The present study aimed to investigate the impact of hardness from 3D printed transfer trays and dental crowding on bracket bonding accuracy. Lower models (no crowding group: Little’s Irregularity Index (LII) < 3, crowding group: LII > 7, n = 10 per group) were selected at random, digitized, 3D printed, and utilized for semiautomated virtual positioning of brackets and tubes. Hard and soft transfer trays were fabricated with polyjet printing and digital light processing, respectively. Brackets and tubes were transferred to the 3D printed models and altogether digitized using intraoral scanning (IOS) and microcomputed tomography (micro-CT) for assessment of linear and angular deviations. Mean intra- and interrater reliability amounted to 0.67 ± 0.34/0.79 ± 0.16 for IOS, and 0.92 ± 0.05/0.92 ± 0.5 for the micro-CT measurements. Minor linear discrepancies were observed (median: 0.11 mm, Q1–Q3: −0.06–0.28 mm). Deviations in torque (median: 2.49°, Q1–Q3: 1.27–4.03°) were greater than angular ones (median: 1.81°, Q1–Q3: 1.05°–2.90°), higher for hard (median: 2.49°, Q1–Q3: 1.32–3.91°) compared to soft (median: 1.77°, Q1–Q3: 0.94–3.01°) trays (p < 0.001), and torque errors were more pronounced at crowded front teeth (p < 0.05). In conclusion, the clinician should carefully consider the potential impact of hardness and crowding on bracket transfer accuracy, specifically in torque and angular orientation.

Objectives To investigate the extension of experimentally induced peri-implantitis lesions under various antiresorptive and antiangiogenic medications. Material and methods Fourty-eight albino rats had randomly received the following medications (dual application, n = 8 each): (1) amino-bisphosphonate (zoledronate) (Zo), (2) RANKL inhibitor (denosumab) (De), (3) antiangiogenic (bevacizumab) (Be), (4) Zo+Be, (5) De+Be, or (6) no medication (Co). Ligature- and lipopolysaccharide-induced peri-implantitis lesions were established at 2 maxillary implants over a period of 16 weeks. Histological (e.g., apical extension and surface area of the inflammatory cell infiltrate—aICT, ICT; defect length; defect width; CD68 positive cells) and bone micromorphometric (μCT) outcomes were assessed. The animal was defined as a statistical unit. Results A total of n = 38 animals (Zo = 6, De = 6, Be = 8, Zo + Be = 6, De + Be = 5, Co = 7) were analyzed. ICT’s were commonly marked by a positive CD68 antigen reactivity. Comparable median aICT (lowest—Zo: 0.53 mm; highest—Be: 1.22 mm), ICT (lowest—De + Be: 0.00 mm2; highest—Co: 0.49 mm2), defect length (lowest—Zo: 0.90 mm; highest—Co: 1.93 mm) and defect width (lowest—De+Be: 1.27 mm; highest—Be: 1.80 mm) values were noted in all test and control groups. Within an inner (diameter: 0.8 mm) cylindric volume of interest, the bone microstructure did not significantly differ between groups. Conclusions The present analysis did not reveal any marked effects of various antiresorptive/ antiangiogenic medications on the extension of experimentally induced peri-implantitis lesions. Clinical relevance The extension of peri-implantitis lesions may not be facilitated by the antiresorptive and antiangiogenic medications investigated.

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