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Adhesive capsulitis of the shoulder
Adhesive capsulitis of the shoulder
Adhesive capsulitis of the shoulder
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Adhesive capsulitis of the shoulder
Other namesFrozen shoulder
The right shoulder and glenohumeral joint.
SpecialtyOrthopedics
SymptomsShoulder pain, stiffness[1]
ComplicationsFracture of the humerus, biceps tendon rupture[2]
Usual onset40 to 60 year old[1]
DurationMay last years[1]
TypesPrimary, secondary[2]
CausesOften unknown, prior shoulder injury[1][2]
Risk factorsDiabetes, hypothyroidism[1]
Differential diagnosisPinched nerve, autoimmune disease, biceps tendinopathy, osteoarthritis, rotator cuff tear, cancer, bursitis[1]
TreatmentNSAIDs, physical therapy, steroids, injecting the shoulder at high pressure, surgery[1]
Frequency2 to 5%[1]

Adhesive capsulitis, also known as frozen shoulder, is a condition associated with shoulder pain and stiffness.[1] It is a common shoulder ailment that is marked by pain and a loss of range of motion, particularly in external rotation.[3] There is a loss of the ability to move the shoulder, both voluntarily and by others, in multiple directions.[1][2] The shoulder itself, however, does not generally hurt significantly when touched.[1] Muscle loss around the shoulder may also occur.[1] Onset is gradual over weeks to months.[2] Complications can include fracture of the humerus or biceps tendon rupture.[2]

The cause in most cases is unknown.[1] The condition can also occur after injury or surgery to the shoulder.[2] Risk factors include diabetes and thyroid disease.[1][4][5]

The underlying mechanism involves inflammation and scarring.[2][6] The diagnosis is generally based on a person's symptoms and a physical exam.[1] The diagnosis may be supported by an MRI.[1] Adhesive capsulitis has been linked to diabetes and hypothyroidism, according to research. Adhesive capsulitis was five times more common in diabetic patients than in the control group, according to a meta-analysis published in 2016.[3]

The condition often resolves itself over time without intervention but this may take several years.[1] While a number of treatments, such as nonsteroidal anti-inflammatory drugs, physical therapy, steroids, and injecting the shoulder at high pressure, may be tried, it is unclear what is best.[1] Surgery may be suggested for those who do not get better after a few months.[1] The prevalence of adhesive capsulitis is estimated at 2% to 5% of the general population.[1] It is more common in people 40–60 years of age and in women.[1]

Signs and symptoms

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Symptoms include shoulder pain and limited range of motion although these symptoms are common in many shoulder conditions. An important symptom of adhesive capsulitis is the severity of stiffness that often makes it nearly impossible to carry out simple arm movements. Pain due to frozen shoulder is usually dull or aching and may be worse at night and with any motion.[7]

The symptoms of primary frozen shoulder have been described as having three[8] or four stages.[9] Sometimes a prodromal stage is described that can be present up to three months prior to the shoulder freezing. During this stage people describe sharp pain at end ranges of motion, achy pain at rest, and sleep disturbances.

  • Stage one: The "freezing" or painful stage, which may last from six weeks to nine months, and in which the patient has a slow onset of pain. As the pain worsens, the shoulder loses motion.
  • Stage two: The "frozen" or adhesive stage is marked by a slow improvement in pain but the stiffness remains. This stage generally lasts from four to twelve[10] months.
  • Stage three: The "thawing" or recovery, when shoulder motion slowly returns toward normal. This generally lasts from 5 to 26 months.[11]

Physical exam findings include restricted range of motion in all planes of movement in both active and passive range of motion.[12] This contrasts with conditions such as shoulder impingement syndrome or rotator cuff tendinitis in which the active range of motion is restricted but passive range of motion is normal. Some exam maneuvers of the shoulder may be impossible due to pain.[13]

Causes

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The causes of adhesive capsulitis are incompletely understood; however, there are several factors associated with higher risk. Risk factors for secondary adhesive capsulitis include injury or surgery leading to prolonged immobility. Risk factors for primary, or idiopathic adhesive capsulitis include many systemic diseases, such as diabetes mellitus, stroke, lung disease, connective tissue diseases, thyroid disease, heart disease, autoimmune disease, and Dupuytren's contracture.[14] Both type 1 diabetes and type 2 diabetes are risk factors for the condition.[14]

Primary

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Primary adhesive capsulitis, also known as idiopathic adhesive capsulitis, occurs with no known trigger. It is more likely to develop in the non-dominant arm.[citation needed]

Secondary

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Adhesive capsulitis is called secondary when it develops after an injury or surgery to the shoulder.[citation needed]

Pathophysiology

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The underlying pathophysiology is incompletely understood, but is generally accepted to have both inflammatory and fibrotic components. The hardening of the shoulder joint capsule is central to the disease process. This is the result of scar tissue (adhesions) around the joint capsule.[14] There also may be a reduction in synovial fluid, which normally helps the shoulder joint, a ball and socket joint, move by lubricating the gap between the humerus and the socket in the shoulder blade. In the painful stage (stage I), there is evidence of inflammatory cytokines in the joint fluid.[14]

The main limiting factor in external rotation is due to the thickening of the coracohumeral ligament, which forms the roof of the rotator cuff and is a primary symptom of adhesive capsulitis. In addition, the coracohumeral ligament contributes to the limitation of internal rotation considering its connection to the supraspinatus and subscapular tendons. As the phases of adhesive capsulitis progress, the glenohumeral (GH) capsule begins to thicken and as a result the contraction of the capsule itself becomes the main reason as to why range of motion will be restricted in all planes of motion.[15]

