Posted by massther on Dec 5, 2013 in Body Talk, News | 0 comments
Author: Erika Kruger
Massage therapists are very familiar with the signs and symptoms of adhesive capsulitis (AC), the chronic fibrosing condition of the shoulder joint capsule, also known as frozen shoulder, shoulder periarthritis, or obliterative bursitis.
But what is not readily known is that diabetes mellitus is one of the risk factors for this condition. In fact according to Dr Gordon Cameron, “(s)ome experts think that shoulder problems in diabetics are so common that they should be regarded as a complication of diabetes and not a coincidental event”.
A variety of conditions involving contractures in joints and peri-articular soft tissue and accompanying joint mobility limitations have been identified in diabetic patients (Friedman 1989). In young, insulin-dependent diabetics it involves mostly the small joints of the hands and is usually less painful while in older diabetics, the large joints of the upper extremities also develop contractures. (Friedman 1989, Smith, Burnett & McNeil 2003:30)
The most disabling of the common musculoskeletal problems in diabetics, is AC. The condition is characterised by progressive, painful restriction of shoulder movement. It develops in up to 20% of diabetic patients (Cameron) and is seen in especially insulin dependent diabetics with type 1 diabetics. According to Walk, the numbers may exceed 35%. Patients with diabetes are also more difficult to treat, take longer to heal and may be left with some residual trouble even with treatment. Furthermore there is a link with the duration of diabetes and the age of the patient (Smith et al 2003:30).
AC is usually classified as either a primary condition or a secondary condition. Primary or idiopathic AC refers to cases where there are no significant and specific reasons for the pain and immobility. It arises spontaneously with no obvious preceding trigger factor. The secondary type of frozen shoulder develops after trauma, surgery or illness. Patients presenting with diabetes as well as a number of other medical conditions such as hyper- and hypothyroidism, cardiovascular disease, tuberculosis and Parkinson’s disease, appear to be predisposed to develop secondary AC.
The natural history of the disease is characterised by three distinct phases: painful, adhesive, and resolution phases (Smith et al 2003:30). The painful phase starts with the gradual onset of an aching shoulder developing into a widespread pain pattern often worst at night and when lying on the affected side. This phase can last anywhere between 2-9 months. During the next phase stiffness starts to become a problem although pain level usually does not alter. The affected shoulder starts to interfere with daily tasks such as dressing, preparing food, carrying bags and working. Muscle wastage may be evident due to lack of use. This stage can last between four to 12 months. During the final or thawing stage there is a gradual improvement in range of movement and a decrease in pain that may however re-appear as stiffness eases. This stage can take up to two years.
In order to understand the relationship between diabetes and AC, it is important to understand the anatomy and the pathogenesis of the condition. AC is a disorder involving the shoulder capsule and the connective tissue around the glenohumeral joint of the shoulder. It presents with inflammation and a thickening of the capsule indicated by increased vascularity visible on magnetic resonance imaging (MRI).
Although the disease causes a contracture of the entire shoulder joint, it appears maximal in the rotator interval (RI) located at the front of the shoulder and particularly around the coracohumeral ligament (Bunker et al 2000:772, Bunker 1997:210). It is this restricted space between the capsule and ball of the humerus that distinguishes AC from a less complicated, painful, stiff shoulder (National Institute of Arthritis and Musculoskeletal and Skin Diseases 2010).
As a result of the contracture, there is progressive loss of mobility with diminished range of motion in all directions but in particular external rotation and abduction (Smith et al 2003:30). This, combined with diminished lubrication of the joint as a result of a lack of synovial fluid in the capsule, leads to chronic pain that can last from five months to three years or more.
The RI is a triangular space defined by a number of landmarks and muscles. It is located between the subscapularis and supraspinatus tendons and the base of the coracoid process and it represents a complex interaction of the fibres of the medial head of the coracohumeral ligament, the superior glenohumeral ligament, the glenohumeral joint capsule, and the supraspinatus and subscapularis tendons (Hunt, Kwon & Zuckerman 2007).
