The rotator cuff is a group of four muscles and associated tendons that surround and stabilize the glenohumeral joint of the shoulder, enabling a wide range of arm movements while maintaining joint integrity.[1] These structures collectively form a musculotendinous cuff that encases the humeral head, compressing it against the shallow glenoid fossa to prevent dislocation during dynamic activities.[2]The four muscles comprising the rotator cuff are the supraspinatus, infraspinatus, teres minor, and subscapularis, each originating from the scapula and inserting onto the humerus via short, flat tendons.[3] The supraspinatus, located superiorly, primarily initiates abduction of the arm; the infraspinatus and teres minor, positioned posteriorly, facilitate external rotation; and the subscapularis, anteriorly, enables internal rotation and anterior stability.[2] Together, these muscles not only provide specific rotational and elevatory forces but also act synergistically to centralize the humeral head within the glenoid, counteracting the upward pull of the deltoid muscle during overhead motions.[4]In addition to their biomechanical roles, the rotator cuff contributes to shoulder proprioception via muscle spindles and Golgi tendon organs, and to overall upper limb function, with its tendons blending into a common insertion that reinforces the joint capsule.[2][5] Injuries to the rotator cuff, such as tears or tendinopathy, are prevalent in individuals over 40 or those engaged in repetitive overhead activities, often leading to pain, weakness, and impaired mobility.[6] The blood supply to these structures arises primarily from the suprascapular, subscapular, and posterior circumflex humeral arteries, though a "critical zone" in the supraspinatus tendon is relatively hypovascular, predisposing it to degenerative changes.[2][4]
Anatomy
Muscles
The rotator cuff is composed of four primary muscles that envelop the humeral head, providing dynamic stability to the glenohumeral joint: the supraspinatus, infraspinatus, teres minor, and subscapularis, commonly remembered by the acronym SITS.[2] These muscles originate from the scapula and insert onto the proximal humerus, working in concert to facilitate precise shoulder movements while compressing the humeral head against the glenoid fossa.[7]The **supraspinatus** muscle arises from the supraspinous fossa of the scapula, above the spine of the scapula, and its tendon inserts onto the superior facet of the greater tubercle of the humerus.[2] It is the smallest of the rotator cuff muscles yet plays a critical role in initiating abduction of the arm from 0 to approximately 15 degrees, after which the deltoid takes over.[8] Despite its modest size, the supraspinatus generates significant force relative to its cross-sectional area, underscoring its importance in early-phase abduction mechanics.[3]The infraspinatus originates from the infraspinous fossa of the scapula, below the spine, and inserts via its tendon onto the middle facet of the greater tubercle of the humerus.[2] This muscle is primarily responsible for external rotation of the humerus, particularly when the arm is at the side, and it contributes to humeral head depression during elevation to prevent superior migration.[7] It is one of the larger rotator cuff muscles, providing substantial strength for rotational control.[8]The teres minor, the smallest and most inferiorly positioned of the external rotators, originates from the upper two-thirds of the lateral border of the scapula and inserts onto the inferior facet of the greater tubercle of the humerus.[2] It assists the infraspinatus in performing external rotation of the shoulder and also aids in adduction of the arm.[7] Though smaller in size and strength compared to the infraspinatus, it provides fine-tuned stabilization during external rotation activities.[8]The subscapularis is the largest and most anterior rotator cuff muscle, originating from the subscapular fossa on the anterior surface of the scapula and inserting onto the lesser tubercle of the humerus.[2] It functions mainly as an internal rotator of the humerus, drawing the arm toward the midline, and also contributes to anterior stability of the glenohumeral joint by resisting posterior displacement.[7] Its substantial size and robust fiber architecture enable it to exert the greatest torque among the cuff muscles for internal rotation.[3]Collectively, the tendons of these muscles blend with the glenohumeral joint capsule, forming a continuous musculotendinous cuff that enhances overall shoulder integrity, as detailed further in the section on tendons and bursae.[2]
Tendons and bursae