Diagnosis

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Adhesive capsulitis can be diagnosed by history and physical exam. It is often a diagnosis of exclusion, as other causes of shoulder pain and stiffness must first be ruled out. On physical exam, adhesive capsulitis can be diagnosed if limits of the active range of motion are the same or similar to the limits to the passive range of motion. The movement that is most severely inhibited is external rotation of the shoulder.[citation needed]

Imaging studies are not required for diagnosis, but may be used to rule out other causes of pain. Radiographs will often be normal, but imaging features of adhesive capsulitis can be seen on ultrasound or non-contrast MRI. Ultrasound and MRI can help in diagnosis by assessing the coracohumeral ligament, with a width of greater than 3 mm being 60% sensitive and 95% specific for the diagnosis. Shoulders with adhesive capsulitis also characteristically fibrose and thicken at the axillary pouch and "rotator interval", best seen as a dark signal on T1 sequences with edema and inflammation on T2 sequences.[16] A finding on ultrasound associated with adhesive capsulitis is hypoechoic material surrounding the long head of the biceps tendon at the rotator interval, reflecting fibrosis. In the painful stage, such hypoechoic material may demonstrate increased vascularity with Doppler ultrasound.[17]

Grey-scale ultrasound can play a key role in timely diagnosis of adhesive capsulitis due to its high sensitivity and specificity. It is also widely available, convenient, and cost efficient. Thickening in the coracohumeral ligament, inferior capsule/ axillary recess capsule, and rotator interval abnormality, as well as restriction in range of motion in the shoulder can be detected using ultrasound. The range of motion is prohibited due to scapulohumeral rhythm changes occurring in the shoulder joint. The altered scapular kinematics can restrict anterior and posterior tilting, downward rotation and depression as well as external rotation. All of these restrictions lead the scapula to be excessively upwardly rotated. The restriction of the scapular posterior tilt is due to tightness in the lower serratus anterior, anterior capsule and the pectoralis minor. Downward rotation and depression are restricted due to the tightness of the rhomboids, upper trapezius and the superior capsule.[18] Respective sensitivity values were 64.4, 82.1, 82.6, and 94.3, and respective specificity levels were 88.9, 95.7, 93.9, and 90.9.[19]

Treatment

[edit]

There is consensus that non-surgical management is the initial treatment of choice for frozen shoulder.[20] There is no strong evidence to favor any particular approach; in fact, some reviews suggest that multi-modal approaches combining several treatments are better.[21] Research in the UK showed that there were three typical approaches to treatment (physiotherapy, manipulation of the shoulder under general anaesthesia, and surgery (arthroscopic capsular release)). All three treatments were deemed effective but they had different benefits and drawbacks, suggesting clinicians and patients should decide together on the most appropriate treatment.[22][23]

The effects of most treatments are primarily short-term, focusing on alleviating symptoms such as shoulder pain and reduced joint movement. Common treatments include exercise, physical therapy, oral analgesics such as paracetamol and nonsteroidal anti-inflammatory drugs, and intra-articular corticosteroid injections. Non-surgical treatment may continue for months, with more complex treatments such as extracorporeal shock wave therapy, movement under analgesia, and hydrodilatation. It is unclear if these treatments lead to a quicker resolution of the disorder, or only manage chronic symptoms. The condition generally resolves itself with or without treatment. If conservative measures have no effect and the condition is long-lasting, or if evidence suggests surgical intervention, there are also several surgical procedures that may alleviate the disorder.[20]

Medication

[edit]

Medications such as nonsteroidal anti-inflammatory drugs can be used for pain control. Oral steroids may provide short-term benefits in range of movement and pain but have side effects such as hyperglycemia. Corticosteroids may also be used by local injection. In the short and medium term, intra-articular corticosteroid injections appear most effective in pain alleviation and increase in range of motion, although the injection does carry complications.[24] Unfortunately, the effects of medication are not long-lasting. Oral corticosteroids in particular should not be used consistently to treat adhesive capsulitis, because of the dangers associated with long-term use and the lack of long-term benefit.[citation needed]

Exercise and physical therapy

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Shoulder stretching and strengthening exercises improve shoulder function and decrease pain. When using intra-articular corticosteroid injections, the effects of exercise on short-term relief were not significant, although individual studies found some benefits.[24] Concerning techniques, posterior glenohumeral mobilization had a large effect; mirror therapy, rotator cuff strengthening, spray & stretch, and end range mobilization had moderate results; continuous passive motion, scapular recognition, scapulothoracic exercises, yijin jing, and lower trapezius strengthening had small effects; and electromagnetic therapy, Kaltenborn mobilization, and instrument assisted soft tissue mobilization had insignificant effects compared to control kinesthetic exercises.[21] It has been found that performing exercises under supervision is more effective than unsupervised exercise at home.[20]

Extracorporeal shock wave therapy has been strongly recommended as a way of reducing pain levels and improving range of motion and functioning in people with Stage 2 and 3 adhesive capsulitis of the shoulder. Laser therapy was also found to have these similar effects for people dealing with Stage 2 adhesive capsulitis. Moderate evidence points to improvements in pain management, range of motion and functional status for interventions such as PNF techniques (stretching), continuous passive motion, dynamic scapular stability exercises, and conventional physiotherapy. Low evidence exists for manual muscle release.[25]

Hydrodilatation or distension arthrography is controversial. However, some studies show that arthrographic distension may play a positive role in reducing pain and improve range of movement and function.[26]

Manipulation of the shoulder under general anesthesia to break up the adhesions is sometimes used.[citation needed]

Regular exercise is a crucial part of the healing stages of adhesive capsulitis. It has been shown that attending physical therapy three times a week is most common for treating adhesive capsulitis.[27] Another useful tool can be anti-inflammatory medications, to provide temporary relief which aids in exercise exertion. The combination of these techniques allow for the most successful healing process. Combination of manual therapy and exercises while in physical therapy has also shown significant effects in decreasing pain, disability, and increasing range of motion of the affected shoulder.[27]

Surgery

[edit]

If conservative measures are unsuccessful, surgery can be trialed. Surgery to cut the adhesions (capsular release) may be indicated in prolonged and severe cases; the procedure is usually performed by arthroscopy. Surgical evaluation of other problems with the shoulder, e.g., subacromial bursitis or rotator cuff tear, may be needed. Resistant adhesive capsulitis may respond to open release surgery. This technique allows the surgeon to find and correct the underlying cause of restricted shoulder movement such as contracture of coracohumeral ligament and rotator interval.

