S REVIEW ARTICLE

Shoulder & Elbow

2017, Vol. 9(2) 75–84
! The Author(s) 2016
Adhesive capsulitis of the shoulder: Reprints and permissions:
[Link]/[Link]
review of pathophysiology and DOI: 10.1177/1758573216676786
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current clinical treatments

Hai V. Le1, Stella J. Lee1, Ara Nazarian2 and

Edward K. Rodriguez1,2

Abstract
Adhesive shoulder capsulitis, or arthrofibrosis, describes a pathological process in which the body forms excessive scar
tissue or adhesions across the glenohumeral joint, leading to pain, stiffness and dysfunction. It is a debilitating condition
that can occur spontaneously (primary or idiopathic adhesive capsulitis) or following shoulder surgery or trauma (sec-
ondary adhesive capsulitis). Here, we review the pathophysiology of adhesive shoulder capsulitis, highlighting its clinical
presentation, natural history, risk factors, pathoanatomy and pathogenesis. Both current non-operative and operative
treatments for adhesive capsulitis are described, and evidence-based studies are presented in support for or against each
corresponding treatment. Finally, the review also provides an update on the gene expression profile of adhesive capsulitis
and how this new understanding can help facilitate development of novel pharmacological therapies.

Keywords
adhesive capsulitis, arthrofibrosis, frozen shoulder, shoulder capsulitis, shoulder pain, shoulder stiffness
Date received: 3rd July 2016; accepted: 9th October 2016

Adhesive capsulitis can be primary or secondary.

Introduction Primary (or idiopathic) adhesive capsulitis can occur
Adhesive shoulder capsulitis, or arthrofibrosis, spontaneously without any specific trauma or inciting
describes a pathological process in which the body event. Secondary adhesive capsulitis is often observed
forms excessive scar tissue or adhesions across the gle- after periarticular fracture dislocation of the glenohum-
nohumeral joint, leading to stiffness, pain and dysfunc- eral joint or other severe articular trauma.5 It can also be
tion.1,2 Painful stiffness of the shoulder can adversely a severe complication after open or arthroscopic shoulder
affect activities of daily living and consequently impair surgery, including rotator cuff repair and shoulder arthro-
quality of life. Simon-Emmanuel Duplay is widely plasty.6 The incidence of adhesive capsulitis in the general
recognized as the first physician to describe this path- population is approximately 3% to 5% but as high as
ology, which he called ‘scapulohumeral periarthritis’. 20% in patients with diabetes. Idiopathic adhesive capsu-
‘Periarthritis’ describes a painful shoulder syndrome litis often involves the nondominant extremity, although
that is distinct from arthritis with general radiographic bilateral involvement has been reported in up to 40% to
preservation of the joint. Earnest Codman later coined 50% of cases.2 Adhesive capsulitis is often regarded as a
the term ‘frozen shoulder’ in 1934 to emphasize the
debilitating loss of shoulder motion in patients afflicted 1
Department of Orthopaedic Surgery, Beth Israel Deaconess Medical
with this condition. He described this condition as ‘dif- Center (BIDMC), Boston, MA, USA
2
ficult to define, difficult to treat and difficult to explain Center for Advanced Orthopaedic Studies, Beth Israel Deaconess
from the point of view of pathology’.3 In a pioneering Medical Center (BIDMC), Boston, MA, USA
histological study published in 1945, Julius Neviaser
Corresponding author:
redefined this condition as adhesive capsulitis, under- Hai V. Le, Beth Israel Deaconess Medical Center (BIDMC), 330 Brookline
lying the inflammatory and fibrotic changes observed in Ave, Boston, MA 02215, USA.
the capsule or adjacent bursa.4 Email: hle6@[Link]
76 S Shoulder & Elbow 9(2)

self-limiting disease that resolves between 1 and 3 years. joint. It is estimated that 70% of patients with adhesive
However, various studies have shown that between 20% shoulder capsulitis are women.15 Additionally, men do
and 50% of patients may go on to develop long-lasting not respond to treatments as well as women.16
symptoms.2,7–9 In this patient population, both non- Demographic studies have shown that most patients
operative and operative interventions are needed to with adhesive capsulitis (84.4%) fall within the age
ensure acceptable functional outcomes. range of 40 years to 59 years.10 A recent meta-analysis
study by Prodromidis and Charalambous17 suggested a
genetic predisposition to adhesive capsulitis, noting a
Review higher predilection of this condition in white patients,
patients with a positive family history, and patients
Diagnosis with HLA-B27 positivity.
