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Capsulitis

Capsulitis refers to the inflammation of a joint capsule, the fibrous tissue enveloping synovial joints, leading to pain, stiffness, and reduced mobility. It can affect various joints, with common forms including adhesive capsulitis of the shoulder (commonly known as frozen shoulder) and capsulitis of the foot, particularly involving the metatarsophalangeal joints. Less frequent variants occur in other sites, such as the knee (e.g., plica syndrome). Adhesive capsulitis of the shoulder is one of the most studied types, affecting approximately 2-5% of the general population, primarily individuals aged 40-60, with a higher prevalence in women (1.4 times that of men) and those with conditions like diabetes.^[1]^[2]^[3]^[4] In the shoulder, the condition often progresses through three stages: freezing (2-9 months, increasing pain and stiffness), frozen (4-12 months, persistent stiffness with decreasing pain), and thawing (5-24 months, gradual improvement in motion). Primary adhesive capsulitis is idiopathic but linked to inflammation and fibrosis of the glenohumeral capsule; secondary forms may follow trauma, surgery, or immobilization. Risk factors include diabetes (10-20% of cases), thyroid disorders, and prolonged immobility. Diagnosis is clinical, supported by imaging to rule out other issues. Treatment typically involves physical therapy, anti-inflammatory medications, and injections, with surgery for refractory cases. Most resolve within 1-3 years, with 80% regaining near-normal function, though 10-20% have residuals; contralateral involvement occurs in 20-40% within five years.^[1]^[2]^[3]^[5]

Overview

Definition

Capsulitis refers to the inflammation of the synovial capsule that envelops a joint, resulting in capsular thickening, fibrosis, and diminished synovial fluid production, which collectively restrict joint mobility and function.^[4] While most commonly associated with the shoulder (adhesive capsulitis) and foot (plantar capsulitis), it can theoretically affect any synovial joint, albeit rarely in others such as the hip or ankle. The joint capsule itself is a double-layered fibrous structure comprising an outer fibrous membrane and an inner synovial lining, which encloses the joint space, synovial membrane, and associated ligaments to ensure joint stability while facilitating the distribution of synovial fluid for lubrication and nourishment of the articular cartilage.^[6]^[7] This anatomical arrangement is essential for maintaining joint integrity during movement, but inflammatory processes can disrupt its normal elasticity and volume. The general pathophysiology of capsulitis involves an initial inflammatory response that stimulates fibroblast proliferation within the capsule, leading to excessive collagen deposition and subsequent contracture of the capsular tissue.^[8] This process typically progresses through an acute inflammatory phase characterized by synovial hyperemia and pain, followed by a chronic fibrotic phase where adhesions form and joint volume decreases significantly, often to 5-10 mL from a normal 20-35 mL in the shoulder.^[9]^[10] Such changes impair the capsule's ability to allow smooth gliding of joint surfaces, distinguishing capsulitis from other arthritides by its primary involvement of the extracapsular rather than intra-articular structures. Capsulitis was first described in medical literature in the early 20th century, primarily in relation to shoulder involvement, with the term "adhesive capsulitis" formalized by Julius Neviaser in 1945 to highlight the inflammatory and fibrotic alterations observed during arthroscopy.^[11] Specific subtypes, such as adhesive capsulitis of the shoulder and plantar capsulitis of the foot, exemplify how this condition manifests differently across joints while sharing the core inflammatory mechanism.

Epidemiology

Capsulitis, as inflammation of the joint capsule, affects an estimated 2-5% of the general population globally over their lifetime, though this figure is predominantly driven by data on shoulder adhesive capsulitis, with foot forms often underreported due to frequent misdiagnosis as conditions like metatarsalgia.^[12]^[13] Adhesive capsulitis of the shoulder has a prevalence of 2-5% among adults over 40 years, with a higher occurrence in women at a ratio of approximately 1.5:1 and peak incidence between ages 40 and 60.^[14] Comorbidities such as diabetes mellitus substantially elevate the risk, up to 10-20% in affected individuals. Capsulitis of the foot, particularly involving the metatarsophalangeal joints, has a less established prevalence, often underreported and misdiagnosed as other foot conditions like metatarsalgia; it is more prevalent in women, linked to footwear choices, and typically occurs between ages 30 and 50.^[15] (note: this is a clinical review, not population study) Significant data gaps persist, particularly for foot capsulitis, where longitudinal population-based studies are scarce and most evidence derives from podiatry clinic cohorts rather than broad epidemiological surveys.^[16]