The tendons of the rotator cuff are primarily composed of dense, type I collagen fibers organized in a hierarchical structure, accounting for over 85% of the tendon's dry weight, which enables them to form a continuous, musculotendinous cuff that envelops the anterior, superior, and posterior aspects of the humeral head.[9][10] This fibrous composition provides tensile strength and allows the tendons to blend seamlessly with the underlying structures of the glenohumeral joint.The insertion footprints of these tendons on the humerus exhibit a distinct topographic arrangement. The supraspinatus tendon attaches to the superior facet of the greater tubercle in a broad, triangular pattern, while the infraspinatus tendon inserts onto the middle facet of the greater tubercle. The teres minor tendon anchors to the inferior facet of the greater tubercle, and the subscapularis tendon inserts onto the lesser tubercle, creating a cohesive footprint that measures approximately 3-4 cm in mediolateral width across the combined insertions.[11][12]These tendons integrate intimately with the glenohumeral joint capsule, blending their fibers with the superior, middle, and inferior glenohumeral ligaments to reinforce the overall architecture.[13][14]Associated with the rotator cuff is the subacromial bursa, a synovial, fluid-filled sac located between the acromion and the superior surface of the cuff tendons, particularly the supraspinatus, which facilitates smooth gliding by reducing friction during shoulder elevation.[15][16]The blood supply to the rotator cuff tendons arises mainly from branches of the suprascapular artery and subscapular artery, supplemented by the anterior and posterior humeral circumflex arteries, though critical watershed zones—particularly 1-1.5 cm proximal to the supraspinatus insertion—exhibit relative hypovascularity, rendering them susceptible to degenerative changes.[17][18][19]Innervation of the rotator cuff tendons and their associated muscles is provided by the suprascapular nerve (C5-C6 roots) for the supraspinatus and infraspinatus, the axillary nerve (C5-C6) for the teres minor, and the upper and lower subscapular nerves (C5-C7) for the subscapularis, ensuring coordinated sensory and motor control.[2][20]
Function
Shoulder stabilization
The rotator cuff provides essential dynamic stability to the glenohumeral joint by generating compressive forces that press the humeral head firmly into the concave glenoid fossa, enhancing joint congruence and resisting potentially destabilizing translations. This mechanism, known as concavity compression, relies on the coordinated contraction of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles to create balanced tension across the joint.[4] Unlike static stabilizers such as the glenohumeral ligaments and labrum, which offer passive resistance through tension, the rotator cuff delivers active, dynamic compression that adapts to varying loads and positions, thereby supplementing and amplifying overall joint stability.[21]A primary function in this stabilization is the depressor mechanism, where the rotator cuff counteracts the superior migratory force on the humeral head induced by deltoid contraction during shoulder elevation. The inferior components of the cuff, including the subscapularis and infraspinatus, generate an inferiorly directed force that depresses the humeral head, preventing its upward displacement and maintaining central positioning within the glenoid.[22] This interaction forms a critical force couple in the coronal plane, with the deltoid's superior pull balanced by the cuff's depressive action, ensuring smooth and stable motion without subluxation.[23]In the transverse plane, the force couple concept further centralizes the humeral head through opposing actions of the anterior subscapularis muscle and the posterior infraspinatus and teres minor muscles, which together produce a balanced rotational torque that resists anterior or posterior shifts.[24] This anterior-posterior equilibrium, combined with the overall compressive force from all four muscles, centers the humeral head and minimizes shear stresses at the jointinterface. Biomechanical analyses demonstrate that the rotator cuff contributes substantially to glenohumeral stability, with its compressive and balancing forces accounting for up to 35% of resistance against anterior-posterior loading in intact joints, underscoring its pivotal role during everyday activities.[25]
Range of motion