The most common surgical technique is arthroscopic capsular release surgery, and it is beneficial to individuals who do not get better with physical therapy treatment. Because this type of surgery is minimally invasive, it allows a faster healing time since it consists of small incisions and a small camera to surgically remove the tissue that is thickened and contracted. This surgery is very detailed which also provides more range of motion to the shoulder post operation.

Another key aspect to surgery is the post-surgical rehabilitation phase. During this phase, physical therapy is utilized to regain range of motion and prevent stiffness. Starting out with rehabilitation there is an emphasis on range of motion exercises such as passive and active assisted which provides mobility to the joints while preventing further stress/damage to the tissues healing. The strengthening phase is where the muscles are put under stress of exercises to build strength and muscle for support of the shoulder. Once the strengthening phase is complete, the individual gets reintroduced gradually to activities of daily living and prior training goals.

Prognosis

[edit]

Most cases of adhesive capsulitis are self limiting, but may take 1 to 3 years to fully resolve. Pain and stiffness may not completely resolve in 20 to 50 per cent of affected people.[14]

Epidemiology

[edit]

Adhesive capsulitis newly affects approximately 0.75% to 5.0% percent of people a year.[28] Rates are higher in people with diabetes (10–46%).[29] Following breast surgery, some known complications include loss of shoulder range of motion and reduced functional mobility in the involved arm.[30] Occurrence is rare in children and people under 40, with the highest prevalence between 40 and 70 years of age.[31] The condition is more common in women than in men (70% of patients are women aged 40–60). People with diabetes, stroke, lung disease, rheumatoid arthritis, or heart disease are at a higher risk for frozen shoulder. Symptoms in people with diabetes may be more protracted than in the non-diabetic population.[32]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Adhesive capsulitis of the shoulder

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Adhesive capsulitis of the shoulder, commonly referred to as frozen shoulder, is a debilitating condition characterized by progressive and significant restriction in both active and passive due to , , and of the . This self-limiting disorder typically unfolds in three distinct stages: the freezing stage (lasting 2–9 months), marked by increasing and gradual loss of motion; the frozen stage (4–12 months), where stiffness peaks but may lessen; and the thawing stage (5–26 months), involving gradual restoration of function. The condition has a prevalence of 2–5% in the general , with higher incidence among women (up to 1.5 times more common than in men) and individuals aged 40–60 years. Risk factors include (with prevalence up to 20% in diabetic patients), disorders, prolonged immobilization, and autoimmune conditions, though the exact etiology remains idiopathic in primary cases and secondary in others linked to trauma or . Pathophysiologically, it involves an initial inflammatory response with synovial proliferation and release, followed by excessive deposition and adhesions that reduce capsular volume by up to 50%, limiting glenohumeral translation and rotation. Diagnosis is primarily clinical, based on history and showing global restriction in shoulder motion (e.g., external limited to less than 50% of normal), with imaging such as MRI used to rule out other pathologies like tears. Treatment is predominantly conservative, with over 90% of cases managed nonoperatively through , which often includes manual therapy techniques (such as joint mobilization) and range-of-motion exercises, oral or intra-articular corticosteroids for pain control, and NSAIDs. For refractory cases, options include joint distension (hydrodilatation), manipulation under , or arthroscopic capsular release, though these are reserved for persistent symptoms beyond 6–12 months. Prognosis is generally favorable, with most patients achieving near-full recovery within 1–3 years, though 7–41% may experience residual mild stiffness or pain long-term, particularly those with comorbidities like . Early intervention can shorten the duration and improve outcomes, emphasizing the importance of multidisciplinary management to mitigate the condition's impact on daily activities and .

Overview

Definition and Classification

Adhesive capsulitis of the , also known as frozen shoulder, is a condition characterized by the gradual onset of shoulder pain and significant restriction in both active and passive , primarily due to the thickening, , and contraction of the glenohumeral joint capsule. This capsular involvement leads to a global decrease in shoulder mobility, often described as a self-limiting disorder that can persist for months to years if untreated. The glenohumeral joint capsule is a loose fibrous envelope that surrounds the articulation between the humeral head and the of the , providing structural integrity while allowing for the shoulder's wide . The term "frozen shoulder" was first coined by Ernest Amory Codman in 1934, who described it as a painful condition of insidious onset marked by stiffness and limitation of motion, distinguishing it from other shoulder pathologies like rotator cuff tears. Earlier, in 1872, Simon Duplay introduced the term "periarthrite scapulo-humerale" ( periarthritis) to refer to a similar painful without destruction, which later evolved into the modern understanding of adhesive capsulitis. Adhesive capsulitis is classified into two main types: primary and secondary. Primary adhesive capsulitis is idiopathic, occurring spontaneously without an identifiable precipitating event or underlying , and is often associated with subtle systemic factors. In contrast, secondary adhesive capsulitis develops in response to known extrinsic factors, such as trauma, prolonged immobilization after or , or systemic conditions including mellitus, disorders, or autoimmune diseases. This classification helps guide clinical evaluation by distinguishing cases requiring investigation for associated comorbidities from those that are truly isolated.

