Histological characteristics of advanced peri-implantitis bone defects in humans

Maria Elisa Galárraga-Vinueza,Frank Schwarz,Ricardo Magini,Reinhard Gruber,Karina Obreja,Stefan Tangl,Marco Bianchini

doi:10.1186/s40729-020-00208-8

Abstract

BackgroundInflammatory osteolysis is the clinical hallmark of peri-implantitis. The morphology of the remaining peri-implant bone and the level of osseointegration, however, remain unknown. Our aim was to characterize advanced peri-implantitis bone defects in humans.MethodsFour patients (3 female and 1 male) were diagnosed with peri-implantitis. A total of 5 implants with machined surfaces and a mean loading time of 12 ± 6 years were removed due to advanced bone loss. The defect extension, the peri-implant bone density (bone area per tissue area in percentage), bone-to-implant contact (%), and the number of filled and empty osteocyte lacunae were calculated based on undecalcified histological specimens.ResultsThe defect extension was on average 4.2 mm (95% CI 0.8–3.4). Remaining peri-implant bone showed a high density of 85.5% (95% CI 79.1–91.3) and covered in total 74% (95% CI 70.5–77.5) of the implant surface. Filled and empty osteocyte lacunae density was on average 191 and 165/mm2 (95% CI 132–251; 103–225), respectively. Histology further revealed signs of ongoing bone formation and resorption.ConclusionThere are signs that suggest that once the original cortical bone is lost due to peri-implantitis, the remaining apical trabecular bone is reinforced and transformed into cortical bone that might take over the functional load.

Highlights

Inflammatory osteolysis is the clinical hallmark of peri-implantitis
Peri-implantitis was defined as the combination of bleeding on gentle probing (BOP) with or without suppuration, probing depths (PD) ≥ 6 mm, and radiographic marginal bone loss (MBL) [2]
The mean defect length amounted to 4.7 mm

Summary

Introduction

Inflammatory osteolysis is the clinical hallmark of peri-implantitis. Our aim was to characterize advanced peri-implantitis bone defects in humans. Considering that the remaining peri-implant bone has to adapt to occlusal load [15], it requires vital osteocytes to translate mechanical forces into molecular signals controlling bone adaptation [16]. It requires vital osteocytes for inflammatory osteolysis [17]. These biological principles let us to hypothesize that the bone in peri-implantitis defects has a high density and contains vital osteocytes

Objectives

Methods

Results

Discussion

Conclusion