Microhardness Recovery Kinetics, Surface Roughness Trajectories, and Erosive Wear Susceptibility of Enamel After Three In-Office Bleaching Protocols: A 28-Day In Vitro Investigation

Background and Objectives: In-office bleaching is one of the most requested aesthetic procedures, but its biomechanical aftermath on enamel—particularly the recovery trajectory of microhardness, surface roughness, and erosive vulnerability—remains incompletely characterised. The present study quantified the 28-day mechanical recovery profile of enamel after three commonly used chairside bleaching protocols and examined inter-relationships between mechanical, topographic and erosive endpoints. Methods: Forty-two human molars and premolars (27 molars, 15 premolars) extracted for clinical reasons and previously catalogued in the institutional biobank were sectioned along the cervical–occlusal axis to obtain matched control and experimental halves. The experimental halves were assigned (n = 14 per group) to Opalescence Quick (45% carbamide peroxide, no light), Opalescence Boost (40% hydrogen peroxide, chemically activated), or BlancOne Ultra+ (35% hydrogen peroxide with light activation). Vickers microhardness (VHN), profilometric roughness (Ra), and erosive wear after a standardised citric-acid challenge were measured at baseline, immediately post-bleaching, and at 24 h, 7 d, 14 d, and 28 d in artificial saliva. Wilcoxon signed-rank, Kruskal–Wallis with Dunn–Bonferroni post hoc, linear mixed-effects models, multiple linear regression, ROC analysis, and Spearman correlations were used (α = 0.05). Results: Immediate VHN drops were −13.2 ± 3.9%, −22.6 ± 3.6%, and −29.6 ± 4.7% for Opalescence Quick, Opalescence Boost, and BlancOne Ultra+, respectively. By 28 days, recovery reached 97.4 ± 2.2%, 96.0 ± 2.9%, and 91.6 ± 2.3% of baseline (p < 0.001). Exponential rate constants were 0.137, 0.075, and 0.092 d−1. Erosive wear after acid challenge was 2.1×, 2.8×, and 3.8× control values. ROC analysis identified Δ-immediate Ra as the strongest predictor of incomplete recovery (AUC = 0.859). Conclusions: Higher-aggression protocols delayed mechanical recovery and amplified erosive susceptibility, with light-activated systems carrying the greatest residual risk. These in vitro findings provide an evidence base for the design of future clinical studies on post-bleaching enamel recovery and remineralisation.