Adhesive shoulder capsulitis is a clinical diagnosis made Adhesive capsulitis is associated with diabetes, thy-
on the basis of medical history and physical exam and is roid disease, cerebrovascular disease, coronary artery
often a diagnosis of exclusion. Other causes of a painful disease, autoimmune disease and Dupuytren’s dis-
stiff shoulder must be excluded before a diagnosis of ease.3,18 Interestingly, both type I and type II diabetic
adhesive capsulitis is rendered, including septic arthritis, patients are at increased risk of developing adhesive
mal-position of orthopedic hardware, fracture malunion, capsulitis, with prevalence of 10.3% and 22.4%,
rotator cuff pathology, glenohumeral arthrosis or cervical respectively.19 Diabetic patients with adhesive capsulitis
radiculopathy. Clinically, patients with this condition usu- have worse functional outcomes compared to their
ally first present with shoulder pain followed by gradual nondiabetic counterparts.16 A nationwide population-
loss of both active and passive range of motion (ROM) based study led by Huang et al.20 showed that, compared
due to fibrosis of the glenohumeral joint capsule.1 Boyle- to the general population, patients with hyperthyroidism
Walker et al.10 observed that the majority of patients have 1.22 times the risk of developing adhesive capsulitis.
(90.6%) reported developing shoulder pain before loss Patients with cerebrovascular disease, especially those
of motion. External rotation is often the first motion surgically treated for subarachnoid haemorrhage, are
affected on clinical examination, with steady global loss more susceptible to developing adhesive shoulder capsu-
of ROM with disease progression. Pain is generally worse litis; in one prospective study of this high risk population,
at the extremes of motion, when the contracted capsule is 23 of 91 patients (25.3%) developed adhesive capsulitis
stretched. Passive ROM is lost with firm painful end- within 6 months.21 Smith et al.22 showed that
points of motion, suggesting a mechanical rather than a Dupuytren’s disease was found in 52% of patients (30
pain-related restriction to motion.1 of 58) with adhesive capsulitis. Although the prevalence
Imaging studies are not necessary for the diagnosis of of adhesive capsulitis is higher in patients with the asso-
adhesive shoulder capsulitis but may be helpful to rule out ciated conditions stated above, further studies are
other causes of a painful and stiff shoulder. Plain films of needed to determine why such relationships exist.
the shoulder may reveal osteopenia in patients with pro-
longed adhesive capsulitis secondary to disuse (i.e. disuse
Natural history
osteopenia).1 Magnetic resonance imaging (MRI) and
magnetic resonance angiography (MRA) may reveal Neviaser and Neviaser23 broke down the natural pro-
thickening of capsular and pericapsular tissues as well as gression of adhesive capsulitis into four stages based on
a contracted glenohumeral joint space.1 Mengiardi et al.11 clinical presentation and arthroscopic appearance.