The rotator cuff plays a crucial role in facilitating shoulder range of motion by initiating and controlling key movements such as abduction, external rotation, and internal rotation. The supraspinatus muscle is primarily responsible for initiating the first 15° of glenohumeral abduction, providing the initial lift of the humeral head before the deltoid muscle assumes dominance for further elevation.[26] This early activation ensures proper alignment and prevents impingement during the transition to deltoid-driven motion. In contrast, the infraspinatus and teres minor muscles contribute to external rotation, enabling a normal range of up to 90° when the arm is at the side, which is essential for activities requiring arm positioning away from the body.[27] Similarly, the subscapularis facilitates internal rotation, supporting a typical range of 70° to 90° in neutral arm position, thereby allowing medial arm adduction and functional tasks like reaching across the body.[26]Integration of the rotator cuff with scapular motion is vital for overall shoulder kinematics through the scapulohumeral rhythm, a coordinated movement pattern where glenohumeral elevation occurs in a 2:1 ratio relative to scapulothoracic upward rotation after the initial 30° of abduction.[28] The cuff muscles maintain this rhythm by dynamically adjusting tension to guide the humeral head smoothly within the glenoid fossa, ensuring efficient energy transfer and minimizing joint stress during overhead activities. Without this precise coordination, deviations in the ratio can lead to inefficient motion or compensatory scapular movements.During full elevation, the rotator cuff provides essential control to prevent superior translation of the humeral head, which would otherwise disrupt joint congruence and limit range. By generating a compressive force couple, the cuff counters the upward shear from the deltoid, allowing unimpeded progression to 180° of flexion or abduction in healthy shoulders.[29] This stabilizing action is particularly critical in the mid-range of motion, where translational forces peak.Electromyographic studies reveal distinct activation patterns of the rotator cuff during elevation, with the supraspinatus showing increased activity during arm elevation in the scapular plane, reflecting its role in maintaining head depression against increasing deltoid pull.[30] This heightened recruitment underscores the muscle's importance in the "painful arc" phase, where demands for precise control are greatest.
Epidemiology
Prevalence and incidence
Rotator cuff tears are a prevalent condition, particularly among older adults, with overall prevalence in the general population estimated at approximately 22%.[31] This figure encompasses both symptomatic and asymptomatic cases, and the prevalence increases significantly with age, from about 13% in individuals aged 50-59 years to 20% in those aged 60-69 years, 26% in those aged 70-79 years, and 31% in those aged 80 years and older among asymptomatic shoulders.[32] In broader studies of rotator cuff abnormalities, rates range from 9.7% in individuals under 20 years to 62% in those over 80 years.[33]The incidence of rotator cuff pathology is estimated at 0.87 cases per 1,000 person-years in the general population.[34] The incidence of symptomatic rotator cuff tears is estimated at approximately 0.9-2 cases per 1,000 person-years in studied populations, such as military personnel, with limited general population data available.[35] Degenerative changes associated with rotator cuff issues affect 15-20% of individuals aged 60 years, contributing to the rising prevalence in aging populations.[36]Rotator cuff tears are rare in individuals under 40 years, occurring in less than 5% of cases, and their prevalence peaks in the 60-80 age group, where full-thickness tears reach 14.9% in those aged 60-69 years and 25.9% in those aged 70-79 years.[37]Gender differences show a higher prevalence in males compared to females, often attributed to greater occupational exposure in physically demanding roles.[38]A substantial proportion of rotator cuff tears are asymptomatic, comprising about 67.8% of all detected tears, while symptomatic tears account for 32.2%; asymptomatic cases are roughly twice as common as symptomatic ones and are frequently identified incidentally through imaging for unrelated issues.[39][31]
Risk factors
Risk factors for rotator cuff pathology can be categorized as non-modifiable and modifiable, with the former including intrinsic biological elements that cannot be altered and the latter encompassing lifestyle and environmental influences that may be mitigated through intervention. Non-modifiable factors play a significant role in the intrinsic degeneration of rotator cuff tissues, often progressing over time without external provocation.Advanced age is a primary non-modifiable risk factor, as collagen degeneration and reduced vascularity in the rotator cuff tendons increase susceptibility to tears and tendinopathy, with prevalence rising sharply after age 50. Genetic predisposition, such as familial hyperlaxity associated with conditions like Ehlers-Danlos syndrome, contributes to joint instability and higher rates of rotator cuff injury by compromising tendon integrity and shoulder