Adhesive Capsulitis (Frozen Shoulder)

Updated: Jul 21, 2022
  • Author: Jefferson R Roberts, MD; Chief Editor: Herbert S Diamond, MD  more...
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Practice Essentials

Adhesive capsulitis and frozen shoulder syndrome (FSS) are two terms that have been used to describe a painful and stiff shoulder. The current consensus definition of a frozen shoulder by the American Shoulder and Elbow Surgeons is "a condition of uncertain etiology characterized by significant restriction of both active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder." [1]  The American Academy of Orthopaedic Surgeons defines this condition as: "A condition of varying severity characterized by the gradual development of global limitation of active and passive shoulder motion where radiographic findings other than osteopenia are absent."

The loss of passive range of motion (ROM) is a critical element in establishing the diagnosis of a true frozen shoulder. Although conditions such as subacromial bursitiscalcifying tendinitis, and partial rotator cuff tears can be associated with significant pain and loss of active ROM, passive ROM is preserved. Therefore, patients with those conditions should not be classified as having a frozen shoulder.

Lundberg divided patients who met the pain and motion requirements of frozen shoulder into two groups: primary and secondary. [2] A patient meets the criteria of primary or secondary FSS if painful, restricted active and passive glenohumeral and scapulothoracic motion occurs for at least 1 month and has either reached a plateau or worsened. This inclusion period for defining frozen shoulder is similar to that described by Binder and colleagues [3, 4] but is shorter than that defined by Lloyd-Roberts and coworkers. [5]

Patients with primary frozen shoulder have no significant findings in the history, clinical examination, or radiographic evaluation to explain their motion loss and pain. Classically, symptoms of primary frozen shoulder have been divided into three phases: freezing (painful), frozen (stiffening), and thawing.

The initial painful phase is marked by a gradual onset of diffuse shoulder pain lasting from weeks to months. The stiffening phase is characterized by a progressive loss of ROM that may last up to 1 year. Most patients lose glenohumeral external rotation, internal rotation, and abduction during this phase. The final, thawing phase is measured in weeks to months and constitutes a period of gradual motion improvement. Once in this phase, the patient may require up to 9 months to regain a functional ROM. [6, 7, 8, 9] See Table 1, below.

Table. 1 Stages of Frozen Shoulder Syndrome  (Open Table in a new window)

Stage Duration 
Stage 1 Freezing (painful) 

Up to 9 months

Stage 2 Frozen (stiffening)

4 months - 20 months

Stage 3 Thawing

5 months- 26 months

Contralateral shoulder 6 months - 7 years after initial onset of symptoms 

Patients with diabetes and younger patients may be more likely to develop contralateral idiopathic adhesive capsulitis. [10]

In contrast to patients with primary FSS, patients with secondary FSS describe an event that preceded the onset of shoulder symptoms, such as the following:

  • Upper extremity trauma (eg, shoulder surgery, rotator cuff tear, proximal humerus facture)
  • Immobilization (eg, cardiothoracic surgery, neurosurgery)
  • Metabolic/endocrine (eg, thyroid disease, diabetes mellitus, autoimmune disease, hyperlipidemia)
  • Neurologic (eg, stroke, Parkinson disease)
  • Cardiac disease (eg, ischemic heart disease, hypertension)
  • Drugs (eg, protease inhibitors, antiretrovirals, immunizations, fluoroquinolones)
  • Malignancy


Codman originally coined the term frozen shoulder to describe a condition with the following signs and symptoms [11] :

  • Slow-onset shoulder pain
  • Localized discomfort near the deltoid insertion
  • Inability to sleep on the affected side
  • Restricted glenohumeral elevation and external rotation
  • A normal radiologic appearance

The inclusion criteria for FSS include painful restriction of active and passive glenohumeral and/or periscapular motion.