Clinical Stages

Adhesive capsulitis of the shoulder, commonly known as frozen shoulder, progresses through three distinct clinical stages: the freezing stage, the frozen stage, and the thawing stage. These stages reflect the temporal evolution of symptoms, from initial pain dominance to stiffness and eventual recovery, allowing clinicians to tailor patient management and education based on disease phase. The overall duration of the condition typically spans 1 to 3 years, though individual variations occur due to factors such as comorbidities and promptness of intervention. The freezing stage, also termed the painful or inflammatory phase, is characterized by escalating shoulder pain that often intensifies at night and with movement, accompanied by a gradual onset of restricted range of motion. This stage generally lasts 2 to 9 months, during which patients experience progressive limitation in both active and passive shoulder motion, marking the beginning of capsular inflammation and adhesions. Recognizing this phase is crucial for early patient reassurance, as it informs prognosis by highlighting the self-limiting nature of the condition while emphasizing the need for pain control to maintain function. In the frozen stage, pain tends to subside compared to the previous phase, but becomes the predominant feature, with severe loss of shoulder that significantly impairs daily activities. This phase endures for 4 to 12 months, reflecting the consolidation of fibrotic changes within the glenohumeral capsule. Staging at this point guides intervention decisions, as the emphasis shifts toward preserving remaining mobility and preventing further , thereby influencing long-term outcomes. The thawing stage involves a gradual return of shoulder motion, with continued reduction in pain and incremental improvements in function over time. Lasting 5 to 26 months, this recovery phase varies widely, often resulting in near-complete restoration of motion in most cases, though some residual limitations may persist. Clinically, identifying the transition to thawing supports optimistic patient education on recovery timelines and encourages adherence to rehabilitative efforts to optimize resolution.

Clinical Features

Symptoms

Adhesive capsulitis of the typically presents with an insidious onset of that gradually intensifies over weeks to months. Patients often describe the as dull and aching, escalating to severe levels, particularly during the initial phase of the condition, and it may radiate down the upper arm but typically does not extend to the or beyond. Secondary neck pain can occur due to compensatory overuse of neck muscles or referred pain from the shoulder condition. This is frequently exacerbated by overhead activities or attempts to reach behind the back, significantly limiting routine movements. A hallmark feature is progressive stiffness in the , which develops alongside the pain and profoundly impacts daily functioning. Individuals report increasing difficulty with basic tasks such as dressing, combing hair, reaching for objects, or driving, often leading to frustration and dependency on others for assistance. Nighttime is particularly disruptive, frequently awakening patients from and contributing to and reduced overall . In the freezing stage, tends to escalate, further compounding these functional limitations. The severity of symptoms is commonly assessed using validated measures, such as the Disabilities of the Arm, Shoulder, and Hand () questionnaire and the Shoulder and Index (SPADI). The evaluates upper extremity through 30 items focusing on intensity and challenges in performing daily activities, demonstrating strong reliability and validity in adhesive capsulitis patients for quantifying functional impairment. Similarly, the SPADI, comprising 13 items on and , captures the subjective burden of and discomfort, showing high responsiveness to changes in shoulder function and specific to this condition. These tools highlight the substantial impact on patients' independence and emotional health, with many reporting persistent interference in work and leisure activities.

Physical Signs

Adhesive capsulitis of the shoulder is characterized by marked restrictions in both active and passive glenohumeral (ROM), with the most pronounced limitations occurring in external rotation, followed by abduction and internal rotation, reflecting a classic global capsular pattern. This pattern distinguishes it from other shoulder disorders, as the loss affects multiple planes without isolated joint involvement. Patients typically exhibit less than 50% of contralateral ROM in external rotation, often quantified using goniometry during clinical assessment to track progression and response to treatment. During , end-range motions provoke significant , particularly when attempting external or overhead abduction, while mid-range movements may be relatively preserved in early stages. is notably absent, unlike in , and there is typically no palpable swelling or to suggest . Muscle strength testing reveals no inherent weakness, as the remains intact, further differentiating it from rotator cuff pathology. Functional assessments, such as the Apley scratch test, demonstrate clear limitations; patients struggle to reach behind their back or overhead due to restricted internal rotation and abduction, often unable to approximate the thoracic spine. This test, performed by having the patient reach across the body or behind the head, highlights the practical impact on daily activities. Bilateral involvement occurs in approximately 40% of cases, with the contralateral shoulder affected either simultaneously or sequentially. These objective signs, combined with the reported in the symptoms section, guide clinicians in confirming the through targeted examination.

Etiology and Epidemiology

Causes and Risk Factors

Adhesive capsulitis of the shoulder, commonly known as frozen shoulder, is frequently idiopathic, with no identifiable underlying cause in the majority of cases. The exact remains unknown, though it is thought to involve an inflammatory process that leads to capsular thickening and without a clear precipitant. Secondary forms of the condition arise from identifiable triggers, including trauma to the , such as fractures or rotator cuff injuries, which can lead to prolonged immobilization and subsequent capsular . Immobilization following events like shoulder surgery—a common complication with a reported incidence of 11%—, or other injuries that restrict shoulder movement is another key secondary cause, as disuse promotes adhesions and stiffness in the . Systemic diseases also contribute, notably diabetes mellitus, where 10% to 20% of affected individuals develop frozen shoulder, thyroid disorders (both hypo- and ), Parkinson's disease, and ischemic heart disease. Several risk factors predispose individuals to the development of adhesive capsulitis. It is more prevalent in females, with a reported ratio of up to 1.5:1 compared to males, and typically affects those aged 40 to 60 years. Endocrine associations, including diabetes and thyroid dysfunction, significantly elevate risk, as do recent findings linking hyperlipidemia and cardiovascular conditions to increased susceptibility. Prolonged shoulder immobilization remains a modifiable risk factor that can exacerbate the progression from inflammation to fibrosis in susceptible individuals.