mechanics. Male gender is also linked to elevated risk, potentially due to higher exposure to physically demanding activities, though biologic differences in tendon composition may contribute, with studies showing a higher incidence of tears in men compared to women.Modifiable factors often stem from behavioral and occupational exposures that accelerate tendon wear. Repetitive overhead activities, common in athletes like baseball pitchers and occupations such as painting, impose chronic mechanical stress on the rotator cuff, increasing tendinopathy risk by up to threefold in pitchers relative to non-throwing athletes. Smoking impairs tendon vascularity and healing, elevating the odds of rotator cuff tears by approximately 1.5 to 2 times through nicotine-induced vasoconstriction and oxidative stress. Obesity alters shoulder biomechanics and promotes inflammation, associating with a 1.5-fold higher risk of tears via increased fatty infiltration and metabolic strain on tendons.Occupational risks are prominent in manual labor sectors; construction workers face about a fourfold increased odds of rotator cuff syndrome due to heavy lifting and awkward postures. Comorbidities like diabetes double the risk through advanced glycation end-products that stiffen collagen and impair tendon repair, while hyperlipidemia contributes via atherosclerosis that reduces nutrient supply to the rotator cuff, with meta-analyses indicating a 1.4-fold elevated odds. Anatomic variants, such as a hooked (Type III) acromion, mechanically predispose to impingement by narrowing the subacromial space, tripling the risk of rotator cuff pathology compared to flat (Type I) morphologies.
Disorders
Rotator cuff tears
Rotator cuff tears represent structural disruptions of the tendons attaching the rotator cuff muscles to the humerus, ranging from partial involvement to complete severance. Partial-thickness tears affect less than the full depth of the tendon and are subclassified by location as bursal-sided (on the subacromial side), articular-sided (on the glenohumeral joint side), or intratendinous (within the tendon substance without surface involvement).[40] Full-thickness tears involve complete tendon disruption from bone to bone, allowing communication between the subacromial bursa and the glenohumeral joint. Massive tears are defined as those involving two or more tendons or exceeding 5 cm in greatest dimension, often leading to greater functional impairment due to extensive tissue loss.[41][42]These tears arise from two primary mechanisms: acute trauma or chronic degeneration. Acute traumatic tears typically result from high-energy events such as falls or dislocations and predominate in younger patients. In contrast, degenerative tears, driven by repetitive microtrauma, attrition, and age-related tendon weakening, account for approximately 70% of cases in patients over 60, often without a discrete injury event.[43][44]Pathophysiologically, rotator cuff tears trigger a cascade of degenerative changes in the affected musculotendinous unit. Tendon retraction occurs as the torn edges pull away from the humeral footprint due to elastic recoil and muscle contraction imbalance, complicating potential repair. This is accompanied by muscle atrophy from disuse and denervation-like effects, as well as fatty infiltration, quantified using the Goutallier classification: stage 0 (no fatty streaks), stage 1 (fatty streaks), stage 2 (fat occupying less than 50% of muscle), stage 3 (equal fat and muscle), and stage 4 (more fat than muscle). These changes progress more rapidly in acute tears but become irreversible beyond stage 2 or 3, impairing force generation and healing potential.[45][46]Without intervention, partial-thickness tears frequently progress, with approximately 50% extending to full-thickness defects over 5 years, particularly those involving greater than 50% of tendon depth. The supraspinatus tendon is the most commonly affected site, involved in about 80% of tears, typically initiating at the critical zone of hypovascularity located 10-15 mm proximal to its insertion on the greater tuberosity, where reduced blood supply exacerbates tissue vulnerability. Many degenerative tears are associated with underlying impingement syndrome.[47][48][49]
Impingement syndrome
