Inflammatory Arthritis of the Shoulder

Definition. Inflammatory arthritis of the shoulder includes rheumatoid arthritis and seronegative, crystal and other inflammatory disorders affecting synovium, cartilage, bone, tendon and bursa. The imaging patterns overlap, so systemic context and exclusion of infection are essential.

Epidemiology. Shoulder symptoms are common in established inflammatory arthritis, but the historical prevalence estimates predate modern disease control. Modern DMARD and biologic therapy has changed the surgical case mix. Involvement is commonly bilateral, although asymmetry and alternative shoulder pathology are common too.

The synovium. Normal synovium is thin, only a few cell layers deep. The bare area is the bone that lies within the capsule but is not covered by cartilage (the surgical neck and the glenoid neck, for example), and it is the site of the initial marginal erosions in RA.

The cuff. An intact rotator cuff allows concentric rotation of the humeral head. A massive tear leads to cuff tear arthropathy, with superior migration or escape of the head.

In RA the synovium is the primary site of pathology, in contrast to OA, where cartilage wear is the primary event. Inflammatory shoulder disease may be synovium-driven, but the phenotype varies.

Synovitis. The rheumatoid synovium undergoes massive hypertrophy and angiogenesis and forms pannus. Hypertrophic, vascular synovium may also produce an effusion and rice bodies.

Erosion and cartilage loss. Inflammatory mediators damage cartilage and marginal and subchondral bone.

Tendon and bursa. The pannus releases enzymes (collagenase, metalloproteinases) that attack the rotator cuff tendons from the undersurface. Supraspinatus is the tendon most commonly affected, the biceps is often inflamed (tenosynovitis) or ruptured, and the subacromial-subdeltoid bursa may be involved.

How often the cuff is torn. Full-thickness tears are common, conventionally reported in roughly a quarter to a half of RA shoulders. The range is wide because the figure depends on disease duration, imaging modality and whether the cohort predates biologic control. What matters operatively is not the population rate but this patient's cuff, because cuff function is one of the variables that selects anatomic against reverse arthroplasty.

The end stage. Central migration, deformity or cuff insufficiency may develop, but none is universal or disease-specific.

Mimics. Infection, CPPD, hydroxyapatite disease and proliferative synovial disorders can look inflammatory.

The seronegative spondyloarthropathies (psoriatic arthritis, ankylosing spondylitis, reactive and enteropathic arthritis) behave differently from RA in ways examiners probe.

Serology and the primary lesion. They are RF- and anti-CCP-negative and HLA-B27-associated. The primary lesion is enthesitis, inflammation where tendon, ligament or capsule inserts into bone, rather than the synovial pannus that drives RA, although a secondary synovitis also occurs.

Radiology. The signature is mixed erosive and proliferative, not purely erosive: alongside the erosions there is new bone formation (enthesophytes, periostitis) and a tendency to ankylosis (bony fusion). Psoriatic arthritis classically produces the pencil-in-cup deformity and can swing between an erosive-mutilating form (arthritis mutilans) and a bone-forming one. Ankylosing spondylitis tends toward a stiff, ankylosed glenohumeral joint, often with supero-lateral humeral-head erosion (the "hatchet" head), and is accompanied by sacroiliitis and spinal disease.

Surgical implications. The arthroplasty decision still hinges on cuff integrity and glenoid bone stock, as in RA, and the perioperative principles are shared: infection risk, osteopenia, holding biologics. Ankylosing spondylitis adds its own hazards:

• A stiff, ankylosed shoulder that is harder to mobilise
• A rigid kyphotic cervical spine that is brittle and difficult to intubate, with a high fracture risk on positioning
• A higher rate of heterotopic ossification after arthroplasty

Medical control. TNF and IL-17 inhibitors are central for axial spondyloarthritis and psoriatic disease, whereas methotrexate, a mainstay in RA, is less effective for axial AS.

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Neer's classic description of the rheumatoid stages guides the decision between soft-tissue procedures (synovectomy) and reconstruction. Larsen grading quantifies radiographic joint destruction.

History. Morning stiffness typically lasts over an hour. Ask about systemic symptoms (fatigue, malaise) and other joints, particularly the hands and feet. Nocturnal pain is common, and function is often poor because stiffness combines with weakness of the cuff.