Prevalence and Demographics

Adhesive capsulitis of the shoulder affects approximately 2% to 5% of the general worldwide, with lifetime estimates in this range based on multiple epidemiological studies. The annual incidence is estimated at approximately 0.2% in adults, though rates vary by age group, with higher figures observed in middle-aged cohorts. Among individuals with , the rises significantly, reaching up to 20% in some cohorts, compared to the lower rates in the nondiabetic . Demographically, the condition predominantly impacts women, who account for about 60% of cases, and peaks in incidence among those aged 40 to 60 years. Certain ethnic groups, such as Asians, exhibit higher rates, with studies indicating an elevated risk compared to other populations. Bilateral involvement occurs in 20% to 30% of patients over the course of the disease, though it is uncommon at initial presentation. Recent studies from 2020 to 2025 have highlighted epidemiological shifts, including associations with COVID-19-related immobility and post-viral syndromes, contributing to a notable increase in incidence during the period. Socioeconomic factors, including access to healthcare, influence reported rates, as lower correlates with delayed diagnosis and potentially underreported cases in underserved populations.

Pathophysiology

Inflammatory Mechanisms

Adhesive capsulitis of the shoulder initiates with an acute inflammatory response in the synovial lining of the glenohumeral capsule, marked by the release of pro-inflammatory cytokines such as transforming growth factor-β (TGF-β) and interleukin-1 (IL-1). These cytokines drive synovial activation and vascular changes, resulting in capsular hyperemia that characterizes the early phase of the condition. During the freezing stage, capsular emerges as a key feature, involving synovial proliferation and infiltration by inflammatory cells, including and mast cells. Mast cells, in particular, interact with to amplify the inflammatory milieu, promoting cellular proliferation and tissue remodeling through the release of mediators that regulate fibroblast activity. In primary idiopathic cases, immune dysregulation contributes to this inflammatory onset, with evidence of altered immune cell function and genetic predispositions. Recent studies, including meta-analyses, have identified associations with (HLA)-B27, showing significantly higher positivity rates in affected individuals compared to controls, suggesting an immunological basis for susceptibility. Systemic indicators of this acute inflammation include elevated levels of (CRP) and (ESR), which reflect the ongoing inflammatory activity without specific diagnostic thresholds. This early inflammatory cascade transitions into subsequent fibrotic processes in the capsule.

Fibrotic Changes

In adhesive capsulitis, the fibrotic phase is marked by progressive capsular thickening, often up to four times the normal thickness, particularly in the rotator interval and axillary recess, where adhesions form between the synovial folds and limit glenohumeral translation. These adhesions, composed of dense fibrous tissue, anchor the capsule walls together, contributing to the characteristic observed in the frozen and thawing stages. Histological examination reveals a proliferation of fibroblasts transitioning into myofibroblasts, which deposit excessive type I and III , forming a rigid scar-like matrix that replaces the normal . This fibroblast-driven process leads to dysregulation of the (ECM), with upregulated expression of profibrotic factors such as transforming growth factor-beta (TGF-β) and disrupted ECM remodeling enzymes like matrix metalloproteinases, perpetuating the fibrotic cascade. Recent single-cell analyses of capsular tissue have identified distinct subpopulations enriched in contractile proteins and ECM components, highlighting their role in sustaining beyond the initial inflammatory trigger. These cellular changes result in a histological picture of hypercellular, hypocellular, or nodular dense , depending on disease stage, with minimal and inflammatory infiltrates in advanced . The cumulative effect of these fibrotic alterations is a substantial reduction in glenohumeral volume, from a normal range of 25-30 mL to as low as 5-10 mL in severe cases, imposing mechanical restrictions on joint motion through capsular and decreased capsular compliance. This volume loss directly correlates with the extent of motion deficit, as the contracted capsule physically impedes articular gliding without involving extrinsic structures.

Diagnosis

Clinical Assessment

The diagnosis of adhesive capsulitis is primarily clinical, relying on a characteristic history and physical examination demonstrating insidious onset of shoulder pain accompanied by significant restriction in both active and passive range of motion (ROM). Key diagnostic criteria include progressive pain of at least one month's duration, global loss of glenohumeral motion with at least 50% reduction in external rotation, abduction, and flexion relative to the contralateral side (or absolute external rotation less than 30 degrees), and absence of other explanatory pathology on radiographs, which typically appear normal. During history-taking, clinicians elicit details on symptom onset, which is usually gradual without acute trauma, though remote minor injury or immobilization may be noted in up to 20% of cases. Night pain that disrupts sleep is a hallmark feature, often described as a deep ache at the deltopectoral region, with symptoms progressing over weeks to months. The duration of pain and stiffness helps integrate findings with clinical staging, while associated comorbidities like are queried as risk factors. Baseline functional assessment using validated tools, such as the Constant-Murley score—which evaluates pain, daily activities, ROM, and strength on a 0-100 scale—is recommended to quantify initial impairment and monitor progress. The protocol emphasizes systematic evaluation of ROM to confirm the . Active and passive motion is tested in all planes: forward flexion, extension, abduction, adduction, internal , and external , with the patient or seated to minimize compensatory scapular movement; a global loss of motion in multiple planes, particularly external , supports the . assesses for tenderness over the , biceps tendon, or posterior capsule, though the is often diffusely stiff without focal swelling. Strength testing is performed to exclude from involvement, and provocative maneuvers like the lift-off test are negative in pure adhesive capsulitis. Differential diagnosis is guided by history and exam to exclude common mimics. pathology is differentiated by predominant weakness and positive impingement signs rather than symmetric stiffness, while cervical radiculopathy typically features , sensory changes, or reflex deficits not seen in adhesive capsulitis; severe inability to move the head is not a typical direct symptom of adhesive capsulitis and may indicate concurrent cervical spine issues (e.g., radiculopathy, stenosis, or muscle spasm) that can mimic or coexist with frozen shoulder. Other considerations like or are ruled out by the absence of , joint deformity, or systemic symptoms.