Despite these criteria, diagnosing FSS can be controversial because there is little consensus on the specific shoulder motion restrictions or duration of symptoms needed to qualify a patient as having a frozen shoulder. Although various authors have classified patients with FSS as those with limited abduction from 45-135º, FSS is still primarily a clinical diagnosis based on clinical motion loss and symptoms.



Frozen shoulder syndrome (FSS) usually affects patients aged 40-60 years. The incidence of FSS is not precisely known; however, it is estimated that 2% to 5% of the general population [12] develops the disease over their lifetime. Men tend to be affected less frequently than women, and there is no predilection for race. In general, bilateral shoulder involvement is rarely simultaneous and instead occurs sequentially.

Diabetes mellitus is an independent risk factor for FSS. A meta-analysis by Zreik concluded that diabetic patients are 5 times more likely to develop adhesive capsulitis compared with non-diabetic controls. They reported a 13.4% overall mean prevalence of adhesive capsulitis in patients with diabetes, and a 30% mean prevalence of diabetes in a population with adhesive capsulitis. Zreik found no significant difference in the prevalence of the disorder with type 1 versus type 2 diabetes, or between patients on insulin therapy and those on oral hypoglycemic agents. [13]  



Duplay was one of the first physicians to present the concept of periarticular tissue pathology rather than periarticular arthritis as the cause of frozen shoulder. [14] Despite a lack of evidence linking frozen shoulder to a specific etiology, various triggers that may predispose patients to this problem appear to exist. A few reported etiologic agents include the following:

  • Trauma
  • Surgery (including but not limited to shoulder surgery)
  • Inflammatory disease
  • Diabetes
  • Regional conditions
  • Various shoulder maladies

In addition, an autoimmune theory has been postulated, with elevated levels of C-reactive protein and an increased incidence of HLA-B27 histocompatibility antigen reported in patients with frozen shoulder versus controls. [15, 16] DePalma proposed that muscular inactivity was a major etiologic factor, [17] while Bridgman identified an increased incidence of FSS in patients with diabetes mellitus. [18] Finally, frozen shoulder also has been associated with the following disorders:

  • Cervical spine disease
  • Parkinson disease [19]
  • Hyperthyroidism [20]
  • Hypothyroidism 
  • Ischemic heart disease

Most patients with FSS have undergone a period of shoulder immobilization. Reasons for immobilization can be diverse; however, the common finding in all of these patients is a period of restricted shoulder motion. In a study of neurosurgery patients who immobilized their shoulders for varying periods, Bruckner noted an incidence of frozen shoulder that was 5-9 times greater than that found in the general population. [21]



Prior to examining the patient, a thorough clinical history should be elicited. Specifically, information should be gathered regarding the following:

  • Onset of symptoms
  • Any antecedent trauma or surgery
  • Affected side(s)
  • Duration of symptoms

The patient should also be queried about any existing medical conditions, particularly diabetes mellitus, thyroid disease, Parkinson disease, stroke, and heart disease. Given the strong association of adhesive capsulitis with diabetes, it is imperative to screen any new patient presenting with possible frozen shoulder syndrome for diabetes or prediabetes. [22] Adhesive capsulitis has also been reported in patients with hyperthyroidism, hypothyroidism, and ischemic heart disease. Questions should be directed toward any upper extremity neurologic complaints, including cervical radiculopathy. Any history of cervical pain or radiculopathy should be thoroughly evaluated during the clinical examination to exclude a diagnosis of cervical spondylosis or cervical disc disease.

Any previous treatments that the patient has received for their condition should be documented, as should the individual's current medication list.


