Document Type : RESEARCH PAPER
Authors
1
Levitetz Department of Orthopedic Surgery, Cleveland Clinic Florida, Weston, FL
2
Department of Orthopedic Surgery, Rothman Orthopedic Institute, PA, USA
10.22038/abjs.2026.95223.4279
Abstract
Objective: Glenohumeral osteoarthritis (OA) is a common degenerative condition, with total shoulder arthroplasty (TSA) often representing the definitive treatment for end-stage disease. Use of glucagon-like peptide-1 receptor agonists (GLP-1RAs) has risen sharply, and recent evidence suggests potential disease-modifying effects and reduced arthroplasty rates in lower-extremity joints. This study evaluated whether GLP-1RAs use influences progression of primary shoulder OA to TSA.
Methods: A retrospective database query was performed to identify patients diagnosed with primary shoulder OA, excluding those with other shoulder pathology. Patients were stratified by preoperative GLP-1RAs prescription, and were 1:1 propensity-score matched to balance relevant comorbidities. Outcomes included incidence of TSA, TSA-free survival (Kaplan-Meier survival analysis), major joint injections, and mean levels of inflammatory biomarkers (CRP, ESR, and cortisol). p<0.05 was set as significance threshold.
Results: After matching, each cohort included 24,669 patients. The GLP-1RAs cohort had a significantly shorter follow-up (731 ± 694 vs 1,220 ± 1,006 days, P<0.001). TSA incidence was higher among GLP-1RAs users (2.25% vs 1.77%; P<0.001), with lower TSA-free survival rates (95.50% vs 97.23%, log-rank P<0.001). A greater proportion of GLP-1RAs patients received major joint injections (18.93% vs 16.87%; P<0.001), with lower mean number of injections per patient (2.48 ± 2.86 vs 2.74 ± 3.23, P<0.001). GLP-1RAs users demonstrated significantly lower average CRP and ESR levels (P<0.001 both), with similar cortisol average values.
Conclusion: Unlike findings reported in hip and knee OA, GLP-1RAs did not appear protective against progression to TSA in primary shoulder OA. Further studies are warranted to clarify the joint-specific mechanisms underlying these differences.
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