Ihtisam Alam, Aravind R Kudva, S Vidhyadhara Shetty, Jayprakash Kukkila
Within the limitations of this in vitro study, blood contamination occurring during setting reduced the shear bond strength of Biodentine to resin composite and increased its discolouration. PDA pretreatment significantly improved bond strength in contaminated specimens only, abolishing the statistically significant contamination penalty, and did so without aggravating colour change.
INTRODUCTION: Calcium silicate cements such as Biodentine are frequently placed in a blood-contaminated field during vital pulp therapy and must subsequently be bonded to an overlying resin composite. Polydopamine (PDA) improves the wettability and bond strength of mineral trioxide aggregate to resin composite, but its effect on blood-contaminated Biodentine is unknown.
AIM: To determine the effect of PDA pretreatment on the shear bond strength (SBS), failure mode and colour change (ΔE) of blood-contaminated and uncontaminated Biodentine bonded to resin composite.
MATERIALS AND METHODS: Seventy-six standardised Biodentine specimens (5 mm diameter × 3 mm) were prepared with blood contamination (present/absent) and PDA pretreatment (present/absent) as the two factors (n = 19 per cell). After adhesive application, bulk-fill composite build-up and 45 days of storage at 37 °C, SBS was measured, failure modes and ΔE was analysed.
RESULTS: Blood contamination significantly reduced SBS [F(1,72) = 18.86, P < 0.001, partial η 2 = 0.21] and the contamination × PDA interaction was significant [F(1,72) = 7.39, P = 0.008, partial η 2 = 0.09], whereas the main effect of PDA was not [F(1,72) = 2.07, P = 0.155]. Simple-effect analysis showed that PDA increased SBS in contaminated specimens (6.44 → 7.77 MPa; mean difference 1.33 MPa, 95% CI 0.43-2.23; P = 0.004) but not in uncontaminated specimens (8.70 → 8.29 MPa; P = 0.368). Without PDA, contamination lowered SBS by 2.26 MPa (P < 0.001), whereas after PDA pretreatment the difference between contaminated and uncontaminated specimens was no longer significant (P = 0.254). Contamination significantly increased ΔE (P < 0.001) whereas PDA did not (P = 0.102); all groups exceeded the clinical acceptability threshold. Failure-mode distribution differed significantly among groups (Fisher-Freeman-Halton exact P = 0.021; Cramér's V = 0.30), cohesive failure within Biodentine predominating in the contaminated groups.
CONCLUSIONS: Within the limitations of this in vitro study, blood contamination occurring during setting reduced the shear bond strength of Biodentine to resin composite and increased its discolouration. PDA pretreatment significantly improved bond strength in contaminated specimens only, abolishing the statistically significant contamination penalty, and did so without aggravating colour change.