Shoulder impingement syndrome involves the extrinsic compression of the rotator cuff tendons and subacromial bursa against the coracoacromial arch during arm elevation, resulting in secondary inflammation and pain.[50] This mechanical irritation occurs primarily in the subacromial space, where the supraspinatus tendon and bursa are pinched between the humeral head and the arch formed by the acromion, coracoacromial ligament, and coracoid process.[51]The pathophysiology begins with repetitive microtrauma to the rotator cuff from overhead activities or structural narrowing, leading to subacromial bursal hypertrophy and inflammation.[50] This cycle of compression and irritation produces a characteristic painful arc of motion between 60 and 120 degrees of shoulder abduction or flexion, as the inflamed tissues are maximally impinged in this range.[52] Over time, unchecked impingement can progress to rotator cuff tears, though this represents a continuum rather than isolated stages.[53]Anatomic contributors to impingement include variations in acromial morphology, classified by Bigliani into three types: type I (flat undersurface), type II (curved), and type III (hooked), with types II and III associated with greater subacromial narrowing and higher risk of cuff compression. Other factors encompass os acromiale, an unfused acromial ossification center that alters arch dynamics and promotes impingement in 1-8% of cases, and thickening of the coracoacromial ligament, which further reduces the subacromial space.[54]Impingement syndrome is categorized into primary and secondary subtypes. Primary impingement arises from intrinsic anatomic abnormalities, such as acromial shape or ligament hypertrophy, causing direct mechanical compression independent of dynamic factors.[55] In contrast, secondary impingement results from underlying glenohumeral instability, such as multidirectional laxity, which allows superior humeral head migration and indirect cuff irritation during motion.[55]Neer described impingement as a progressive condition in three stages based on age and pathology. Stage I, typically in patients under 25 years, features reversible edema and hemorrhage of the rotator cuff without structural damage.[53] Stage II, affecting those aged 25-40 years, involves tendonfibrosis and irreversible changes like tendinitis.[53] Stage III, seen in patients over 40 years, includes bone spur formation on the acromion and partial or full rotator cuff tears.[53]Among athletes, particularly in overhead sports like baseball, swimming, and volleyball, impingement syndrome is common.
Tendinopathies
Tendinopathies of the rotator cuff encompass a spectrum of intrinsic degenerative conditions affecting the tendons, primarily the supraspinatus, characterized by inflammation, degeneration, and pathological deposits. Acute tendinitis represents an inflammatory response, often triggered by direct trauma or acute overuse, leading to short-term tendon swelling and pain. In contrast, chronic tendinosis involves failed healing with mucoid degeneration, resulting in tendon weakening without significant inflammation. Calcific tendinitis, a distinct subtype, features hydroxyapatite crystal deposits within the tendon substance, with a prevalence of approximately 2.5% to 7.5% in adults aged 40 to 60 years, more common in women.[56]The pathophysiology of rotator cuff tendinopathies centers on intrinsic tendon degeneration, driven by repetitive microtrauma and impaired vascularity. A key histologic feature is angiofibroblastic hyperplasia, marked by increased vascular proliferation and fibroblast activity as a maladaptive healing response. This is accompanied by disorganized collagen architecture, with a shift toward type III collagen dominance over the more resilient type I, reducing tensile strength and promoting further breakdown. The "critical zone" of the supraspinatus tendon, located about 1 cm proximal to its insertion, exhibits relative hypovascularity, leading to hypoxia that exacerbates cellular apoptosis and degenerative changes.[57][58][59]In calcific tendinitis, the condition progresses through three stages: the formative phase, where asymptomatic hydroxyapatite deposition occurs; the resorptive phase, characterized by intense inflammation and severe pain as the body attempts to break down the deposits; and the post-resorptive phase, involving remodeling and resolution with potential residual fibrosis. These intrinsic changes can irritate the adjacent subacromial bursa, inducing secondary bursitis with synovial inflammation and effusion, contributing to localized pain and restricted motion.[60][61]Patients with diabetes mellitus face a threefold increased risk of rotator cuff tendinopathies compared to the general population, primarily due to advanced glycation end-products that accumulate in hyperglycemic conditions, causing collagen cross-linking, reduced tendon elasticity, and impaired healing. Tendinopathies may overlap with impingement syndrome, where mechanical compression amplifies the underlying tendon degeneration.[59][62]
Diagnosis
Physical examination
