Frozen shoulder – etiology, pathogenesis and natural course

Authors: R Norlin

References: SECEC 2005

The Stiff Shoulder


Frozen shoulder – etiology, pathogenesis and natural course


R. Norlin

University Hospital Linköping, Sweden


The term frozen shoulder (FS) is used to describe a clinical condition with restricted active and passive range of motion in all directions, both flexion, abduction and rotation.



Many authors have tried to define this condition of pain and limited glenohumeral motion:


          Duplay          1872             Periarthrite scapulohumerale

          Dickson & Crosby      1932             Periarthritis of the shoulder

          Pasteur                   1932             enosynovitis LHB

          Codman                  1934             Uncalcified tendonitis

          Lippman                  1943             Scarring of LHB

          Nevasier                  1945             Adhesive capsulitis

          Moseley                  1945             Varied symptoms, periarthritis


Once Nevasier, Moseley and other had come to a better understanding of the syndrome, more detailed studies deepened the knowledge of adhesive capsulitis:


          Withers                   1949             Involvement of subacromial bursa

          Simmonds                1949             Inelastic fibrous tissue


Different theories and speculations in aetiology started to be published.  DePalma (1952) discussed the possibility of muscular inactivity to be the main course for the development of FS.  Meulengracht & Schwartz (1952) found that 18% of the FS patient also suffered from Dupuytren’s contracture.  Nevasier (1962) described the typical decrease in joint volume using arthrography.  Lundberg carefully studied FS from different aspects and published theories on change in glucosaminoglycans in the affected shoulder (1970).  Several other theories were discussed, such as autoimmune mechanisms (McNab 1971), association with other shoulder problems (De Seze 1974) and association with different neurologic conditions (Bruckner & Nye 1981).


The increased appearance of FS in diabetic patients was first described by Bridgeman 1972.


Treatment was initially a challenge.  However, Andren & Lundberg (1965) studied the beneficial effect of mobilisation, using arthrography.



The definition, also defined by Lundberg, is:

-                     shoulder joint elevation of ≤135°

-                     restriction of motion is localised to the glenohumeral joint

-                     history, clinical and radiological examination show no other explanation


As in all situations where not all facts are known, many different ways of classifying may exist.

Perhaps it is wise to use the initial classification of Lundberg (1969):

-                     Primary Frozen shoulder

-                     Secondary Frozen shoulder


But not even this is clear – these groups need to be subdivided:


          -        Primary Frozen shoulder                 -        Diabetic

                                                                   -        No other explanation


          -        Secondary Frozen shoulder   -        Post-traumatic

                                                                   -        Latrogenic

                                                                   -        Other


There exists, of course, other types of classification.  In some, the diabetic frozen shoulder is a secondary type.  The secondary may be divided into extrinsic (causes outside the joint) and intrinsic (causes inside the joint).



When looking at secondary frozen shoulder, the cause of the syndrome is usually easy to define.


In the posttraumatic cases there is clear evidence of a trauma and usually also structural changes within or adjacent to the joint, such as fractures, chondral lesions, avascular necrosis or tendon injuries.  Scarring following traumatic tissue injury is another cause.


The iatrogenic cases occur following treatment, usually surgery.  In these cases extreme scarring following tissue repair may occur or surgical mistakes such as over tightening of soft tissue may be responsible for the following limitation in range of movement.


The problem of identifying the true etiology arises when we look at primary frozen shoulder.  Today, no comprehensive etiological model exists!


There are three different modalities of outcome following primary FS:

-                     40% restore the range of motion (ROM) and are pain free

-                     45% regain functional ROM but show residual symptoms

-                     15% show persisting stiffness with marked handicap (Noel et al 2000, Shaffer et al 1992).  Perhaps are these different outcome patterns signs of different types or subsets of primary FS?


The association with metabolic diseases is most well known regarding diabetes mellitus (both insulin-dependent and non-insulin-dependent types), especially retinopathy, but exists also with hypo- and hyperthyroidism (Balci et al 1999, Massoud et al 2002).  In diabetes, up to 40% incidence of FS has been reported.