The floor of the RI is formed by the cartilage of the humeral head, and it is roofed by the RI capsule which is principally made up of coracohumeral ligament linking the subscapularis and supraspinatus tendons. The coracohumeral ligament bridges the RI and its contents – the tendon of the long head of the biceps and the superior glenhumeral ligament (Krief 2005, Gaillard 2008).
According to Hunt et al (2007) the RI has, over the past two decades, become accepted as a distinct anatomic entity. It plays an important role in the proper functioning and biomechanical stability of the glenohumeral joint to prevent the long head of the biceps tendon from dislocating anteriorly (Hunter et al 2007, Cole, Mazzocca, & Meneghini 2003, Gaillard). The RI checks against excessive flexion, extension, adduction, external rotation. It stabilizes against inferior translation of the humeral head in the adducted shoulder as well as against posterior translation of the humeral head in the flexed or abducted /externally rotated shoulder (Bhardwaj 2008).
The pathogenesis of AC is caused by the combination of fibrosis and inflammation.
Despite the name of the condition, Bunker et al (2000:772) point out that shoulder arthroscopes in patients with frozen shoulder have shown that although the capsule is contracted, there are no adhesions. In fact in a 2009 article Bunker suggests that it is time to drop the name frozen shoulder and even AC and replace it with the term contracture of the shoulder.
However arthroscopies do show that the RI is damaged or in cases even destroyed by granulating scar tissue of the synovial membrane of the joint. Synovitis showing up as tiny purplish-red spots caused by the release of a very small quantity of blood from capillaries, is also visible in the joint as well as just beneath the biceps insertion in the subscapular recess (Bunker 1997:211).
This is confirmed by surgical exploration showing the capsule to be thickened and scarred and peeling “from the humeral head like adhesive plaster from skin” (Neviaser in Bunker 1997:211). Instead of the normal palpable sulcus or shallow groove, there appears a vascular area of nodular thickening (Bunker 1997:211).
Histological and immunocytochemical studies show elevated levels of cytokines or cell-to-cell signalling proteins, in the area (Bunker et al 2000:772). Cytokines and other cellular growth factors function to regulate the growth and function of fibroblasts in connective tissue and to control healing in damaged tissues. These cell messengers are derived from a variety of cells including lymphoid cells, platelets, epithelial cells, endothelial cells and fibroblasts.
In AC too many fibroblasts are produced (fibroblastic proliferation) and too much collagen is laid down. Thick collagen bands cause reduced volume in the glenohumeral joint and form a checkrein to movement when the arm is placed in extemal rotation (Bunker 1997:211). It is also suspected that this pathological cytokine response leads to the formation of new blood vessels (angiogenesis) within the capsule (Bunker et al 2000:773, Bunker 1997:211).
At the same time, Bunker et al (2000:773) posits, there may be a failure of collagen remodelling. This imbalance between aggressive healing, scarring, contracture and a failure to remodel the tissue may lead to the protracted stiffening of the capsule.
Also combined with the fibrosis is an inflammatory healing response within the shoulder capsule indicated by the presence of chronic inflammatory cells (mast cells, T cells, B cells and macrophages) and specifically resistin, an adipokine expressed in bonemarrow (Bunker et al 2000:773). This is of particular interest in the case of frozen shoulder. According to Walk resistin has been shown to mediate inflammation by up-regulating specific cytokines which have been implicated in the pathophysiology of frozen shoulder. However, according to Walk, there are still numerous questions to be answered as to how the mechanisms behind this complex process of cytokinetic signaling work.
Walk summarizes the development of AC as follows:
An underlying metabolic disorder of some sort, leads to increased bone turnover, specifically at the site of the humeral head. Through increased bony turnover, resistin-secreting adipocytes come into closer proximity to the articular surface of the humeral head, creating a very pro-inflammatory environment within the capsule. A minor injury (if any at all) leads to a hyper-inflammatory response due to the increased presence of resistin which drives other cytokines involved in inflammation and fibrosis.
Although statistics show a direct link between AC and diabetes mellitus, the exact nature of the influence of the one on the other is not known. Theories abound however and Walk mentions a few:
• Diabetics are known to suffer from soft tissue changes and osteopaenia throughout the disease progression. Walk hypothesizes that although the pathophysiology behind this is still largely unknown, these changes may lead to various musculoskeletal problems including AC, but the jury on this theory is still out.
