Influence of antiresorptive/antiangiogenic therapy on the extension of experimentally induced peri-implantitis lesions

Abstract

ObjectivesTo investigate the extension of experimentally induced peri-implantitis lesions under various antiresorptive and antiangiogenic medications.Material and methodsFourty-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.ResultsA 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.ConclusionsThe present analysis did not reveal any marked effects of various antiresorptive/ antiangiogenic medications on the extension of experimentally induced peri-implantitis lesions.Clinical relevanceThe extension of peri-implantitis lesions may not be facilitated by the antiresorptive and antiangiogenic medications investigated.