reported that MRA findings of coracohumeral ligament In Stage I, patients present with a primary complaint
(CHL) ligament thickness  4 mm (95% specificity, 59% of shoulder pain, especially at night, although they have
sensitivity) or capsule thickness  7 mm (86% specificity, preserved motion. Arthroscopically, there is evidence of
64% sensitivity) may aid in the diagnosis of adhesive cap- synovitis without adhesions or contractures. In Stage
sulitis. Dynamic sonography may reveal thickening of the II, patients begin to develop stiffness. Synovitis is
joint capsule and limited sliding movement of the supras- again observed on arthroscopy, although there is also
pinatus tendon.12 These findings correlate with intraopera- some loss of the axillary fold, suggestive of early adhe-
tive direct visualization, documenting thickening of sion formation and capsular contracture. Stage III is
primarily the rotator interval and CHL.13,14 characterized by profound global loss of ROM and
pain at the extremes of motion. During this stage,
also known as the maturation stage, synovitis is
Risk factors
resolved but the axillary fold is obliterated as a result
Risk factors for adhesive capsulitis include female sex, of significant adhesions. Finally, in Stage IV or the
age over 40 years, preceding trauma, HLA-B27 positiv- chronic stage, there is persistent stiffness but minimal
ity and prolonged immobilization of the glenohumeral pain as synovitis has resolved. With pain controlled,
 S Le et al. 77

patients may begin to exhibit slow improvement transform into smooth muscle phenotype (myofibro-
in shoulder mobility. Advanced adhesions and restric- blasts), which is assumed to be responsible for capsular
tion of the glenohumeral joint space are observed contracture. There are altered levels of matrix metallo-
arthroscopically. proteinases (MMPs), which are involved in scar tissue
Histologically, Stage I is characterized by inflamma- remodelling. For example, MMP-14 is expressed in
tory cell infiltration of the synovium, Stage II by syn- control patients but not at all in patients with adhesive
ovial proliferation and Stage III by dense collagenous capsulitis.29 MMP-14 is an activator of MMP-2,
tissue within the capsule,1 supporting the theory that involved in collagen degradation, and this may result
inflammation leads to reactive fibrosis. in excessive collagen production compared to break-
Adhesive capsulitis is often regarded as a self-limit- down. Expression of MMP-1 and MMP-2 is lowered
ing disease that resolves in approximately 1 years to in patients with adhesive capsulitis; at the same time,
3 years. Neviaser’s four classical stages of adhesive cap- expression of tissue inhibitor of metalloproteinases
sulitis are sometimes reclassified as the ‘painful phase’, (TIMPs) such as TIMP-1 and TIMP-2 is elevated.30
‘stiff phase’, and ‘thawing phase’, implying that this Those findings support the notion that adhesive capsu-
condition resolves spontaneously. However, as previ- litis is the result of an imbalance between extracellular
ously noted, approximately 20% to 50% of patients matrix tissue degradation, remodelling and regener-
may have enduring symptoms,2 making non-operative ation. Future therapy may directly inhibit fibrogenesis
and operative interventions necessary. or promote remodelling of fibrotic tissue.
It is now generally accepted that the development of
adhesive capsulitis involves an inflammatory as well as
Pathoanatomy
fibrotic process. Corroborating this are studies demon-
Contracture of the glenohumeral capsule is the hall- strating elevated inflammatory cytokines including
mark of adhesive capsulitis. Findings include loss of interleukin (IL)-1a, IL-1b, tumour necrosis factor
the synovial layer of the capsule, adhesions of the axil- (TNF)-a, cyclooxygenase (COX)-1 and COX-2 in cap-
lary to itself and to the anatomical neck of the humerus, sular and bursal tissues of patients with adhesive cap-
and overall decreased capsular volume.1 In particular, a sulitis compared to controls.31 Thus, it might be argued
thickened and fibrotic rotator interval, a structure that that adhesive capsulitis is primarily an inflammatory
is critical to glenohumeral joint stability, is associated process that eventually leads to fibrotic changes.
with adhesive capsulitis.24 The rotator interval is bor- Almost all of the samples obtained from the rotator
dered by the supraspinatus tendon superiorly, subsca- interval of patients with adhesive capsulitis contain
pularis tendon inferiorly, transhumeral ligament inflammatory cells, including T cells, B cells, macro-
laterally and coracoid process medially. The rotator phages and mast cells.32 Mast cells are known to regu-
interval contains the CHL, biceps tendon and the gle- late fibroblast proliferation in vivo and may act as an
nohumeral capsule. A contracted CHL is considered intermediary between the inflammatory and subsequent
the essential finding in adhesive capsulitis. The CHL fibrotic processes.
