1.2. Diagnosis

Autoimmunity and the overall systemic and articular inflammatory load drive the destructive phase of the disease, which can be detected by conventional radiography or other imaging techniques. But the joint destruction is rarely visible in the early stages of the disease [16]. In the last decade, the use of disease-modifying antirheumatic drugs (DMARDs), particularly methotrexate (MTX) and the availability of new biologic agents have dramatically enhanced the success of RA management [17, 18]. It was shown that early therapeutic intervention improves clinical and radiological outcomes [19]. Up to now it was not possible to effectively investigate the efficacy of early interventions in terms of their ability to prevent later stage RA, since there are not enough data or accepted criteria to group such patients with early disease. In 1987, American College of Rheumatology (ACR) published the criteria for diagnosis [20]. The criteria required four or more of the following: (a) morning stiffness for at least 1 hour for at least 6 weeks, (b) soft-tissue swelling of three or more joints at least 6 weeks, (c) swelling of the proximal interphalangeal, metacarpophalangeal or wrist joints for at least 6 weeks, (d) symmetric joint swelling for at least 6 weeks, (e) rheumatoid nodules, (f) RF positive blood test and (g) radiographic changes like erosions or osteopenia in hand and wrist joints. These criteria are widely accepted for the diagnosis, but have a limitation in that they were derived for trying to discriminate patients with RA from those with a combination of other rheumatologic diagnosis. Early identification in the patients was not possible with the use of these criteria. In 2010, a joint working group of the ACR and the European League Against Rheumatism (EULAR) was formed to develop a new classification for RA. The newly developed criteria's were designed also as a referral tool for primary care physicians. The number of joints involved, small or large joints, serology (RF, negative or positive ACPA, CRP, ESR) and the duration of symptoms are noted. Every possibility has different points. If the patient has more than six points, the patient has a definitive RA [17] (Table 1).



\* Score-based algorithm: add score of categories A–D.

\*\*A score of ≥6/10 is needed for classification of a patient as having definite rheumatoid arthritis.

† At least one test is needed for classification.

1. Introduction

170 Advances in Shoulder Surgery

1.1. Epidemiology

1.2. Diagnosis

Rheumatoid arthritis (RA) is an inflammatory process that may lead to disability as a result of joint destruction. The prevalence of RA is less than 1% in the general population and women are affected three times more as men but this sex difference weakens in the elderly. The onset of the disease is mostly during the fourth and fifth decades. Family studies have indicated a genetic predisposition with an increased frequency of the disease among the first-degree relatives and twins [1]. An association with human leukocyte antigen (HLA)-DR4 was shown in 70% of the Caucasian and Japanese patients compared to 28% of the controls [2, 3]. The discovery of rheumatoid factor (RF) in 1940s, led to hopes that blood tests could provide gold standard biomarkers in the recognition of the disease [4]. Approximately 70% of RA patients have a positive RF or anti-cyclic citrullinated peptide antibodies (ACPA) along with elevated

New Genome-Wide Association Studies (GWAS) showed a total of 101 single nucleotide polymorphisms (SNPs) associated with immune dysregulation and inflammation. T-reg cells seem to be defective in RA patients [8]. Also, GWAS studies identified potential therapeutic targets. One study showed RA risk in a special pathway, which is called kappa B signaling pathway (NF-kB). Engagement of CD40 is one of the ways this pathway can be triggered and can be targeted for treatment [9]. Another new treatment method focuses on the Janus kinase (JAK) pathway [10]. This pathway is the main signaling mechanism in response to many cytokines involved in RA, including IL-6 [11]. Human leukocyte antigen (HLA) class II locus is associated less with the risk of developing ACPA and more ACPA-positivity to have RA [12]. In the recent years, environmental factors like smoking and pulmonary inflammation was shown to be associated with the emergence of the disease [13]. By using new methods that integrate genetic data with biochemical pathways and cell types involved in the disease, real progress has been made about RA pathophysiology like where and when immune tolerance is broken, which results in synovial inflammation and bone destruction [14]. Environmental factors needs to be

recognized and their role in breaking RA tolerance should be investigated further [15].