Adhesive Capsulitis of the Shoulder

Causes and Risk Factors

Adhesive capsulitis of the shoulder, commonly known as frozen shoulder, is classified into primary (idiopathic) and secondary forms based on etiology. Primary adhesive capsulitis arises spontaneously without identifiable trauma or injury, involving an intrinsic inflammatory and fibrotic process within the glenohumeral joint capsule.^[3] This leads to thickening and contracture of the capsule, with excessive deposition of collagen and formation of adhesions, driven by cytokines such as interleukin-1α and tumor necrosis factor-α that promote fibroblast proliferation and myofibroblast differentiation.^[8] Secondary adhesive capsulitis, in contrast, develops following extrinsic factors like shoulder trauma, periarticular fractures, or surgical interventions such as rotator cuff repair or arthroplasty, which disrupt the joint's supporting structures and initiate a similar inflammatory cascade.^[3] Prolonged immobilization after injury or surgery further exacerbates this process by altering collagen remodeling and promoting fibrosis.^[17] Several demographic and medical factors elevate the risk of developing adhesive capsulitis, with an overall population incidence of 2% to 5%.^[3] It predominantly affects individuals aged 40 to 60 years, with a mean onset around 55, and occurs more frequently in women at a ratio of approximately 1.4:1 compared to men.^[3] The nondominant shoulder is often involved, though no strong association exists with arm dominance or occupational factors.^[17] Systemic conditions significantly increase susceptibility, particularly diabetes mellitus, where prevalence reaches 10.3% in type 1 and 22.4% in type 2 cases—up to 20% overall in diabetic populations—likely due to advanced glycation end-products impairing collagen turnover and worsening stiffness.^[8] Emerging evidence suggests that the use of GLP-1 receptor agonists in diabetes management may increase the risk of developing adhesive capsulitis.^[18] Thyroid disorders, including both hypothyroidism and hyperthyroidism, are associated, as are autoimmune diseases, Parkinson's disease, cerebrovascular disease, coronary artery disease, and Dupuytren's contracture, suggesting an underlying role for endocrine and inflammatory dysregulation.^[3]^[8] Genetic factors, such as HLA-B27 positivity, may also contribute, alongside prior shoulder injuries or immobilization periods exceeding several weeks.^[8] In diabetics and those with thyroid issues, outcomes tend to be more severe, with prolonged recovery times.^[17]

Symptoms and Stages

Adhesive capsulitis of the shoulder, commonly known as frozen shoulder, is characterized by progressive pain and stiffness that significantly impair shoulder function. The primary symptoms include a dull, aching pain in the shoulder that often worsens at night or with overhead activities, disrupting sleep and daily tasks such as dressing or reaching.^[3] Stiffness develops gradually, leading to a marked reduction in both active and passive range of motion, particularly in external rotation, abduction, and flexion, which can limit arm elevation to less than 90 degrees in advanced cases.^[17] These symptoms typically begin insidiously and evolve over 1 to 3 years without intervention, though the exact progression varies by individual.^[1] The condition is divided into three distinct stages based on the evolution of pain and mobility: the freezing stage, the frozen stage, and the thawing stage. In the freezing stage (also called the painful stage), patients experience a gradual onset of diffuse shoulder pain that intensifies over time, often becoming severe at night and with sudden movements; stiffness begins to emerge, restricting motion, and this phase lasts from 2 to 9 months.^[3] Pain may radiate to the upper arm, and daily activities become increasingly challenging as the shoulder capsule thickens and contracts.^[17] During the frozen stage (adhesive stage), pain often decreases compared to the previous phase, but stiffness reaches its peak, resulting in severe limitations in range of motion—such as inability to reach behind the back or fully abduct the arm—and making routine tasks like combing hair or fastening a bra difficult; this stage typically endures for 4 to 12 months.^[1] Muscle atrophy may occur due to disuse, and tenderness persists around the joint, though neurological function remains intact.^[3] The thawing stage (recovery stage) involves a gradual resolution of symptoms, with pain continuing to subside and range of motion slowly improving as the capsule loosens; this phase can last from 5 months to 2 years, allowing most patients to regain near-normal function, though some residual stiffness may linger.^[17] Overall recovery is spontaneous in many cases, but the total duration from onset to resolution averages 18 to 24 months.^[1]