Examination. Look for wasting of the spinati and a boggy swelling anteriorly, and feel for warmth, effusion and tenderness. Cuff strength is often reduced, from pain or from a tear; lag signs indicate a massive tear.

RA or OA? Rheumatoid disease may produce synovitis, periarticular osteopenia, marginal erosions, cartilage loss, cuff and biceps pathology, and central migration; the combination and severity vary with disease duration and control. Primary OA more often shows osteophytes, sclerosis and asymmetric glenoid wear, but posterior wear is not universal and cuff status must be assessed independently.

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Blood tests. The laboratory screen:

• ESR and CRP - markers of active inflammation
• RF and anti-CCP - specific for RA
• Full blood count - anaemia of chronic disease, or leukopenia (Felty's)

Radiographs. AP, Grashey and axillary lateral views. The rheumatoid findings:

• Periarticular osteopenia ("washed out"), which affects fixation and fracture risk
• Marginal erosions
• Symmetric joint space narrowing
• Central migration of the head (acetabularisation)
• A high-riding head, which indicates a massive cuff tear

CT and MRI. Together they guide the choice between anatomic and reverse arthroplasty. CT is essential for glenoid version and bone stock, including central erosion; MRI is essential for rotator cuff integrity, which is critical for implant choice.

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Synovial fluid. Aspirate when the diagnosis is unclear or infection (septic arthritis) is suspected. Rheumatoid fluid is inflammatory, with a white cell count of 2,000-50,000, and is cloudy, of low viscosity and low in glucose.

Before surgery. The preoperative work-up:

• Disease control and medication - review the DMARD schedule with the rheumatologist and coordinate systemic treatment
• Cervical spine - flexion-extension radiographs to rule out atlantoaxial instability when neck symptoms, neurology or risk factors indicate them; respiratory risk is likewise assessed as clinically indicated
• Cardiac - risk stratification
• Skin - inspect its integrity and healing risk
• Glenoid and humeral bone - plan fixation and reconstruction
• Sepsis - culture or biopsy when the diagnosis is uncertain

Rice bodies are a marker of chronic inflammatory synovitis, and they carry an important "do not miss".

What they are. Small, smooth, white, ovoid intra-articular or intra-bursal loose bodies that resemble grains of polished rice, also called "melon-seed bodies". They are made of fibrin, collagen and degenerated or infarcted synovial fragments, formed when chronically inflamed hypertrophic synovium sheds and the fragments become encased in fibrin. They can fill the glenohumeral joint and, characteristically at the shoulder, the subacromial-subdeltoid bursa.

The tuberculosis caveat. The common associations are rheumatoid arthritis and juvenile idiopathic arthritis, but rice bodies are classically described in tuberculous and atypical-mycobacterial synovitis and tenosynovitis. Finding them, especially in a monoarticular or atypical presentation, should always prompt exclusion of tuberculosis.

Imaging. Rice bodies are largely radiolucent and poorly seen on plain radiographs, being isodense to fluid, so a plain film mostly shows the background arthropathy. They are best demonstrated on MRI, as myriad small bodies of low-to-intermediate T1 and low T2 signal within a distended joint or bursa, or on ultrasound.

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Management. Rice bodies are removed at synovectomy, open or arthroscopic, together with the diseased synovium; recurrence tracks ongoing synovitis, so disease control matters. Always send the synovium and bodies, and the fluid, for acid-fast staining, mycobacterial culture and histology to exclude an infective (mycobacterial) cause before attributing them to RA alone.

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Choosing the operation. Implant choice depends on the cuff and the bone, and on the deltoid, deformity and the patient's goals as well; cuff status alone does not select one arthroplasty.

Medical management. NSAIDs, DMARDs (methotrexate) and biologics (TNF-alpha inhibitors), with regular monitoring. Physiotherapy is gentle range of motion, avoiding aggressive strengthening if the cuff is fragile. Corticosteroid injection has a limited role because of the risk of infection and cuff atrophy.

Arthroscopic synovectomy. Indicated in the wet stage (active synovitis) with a preserved joint space and an intact cuff. The goal is to reduce pain and slow enzymatic destruction; it does not stop long-term progression. Reported pain relief is good in the short term, but the published series are small and uncontrolled and no study on this page quantifies it, so counsel improvement rather than a percentage.

Hemiarthroplasty. Indicated for severe glenoid bone loss and cuff tear arthropathy (historical). Pain relief is less reliable, with metal articulating on eroded bone.