Surgical Indications

Refractory shoulder periscapular pain and limited glenohumeral motion that persists despite attempted conservative treatment are indications for surgery. Conservative treatment can include the following:

  • A course of prednisone [23]

  • A course of a nonsteroidal anti-inflammatory drug when not on prednisone

  • A subacromial or glenohumeral intra-articular injection at least once but not more than twice within a 3-month period

  • Physical therapy for range of motion of the shoulder [24, 25, 26]

  • A physician-directed home therapy program has been shown to have efficacy in helping restore range of motion [27]  


Relevant Anatomy

Critical to the understanding of frozen shoulder syndrome is the concept that shoulder function involves not only the glenohumeral joint but also scapulothoracic articulation. Clinicians must understand the essential role that the scapula plays in facilitating glenohumeral motion. Scapulothoracic and glenohumeral motion occur simultaneously following initial arm abduction. In healthy individuals, approximately one third of arm elevation in abduction is attributed to scapulothoracic motion, while two thirds is provided by glenohumeral motion.

The glenohumeral joint is enclosed by the joint capsule and is surrounded by two sleeves of muscles. The capsule normally is a loose structure with a surface area nearly twice as large as that of the humeral head. The rotator cuff tendons adjacent to the joint capsule thicken the capsule anteriorly, posteriorly, and superiorly, while the glenohumeral ligaments represent further areas of joint capsule thickening.

Histologically, the capsule consists of bundles of type I collagen. Synovial cells line the inner surface of the capsule and enclose the long head of the biceps tendon.



Contraindications to surgical intervention for recalcitrant frozen shoulder include the following:

  • Concomitant neurologic complaints or abnormalities originating from the cervical spine

  • An inadequate trial of conservative therapy (< 3 mo)

  • Ongoing infection of any type [28]

  • Isolated capsular release in the face of adhesive capsulitis and concomitant glenohumeral arthritis (in this situation, capsular release or lengthening should be performed in conjunction with total shoulder arthroplasty)

  • An ongoing oncologic process involving the affected shoulder



Immune, inflammatory and fibrotic changes appear to be involved in the pathophysiology of FSS. [29] The current hypothesis posits inflammation in the joint capsule [30]  followed by development of adhesions and fibrosis of the synovial lining. [31] Thickening and contraction of the glenohumeral joint capsule and formation of collagenous tissue surrounding the joint reduces joint volume. 

Biomarkers in synovial fluid suggest chronic inflammation is present. [32] The following markers have been identified in FSS [33, 34] :

  • Intercellular adhesion molecule–1 (ICAM-1; CD54)
  • Transforming growth factor–beta (TGF-β)
  • Tumor necrosis factor–alpha (TNF-α)
  • Interleukin-1 (IL-1) alpha and beta
  • IL-6
  • Platelet-derived growth factor (PDGF)

Matrix metalloproteinases are involved in the construction of extracellular matrix and in the various cytokines that control collagen deposition. Drugs that inhibit matrix metalloproteinase can induce conditions very similar to FSS and Dupuytren disease. [12]

Following the synovial inflammatory process, a high number of fibroblasts and myofibroblasts suggest a fibrotic process in the capsule. The condition is thought to result from progressive fibrosis and eventual contracture of the capsule of the glenohumeral joint, which causes pain and stiffness. [34, 35]

Microvascular diseases such as diabetes mellitus may cause abnormal collagen repair, which predisposes patients to FSS. [36] Increased glycosylation of collagen protein and increased formation of abnormal glycation end products and their subsequent accumulation have a detrimental effect on cellular and extracellular processes that might facilitate adhesion and fibrosis. [37] Neovascularization with vascular endothelial growth factor (VEGF) staining has also been identified in diabetic tissue samples. [12]



FSS has a favorable natural history. It is generally a self-limiting condition that can be treated with physical therapy and typically resolves in 1-3 years. [38]  Time to recovery does not differ between primary and secondary FSS. No difference in pain and disability of FSS in patients with and without diabetes has been reported. [39]  Patients with FSS do not have a lower shoulder activity level than sex- and age-matched controls. [40]  

However, several studies have demonstrated long-term pain and shoulder stiffness following conservative treatment. Long-term disability has been reported in 15%, [8]  permanent functional loss in 7-15%, and persistent symptoms in 40%. [41]