Other factors that have been reported are neuropathy and reflex sympathetic dystrophy (Rizk & Pinals 1982), chronic airway obstruction (Engelman 1966, Saha 1966), various medications (Weber et al 1995) and ischemic heart disease (Wright & Haq 1976).


Dupuytren’s disease is again shown to be related to FS.  Dupuytren’s disease is significantly more common than usual among male relatives to FS patients and the microscopic changes in the anterior capsule and coracohumeral ligament are very similar to those in Dupuytren’s disease of the hand (Bunker & Anthony 1995, Smith et al 2001).  They show that half of the patients with FS also show signs of Dupuytren’s!  Similarities with Dupuytren’s are also shown when analysing the fibrotic capsule for cytokines and proteinases (Bunker et al 2000).


Pathoanatomically there is an involvement of the capsule in the glenohumeral joint.  The capsule volume is reduced and this is the cause for the restricted range of motion (Itoi & Tabata 1992). 


Look arthroscopically in the joint is technically more difficult than in a normal shoulder.  The dense capsule is difficult to penetrate and the tight joint with marked reduced volume is demanding to visualise without compromising the joint surfaces.  The capsule is tight and its synovial surface is showing signs of vascular inflammation.  Usually, no intra articular adhesions are seen. 



Primary frozen shoulder is usually considered to be a self limiting disease which usually lasts for 18-24 months but will usually heal with minor residual handicap.


This is the result of a recent study (Diercks & Stevens 2004) showing the increase of Constant score with time when treated with “supervised neglect” – (and also showing that physiotherapy may perhaps be harmful to the patient):


The pattern in which FS usually is developed may be described as three time periods of six months each:

-        1st period:      Freezing

-        2nd period:     Frozen

-        3rd period:      Thawing


1.                  The freezing stage shows an insidious onset where pain is dominating the clinical picture.  Quite often, subacromial impingement is initially suspected because of the involvement of the subacromial bursa.  At the end of this period range of motion becomes limited in the typical way and diagnosis is usually no longer a problem.

2.                  The frozen period shows reduction of pain but the restricted mobility remains.

3.                  The thawing includes successive reestablishment of normal or near normal range of motion.


However, this time plane is an approximation of the most common time course of this disease.  It may vary greatly between different patients.


End results: As shown above most patients regain function range of motion but 10-15% suffer from remaining handicap, both pain and restricted motion.  However, 10 years after FS further improvement may be seen (Dudkiewicz et al 2004).


Recurrence of primary frozen shoulder is extremely rare.  Only three cases have been published in the literature (Rowe & Leffert 1988, Cameron et al 2000).



1.                  Andren L, Lundberg BJ.  Treatment of rigid shoulder by joint distension during arthrography.  Acta Orthop Scan 36:46-53, 1965.

2.                  Balci N, Balci MK, Tuzuner S.  Shoulder adhesive capsulitis and shoulder range of motion in type II diabetes mellitus: association with diabetic complications.  J Diabetes Compl 13:135-140, 1999.

3.                  Bruckner FE, Nye CJS.  A prospective study of adhesive capsulitis of the shoulder in a high risk population.  Q J Med 198:191-204, 1981.

4.                  Bunker FE, Anthony PP.  the pathology of frozen shoulder.  A Dupuytren-like disease.  JBJS Br 77:677-638, 1995.

5.                  Bunker, TD, Reilly J, Baird KS, Hamblen DL.  Expression of growtrh factors, cytokines and matrix metalloproteinases in frozen shoulder.  JBJS Br 82:768-773, 2000.

6.                  Cameron RI, McMillan J, Kelly IG.  Recurrence of a “primary frozen shoulder”: a case report.  J Shoulder Elbow Surg 9:65-67, 2000.

7.                  Codman EA.  The Shoulder.  Boston: Thomas Todd Co., 1934.

8.                  Diercks RL, Stevens M.  Gentle thawing of the frozen shoulder.  J Shoulder Elbow Surg 13:499-502, 2004.

