. However, patients with verified structural healing achieve significantly superior active elevation, higher external rotation and abduction strength, and better long-term Constant scores compared to those with unhealed defects.

10. Complications

Complications associated with rotator cuff repair are categorized by chronological onset:

11. Pearls and Pitfalls

• Footprint Decortication Pearl: Lightly decorticate the greater tuberosity using a motorized burr or microfracture awl down to punctate bleeding bone without creating a deep trough in the cortical plate. Aggressive troughing removes the dense cortical shell required for secure anchor purchase.
• Deadman’s Angle Pearl: Suture anchors placed along the medial footprint must be inserted at Burkhart’s 45° “deadman angle” relative to the cortical bone surface. Inserting anchors perpendicular or obtuse to the bone creates a cantilever pullout force that predisposes to early cyclic displacement.
• Interval Slide Pearl: For retracted tears with limited excursion, perform an anterior slide (releasing the coracohumeral ligament and rotator interval) and, if necessary, a posterior slide (between the supraspinatus and infraspinatus). These releases mobilize the tendon lateral to the glenoid without disrupting dorsal muscular vascularity.
• Biceps Management Pearl: Routinely address an unstable, subluxated, or severely frayed long head of the biceps tendon with tenotomy or tenodesis. Addressing the biceps eliminates a primary anterior pain generator and improves arthroscopic visualization of the subscapularis footprint.
• Overtensioning Pitfall: Forcibly pulling a retracted tendon stump directly to the lateral footprint under high tension causes suture strangulation and ischemic necrosis at the musculotendinous junction (Type 2 failure). If tension remains elevated after complete releases, medializing the footprint 3 to 5 mm onto the articular margin provides a durable, tension-free repair.
• Aggressive Acromioplasty Pitfall: Overzealous resection of the anterior-inferior acromion compromises the anterolateral deltoid origin and risks an acromial stress fracture without conferring clinical outcome benefits. Limit acromioplasty to removing prominent mechanical enthesophytes (Bigliani Type III).
• Missed Subscapularis Pitfall: Failing to inspect the upper border of the subscapularis tendon from a posterior portal is a common diagnostic error. Look for the “comma sign” (displaced medial sling of the coracohumeral ligament) and visualize the tendon in dynamic internal and external rotation. Unrepaired subscapularis tears leave the anterior force couple disrupted, causing posterosuperior repairs to fail.

12. Controversy

Key clinical controversies continue to shape modern rotator cuff management:

• Single-Row vs. Double-Row Fixation: Double-row transosseous-equivalent constructs provide superior footprint contact area, higher load-to-failure, and significantly lower structural re-tear rates on postoperative imaging in tears greater than 2 to 3 cm. However, multiple Level I randomized controlled trials demonstrate equivalent patient-reported outcome measures (ASES, Constant scores) between single-row and double-row repairs in small-to-medium tears, questioning whether the added implant costs and operative time are justified in routine cases.
• Routine Subacromial Decompression: Neer’s original impingement concept prompted routine anterior acromioplasty during cuff repair. High-level randomized controlled trials have demonstrated that adding routine acromioplasty does not improve functional outcomes, pain scores, or structural healing rates compared with repair alone. Modern consensus limits acromioplasty to distinct, symptomatic anterior-inferior spurs.
• Biological Augmentation: The application of platelet-rich plasma (PRP), bone marrow aspirate concentrate (BMAC), and extracellular matrix xenografts or synthetic patches aims to enhance biological healing at the tendon-bone interface. While certain trials report modest reductions in re-tear rates for large tears, substantial heterogeneity in preparation techniques, leukocyte concentrations, and delivery protocols has prevented universal clinical consensus.
• Management of Asymptomatic Tears: With over 30% to 50% of asymptomatic full-thickness tears exhibiting structural propagation and potential progression to irreversible muscle fatty degeneration over 2 to 5 years, some clinicians advocate early prophylactic repair in active patients. Conversely, others recommend conservative surveillance because many asymptomatic tears remain functionally compensated, avoiding the morbidity and costs of overtreatment.

13. Evidence-Based Synthesis

Modern clinical decision-making is grounded in high-quality randomized controlled trials and prospective registry analyses, corroborated by seminal biomechanical and anatomical descriptions.

14. References

• Moosmayer S, Lund G, Seljom US et al. Tendon repair compared with physiotherapy in the treatment of rotator cuff tears: a randomized controlled study in 103 cases with a five-year follow-up. J Bone Joint Surg Am. 2014. doi:10.2106/JBJS.M.01393 [Level I: Randomized Controlled Trial]
• Longo UG, Risi Ambrogioni L, Candela V et al. Conservative versus surgical management for patients with rotator cuff tears: a systematic review and META-analysis. BMC Musculoskelet Disord. 2021. doi:10.1186/s12891-020-03872-4 [Level I: Systematic Review / Meta-Analysis]
• Kukkonen J, Joukainen A, Lehtinen J et al. Treatment of non-traumatic rotator cuff tears: A randomised controlled trial with one-year clinical results. Bone Joint J. 2014. doi:10.1302/0301-620X.96B1.32168 [Level I: Randomized Controlled Trial]
• Lowry V, Lavigne P, Zidarov D et al. A Systematic Review of Clinical Practice Guidelines on the Diagnosis and Management of Various Shoulder Disorders. Arch Phys Med Rehabil. 2024. doi:10.1016/j.apmr.2023.09.022 [Level I: Systematic Review / Meta-Analysis]
• Boileau P, Brassart N, Watkinson DJ et al. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal?. J Bone Joint Surg Am. 2005. doi:10.2106/00004623-200506000-00007 [Level IV: Clinical Case Series / Cohort Study]

15. Master Class Pro-Tip

Master Class Surgical Pearl: When repairing retracted U-shaped or L-shaped rotator cuff tears, never attempt to pull the apex of the tendon directly to the lateral footprint, which produces excessive mechanical tension and early failure. First perform extensive intra-articular and subacromial releases of the coracohumeral and glenohumeral ligaments, followed by side-to-side margin convergence sutures to close the longitudinal split and advance the tendon margin laterally. Once margin convergence transforms the large defect into a smaller, transverse tear with restored force couples, perform a low-tension double-row transosseous-equivalent footprint repair to bleeding decorticated bone.

Master Class Surgical Pearl: Rotator Cuff Reconstruction