Autoimmunity and the overall systemic and articular inflammatory load drive the destructive phase of the disease, which can be detected by conventional radiography or other imaging techniques. But the joint destruction is rarely visible in the early stages of the disease [16]. In the last decade, the use of disease-modifying antirheumatic drugs (DMARDs), particularly methotrexate (MTX) and the availability of new biologic agents have dramatically enhanced the success of RA management [17, 18]. It was shown that early therapeutic intervention improves clinical and radiological outcomes [19]. Up to now it was not possible to effectively investigate the efficacy of early interventions in terms of their ability to prevent later stage RA, since there are not enough data or accepted criteria to group such patients with early disease. In 1987, American College of Rheumatology (ACR) published the criteria for diagnosis [20]. The criteria required four or more of the following: (a) morning stiffness for at least 1 hour for at least 6 weeks,

erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) [5–7].

Table 1. The 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis [17].

Joint status of the RA patients was needed to be evaluated after biological agent administration for remission of the disease. Joint destruction pattern under biologic agents were widely discussed. Fukae et al. [21] had shown under X-ray imaging of fingers, Yoshimi et al. [22] by ultrasound and Suzuki et al. [23] evaluated the synovitis of the hand by the help of MRI. Yonemoto et al. had chosen the 18F-fluorodeoxyglucose positron emission tomography for the evaluation of the destruction. They shared the results of the previous studies of the authors mentioned that even though clinical status of the patient may improve, the synovitis thus destruction was only slowed [24].

primary diagnostic tools for evaluating the glenohumeral joint (GH). According to prospective study of Kojima et al., RA patients were evaluated for their range of motion of large joints and the effect on the daily activities. Disability of daily activities like dressing, arising, eating, walking

The Rheumatoid Shoulder: Current Surgical Treatments http://dx.doi.org/10.5772/intechopen.71452 173

Medial migration and remodeling of the humeral head with medialization of the GH joint due to bony erosion are common radiographic findings in RA [35]. The rotator cuff insufficiency

Larsen defined the widely used radiographic classification of rheumatoid shoulder in 1977. According to this classification, in stage 0: there is no sign on plain X-ray; stage I: arthritic changes with osteopenia and periarticular tissue swelling; stage II: narrowing of the joint space and erosions; stage III: cysts, increased loss of joint space, superior migration of the humeral head because of rotator cuff insufficiency; stage IV: loss of contours of the articular surface, flattening of the humeral head, medialization of the glenoid; and stage V: severe bony deformation with loss of joint contours and superior migration of the humeral head [36]. Ultrasonography (USG) is also a helpful tool in the shoulder joint. Thus radiography gives limited information about the soft tissue changes, USG could show possible pathologies of the periarticular tissues, especially at the beginning of the disease. It is easy to detect inflammatory changes in the subacromial space like bursitis, tendinitis of the long head of the biceps tendon and rotator cuff tears [37]. Magnetic resonance imaging (MRI) and computerized tomography (CT) are not needed for classification of the disease. But they are useful to answer some special questions like tumoral infiltration, fatty infiltration of the muscles and preoperative planning of shoulder arthroplasty [38, 39]. Evaluation of the degree of periarticular soft tissues is important when deciding on the best treatment

Amundsen et al. investigated the arthroplasty mortality rates for various aetiologies. A total of 214 RA patients were included and on the postoperative 90th day and first year, significantly higher mortality rate was encountered. Even though the highest mortality rate was encountered for fracture patients, RA patients' increased mortality rate must be kept in mind for

Best treatment strategy takes into account the overall condition of the patient and the involvement of other joints. There might be need for lower limb surgery and the use of walking aids. Sometimes the involvement of other, distal joints in the upper arm affects the timing of shoulder

In RA, synovium produces chemokines and cytokines, which are responsible for pain and swelling of the joint and later for the articular destruction [41]. Synovectomy is a treatment method aimed for pain relief and treatment of joint swelling before bony erosions occur [42].

and personal hygiene was strongly correlated with shoulder abduction limitations [34].

provokes superior migration of the humeral head with medialization.

strategy [33].

surgical intervention [40].

surgery/reconstruction.