ligament is placed under tension with maximal external Recent studies have sought to link molecular patho-
rotation;25 therefore, it is the main target of operative genesis with known risk factors and genetic susceptibil-
treatment of adhesive capsulitis. Patients with adhesive ity for adhesive capsulitis. Cytogenetic analysis study
capsulitis have stiffer CHL ligament in the affected has revealed elevated fibrogenic (MMP-3) as well as
shoulder compared to the non-affected shoulder as inflammatory (IL-6) cytokines in patients with adhesive
measured by shear-wave elastography.26 MRA and capsulitis.33 Ling et al.34 found that specific single-
MRI studies reveal that the CHL is also thickened peptide polymorphisms (SNP) of IL-6 (rs1800796
(4.1 mm versus 2.7 mm) in patients with adhesive cap- SNP) and MMP-3 (rs650108 SNP) are associated
sulitis.11,27 Likewise, the capsule in the rotator interval with severity and susceptibility of shoulder stiffness
is thicker (7.1 mm versus 4.5 mm) and the volume of the following rotator cuff repair, demonstrating a genetic
axillary recess is smaller (0.53 mL versus 0.88 mL) com- predisposition for secondary adhesive capsulitis.
pared to controls.11 Kim et al.35 reported that intercellular adhesion
molecule-1 (ICAM-1), a transmembrane protein on
endothelial cells and leukocytes that facilitate leukocyte
Pathogenesis endothelial transmigration, is increased in capsular
Adhesive capsulitis has long been considered to be a tissue, synovial fluid and serum of patients with
primarily fibrotic disorder similar to Dupuytren’s dis- adhesive capsulitis. Interestingly, the ICAM-1 level is
ease because the histology of affected specimens pri- also elevated in diabetes mellitus. This observation pro-
marily show fibroblasts mixed with type I and type vides a potential molecular link between the two con-
III collagen.28 These fibroblasts were observed to ditions.35 Raykha et al.36 reported elevated expression
78 S Shoulder & Elbow 9(2)

of IGF-2 and b-catenin in Dupuytren’s disease and of patients (five of 75) required surgical intervention.
adhesive capsulitis. Home self-exercise has been shown to be equally effect-
Other molecules that have been shown to be elevated ive or superior to supervised stretching-exercise.46,47
in local tissues obtained from adhesive shoulders include Posterior glide mobilization technique is considered to
mitogen-activated protein kinases (ERK and JNK), NF- provide improved external rotation compared to an
kappa B, CD29 (b-1 integrin) and VEGF.37 Markers for anteriorly directed technique.48 Physical therapy can
blood vessels (CD34) and nerves]nerve growth factor be combined with ultrasonic therapy, transcutaneous
receptor p75, growth associated protein 43 (GAP43), electrical nerve stimulation, short-wave therapy, low-
protein gene product 9.5 (PGP9.5)] are also elevated. level laser therapy and hydrotherapy. More aggressive
This suggests concluded that both neoangiogenesis and treatment modalities should be employed in refractory
neoinnervation occur in adhesive capsulitis, and the cases after 4 months of physical therapy because those
latter process may explain why adhesive capsulitis is patients are likely to fail non-operative treatment.49
unbearably painful.38 One key growth factor involved
in adhesive capsulitis is TGF-b.39 Watson et al.40 Pharmacological therapy. Pharmacological therapy,
demonstrated that overexpression of TGF-b1 using an including non-steroidal anti-inflammatory drugs
adenovirus vector in the knee joints of rats lead to devel- (NSAIDs) and systemic or intra-articular corticoster-
opment of adhesive capsulitis as early as within 5 days. oids, provides symptomatic management and serves
as an adjunct to physical therapy. Both COX-1 and
COX-2 expressions are elevated in capsular and
Non-operative management
bursal tissues of patients with adhesive capsulitis,31
The goal of treatment of adhesive capsulitis is to restore and these anti-inflammatory agents target synovitis as
the shoulder to a painless and functional joint.41,42 the source of pain. Pain management is a key feature to
