Shoulder Osteoarthritis

Definition Glenohumeral osteoarthritis (GHOA) is a chronic, degenerative condition characterized by the progressive loss of articular cartilage, subchondral sclerosis, cyst formation, and osteophyte development. It leads to significant pain, stiffness, and functional limitation. While often considered a disease of "wear and tear", the pathophysiology involves a complex interplay of mechanical, biochemical, and genetic factors. It is the end-stage of joint failure.

Epidemiology

• Prevalence: Symptomatic glenohumeral OA affects roughly 3-5% of people over 60 years; radiographic changes are far more common (up to ~30% of the elderly).
• Sex: Primary GHOA affects men and women in broadly similar numbers (approximately 1:1), in contrast to the female predominance of hand and knee OA.
• Bilateralism: A substantial minority develop clinically significant bilateral disease over time.
• Trend: Shoulder arthroplasty is among the fastest-growing joint replacements globally, driven largely by the expansion of reverse TSA indications.
• Age Distribution: An increasing younger cohort (50-60 years) presents with end-stage disease ("the young OA patient"), posing a biological and mechanical dilemma for reconstruction longevity.

Pathophysiology of Progression The disease follows a predictable pattern of degeneration, often described in four stages:

1. Cartilage Fibrillation: Initial softening and focal loss of cartilage, usually starting on the glenoid center. This asymptomatic phase can last years.
2. Posterior Erosion: As the anterior capsule tightens and the posterior capsule stretches, the humeral head subluxates posteriorly. This eccentric loading causes preferential wear of the posterior glenoid rim. This creates the classic Walch B2 (Biconcave) deformity, where the humeral head carves a second articular surface ("Neoglenoid") while the anterior native surface ("Paleoglenoid") remains relatively preserved.
3. Osteophyte Formation: Large osteophytes form in the inferior recess of the joint. The inferior humeral osteophyte, known as the "Goat's Beard", effectively increases the articular surface area to distribute load but mechanically blocks adduction and rotation. These osteophytes can become massive, obliterating the axillary pouch and wrapping around the surgical neck.
4. Contracture and Stiffness: The subscapularis muscle and anterior capsule become fibrotic and contracted. This leads to the characteristic fixed internal rotation contracture (loss of External Rotation). The patient loses the ability to "cock the arm" for throwing or reach behind the head. The posterior capsule becomes attenuated and lax.

Etiology Details

• Primary: Idiopathic osteoarthritis is the most common form. There is a strong genetic component.
• Secondary Causes:
  • Post-traumatic: Intra-articular fractures (Head split, impression fractures) or previous dislocation damage. Malunion of tuberosities can also alter mechanics leading to eccentric wear.
  • Capsulorraphy Arthropathy: A specific iatrogenic form of OA caused by historical instability surgeries (Putti-Platt, Magnuson-Stack) where the anterior structures were over-tightened, forcing the head posteriorly and grinding out the joint (like a mortar and pestle).
  • Metabolic: Hemochromatosis ("Iron Fist, Iron Shoulder"), Gout, CPPD (Chondrocalcinosis).
  • Osteonecrosis: Collapse of the humeral head leading to secondary glenoid wear. Common after prolonged steroid use or alcohol abuse.
  • Post-infectious: Cartilage destruction from previous septic arthritis (Chondrolysis). Prior history of staph aureus infection is a red flag.
  • Inflammatory: Rheumatoid Arthritis (RA), Psoriatic Arthritis, Ankylosing Spondylitis.
    • RA Specifics: RA causes concentric central erosion ("Acetabularization") due to pannus, rather than posterior wear. The bone is osteopenic. The cuff is often thin or torn.
  • Neuropathic: Charcot arthropathy (Syringomyelia, Diabetes). Characterized by massive destruction and debris.

Molecular Pathogenesis At a cellular level, OA is an active metabolic disorder, not just passive wear.

• Cytokines: IL-1 and TNF-alpha drive catabolic enzymes (MMPs) which degrade the collagen type II matrix.
• Chondrocytes: Undergo senescence and apoptosis.
• Subchondral Bone: Increases in stiffness (sclerosis), transferring more load to the cartilage, accelerating wear (a vicious cycle).
• Osteophytes: Driven by TGF-beta and BMPs in an attempt to stabilize the joint surface area.