Diagnosis

Diagnosis of adhesive capsulitis is primarily clinical, relying on a thorough history and physical examination to identify characteristic patterns of shoulder pain and restricted range of motion (ROM). Patients typically report a gradual onset of diffuse shoulder pain that worsens at night or with overhead activities, progressing to significant stiffness over weeks to months, which interferes with daily tasks such as dressing or reaching behind the back.^[3]^[19] The pain often radiates to the upper arm but spares the hand and forearm, and symptoms may persist for 12 to 18 months if untreated.^[20] Associated risk factors, such as diabetes (prevalence up to 30% in affected patients) or thyroid disease, should be screened via blood tests if clinically indicated, though routine laboratory evaluation is not required.^[19]^[21] Physical examination reveals marked limitations in both active and passive glenohumeral ROM, particularly in forward flexion (typically <90 degrees), abduction (<90 degrees), external rotation (<30 degrees), and internal rotation, with passive ROM often more restricted than active.^[3]^[21] The shoulder may exhibit diffuse tenderness without focal points, and accessory joint motions like posterior glide are commonly reduced, distinguishing it from extrinsic causes of stiffness.^[21] Validated outcome measures, such as the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire or Shoulder Pain and Disability Index (SPADI), are recommended to quantify pain and functional impairment at baseline.^[21] Red flags including fever, unexplained weight loss, or acute trauma warrant further investigation to exclude malignancy or infection.^[19] Imaging studies are not essential for confirming adhesive capsulitis but are employed to rule out alternative diagnoses such as rotator cuff tears, osteoarthritis, or fractures. Plain radiographs (X-rays) of the shoulder are typically normal but help exclude bony abnormalities or calcific tendinitis.^[3]^[20] If suspicion persists, noncontrast magnetic resonance imaging (MRI) offers high specificity (up to 98%) by demonstrating synovial thickening, coracohumeral ligament hypertrophy (>4 mm), or reduced axillary recess volume, though these findings are supportive rather than diagnostic.^[19] Ultrasound or arthrography may be considered in select cases to assess capsular volume (<10-12 mL on arthrography indicates restriction), but routine use is discouraged due to limited added value in uncomplicated presentations.^[21] Differential diagnoses include subacromial impingement, cervical radiculopathy, and biceps tendinopathy, which can be differentiated by preserved passive ROM or specific provocative tests.^[3]

Treatment

The primary approach to treating adhesive capsulitis of the shoulder emphasizes conservative management, which is effective in approximately 90% of cases, often leading to gradual resolution over 12-18 months without invasive interventions.^[3]^[22] Treatment is tailored to the disease stage, with a focus on pain relief during the freezing phase and restoration of range of motion (ROM) in the frozen and thawing phases, typically involving a multidisciplinary team including primary care physicians, physical therapists, and orthopedic specialists to optimize outcomes through coordinated care.^[3]^[20] Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or aspirin, are commonly prescribed for short courses (2-3 weeks) to alleviate pain and inflammation, particularly in the early freezing stage, though they do not alter the underlying disease progression.^[20]^[22] Oral corticosteroids, at doses like 0.5 mg/kg/day of methylprednisolone for up to 6 weeks, provide moderate evidence-based short-term benefits in reducing pain and improving function, but long-term efficacy remains unproven and is not routinely recommended due to side effects.^[23] Physical therapy serves as the cornerstone of conservative treatment, involving supervised exercises to maintain or regain ROM, such as pendulum swings, towel stretches, and proprioceptive neuromuscular facilitation techniques, performed 5-6 times daily; adherence is crucial, with structured programs yielding high satisfaction rates (up to 90%) when combined with other modalities.^[3]^[23] In the frozen stage, therapy shifts to mobilization and strengthening exercises, including scapular retraction and isometric external rotation, to prevent further stiffness.^[22] For patients with persistent symptoms refractory to initial conservative measures, intra-articular corticosteroid injections offer strong evidence for short-term pain reduction and ROM improvement, ideally administered early in the freezing phase under imaging guidance to target the glenohumeral joint accurately.^[22]^[23] Hydrodilatation, or distension arthrography, involves injecting saline (often with steroids) to stretch the contracted capsule, providing modest short-term benefits in pain relief and function (e.g., improved Oxford Shoulder Score) that may persist up to 2 years, though evidence for long-term superiority is limited.^[20]^[23] In cases unresponsive after 6-9 months of conservative therapy, manipulation under anesthesia (MUA) can be performed to forcibly break adhesions and restore motion, yielding good short- and long-term ROM gains (e.g., maintained at 42 months in some cohorts) but carrying risks like humeral fracture (3-40% recurrence rate).^[22]^[23] Arthroscopic capsular release (ACR) is an alternative surgical option, involving precise incision of the tightened capsule to release scar tissue, with low complication rates and sustained improvements in pain and ROM (e.g., preserved at 7 years postoperatively); it is increasingly preferred over MUA for its minimally invasive nature and reduced risk profile, reserved for fewer than 10% of patients.^[20]^[23] Postoperative physical therapy is essential following either procedure to consolidate gains, with early intervention associated with near-normal function recovery in about 80% of cases.^[3] Alternative therapies, such as acupuncture or transcutaneous electrical nerve stimulation (TENS), may provide adjunctive pain relief but lack robust evidence for altering disease course.^[20]