Because some patients with adhesive capsulitis improve allow patients to tolerate physical therapy to improve
spontaneously, treatment varies greatly from benign ROM. There have been few studies evaluating the
neglect to invasive open capsulotomy. There is no uni- effectiveness of NSAIDs for the treatment of adhesive
versal treatment algorithm, and therefore treatment capsulitis. NSAIDs are generally recommended for
should be patient-specific. short-term pain relief during the early inflammatory
stages of adhesive capsulitis.3,50 Rhind et al.51 per-
Physical therapy. For patients with early stages of adhe- formed a double-blinded study comparing the effective-
sive shoulder capsulitis, physical therapy is the first line ness of naproxen to indomethacin in the treatment of
of treatment. In general, physical therapy is simultan- adhesive capsulitis. Patients in both groups demon-
eously combined with other treatment modalities, as strated improved pain relief but no objective improve-
a Cochrane study concludes that there is little overall ment in shoulder mobility. Additionally, 70% (14 of 20)
evidence to support physical therapy alone in the treat- of patients taking naproxen and 76% (16 of 21) of
ment of adhesive capsulitis.43 Although early mobiliza- patients taking indomethacin reported side effects,
tion with physical therapy is recommended, the most commonly nausea and headache.51
technique (i.e. gentle therapy versus aggressive therapy Four randomized controlled trials (RCTs) have been
beyond the pain limits) and frequency of therapy published, evaluating the effectiveness of oral cortico-
remain controversial. Diercks and Stevens44 reported steroids in the treatment of adhesive capsulitis.52–55
that only 63% of patients undergoing intensive physical Binder et al.54 compared the treatment group (10 mg
therapy demonstrated improvement in shoulder func- of prednisone daily for 4 weeks, followed by 5 mg for
tion compared to 90% who did pendulum and gentle 2 weeks) to the nontreatment group. All patients were
exercises, improvement in shoulder function at 2-year encouraged to carry out pendulum exercises at home.
follow-up compared to 90% who did pendulum and The only statistically significant difference between the
gentle exercises. On the other hand, Vermeulen two groups was pain at night, although this was short
et al.45 showed no difference between gentle (low- lived. There was no difference in pain with movement,
grade) and aggressive (high-grade) mobilization tech- pain at rest or ROM.54 Buchbinder et al.55 utilized a
niques. Many clinicians would not recommend physical higher dose of prednisone over a shorter duration
therapy until the patients are beyond phase I, or the (30 mg of prednisolone daily for 3 weeks) and showed
painful phase, of adhesive capsulitis, when supervised greater improvement in pain at 3 weeks compared to
or self-directed mobilization becomes more tolerable. the placebo group. Improvements in disability, ROM
In a prospective nonrandomized study, Griggs et al.16 and participant-rated score were also statistically sig-
documented satisfactory outcomes in 90% of patients nificant; however, these improvements were not sus-
(64 of 75) with phase-II adhesive shoulder capsulitis tained beyond 6 weeks. Interestingly, at 12 weeks, the
undergoing a stretching exercise programme; only 7% placebo group tended to do better than the treatment
 S Le et al. 79

group, which the authors attributed to rebound symp- Suprascapular nerve block. Suprascapular nerve block
toms after cessation of prednisolone.55 (SSNB) can be performed in the hospital or office set-
ting to provide temporary pain relief to facilitate mobil-
Corticosteroid intra-articular injection. Intra-articular ization. The suprascapular nerve provides sensory
corticosteroid injection has been observed to offer fibres to approximately 70% of the glenohumeral
faster and superior improvement in symptoms com- joint.65 A double-blinded RCT by Dahan et al.66 con-
pared to oral steroid treatment.56,57 Intra-articular ster- cluded that patients receiving three successive bupiva-
oid injection decreases fibromatosis and myofibroblasts caine SSNBs experienced improved short-term pain but
