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.