2. Current surgical treatments

2.1. Synovectomy and bursectomy

In multiple-joint involvement type of the disease, shoulder joint is commonly involved. But it is rarely affected in monoarticular fashion. The clinical presentation may be different in every patient. It can be symmetrical, episodic and silent between periods of remission. The clinical presentation may start with musculoskeletal pain, fever, fatigue or malaise. At the same time, other joints may present with erythema, pain and stiffness after inactivity. In the early stages of this disease, inflammatory changes of the subacromial soft tissue like bursitis, tenosynovitis of the long head of the biceps tendon resulting in defects of the rotator cuff. Rotator cuff is affected both by the synovial proliferations of the glenohumeral joint and the synovitis of the subacromial bursa. The starting point of the destruction of the rotator cuff is often a partial defect of the supraspinatus tendon at the attachment side to the humeral head. The intraoperative rate of this pathology lies between 30 and 90% of the cases, intratendinous defects between 20 and 40%, partial defects and simply thinning-out is found 80% of the cases [25]. Glenohumeral joint, at the beginning, is not really painful because of the large intracapsular space. The first cartilage bone change starts from humeral head that leads to deformation of the head [26]. Pain originates from the capsule, that is sensitive to stretch and distension. The increase in the synovial fluid and hypertrophy of the synovium leads to increase in intra-articular pressure. To overcome this condition, the shoulder is positioned in slight flexion and internal rotation. By this way, the capsular volume is increased [1].

The initial presentation around the shoulder is pain and loss of motion. With the progression of the disease, loss of elevation and external rotation are noted. The initial presentation of the disease can be subacromial bursitis with giant rice bodies in some patients, which may mimic impingement syndrome [27]. Villous synovial hypertrophic tissues (pannus) may result in crepitation and pain during motion. At the inflammatory phase, the patient experiences a constant aching even at rest and being worst at night. In rare cases, scapulothoracic bursa can become inflamed and painful [28]. It should be kept in mind that, in rheumatoid shoulder, the affected joint is not only the GH joint, also acromioclavicular joint (AC) is affected. It was found that in RA patients, AC joint is affected more frequently than the GH joint, but in half of the patients both joints are involved. This should be remembered when treating painful rheumatoid shoulder [29].

The shoulder joint is affected in approximately 60% of hospitalized patients with RA [30, 31]. The pain around the shoulder area was reported in 50% of newly diagnosed RA patients [32]. The degree of dysfunction of the shoulder is related to the severity of the rheumatoid disease [33]. It was reported that 48% of RA patients developed glenohumeral erosive changes and 13% developed pathologic joint space narrowing. Plain radiographs of the rheumatoid shoulder are the primary diagnostic tools for evaluating the glenohumeral joint (GH). According to prospective study of Kojima et al., RA patients were evaluated for their range of motion of large joints and the effect on the daily activities. Disability of daily activities like dressing, arising, eating, walking and personal hygiene was strongly correlated with shoulder abduction limitations [34].

Medial migration and remodeling of the humeral head with medialization of the GH joint due to bony erosion are common radiographic findings in RA [35]. The rotator cuff insufficiency provokes superior migration of the humeral head with medialization.

Larsen defined the widely used radiographic classification of rheumatoid shoulder in 1977. According to this classification, in stage 0: there is no sign on plain X-ray; stage I: arthritic changes with osteopenia and periarticular tissue swelling; stage II: narrowing of the joint space and erosions; stage III: cysts, increased loss of joint space, superior migration of the humeral head because of rotator cuff insufficiency; stage IV: loss of contours of the articular surface, flattening of the humeral head, medialization of the glenoid; and stage V: severe bony deformation with loss of joint contours and superior migration of the humeral head [36]. Ultrasonography (USG) is also a helpful tool in the shoulder joint. Thus radiography gives limited information about the soft tissue changes, USG could show possible pathologies of the periarticular tissues, especially at the beginning of the disease. It is easy to detect inflammatory changes in the subacromial space like bursitis, tendinitis of the long head of the biceps tendon and rotator cuff tears [37]. Magnetic resonance imaging (MRI) and computerized tomography (CT) are not needed for classification of the disease. But they are useful to answer some special questions like tumoral infiltration, fatty infiltration of the muscles and preoperative planning of shoulder arthroplasty [38, 39]. Evaluation of the degree of periarticular soft tissues is important when deciding on the best treatment strategy [33].

Amundsen et al. investigated the arthroplasty mortality rates for various aetiologies. A total of 214 RA patients were included and on the postoperative 90th day and first year, significantly higher mortality rate was encountered. Even though the highest mortality rate was encountered for fracture patients, RA patients' increased mortality rate must be kept in mind for surgical intervention [40].

Best treatment strategy takes into account the overall condition of the patient and the involvement of other joints. There might be need for lower limb surgery and the use of walking aids. Sometimes the involvement of other, distal joints in the upper arm affects the timing of shoulder surgery/reconstruction.