in adhesive shoulders.58 Bulgen et al.59 reported that not shoulder function compared to patients receiving
intra-articular methylprednisolone injection provided placebo injections at 1-month follow-up. In another
more rapid improvement in pain and ROM compared RCT study, SSNB (9.5 mL 0.5% bupivacaine, 20 mg
to physiotherapy, ice therapy and no treatment. of triamcinolone) offered greater pain control and
However, there was no difference between the groups improved ROM at 3-month follow-up compared to
at 6 months.59 Van der Windt et al.60 observed that intra-articular corticosteroid injection (20 mg of triam-
77% of patients (40 of 52) treated with one to three cinolone).67 More recently, Ozkan et al.65 reported that
intra-articular injections of 40 mg of triamcinolone acet- SSNB is a feasible therapeutic option for patients with
onide had improved pain and shoulder disability scores adhesive capsulitis refractory to intra-articular steroid
compared to only 46% (26 of 56) in patients treated with injections.65 Using electromyography to guide the
physiotherapy (two times weekly for 6 weeks). This dif- SSNB is superior to SSNB by palpating anatomical
ference was sustained at 1-year follow-up. Adverse landmarks.68
effects were more commonly reported in women, includ-
ing facial flushing and irregular menstrual bleeding.60
Hydrodilation
More recently, Ryans et al.61 published a RCT study
demonstrating that intra-articular injection of 20 mg of Hydrodilation, otherwise known as distention arthro-
triamcinolone led to improved self-assessment of global graphy or brisement, describes a process in which cap-
disability at 6 weeks, whereas physical therapy improved sular distention is achieved by injection of air or fluid
passive external rotation at 6 weeks. Interestingly, the under fluoroscopy and local anesthetic to stretch
group that received both triamcinolone injection and the contracted capsule and thereby increasing the intra-
standardized physical therapy did not have combined capsular volume.69,70 In a level II RCT by Quraishi
benefits of both treatment modalities (or interaction et al.,71 an improved Constant score and visual ana-
effect). At 16 weeks, all groups had similar improve- logue scale (VAS) pain score was observed in the
ments in all outcome measures.61 hydrodilation group compared to the manipulation
under anesthesia (MUA) plus intra-articular triamcino-
Sodium hyaluronate intra-articular injection. Sodium hyalur- lone group. There was no difference in ROM between
onate is an unbranched polysaccharide considered to be the two groups.71 Hydrodilation with normal saline and
chondro-protective62 and has been shown to provide corticosteroid (40 mg of methylprednisolone acetate)
equivalent outcomes to intra-articular corticosteroid provides improved pain, range of active motion,
injection.18 Pharmacologically, hyaluronate has ‘meta- shoulder-specific disability measure and patient prefer-
bolic effects on articular cartilage, synovial tissue and ence measure compared to placebo (arthrogram)
synovial fluid’.62 Additionally, using dynamic MRI at 3 weeks.72 In a Cochrane review by Buchbinder
enhanced with Gd-DTPA, Tamai et al.63 demonstrated et al.73 that included five clinical trials, it was concluded
that hyaluronate injection leads to a lower coefficient of that hydrodilation with steroid and saline may improve
enhancement (a measurement of synovitis) in the syno- pain at 3 weeks and disability at up to 12 weeks; how-
vium of patients with adhesive capsulitis. A systematic ever, there may be no difference in pain and disability
review by Harris et al.,18 which included four level I and compared to steroid injection alone.
three level IV studies, concluded that sodium hyaluron-
ate injection leads to improved ROM, constant scores Other nonoperative therapies. Whole-body cryotherapy
and pain at short-term follow-up. Additionally, hyalur- (WBC) involves the exposure of the unclothed body
onate is found to be safe with no reported complica- in a chamber that circulates very cold air maintained
tions.18 Rovetta and Monteforte64 reported that a between –110  C to –140  C for 2 minutes to 3 minutes.