Imaging and Laboratory Evaluation

Plain radiographs of the are typically normal in adhesive capsulitis but serve primarily to exclude alternative pathologies such as , fractures, or ; mild may occasionally be observed due to disuse in prolonged cases. provides a dynamic, non-invasive assessment of the glenohumeral , detecting capsular thickening greater than 4 mm in the axillary recess and reduced volume in this area, which correlates with restricted ; it also evaluates the for thickening exceeding 2.2 mm and identifies synovial proliferation as hypoechoic tissue with increased vascularity on Doppler imaging. Magnetic resonance imaging (MRI) is considered the gold standard for visualizing changes in adhesive capsulitis, demonstrating synovial proliferation, capsular thickening (often >4 mm in the axillary recess), and signal alterations including T2-weighted hyperintensity indicative of , particularly in the inferior glenohumeral and rotator interval. Recent 2023 reviews affirm MRI's high diagnostic utility for confirming these features and differentiating from other shoulder disorders. Laboratory evaluation focuses on identifying associated systemic conditions rather than direct diagnostic markers for adhesive capsulitis; fasting glucose and HbA1c levels are recommended to screen for undiagnosed diabetes mellitus, a major risk factor present in up to 10-20% of cases. , including TSH, are advised given the established association with thyroid dysfunction, which may contribute to the condition's . or may be mildly elevated but lack specificity. Arthrography, often performed as MR or conventional contrast injection, quantifies reduced glenohumeral joint volume—typically less than 8-10 mL in affected shoulders compared to 20-30 mL in normal joints—confirming capsular contraction and aiding in treatment planning such as hydrodilatation.

Management

Nonsurgical Treatments

Nonsurgical treatments form the cornerstone of management for adhesive capsulitis, with approximately 90% of cases achieving resolution without surgical intervention through a multimodal approach combining pain relief, physical therapy, and targeted injections. This strategy emphasizes early intervention to alleviate pain and restore range of motion (ROM), particularly during the freezing stage, while minimizing risks associated with more invasive procedures. Recent guidelines recommend initiating conservative measures promptly, as delayed treatment can prolong recovery. Pharmacological options primarily target and in the initial phases. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or celecoxib, provide symptomatic relief by reducing and improving short-term function, with studies showing significant reduction within weeks of use. Oral corticosteroids offer a more potent effect than NSAIDs, accelerating relief and functional recovery in the early stages, though their benefits are typically limited to 4-6 weeks and should be used judiciously to avoid systemic side effects. Evidence from 2024 reviews confirms their short-term efficacy in decreasing scores and enhancing ROM, but long-term use is not recommended due to potential complications like gastrointestinal issues. Physical therapy is essential for restoring shoulder mobility and preventing further stiffness, often starting with gentle exercises to avoid exacerbating . Pendulum exercises, which involve allowing the to swing freely in a , promote passive mobilization of the without active . Manual therapy, including joint mobilization techniques such as glenohumeral glides and capsular , combined with active-assisted ROM exercises, has demonstrated improvements in external rotation and overall function when performed regularly, with fair evidence from systematic reviews supporting the use of manual mobilization techniques in combination with exercise to increase range of motion and function. According to 2025 clinical practice guidelines, is most effective when integrated with other modalities, such as injections (Grade B evidence), yielding better outcomes in reduction and ROM gains compared to therapy alone. Intra-articular corticosteroid injections deliver targeted anti-inflammatory effects directly into the glenohumeral joint, significantly improving pain and ROM for up to 6 months in many patients (Grade B evidence). These injections, often ultrasound-guided, provide faster symptom relief than oral medications, with meta-analyses from 2024 indicating moderate efficacy in over 50% of cases, particularly when administered in the freezing phase. Hydrodilatation, or distension arthrography, involves injecting saline or local anesthetic to stretch the contracted capsule, with studies reporting improvements in pain and range of motion in many patients, though benefits may be transient and comparable to other treatments like corticosteroid injections (Grade B evidence). Suprascapular nerve blocks offer effective pain control by interrupting nerve signals, with studies showing sustained relief for 12 weeks or more when combined with therapy, outperforming physical therapy alone in early pain management (Grade B, very low evidence). Emerging therapies like (PRP) injections represent a promising alternative to corticosteroids, with a 2024 randomized demonstrating superior long-term pain reduction and functional improvements at compared to steroids, though evidence remains limited and PRP is not yet standard per recent reviews. PRP works by delivering growth factors to promote tissue repair, showing durable effects on ROM and disability scores without the rebound inflammation sometimes seen with corticosteroids. Home exercise programs and further support these interventions by encouraging adherence to daily and activity modification, enhancing overall recovery rates in outpatient settings.