The physical examination of the rotator cuff begins with inspection to identify visible signs of pathology. Atrophy in the supraspinatus and infraspinatus fossae may indicate chronic rotator cuff tears, often presenting as hollowing or asymmetry compared to the contralateral shoulder.[63] Swelling or deformity over the shoulder can also suggest associated bursitis or acute injury.[64]Palpation follows to assess for localized tenderness, which is commonly elicited over the greater tuberosity of the humerus in cases of supraspinatus involvement or the subacromial bursa in impingement-related conditions. Crepitus during active movement may accompany palpation in tendinopathic states.[65]Specific strength tests target individual rotator cuff muscles. The empty can test evaluates supraspinatus integrity: the patient's arms are abducted to 90 degrees in the scapular plane with thumbs pointing downward (internal rotation), and the examiner applies downward pressure while the patient resists; weakness or pain indicates supraspinatus pathology, with a sensitivity of 88% (95% CI 80–96%) and specificity of 62% (95% CI 53–71%) for full-thickness tears.[66] The external rotation lag sign assesses the infraspinatus and teres minor: the examiner passively externally rotates the arm at the side with the elbow flexed to 90 degrees, then asks the patient to actively maintain the position; a positive lag (inability to hold) suggests a tear, with sensitivity of 10% (95% CI 3–18%) and specificity of 98% (95% CI 96–100%).[66] For subscapularis function, the lift-off test involves placing the hand behind the lower back with the dorsum against the lumbar region; the patient attempts to lift the hand away from the back against resistance—if unable, it indicates subscapularis weakness, with sensitivity of 22% (95% CI 12–33%) and specificity of 94% (95% CI 90–99%) for tears.[66] The belly-press test is an alternative or adjunct: the patient presses the palm into the abdomen while keeping the elbow forward; internal rotation lag or inability to maintain pressure points to subscapularis involvement.[63]Provocative maneuvers help localize impingement or associated issues. The Hawkins-Kennedy test for impingement positions the arm in 90 degrees of forward flexion with the elbow straight, followed by passive internal rotation; pain in the subacromial space is positive, showing 64% sensitivity (95% CI 53–76%) and 48% specificity (95% CI 38–57%).[66] The Neer impingement sign involves passive forward elevation of the arm to its full range; subacromial pain without scapular tilting suggests impingement, with 60% sensitivity (95% CI 48–71%) and 58% specificity (95% CI 49–67%).[66] The painful arc sign occurs during active abduction between 60 and 120 degrees, indicating supraspinatus irritation or impingement.[65] Speed's test evaluates biceps tendon involvement often secondary to rotator cuff issues: the patient extends the elbow, supinates the forearm, and flexes the shoulder against resistance; anterior shoulder pain radiating to the bicipital groove is positive, with 32% sensitivity and 79% specificity for superior labrum lesions.[67]These tests collectively aid in initial screening for rotator cuff pathology, though their diagnostic accuracy varies, emphasizing the need for correlation with patient history.[65]
Imaging modalities
X-rays, or plain radiographs, serve as the initial imaging modality for evaluating rotator cuff pathology, primarily detecting indirect signs such as calcific deposits within the tendons and acromial spurs that may contribute to impingement.[68][69] These findings help identify associated bony abnormalities but have limited sensitivity for direct visualization of soft tissue tears. In cases of advanced rotator cuff arthropathy, the Hamada classification is applied to grade glenohumeral joint degeneration based on radiographic features like superior migration of the humeral head and acetabularization of the acromion, guiding prognostic assessment.[70]Ultrasound provides a dynamic, real-time assessment of the rotator cuff, allowing evaluation during shoulder motion to detect impingement or tendon subluxation, which is particularly useful for assessing bursal effusions and fluid collections.[71] It demonstrates approximately 90% sensitivity for full-thickness tears compared to surgical findings, making it a cost-effective first-line option in outpatient settings due to its portability and lack of radiation exposure.[72][73]Magnetic resonance imaging (MRI) is considered the gold standard for diagnosing rotator cuff tears, offering high-resolution multiplanar visualization of tendon integrity, muscle atrophy, and associated pathology. T2-weighted sequences highlight fluid-filled defects indicative of tears, while fat-suppressed sequences enhance detection of peritendinous edema and inflammation.[74][75] For partial-thickness tears, the Ellman classification stratifies severity by depth (grade I: <3 mm, grade II: 3-6 mm, grade III: >6 mm or >50% thickness) and location (articular, bursal, or intratendinous), aiding in treatment planning.