Glenoid retroversion associates with deltoid muscle asymmetry in Walch B-type glenohumeral osteoarthritis.

Background: The etiologies of glenohumeral osteoarthritis (GHOA) and eccentric glenoid wear within GHOA are unknown, but muscular imbalance may play a role. The purpose of the present study was to determine the relationship between deltoid muscle area, GHOA, and eccentric glenoid wear. We hypothesized that patients with GHOA would have overall deltoid atrophy as compared with controls and that increasing posterior deltoid areas would associate with glenoid retroversion in the Walch B-type (eccentric) GHOA group.

Methods: The study was a retrospective review of computed tomography imaging studies. We included a control group of subjects without GHOA and a group of individuals with GHOA before undergoing total shoulder arthroplasty. We assigned Walch types via consensus. Cross-sectional area was measured for the anterior and posterior deltoid musculature demarcated via the scapular line, normalized to the total deltoid area. Absolute and normalized total, anterior, and posterior deltoid areas were compared between controls and the entire GHOA group. Normalized anterior and posterior deltoid areas were compared between Walch A-type and B-type GHOA patients within the GHOA group. Univariate linear regression was used to evaluate for an association between glenoid retroversion and normalized posterior deltoid areas in controls, Walch A-type, and Walch B-type patients. Multivariate linear regression analysis was used to evaluate the effects of normalized posterior deltoid area, age, sex, and height on glenoid retroversion within the Walch B-type subgroup.

Results: We included 99 patients with GHOA and 47 controls. The control and GHOA patients did not differ in absolute deltoid areas (21.8 ± 8.8cm vs. 20.6 ± 7.9cm;  = .488). Patients with GHOA had a statistically significant increase in normalized posterior deltoid area (0.50 ± 0.10 vs. 0.46 ± 0.10;  = .032) and a reciprocal decrease in normalized anterior deltoid area (0.50 ± 0.10 vs. 0.54 ± 0.10;  = .040) compared with controls. Walch A-type and B-type patients did not differ in normalized posterior deltoid areas (0.50 ± 0.11 vs. 0.50 ± 0.10;  = .780). Normalized posterior deltoid area positively associated with glenohumeral retroversion in Walch B-type GHOA (R = 0.102;  = .020), a relationship maintained in multivariate linear regression, using gender, age, and height as covariates (standardized beta = 0.309,  = .027).

Conclusion: GHOA is not associated with deltoid atrophy, calling into question the suggestion that periarticular muscular atrophy in GHOA is secondary to disuse. Increasing normalized posterior deltoid area associates with increased glenoid retroversion in patients with Walch B-type glenoid morphology. Muscular imbalance may play a role in the etiology or progression of the glenoid deformity observed in eccentric GHOA.