Microbial and host‐derived biomarker changes during ligature‐induced and spontaneous peri‐implantitis in the Beagle dog

Abstract

Objective To evaluate microbial and host‐derived biomarker changes during experimental peri‐implantitis in the Beagle dog. Background Limited data exist on the microbial and biomarker changes during progressive bone loss as result of experimental peri‐implantitis. Methods In total, 36 implants (ndogs = 6) were assessed over 3 episodes of ligature‐induced peri‐implantitis followed by a period of spontaneous progression. Implants with hybrid (H) and completely rough (R) surface designs were used. Clinical and radiographic parameters were recorded at 4 timepoints. Peri‐implant sulcus fluid was collected from the buccal and lingual aspects of the implants. The presence of 7 bacterial species and 2 host‐derived biomarkers was assessed during the study period. Results Total bacterial counts were significantly correlated with marginal bone loss (MBL) (r = .21; P = .009). Further, Phorphyromonas gulae (Pg) and Tannerella forsythia (Tf) were commonly correlated with MBL, suppuration (SUP) and the sulcular bleeding index scores (mSBI) (P < .05). Other bacteria were further correlated with SUP, mSBI, and MBL. While the analyzed bacteria dropped, Prevotella intermedia (Pi) further increased during the spontaneous progressive phase (P < .05). Total bacterial load did not differ significantly between H and R implants. Host‐derived IL‐10 was undetected along the study period. IL‐1β positively correlated with probing pocket depth (r = .18; P = .03). During spontaneous progression, H implants displayed statistically significant lower levels of IL‐1β (P = .003). Conclusion Experimental peri‐implantitis is associated with an increase in bacterial counts. While Pg and Tf are associated with ligature‐induced disease progression, Pi augmented its load during the spontaneous progressive phase. IL‐1β is associated with pocket probing depth and influenced by implant surface characteristics during the spontaneous progression phase.

Inflammasomes in Alveolar Bone Loss

“…Radiographic bone loss greater than or equal to 2 mm beyond the crestal bone level from the initial surgery, or greater than or equal to 3 mm apical to the most coronal part of the intraosseous portion of the implant is observed in periimplantitis, with even greater progression than that in periodontitis (273). Similar to periodontitis, peri-implantitis exhibits higher IL-1b levels in diseased tissues, and these changes may persist despite nonsurgical therapy (274)(275)(276). Genetic polymorphisms in IL1B are related to the risk of periimplantitis and contribute to increased clinical parameters, such as peri-implant pocket depth, plaque index, and clinical attachment level (277).…”

One‐year outcomes of dental implants with a hybrid surface macro‐design placed in patients with history of periodontitis: A randomized clinical trial

“…Even though in the microbiological analysis using real-time PCR, there were no differences between the tested implants regarding the total bacterial counts, during the spontaneous progression phase, hybrid implants presented significantly lower levels of IL-1B. This differential biofilm pathogenicity associated with hybrid implants may be relevant on susceptible patients such as those evaluated in the present study (Monje et al, 2021).…”

What is the influence of implant surface characteristics and/or implant material on the incidence and progression of peri‐implantitis? A systematic literature review

“…The 25 included publications (Albouy et al, 2008, 2009, 2012; Almohandes et al, 2019; Berglundh et al, 2007; Carcuac et al, 2013, 2015, 2020; Cook, & Rust‐Dawicki, 1995; Favero et al, 2020; Fickl et al, 2015; Godoy‐Gallardo et al, 2016; Gotfredsen et al, 2002; Huang et al, 2018; Madi et al, 2013; Martins et al, 2004, 2005; Monje et al, 2019, 2020; Monje, Insua, Monje, et al, 2018; Monje, Insua, Rakic, et al, 2018; Namgoong et al, 2015; Roehling et al, 2019; Tillmanns et al, 1997, 1998) on pre‐clinical in vivo experiments (Table 1)—published between 1995 and 2020—are reporting on 18 different experiments, all involving healthy dogs (5–14 animals per experiment) and the experimentally induced peri‐implantitis model. Implant installation was performed after a healing period of 2–3 months post‐extraction of mandibular teeth.…”