Normal Anatomy

• Version: The glenoid is naturally retroverted ~2-8 degrees relative to the scapular body, but the scapula is anteverted on the chest wall.
• Mismatch: The radius of curvature of the glenoid is larger than the humeral head (Mismatch ratio), allowing translation. In OA, this mismatch is lost as the joint becomes congruent and stiff.

Pathoanatomy of OA

• Glenoid: Retroversion is the hallmark. The posterior lip wears down, creating a slope that pushes the head out the back.
• Humerus: Flattens and enlarges (hypertrophic OA).
• Soft Tissues:
  • Subscapularis: Shortened/Contracted.
  • Posterior Capsule: Stretched/Attenuated.
  • Biceps: Often frayed or subluxed/dislocated medially.

Imaging Protocol and Interpretation

Deep Infection (PJI)

• Incidence: Under 1% for primary cases, higher for revision.
• Organism: Cutibacterium acnes (formerly Propionibacterium) is the dominant pathogen. It is a slow-growing anaerobe that colonizes the hair follicles (dermoglandular unit).
• Diagnosis: Difficult. ESR/CRP often normal. X-rays may show nonspecific loosening. Definitive diagnosis requires tissue culture held for 14 days.
• Prevention: Benzoyl peroxide prep pre-op, minimizing traffic, laminar flow, vancomycin powder (debated).

Glenoid Loosening

• Incidence: The most common mode of long-term failure in aTSA.
• Mechanism: "Rocking horse" phenomenon. If the head is not centered (due to cuff imbalance or uncorrected retroversion), eccentric loading occurs at the glenoid edge, toggling the component until the cement bond fails.
• Radiology: Radiolucent lines over 2mm around the pegs/keel.

Subscapularis Failure

• Mechanism: Rupture of the repair or failure to heal.
• Consequence: Anterior instability (dislocation), loss of active internal rotation, pain.
• Risk Factors: Aggressive early rehab, poor tissue quality, over-tensioning.
• Pectoralis Major Transfer: Salvage option for irreparable subscapularis.

• Survival: ~90% at 10 years, 80% at 15 years.
• Function: aTSA provides better range of motion (internal/external rotation) compared to Reverse TSA.
• Constraint: aTSA allows the patient to do more "normal" activities but heavy loading is discouraged to protect the glenoid.

Global Epidemiology

• Symptomatic GHOA affects ~3-5% of adults over 60; radiographic disease is far more prevalent. Demand for shoulder arthroplasty is rising faster than for hip or knee, driven chiefly by expanding reverse TSA indications across high-income health systems.
• Younger, higher-demand patients (under 60) form a growing share of arthroplasty referrals worldwide and consistently show higher revision rates.

Society Guidance, Side by Side

Registry Evidence (Joint Picture)

• Revision rate: National joint registries (AOANJRR, NJR UK, the Nordic registries) report cumulative revision of primary shoulder arthroplasty for OA in the region of ~5-10% at 10 years.
• Age effect: Younger patients (under 55) have roughly double the revision risk of patients over 75 — consistent across registries.
• Prosthesis choice: Total shoulder arthroplasty has lower revision rates than hemiarthroplasty for OA. Reverse TSA revision rates are broadly comparable to anatomic TSA in the short-to-medium term, but very long-term (over 15 years) data remain richest for anatomic TSA.
• Fixation: Cemented all-polyethylene glenoids show superior survivorship to uncemented metal-backed glenoids in anatomic TSA (metal-backed designs failed through polyethylene dissociation and construct over-stiffening).

High- vs Limited-Resource Practice Variation

• Well-resourced settings: Routine preoperative 3D CT planning, patient-specific instrumentation or navigation, and an increasing default to reverse TSA for elderly and deformed glenoids.
• Resource-limited settings: CT and modern implants may be scarce; hemiarthroplasty or non-operative management retains a larger role, and stemmed cemented implants are often preferred for availability and cost.

Exam-Ready Practice Points

• Quote a revision figure in the "~5-10% at 10 years" range and note the strong age effect.
• Understand why metal-backed glenoids fell out of favour (polyethylene dissociation, construct over-stiffening).
• Reverse TSA usage is expanding rapidly, but anatomic TSA remains the functional benchmark for the intact-cuff patient with adequate glenoid bone stock.
• Higher-volume surgeons and centres have lower complication rates (volume-outcome relationship).
• Indications for hemiarthroplasty are now narrow (very young patients for bone preservation, insufficient glenoid bone stock, or AVN with a spared glenoid).