9.                  DePalma AF.  Loss of scapulohumeral motion.  Ann Surg 135:193-204, 1952.

10.              De Seze.  Les epaules douloureuses et les epaules bloquees.  Concours medical 96;5329-5357, 1974.

11.              Dickson JA, Crosby EH.  Periarthritis of the shoulder: an analysis of two hundred cases.  JAMA 99:2252-2257, 1932.

12.              Dudkiewicz I, Oran A, Salai M, Palti R, Pritsch M.  Idiopathic adhesive capsulitis: long-term results of conservative treatment.  Isr Med Assoc J 6:524-526, 2004.

13.              Duplay ES.  De la periarthrite scapulohumeral et des raiduers de l’epaule qui en son la consequence.  Arch Gen Med 20:513-542, 1872.

14.              Engelman RM.  Shoulder pain as a presenting complaint in upper lobe bronchogenic carcinoma.  Conn Med 30:273-276, 1966.

15.              Itoi E, Tabata S.  range of motion and arthrography in the frozen shoulder.  J Shoulder Elbow Surg 1:106-112, 1992.

16.              Lippman RK.  Frozen shoulder: Bicipital tenosynovitis.  Arch Surg 47:283-296, 1943.

17.              Lundberg BJ.  The frozen shoulder.  Acta Orthop Scand suppl 119;1-59, 1969.

18.              Lundberg BJ.  Glycosaminglycans of the normal and frozen shoulder-joint capsule.  Clin Orthop Relat Res 69:279-84, 1970.

19.              MacNab I.  the painful shoulder due to rotator cuff tendonitis.  RI Med J 54:367-374, 1971.

20.              Massoud SN, Eyiyemi OP, Ofer L, Copeland SA: Operative management of frozen shoulder in patients with diabetes.  J Shoulder Elbow Surg 11:609-613, 2002.

21.              Meulengracht E, Schwartz M.  Course and prognosis of periarthritis humeroscapularis.  Acta Med Scand 143:350-360, 1952.

22.              Moseley HF.  Shoulder lesions.  Sprinfield, IL: Charles C Thomas, 1945.

23.              Nevasier JS.  Adhesive capsulitis of the shoulder.  JBJS 27:211-222, 1945.

24.              Nevasier JS.  Arthrography of the shoulder joint.  JBJS 44:1321-1330, 1962.

25.              Noel E, Thomas T, Schaeverbake T, Thomas P, Bonjean M, Revel M.  Frozen shoulder.  Joint Bone Spine 67:393-400, 2000.

26.              Pasteur F.  Les algies do l’epaule et la physiotherapie.  J Radiol Electrol 16:419-426, 1932.

27.              Rizk TE, Pinals RS.  Frozen shoulder.  Semin Arthrop Rheumatol 11:440-452, 1982.

28.              Rowe CR, Leffert RD.  Idiopathic chronic adhesive capsulitis (frozen shoulder).  In: Rowe CR, editor.  The shoulder.  New York: Churchill Livingstone p 155-163, 1988.

29.              Saha NC.  Painful shoulder in patients with chronic bronchitis and emphysema.  Am Rev Respir Dis 94:455-456, 1966.

30.              Shaffer B, Tibone JE, Kerlan RK.  Frozen shoulder.  A long-term follow-up.  JBJS AM 74:738-746, 1992.

31.              Simmonds FA.  Shoulder pain with particular reference to the frozen shoulder.  JBJS 31:834-838, 1949.

32.              Smith SP, Devaraj VS, Bunker TD.  The association between frozen shoulder and Dupuytren’s disease.  J Shoulder Elbow Surg 10:149-151, 2001.

33.              Weber M, Prim J, Bugglin R, Michel BA, Gerber H.  Long term follow up of patients with frozen shoulder.  Clin Rheumatol 14:686-691, 1995.

34.              Withers RJW.  The painful shoulder: review of one hundred personal cases with remarks on the pathology.  JBJS 31:414-417, 1949.

35.              Wright V, Haq A.  Periarthritis of the shoulder: 2. Ann Rheum Dis 35:220-226, 1976.


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