• Even a link between the connective tissue changes seen in diabetics and the accumulation of an agent such as sorbitol, a plant alcohol used as a sweetener, in the extracellular matrix changing the physical properties of that tissue has been put forward.
• Another theory is that there is an alteration of the structure of collagen itself causing resistance to enzymatic breakdown.
• Diabetic complications have also been attributed to a state of chronic low-grade inflammation by specific cytokines.
Cameron puts forward these hypotheses:
• Diabetes can damage blood vessels and a poor blood supply results in scarring.
• Slow healing and impaired nerve function are also common in diabetic patients and contribute to the fact that the AC pain takes longer to settle than it does in other, non-diabetic, patients.
• Damage in the body’s elastic tissues may be a result of diabetes.
Smith et al (2003:30) states that the most obvious factor in the prevalence and worsening of rheumatic conditions in diabetics is poor glycaemic control.
As Bunker (2009:4) puts it, AC or Contracted (Frozen) Shoulder is an enigmatic condition and although the last two decades have seen advances made in our understanding of the condition, there is still a long way to go before we have a full understanding thereof. This includes the relationship with diabetes. Studies showing clear evidence for the proposed theories still needs to be done but it is important that massage therapists should be aware of the relationship between AC and diabetes when designing treatment plans.
BIBLIOGRAPHY
1. Bunker, T.D. (1997). Frozen shoulder: unravelling the enigma in The Annals of The Royal College of Surgeons of England, 79: 210-213
2. Bunker, T.D. (2009). Time for a new name for frozen shoulder—contracture of the shoulder. Shoulder & Elbow 2009(1) pp 4–9
3. Bunker, T. D., Reilly, J., Baird, K.S. & Hamblen, L.D. (2000) Expression of growth factors, cytokines and matrix metalloproteinases in frozen shoulder.The Journal of Bone and Joint Surgery [Br], 82-B:768-73.
4. Bhardwaj, R.G. (2008). Anatomy and Pathology of the Rotator Interval. The Bone Pit
http://www.bonepit.com/Lectures/Anatomy%20and%20Pathology%20of%20the%20Rotator%20Interval%20%20%20%20R.%20Grace%20Bhardwaj.pdf
5. Cameron, G. Frozen Shoulder and Diabetes. The Diabetes Monitor http://www.diabetesmonitor.com/b240.htm
6. Cole, B.J., Mazzocca, A.D. & Meneghini, R.M. (2003). Indirect Arthroscopic Rotator Interval Repair. Arthroscopy: The Journal of Arthroscopic and Related Surgery, 19(6), e28-e31.
7. Friedman, N. (1989) Abstract: Periarthrosis of the Shoulder Associated with Diabetes Mellitus. American Journal of Physical Medicine & Rehabilitation.
8. Gaillard, F (2008). Rotator Cuff Interval. Radiopedia.org http://radiopaedia.org/articles/rotator_cuff_interval
9. Hunt, S.A., Kwon, Y. W. & Zuckerman, J.D (2007). The Rotator Interval: Anatomy, Pathology, and Strategies for Treatment in Journal of the American Academy of Orthopaedic Surgeons, 15(4), 218-227.
10. Krief, O.P. (2005). MRI of the Rotator Interval Capsule in American Journal of Roentgenology, 184, 1490-1494 http://www.ajronline.org/cgi/content/full/184/5/1490
11. National Institute of Arthritis and Musculoskeletal and Skin Diseases, 2010. Shoulder Problems. NIAMS. http://www.niams.nih.gov/health_info/shoulder_problems/
12. Smith, L.L., Burnett, S.P., McNeil, J.D. Musculoskeletal manifestations of diabetes mellitus in British Journal of Sports Medicine 37, 30–35 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1724591/pdf/v037p00030.pdf
13. Walk, M. A Contemporary Perspective on the Etiology of Primary Adhesive Capsulitis http://www.kaiserhaywardptfellowship.com/PDF/Etiology%20Adhesive%20Capsulitis%20WALK%202008.pdf