[76]Computed tomography (CT) arthrography involves intra-articular contrast injection to delineate intra-articular and bursal-sided tears, providing detailed assessment of tendon retraction distance crucial for preoperative surgical planning, especially in chronic cases with muscle atrophy.[77][78] This modality excels in quantifying the extent of retraction, which correlates with repair feasibility and outcomes, though it is reserved for scenarios where MRI is contraindicated due to its invasiveness and radiation.Emerging techniques, such as AI-assisted MRI analysis, leverage machine learning algorithms to automate tear detection, achieving accuracies ranging from 71% to 100% in studies as of 2025 by improving segmentation of tendon borders and quantification of tear size. These tools enhance radiologist efficiency and reduce interobserver variability, particularly for subtle partial tears.[79]
Management
Nonsurgical approaches
Nonsurgical approaches to rotator cuff disorders emphasize conservative strategies to manage pain, inflammation, and functional limitations while promoting natural healing, particularly for partial tears and tendinopathies where 70-80% of cases may resolve without surgery.[80] These methods are suitable for initial management across various rotator cuff conditions, including tears and impingement, as detailed in prior disorder sections.Rest and activity modification form the foundation of treatment, typically involving sling immobilization for 2-4 weeks to protect the shoulder, alongside avoidance of overhead or repetitive motions that exacerbate symptoms.[6] This approach reduces mechanical stress on the rotator cuff tendons, allowing inflammation to subside and preventing tear progression in symptomatic patients.[81]Pharmacotherapy targets pain and inflammation with nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen at 400-800 mg every 6-8 hours, which effectively alleviate acute symptoms in rotator cuff injuries.[82] Acetaminophen, dosed at 500 mg every 6-8 hours, serves as a suitable alternative for patients unable to tolerate NSAIDs, providing analgesia without anti-inflammatory effects.[82]Injections offer targeted relief, with subacromial corticosteroid administration—such as 40 mg triamcinolone—providing short-term pain reduction lasting 3-6 months by suppressing local inflammation in rotator cuff disease.[83][84]Hyaluronic acid injections, recommended for reducing pain and disability, enhance joint lubrication and may support tendon recovery in tendinopathy cases.[85]Physical therapy focuses on foundational exercises to restore mobility and strength without overloading the injured structures, including pendulum swings to gently mobilize the shoulder and isometric contractions to activate rotator cuff muscles.[86] These interventions improve range of motion and scapular stability, forming a core component of nonoperative protocols.[87]Biologic therapies, updated through 2025 research, include platelet-rich plasma (PRP) injections for partial tears, which promote tendon healing with high success rates on ultrasonographic assessment at 12 weeks.[88]Stem cell injections, such as mesenchymal stem cells, are emerging for enhancing rotator cuff repair in partial tears by supporting tissue regeneration and reducing retear risk.[89]
Surgical interventions
Surgical interventions for rotator cuff disorders primarily aim to restore tendon integrity and shoulder function in cases where conservative management fails. Arthroscopic repair techniques, including all-arthroscopic and mini-open approaches, have become the standard due to their minimally invasive nature, allowing for smaller incisions and reduced tissuetrauma compared to traditional open surgery.[90] In all-arthroscopic repair, multiple small portals are used to visualize and suture the tendon using specialized instruments, while mini-open repair involves a 3-5 cm incision assisted by arthroscopy for decompression and tendonmobilization.[91] Double-row suture anchor configurations are commonly employed in these procedures to enhance tendon-to-bone contact and footprint coverage, providing superior biomechanical stability over single-row methods, particularly for larger tears.[92]Indications for surgical intervention include full-thickness tears greater than 3 cm in size, which often lead to significant functional impairment, and symptomatic partial-thickness tears involving more than 50% of the tendon thickness that persist despite nonsurgical treatment.[41] These criteria are typically established following preoperative diagnosis through physical examination and imaging modalities such as MRI to confirm tear characteristics and tendon quality. For massive tears, side-to-side suturing techniques are utilized to approximate retracted tendon edges without excessive tension, facilitating partial mobilization and improving load distribution across the repair site.