Anatomic total shoulder arthroplasty. Needs an intact rotator cuff and adequate glenoid bone stock, and gives superior pain relief to hemiarthroplasty.

Reverse total shoulder arthroplasty. Indicated for a rotator cuff tear, severe glenoid erosion or the elderly patient, and becoming standard for many RA shoulders.

Anatomic TSA. Use a deltopectoral approach and handle the fragile soft tissues gently. The subscapularis is often thin and friable and needs careful takedown and repair. Central wear may need eccentric reaming or an augmented glenoid component, and pegged ingrowth components are preferred over cemented ones for better bone preservation.

Reverse TSA. Also deltopectoral. If central erosion is severe, medialise the reaming or use bone graft, and use long-peg baseplates in osteopenic bone. A "stove-pipe" humerus often requires a cemented stem. Deltoid tension is key.

Rehabilitation. The protocol runs in phases:

1. 0-6 weeks - sling, passive range of motion only to protect the subscapularis repair, pendulums
2. 6-12 weeks - active assisted range of motion, pulleys
3. 3-6 months - active range of motion, gentle strengthening
4. 6 months onwards - full activity

In RA. Soft-tissue repairs such as the subscapularis take longer to heal. Osteopenia makes aggressive passive stretching a fracture risk, and the skin needs care with dressings and tape because it tears.

Pain and function. Arthroplasty, anatomic or reverse, gives reliable and substantial pain relief in RA: the Mayo series recorded significant long-term relief with both anatomic TSA and hemiarthroplasty (p less than 0.0001). Function is less predictable than in OA, because of the muscles and cuff.

Reading the survivorship figures. Be careful here: the arthroplasty registries do not separate inflammatory arthritis cleanly, and the RA-specific series are small or historical.

Anatomic TSA and hemiarthroplasty. The Mayo cohort (Sperling, operated 1976-1991) shows durable pain relief with anatomic TSA and a lower revision risk than hemiarthroplasty when the cuff was intact. Radiographic glenoid lucency was nonetheless present in 72% of those TSAs, and glenoid erosion in 98% of hemiarthroplasties. Hemiarthroplasty brings lower satisfaction and ongoing glenoid-sided pain, with progressive erosion the predictable failure mode.

Reverse TSA. There are no long-term RA-specific survivorship data. The Young series is 18 shoulders at a mean 3.8 years with no revisions, which is far too short to quote a ten-year figure.

Overall. Surgery significantly improves quality of life, but complication rates (infection, fracture) are higher than in OA.

Global epidemiology:

• RA affects roughly 0.5–1% of adults worldwide; shoulder symptoms develop in the majority over the disease course and involvement is frequently bilateral.
• Female-to-male ratio approximately 3:1; peak onset in the fourth-to-sixth decades.
• Widespread early use of methotrexate and biologic DMARDs has reduced the incidence of end-stage erosive shoulder disease and of synovectomy/early arthroplasty compared with historical cohorts — a trend seen across high-income health systems.

These are legitimate debates, and examiners reward a balanced answer that acknowledges the uncertainty rather than a dogmatic one.

Anatomic TSA or reverse in the cuff-intact RA shoulder. With an intact cuff, anatomic TSA gives better rotation and preserves bone, but progressive cuff attrition is intrinsic to RA and may cause later glenoid loosening ("rocking horse"). Some surgeons favour primary reverse arthroplasty in older RA patients to pre-empt this, accepting reduced rotation and notching. No high-level trial resolves the trade-off.

Holding biologics. The optimal hold interval is extrapolated from low-grade, mostly retrospective data; recommendations are consensus (Guideline-level), and the magnitude of infection reduction is uncertain. Over-holding risks a disabling flare.

Continuing or stopping methotrexate. Continuing is now standard, but practice still varies in patients with renal impairment or concurrent high-dose steroids.

The role of synovectomy. Its value in the biologic era is debated, and it is increasingly limited to medically refractory synovitis with preserved cartilage.

The glenoid component in soft bone. Whether to implant a glenoid (better pain relief) or accept hemiarthroplasty or ream-and-run (lower loosening risk) in severely osteopenic, eroded glenoids remains individualised.

Cervical spine clearance. Routine flexion-extension films before every RA arthroplasty are traditional teaching, but selective imaging guided by symptoms and examination is increasingly advocated.