Surgical Interventions

Surgical interventions for adhesive capsulitis of the shoulder are reserved for the small subset of patients—typically less than 10%—who experience persistent symptoms despite adequate conservative management. Indications include failure of nonsurgical therapies after 6-12 months, accompanied by severe functional impairment such as significant limitations in daily activities due to restricted (ROM). Manipulation under anesthesia (MUA) involves forcefully stretching the to restore ROM while the patient is under general , often combined with immediate post-procedure to maintain gains. This procedure targets the contracted capsule by breaking adhesions through controlled external rotation, abduction, and flexion maneuvers. However, MUA carries risks including humeral shaft fracture, glenoid fracture, and , particularly in patients with or advanced age. Arthroscopic capsular release is the most commonly performed surgical option, involving minimally invasive excision of the tightened glenohumeral capsule, including release of the rotator interval and to alleviate adhesions. Performed as an outpatient procedure under regional or general , it allows direct visualization and precise cutting of fibrotic tissue using or electrocautery. Studies report significant improvements in pain and ROM, with over 80% of patients achieving substantial functional gains within 2-6 weeks postoperatively, followed by aggressive rehabilitation protocols emphasizing early . Open capsular release is rarely utilized, reserved for cases with extensive extracapsular fibrosis or when arthroscopic access is inadequate, such as in revision surgeries. This approach involves a deltopectoral incision to directly incise and excise the thickened capsule, followed by similar postoperative rehabilitation to prevent re-adhesion. Recent 2025 research highlights the potential of combined MUA with hydrodilatation, where saline and corticosteroid are injected to distend the joint capsule during manipulation; a study comparing this approach to arthroscopic capsular release found improvements in early ROM gains, though arthroscopic release offered superior overall outcomes in pain relief and satisfaction. Postoperatively, all surgical approaches emphasize structured rehabilitation, including pendulum exercises and progressive strengthening, typically starting within 24-48 hours to optimize recovery.

Prognosis

Recovery Patterns

Adhesive capsulitis of the shoulder follows a self-limiting , with the majority of cases resolving spontaneously over 1 to 3 years, during which approximately 94% of patients with idiopathic forms achieve full functional recovery and normal without any intervention. The condition typically progresses through three distinct stages: the freezing stage, lasting 2 to 9 months and dominated by escalating pain with gradual onset of stiffness; the frozen stage, enduring 4 to 20 months, where stiffness peaks but pain often diminishes; and the thawing stage, spanning 5 to 26 months, marked by progressive improvement in mobility as the capsular restrictions loosen. These stage durations contribute to the overall trajectory, emphasizing the protracted but predictable course of the disorder. Resolution of adhesive capsulitis is commonly assessed by substantial restoration of shoulder and significant reduction in . Secondary forms of the condition, such as those associated with trauma or systemic diseases, may have a less favorable with more prolonged and , along with delayed treatment initiation tending to extend the recovery timeline beyond the typical 1- to 3-year window. In the long term, 7% to 15% of patients may retain mild residual or limitations in overhead motion even after several years, though severe is rare. Recent analyses from 2024 to 2025 confirm an average disease course of for symptom resolution under conservative management, underscoring the variability while highlighting the potential for to accelerate thawing in select cases.