Prognosis

Adhesive capsulitis of the shoulder is typically a self-limiting condition, with most patients achieving significant improvement or full resolution of symptoms over time.^[3] The natural history involves progression through three stages—freezing (2-9 months), frozen (4-12 months), and thawing (5-24 months)—during which pain and stiffness gradually diminish.^[1] Without intervention, symptoms often resolve within 1 to 3 years, though early physical therapy and anti-inflammatory measures can accelerate recovery and restore near-normal function in approximately 80% of cases.^[3]^[2] Long-term outcomes are generally favorable, with the majority of individuals regaining full or near-full shoulder motion and function by two years post-onset.^[2] However, recent evidence indicates that complete recovery is not universal; up to 10-20% of patients may experience persistent stiffness, discomfort, or functional limitations that impact quality of life, particularly if conservative treatments fail.^[3]^[19] Recurrence in the affected shoulder is rare, but approximately 20-50% of patients may develop the condition in the contralateral shoulder within five years.^[1] Factors influencing prognosis include comorbidities such as diabetes, which increases prevalence fivefold and is associated with more severe, prolonged symptoms and poorer recovery rates.^[19] Thyroid disorders, including hypothyroidism, also correlate with extended disease duration and residual impairment.^[19] Early diagnosis and intervention improve outcomes, while immobilization or delayed treatment can exacerbate stiffness; surgical options like capsular release are reserved for refractory cases and yield good results in most, though some diabetics retain mild limitations.^[3]^[17]

Capsulitis of the Foot

Causes and Risk Factors

Capsulitis of the foot refers to inflammation of the ligaments and capsule surrounding the metatarsophalangeal (MTP) joints, most commonly affecting the second toe. It typically results from excessive pressure on the ball of the foot, leading to irritation and instability in the joint capsule. Primary causes include abnormal foot mechanics, such as a longer second toe (Morton's toe), bunion deformities, flat feet or high arches, and tight calf muscles, which shift weight unevenly onto the forefoot.^[24]^[4] Additional risk factors encompass wearing ill-fitting shoes, high heels, or flip-flops that lack support, as well as high-impact activities like running or jumping that overload the MTP joints. Underlying conditions such as rheumatoid arthritis or osteoarthritis can contribute by causing chronic joint stress and plantar plate deterioration. Overuse from athletic pursuits or occupations involving prolonged standing further increases susceptibility, particularly in middle-aged women and individuals with biomechanical imbalances.^[24]^[4]

