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 shoulder OA affects approximately 3-5% of the population over 60 years. Radiographic changes are much more common, present in up to 30% of elderly patients.
• Gender: Women are more commonly affected than men (unlike hip OA which is more balanced).
• Bilateralism: Up to 15-20% of patients will develop bilateral disease requiring intervention.
• Trend: The demand for shoulder arthroplasty is the fastest growing of all joint replacements, with volume increasing by over 300% over the last two decades.
• Age Distribution: We are seeing a younger demographic (50-60 year olds) presenting with end-stage disease ("The Young OA Patient"), posing a unique biological and mechanical dilemma for longevity of reconstruction.

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.

• Trends: AOANJRR data shows rTSA volume exceeds aTSA volume since 2019. This is driven by expanded indications for rTSA (fracture, elderly OA).
• Prostheses: Cemented all-poly glenoids remain the gold standard for aTSA in Australia with best long-term survivorship.

Registry Data Insights (AOANJRR)

• Revision Rate: The cumulative percent revision of primary shoulder arthroplasty for OA is approximately 10% at 10 years.
• Age Effect: Younger patients have significantly higher revision rates. Patients under 55 years have nearly double the risk of revision compared to those over 75 years.
• Prosthesis Choice:
  • Total Shoulder Arthroplasty (TSA) has lower revision rates than Hemiarthroplasty for OA.
  • Reverse TSA revision rates for OA are comparable to Anatomic TSA in the short term, but long term data (over 15 years) is still maturing compared to the 20+ year data we have for Anatomic.
• Fixation: Cemented glenoid components have superior survivorship compared to uncemented metal-backed glenoids in Anatomic TSA.

Practice Points for the Fellowship Exam

• Be able to quote the "10% at 10 years" figure.
• Understand why metal-backed glenoids failed in the past (polyethylene dissociation, over-stiffening of construct).
• Recognize that while Reverse TSA usage is exploding, Anatomic TSA remains the functional gold standard for the "young" (60-75) patient with an intact cuff.
• Be aware of the "Volume-Outcome" relationship in shoulder arthroplasty (surgeons doing over 10 per year have significantly lower complication rates).
• Know the indications for a Hemi-arthroplasty are now extremely limited in Australia (Concept of "Hemi is for Head, Total is for Training, Reverse is for Revision" is outdated - Reverse is now workhorse).