Influencing Factors

The prognosis of adhesive capsulitis is generally favorable, with most patients achieving substantial recovery over 1 to 3 years through conservative management, but several patient-specific factors can significantly alter the trajectory, duration, and completeness of recovery. stands out as a major adverse influencer, with systematic reviews indicating that individuals with diabetes experience worse multidimensional clinical scores, greater pain persistence, and reduced compared to non-diabetics, often requiring closer monitoring and potentially more aggressive interventions. This association is attributed to impaired remodeling and higher rates of in diabetic patients, often leading to prolonged symptoms and higher rates of incomplete resolution. Duration of symptoms at also critically affects outcomes; chronic cases (beyond 6-12 months) are linked to poorer responses to nonoperative treatments, with systematic recommending early intervention to mitigate progression and improve functional recovery. Similarly, bilateral involvement signals a higher-risk profile, correlating with extended recovery times and reduced likelihood of full spontaneous resolution, as bilateral disease may reflect underlying systemic vulnerabilities. Demographic and clinical variables further modulate . Age shows mixed effects across studies: one of nonoperative outcomes found patients aged 60 years or older had better recovery rates, possibly due to less demanding physical lifestyles, while others report older age as a negative predictor for surgical interventions like manipulation under , with slower gains in motion. Severity of initial restriction, particularly in external , predicts slower improvement, with severe limitations at baseline explaining up to 10-15% of variance in long-term shoulder function. Certain comorbidities provide additional nuance, though evidence varies. and anxiety have been associated with variations in patient-reported outcome improvements during the natural course, potentially through inflammatory pathways, but their independent impact remains multifactorial and requires further validation. In contrast, thyroid disorders do not consistently worsen outcomes, with most studies showing no significant difference in or treatment response compared to euthyroid patients. Overall, these factors underscore the importance of individualized prognostic counseling, prioritizing early multidisciplinary care for high-risk groups to optimize recovery.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK532955/
  2. https://www.mayoclinic.org/diseases-conditions/frozen-shoulder/symptoms-causes/syc-20372684
  3. https://www.aafp.org/pubs/afp/issues/2011/0215/p417.html
  4. https://orthoinfo.aaos.org/en/diseases--conditions/frozen-shoulder
  5. https://emedicine.medscape.com/article/1261598-overview
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC9866675/
  7. https://www.dynamed.com/condition/adhesive-capsulitis-of-shoulder
  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC5384535/
  9. https://jeo-esska.springeropen.com/articles/10.1186/s40634-020-00307-w
  10. https://emedicine.medscape.com/article/1261598-treatment
  11. https://www.aafp.org/pubs/afp/issues/2019/0301/p297.html
  12. https://www.mayoclinic.org/diseases-conditions/frozen-shoulder/diagnosis-treatment/drc-20372690
  13. https://www.sciencedirect.com/science/article/abs/pii/S1058274607004867
  14. https://radiopaedia.org/articles/adhesive-capsulitis-of-the-shoulder?lang=us
  15. https://www.kenhub.com/en/library/anatomy/the-shoulder-joint
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC1315655/
  17. https://www.orthobullets.com/shoulder-and-elbow/3059/adhesive-capsulitis-frozen-shoulder
  18. https://www.jospt.org/doi/10.2519/jospt.2013.0302
  19. https://www.health.harvard.edu/pain/how-to-thaw-a-frozen-shoulder
  20. https://my.clevelandclinic.org/health/diseases/frozen-shoulder-adhesive-capsulitis
  21. https://www.brighamandwomens.org/assets/BWH/patients-and-families/rehabilitation-services/pdfs/shoulder-adhesive-capsulitis.pdf
  22. https://www.bswhealth.com/conditions/frozen-shoulder
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC10986124/
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC2633286/
  25. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-023-06268-2
  26. https://doi.org/10.2522/ptj.20080341
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC2682415/
  28. https://www.schoudernetwerk.nl/SNNbestanden/ProjectFrozenShoulder/FS.Guidelines-AdhesiveCapsulitis.Kelleyetal.JOSPT.2013.pdf
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC2373295/
  30. https://now.aapmr.org/adhesive-capsulitis/
  31. https://www.hss.edu/health-library/conditions-and-treatments/list/frozen-shoulder
  32. https://pubmed.ncbi.nlm.nih.gov/28132086/
  33. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-024-07614-8
  34. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2024.1363018/full
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC8024456/
  36. https://journals.lww.com/md-journal/fulltext/2019/09270/the_impact_of_pre_existing_shoulder_diseases_and.38.aspx
  37. https://www.researchgate.net/publication/323374065_Asian_ethnicity_a_risk_factor_for_adhesive_capsulitis
  38. https://www.sciencedirect.com/science/article/pii/S2666638323001822
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC9248121/
  40. https://josr-online.biomedcentral.com/articles/10.1186/s13018-024-05360-0
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC10092900/
  42. https://academic.oup.com/mr/article/34/3/439/7252234
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC6478286/
  44. https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2024.1248612/full
  45. https://onlinelibrary.wiley.com/doi/10.1155/2018/7274517
  46. https://pubmed.ncbi.nlm.nih.gov/27490134/
  47. https://www.researchgate.net/publication/295833770_Is_There_a_Genetic_Predisposition_to_Frozen_Shoulder_A_Systematic_Review_and_Meta-Analysis
  48. https://journals.lww.com/md-journal/fulltext/2024/11010/impact_of_immune_cells_on_the_risk_of_frozen.82.aspx
  49. https://pubmed.ncbi.nlm.nih.gov/32379116/
  50. https://www.researchgate.net/publication/369046307_Evaluation_of_serological_factors_in_29_patients_with_frozen_shoulder_a_cohort_study
  51. https://www.mdpi.com/2075-4418/13/22/3410
  52. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-016-1190-9
  53. https://www.nature.com/articles/s41467-024-45341-9
  54. https://www.researchsquare.com/article/rs-6289785/latest.pdf
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC3785028/
  56. https://emedicine.medscape.com/article/1261598-clinical
  57. https://emedicine.medscape.com/article/1261598-differential
  58. https://emedicine.medscape.com/article/1261598-workup
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC10201101/
  60. https://ajronline.org/doi/10.2214/ajr.164.6.7754892
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC7458737/
  62. https://www.aafp.org/pubs/afp/issues/1999/0401/p1843.html
  63. https://radiopaedia.org/articles/glenohumeraljoint-hydrodilatation?lang=us
  64. https://www.mdpi.com/2077-0383/10/21/5185
  65. https://www.e-arm.org/journal/view.php?number=4407
  66. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-024-07275-7
  67. https://www.massgeneral.org/assets/MGH/pdf/orthopaedics/sports-medicine/physical-therapy/rehabilitation-protocol-for-frozen-shoulder.pdf
  68. https://www.health.harvard.edu/stretching-exercises-frozen-shoulder
  69. https://pmc.ncbi.nlm.nih.gov/articles/PMC10949050/
  70. https://pubmed.ncbi.nlm.nih.gov/40978863/
  71. https://pmc.ncbi.nlm.nih.gov/articles/PMC10788845/
  72. https://journals.lww.com/joacp/fulltext/2023/39020/suprascapular_nerve_block__ssnb__improves_the.5.aspx
  73. https://www.sciencedirect.com/science/article/pii/S2773157X24002273
  74. https://www.uptodate.com/contents/frozen-shoulder-adhesive-capsulitis
  75. https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/s12891-024-07629-1
  76. https://pmc.ncbi.nlm.nih.gov/articles/PMC5917053/
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC4738186/
  78. https://uvahealth.com/treatments/adhesive-capsulitis-closed-manipulation
  79. https://www.sciencedirect.com/science/article/pii/S266663832300275X
  80. https://www.jshoulderelbow.org/article/S1058-2746%2810%2900528-8/pdf
  81. https://www.sciencedirect.com/science/article/pii/S1877056819300866
  82. https://californiashoulder.com/frozen-shoulder/
  83. https://www.jojs.in/abstractArticleContentBrowse/JOJS/70/7/2/40947/abstractArticle/Article
  84. https://pmc.ncbi.nlm.nih.gov/articles/PMC3293960/
  85. https://link.springer.com/article/10.1007/s40141-025-00516-3
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC12276553/
  87. https://pubmed.ncbi.nlm.nih.gov/34589691/
  88. https://link.springer.com/article/10.1007/s00402-015-2341-4
  89. https://pmc.ncbi.nlm.nih.gov/articles/PMC3631491/
  90. https://www.sciencedirect.com/science/article/pii/S2666638324004948
  91. https://bmjopen.bmj.com/content/12/11/e056563
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC9998727/
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