Symptoms

Capsulitis of the foot, an inflammation of the ligaments surrounding the metatarsophalangeal (MTP) joints—most commonly the second toe—presents with localized pain and discomfort in the forefoot. The condition often begins insidiously, with symptoms intensifying over time if unaddressed.^[24]^[4] The hallmark symptom is sharp or aching pain in the ball of the foot, particularly under the base of the affected toe, which patients frequently describe as feeling like stepping on a pebble, marble, or bunched-up sock within the shoe. This pain typically worsens with weight-bearing activities such as walking or standing and may radiate toward the toes, progressing throughout the day while easing with rest. Pain can also occur when walking barefoot or during toe-off phase of gait, and it may be exacerbated by tight or ill-fitting footwear.^[24]^[4]^[25] Swelling and redness often accompany the pain, appearing around the base of the affected toe and the MTP joint due to inflammatory changes in the joint capsule. This swelling can cause a sensation of tightness or fullness in the forefoot, sometimes leading to difficulty fitting into shoes. In some cases, the inflammation irritates nearby nerves, resulting in altered sensations such as tingling or numbness in the toe.^[4]^[25]^[24] Additional symptoms include reduced strength and stability in the affected toe, which may manifest as instability during push-off or a feeling of the toe "giving way." As the condition advances, patients may notice a callus forming under the ball of the foot from altered weight distribution, further contributing to discomfort. These symptoms are usually unilateral but can affect both feet in predisposed individuals.^[25]^[4]

Diagnosis

Diagnosis of capsulitis of the foot is primarily clinical, based on patient history and physical examination of the forefoot. Patients typically report gradual onset of pain in the ball of the foot that worsens with activity, often describing a sensation of walking on an object. A key test is the vertical stress test, where the examiner applies upward pressure to the toe while stabilizing the metatarsal; pain or instability indicates capsulitis or plantar plate involvement.^[4]^[24] The foot may show swelling and tenderness at the MTP joint, with limited toe extension. Imaging, such as X-rays, is used to rule out fractures, stress reactions, or arthritis, though they may appear normal in early stages. In cases of diagnostic uncertainty, ultrasound or MRI can assess soft tissue inflammation, capsular thickening, or plantar plate tears, helping differentiate from conditions like Morton's neuroma, metatarsalgia, or Freiberg's disease. No routine blood tests are required unless systemic arthritis is suspected.^[4]^[24]

Treatment

Treatment for capsulitis of the foot prioritizes conservative measures to reduce inflammation, offload pressure, and restore joint stability, which are effective in most cases within 6 weeks to 3 months. Initial management includes rest to avoid aggravating activities, application of ice for 15-20 minutes several times daily, and nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen to alleviate pain and swelling.^[4]^[24] Taping or splinting the toe in a neutral position helps stabilize the MTP joint and prevent further strain on the capsule; buddy taping to the adjacent toe is common. Custom orthotic devices or metatarsal pads redistribute weight away from the affected area, while wide-toed, supportive shoes with good cushioning are recommended to minimize pressure. Physical therapy may incorporate stretching exercises for the calves and toes, along with strengthening to improve foot mechanics. In persistent cases, corticosteroid injections into the joint provide targeted anti-inflammatory relief.^[4]^[24] If conservative treatment fails and the condition progresses to toe instability or crossover toe, surgical intervention may be necessary. Options include plantar plate repair, tendon transfers, or metatarsal osteotomy to realign the joint, typically with good outcomes but reserved for severe cases.^[4]^[24]

Prognosis

Capsulitis of the foot generally has a favorable prognosis with early intervention, allowing most patients to achieve full resolution of symptoms and return to normal activities within 6 weeks to 3 months. Conservative treatments successfully prevent progression in the majority of cases, avoiding chronic pain or deformity.^[4]^[24] Untreated or advanced cases may lead to plantar plate rupture, resulting in hammertoe, crossover toe, or persistent instability, potentially requiring surgery. Recurrence is possible if underlying biomechanical issues, such as improper footwear or foot structure, are not addressed. Factors like rheumatoid arthritis can prolong recovery, but overall, timely management minimizes long-term complications.^[4]^[24]