combined injection of 20 mg of sodium hyaluronate WBC is assumed to provide anti-inflammatory and
plus 20 mg of triamcinolone acetonide with physiother- analgesic effects to the body. Ma et al.74 compared
apy yielded better improvements in shoulder pain and physical therapy alone versus physical therapy with
joint motion compared to triamcinolone injection with WBC, noting that the group receiving physical therapy
physiotherapy. with WBC demonstrated higher improvement in VAS,
80 S Shoulder & Elbow 9(2)

active ROM (flexion, abduction, internal rotation and and hydrodilation, it allows for direct visualization of
external rotation) and self-assessed functional score the tightened CHL, thickened rotator interval and con-
using the American Shoulder and Elbow Surgeons tracted capsule to ensure adequate release. The stand-
Standardized Shoulder Assessment Form. Joo et al.75 ard arthroscopic capsulotomy is anteroinferior capsular
reported their prospective controlled trial evaluating release. The utility of posterior capsular release (or
the effects of intra-articular administration of botulinum extended capsular release) remains controversial.86–88.
toxin type A (BoNT-A) compared to intra-articular Smith et al.89 found that 50% and 80% of patients
triamcinolone in patients with adhesive capsulitis. Both had good pain relief within 1 and 6 weeks of arthro-
groups had significant improvements from baseline in scopic capsular release, respectively. On average, it
pain and ROM, although there was no difference takes 16 days to achieve good pain relief, from a VAS
between the two study groups. BoNT-A is more expen- score of 6.6 down to 1. Of the 136 patients in that study,
sive but allows the patient to avoid steroid-induced side only one patient had surgical site infection treated with
effects.75 oral antibiotics.89 In their series, Le Lievre and
Murrell90 observed that all 43 patients had improve-
ment in pain frequency and severity, shoulder function
Operative management and ROM at a long-term follow-up of 7 years. Patients
Surgical options for treatment of adhesive shoulder who tend to do more poorly with arthroscopic capsular
capsulitis are generally reserved for patients with per- release are female, > 50 years old and have type 2
sistent symptoms refractory to conservative manage- diabetes mellitus.91 Diabetic patients with adhesive
ment. These options include MUA and arthroscopic capsulitis do show improved shoulder function as mea-
or open capsulotomy. sured by the modified Constant scores after arthro-
scopic capsular release, although their results are not
Manipulation under anesthesia. MUA relies on aggressive as good compared to their nondiabetic counter-
mobilization of the shoulder joint in a controlled setting parts.92,93 At 1 year, the recurrence can be up to 11%
beyond the normal pain thresholds to tear apart the following arthroscopic capsular release.83
adhesions and stretch the contracted capsule. Often Postoperative adhesive capsulitis is a dreaded com-
regarded as a safe procedure, there have been reported plication following arthroscopic or open shoulder sur-
incidences of hemarthrosis, capsular tear, labral detach- gery, including capsulotomy procedures. There is a fine
ment, SLAP (superior labral anterior and posterior) balance between immobilization to allow the surgical
lesion, and humeral or glenoid fracture following construct, fracture or surrounding soft tissue to heal at
MUA.3,76,77 Additionally, the effectiveness of MUA the same time as promoting early mobilization to pre-
remains a topic of debate. Melzer et al.78 observed vent arthrofibrosis. Some surgeons would argue that
that patients receiving pharmacotherapy and physio- the best treatment for adhesive capsulitis is prevention
therapy did better than patients undergoing MUA by providing adequate postoperative pain management
with regards to subjective personal rating and ROM. to allow patients to comfortably engage in physical
On the other hand, Placzek et al.79 argued that MUA is therapy. Yamaguchi et al.94 placed intra-articular bupi-
a feasible treatment option for adhesive capsulitis, vacaine pain catheter following their arthroscopic cap-
documenting improved passive ROM and VAS pain sular release. It was concluded that postoperative intra-
score following translational manipulation of the gle- articular analgesia provided statistically significant
nohumeral joint under brachial plexus block. MUA postoperative pain relief and near-complete restoration
alone bears equivalent improvements in mobility and of shoulder ROM, with an average follow-up of
pain compared to MUA with intra-articular steroid 22.4 months.94 Likewise, postoperative analgesia can
injection [1 mL of betamethasone (6 mg/mL) and also be achieved via cervical epidural infusion95 or
4 mL of lidocaine (10 mg/mL)].80 In one RCT, MUA interscalene block following arthroscopic release.96,97
with home exercises provided comparable outcomes to
home exercises alone.81 MUA has been shown to be less Open capsulotomy. Open capsulotomy is rarely per-
effective in diabetic patients with adhesive shoulder formed for recalcitrant adhesive shoulder capsulitis
capsulitis.82 because arthroscopic capsular release results in smaller
surgical wounds and shorter postoperative recovery.