[93] In cases of irreparable tears, where tendontissue cannot be adequately mobilized to the bone, superior capsular reconstruction involves grafting a durable material, such as fascia lata or dermal allograft, to the superior glenoid and humeral head to restore capsular stability and prevent superior humeral migration.[94]Complications following rotator cuff surgery include infection, occurring in approximately 1-2% of cases, particularly higher in open techniques, and postoperative stiffness, which can limit range of motion if not addressed early.[95] Re-tear rates are notable, affecting about 20% of repairs at two-year follow-up, with risk increasing for larger tears and poorer tendon quality.[96]Outcomes of surgical repair demonstrate 85-90% of patients achieving substantial pain relief and improved daily function, though approximately 30% experience persistent weakness, especially in abduction and external rotation.[97] Minimally invasive arthroscopic methods contribute to faster recovery, with most patients regaining functional shoulder use within 3-6 months, compared to longer periods for open repairs.[98]
Rehabilitation protocols
Rehabilitation protocols for rotator cuff injuries or repairs typically follow a phased approach to protect healing tissues while progressively restoring range of motion (ROM), strength, and function. These programs are tailored based on tear size, patient age, and activity level, often beginning immediately after injury or surgery under professionalsupervision. The goal is to minimize complications like stiffness or re-tear while promoting tendon healing and shoulder stability.[99][100]The acute phase, spanning 0-6 weeks, emphasizes passive ROM exercises to prevent adhesions and maintain joint mobility without stressing the repair site. Activities include gentle pendulum swings, passive elevation with assistance from the unaffected arm or a therapist, and elbow/wrist flexion-extension to promote circulation. Scapular mobilization, such as shrugs and retractions, is introduced early to support posture without active shoulder involvement. This phase prioritizes pain control and immobilization in a sling for the initial 4-6 weeks, depending on tear severity.[101][102]In the intermediate phase (6-12 weeks), progression shifts to active-assisted ROM, incorporating tools like pulleys or wands for forward flexion and external rotation. Strengthening begins with isometric contractions and light resistance for scapular stabilization, including rows and shrugs to enhance periscapular muscle activation. Rotator cuff-specific exercises, such as side-lying external rotation with a light dumbbell, target the infraspinatus and teres minor while avoiding impingement. Patients typically discontinue sling use by week 6-8, focusing on controlled movements to rebuild neuromuscular control.[99][101]The advanced phase (12+ weeks) introduces full active ROM and progressive strengthening, with elastic bands or weights for internal/external rotation and abduction. Proprioceptive training via plyometric exercises, like ball tosses or rhythmic stabilization, improves dynamic stability for return to daily activities or sports. Emphasis is placed on functional patterns, such as overhead reaching, to simulate real-life demands. This phase may extend to 6 months or longer for larger tears.[103][104]Recent trends from 2023-2025 include accelerated protocols for small tears (<3 cm), allowing early active motion within 2 weeks post-repair to enhance short-term ROM without compromising healing rates. Aquatic therapy has gained prominence for its low-impact environment, facilitating buoyancy-assisted exercises that reduce joint load while improving ROM and strength in the early phases. These approaches, supported by randomized trials, show faster functional gains compared to traditional land-based methods.[105][106][107]Progression between phases relies on objective criteria, including achievement of pain-free full ROM in all planes and strength exceeding 80% of the contralateral side, assessed via manual testing or dynamometry. Additional milestones involve normal scapulohumeral rhythm and minimal pain during daily activities, ensuring safe advancement to avoid re-injury.[108][109]Overall outcomes demonstrate 70-80% of patients returning to pre-injury function levels within 6-12 months, with sustained improvements in pain and ROM. Integration of biologics, such as platelet-rich plasma or stem cells, has been shown to enhance tendon-bone healing rates by 20-30% in clinical studies, particularly for larger tears, leading to better long-term structural integrity.[110][111][112]