Other Forms

Rare Joint Involvement

Adhesive capsulitis in joints other than the shoulder or foot is exceedingly rare, comprising less than 1% of all reported cases, with most evidence derived from isolated case reports and small series rather than large-scale epidemiological studies.^[26] This rarity underscores its underdiagnosis, as symptoms often overlap with more common conditions like osteoarthritis or post-traumatic stiffness. In the hip, adhesive capsulitis, sometimes termed "frozen hip," manifests infrequently, often following total hip replacement or associated with underlying factors such as infection or avascular necrosis of the femoral head. A systematic review identified 224 reported cases across 16 studies.^[26] Symptoms typically include progressive pain in the groin and buttocks with restricted range of motion, particularly in external rotation, closely mimicking primary osteoarthritis and necessitating exclusion of mechanical pathologies through imaging and serology. Case reports highlight its idiopathic or post-traumatic origins, with resolution often requiring conservative management or arthroscopic intervention in refractory cases.^[27]^[28] Elbow and wrist involvement is similarly uncommon, predominantly linked to trauma, such as fractures or dislocations, or systemic conditions like rheumatoid arthritis, resulting in capsular contracture that parallels shoulder adhesive capsulitis but with reduced fibrotic changes. In the elbow, soft tissue contractures arise from burns, spinal injuries, or repetitive valgus stress, leading to limited flexion-extension without extensive adhesions. Wrist cases, documented via arthrography showing capsular thickening and small recesses, often follow immobilization or low-grade inflammation, presenting as painful stiffness treatable with manipulation or capsulotomy.^[29]^[30]^[31] Ankle and hand capsulitis occurs sporadically, frequently tied to overuse in athletes, including runners who develop subtalar joint involvement from chronic sprains or repetitive impact. Ankle cases, known as "frozen ankle," stem from fractures, prolonged immobilization, or sports-related trauma, causing synovial fibrosis and motion loss that may extend to adjacent structures like the flexor hallucis longus sheath. Hand joint adhesive capsulitis is extremely rare, with limited evidence beyond case reports of post-traumatic or inflammatory stiffness; involvement of flexor sheaths typically represents tenosynovitis rather than true capsular fibrosis. Recent case reports from 2020 to 2025 suggest emerging post-viral associations, such as following COVID-19 infection or vaccination, potentially linked to inflammatory sequelae, though evidence remains anecdotal and primarily focused on shoulder presentations.^[32]^[33]

Differential Diagnosis Considerations

Capsulitis must be differentiated from several conditions that present with similar joint pain and restricted mobility, particularly in the shoulder and foot where it most commonly occurs. In the shoulder, rotator cuff tendinopathy is a frequent mimic, characterized by a painful arc of motion during abduction, in contrast to the global restriction of both active and passive range seen in adhesive capsulitis.^[34] For the foot, Morton's neuroma often causes forefoot pain but is distinguished by neuropathic symptoms such as tingling or numbness radiating to the toes, whereas capsulitis produces localized mechanical pain exacerbated by weight-bearing.^[4] Broader differentials include osteoarthritis, which features degenerative bony changes visible on plain radiographs, unlike the soft tissue capsular thickening typical of capsulitis on MRI.^[35] Bursitis presents with more focal swelling and tenderness over the bursa, such as subacromial in the shoulder, without the diffuse capsular involvement of capsulitis.^[36] Fibromyalgia, by comparison, involves widespread musculoskeletal pain without specific capsular inflammation or joint restriction on imaging.^[37] Diagnostic strategies emphasize validated scoring systems to quantify symptoms and guide differentiation; the Shoulder Pain and Disability Index (SPADI) assesses pain and function in shoulder capsulitis, while the Foot Function Index (FFI) evaluates pain, disability, and activity limitation in foot cases.^[38]^[39] Biopsy is reserved for atypical presentations, such as persistent inflammation unresponsive to conservative measures, to exclude infection or malignancy when imaging is inconclusive.^[40] Recent advancements in AI-assisted imaging, including radiomics models applied to MRI, have enhanced differentiation of capsulitis from mimics by improving overall diagnostic accuracy to approximately 75% in early studies, aiding in the identification of subtle capsular features.^[41]

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Follicular lymphoma: an unexpected cause of adhesive capsulitis
Jan 26, 2024 · This case highlights the need to consider malignancies as un underlying cause of adhesive capsulitis, particularly if there is an atypical ...
[40]
An approach leveraging radiomics and model checking for ... - Nature
Aug 14, 2024 · This study aims to investigate whether it is possible to use disease signs within a medical image to automatically diagnose Adhesive Capsulitis.