Arthroscopic capsulotomy. Arthroscopic capsular release is The open procedure remains an option when arthro-
an effective and safe method for treatment of adhesive scopic capsular release has failed in improving pain
shoulder capsulitis.83–85 Arthroscopic capsulotomy has and ROM for adhesive capsulitis. Release of the CHL
two key advantages. First, diagnostic arthroscopy con- and rotator interval have been found to restore motion
firms the diagnosis and rules out other potential causes and improve pain.13 In their series of 25 patients who
of a painful stiff shoulder. Second, compared to MUA failed MUA, Omari and Bunker14 performed open
 S Le et al. 81

capsular release and noted improvement in both pain capsular adhesions and accumulation of collagen
and function at mean follow-up of 19.52 months. within the capsule. More recently, the internal fixation
model of adhesive capsulitis in rats have been shown
Future therapies. As we continue to gain better insight to result in sustained in vivo kinematic changes.103 This
into the pathophysiology of adhesive capsulitis, there animal model, which allows for long-term functional
is equal interest in developing novel non-operative measurements, should pave the way for the testing of
therapeutic interventions for treating this debilitating new pharmacological therapies.
condition.
One recurring theme in medicine is to apply a
successful treatment of one disease to another disease
Conclusions
that shares similar pathophysiology. Collagenase is an Adhesive capsulitis of the shoulder remains an unre-
enzyme isolated from the bacterium Clostridium histy- solved clinical problem. No present treatment protocols
lyticum and breaks down the peptide bonds in collagen. are universally effective, and there is a strong need for
Collagenase has been approved by the Food and Drug further research and development of more effective
Administration (FDA) for the treatment of two fibrotic treatment strategies. Morbidity from this condition
tissue disorders, Dupuytren’s disease and Peyronie’s has significant individual and societal cost, and disabil-
disease, with good functional outcomes. As previously ity is always long-lasting, if not permanent. There are
illustrated, adhesive capsulitis is very similar to few validated animal models, and investigational pro-
Dupuytren’s disease, both histologically and molecu- gress has been slow. The recent development of a new
larly. Although collagenase has been FDA-approved validated animal study should lead the way to develop-
for use in Dupuytren’s since 2010, only recently have ment of novel therapies. New treatments for adhesive
there been studies investigating the efficacy of off-label capsulitis, if developed, could also serve to address
use of collagenase injection in patients with adhesive other aetiologies of arthrofibrosis.
shoulder capsulitis. This is known as enzymatic capsu-
lotomy. In a phase 2 placebo-controlled double-blind
RCT, Badalamente and Wang98 reported that extra- Declaration of Conflicting Interests
articular collagenase injection into the anterior shoul- The author(s) declared no potential conflicts of interest with
der capsule (midway between the bicipital groove and respect to the research, authorship, and/or publication of this
coracoid at maximal external rotation) results in article.
improved functional score, shoulder motion and pain
compared to injection of placebo (0.9% saline/2 mM
Funding
CaCl2). Patients also benefited from subsequent injec-
The author(s) received no financial support for the research,
tions. Improvements were sustained at a follow-up of
authorship, and/or publication of this article.
1.8 years. Side effects include tenderness and ecchym-
osis at the injection sites, which resolved between 7 and
14 days.98 MRI obtained 3 months after collagenase References
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