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In Vitro Effects of Streptococcus oralis Biofilm on Peri-Implant Soft Tissue Cells.

ABSTRACT: Human gingival epithelial cells (HGEps) and fibroblasts (HGFs) are the main cell types in peri-implant soft tissue. HGEps are constantly exposed to bacteria, but HGFs are protected by connective tissue as long as the mucosa-implant seal is intact. Streptococcus oralis is one of the commensal bacteria, is highly abundant at healthy implant sites, and might modulate soft tissue cells-as has been described for other streptococci. We have therefore investigated the effects of the S. oralis biofilm on HGEps and HGFs. HGEps or HGFs were grown separately on titanium disks and responded to challenge with S. oralis biofilm. HGFs were severely damaged after 4 h, exhibiting transcriptional inflammatory and stress responses. In contrast, challenge with S. oralis only induced a mild transcriptional inflammatory response in HGEps, without cellular damage. HGFs were more susceptible to the S. oralis biofilm than HGEps. The pro-inflammatory interleukin 6 (IL-6) was attenuated in HGFs, as was interleukin 8 (CXCL8) in HGEps. This indicates that S. oralis can actively protect tissue. In conclusion, commensal biofilms can promote homeostatic tissue protection, but only if the implant-mucosa interface is intact and HGFs are not directly exposed.

SUBMITTER: Ingendoh-Tsakmakidis A

PROVIDER: S-EPMC7290395 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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In Vitro Effects of Streptococcus oralis Biofilm on Peri-Implant Soft Tissue Cells.

Ingendoh-Tsakmakidis Alexandra A Eberhard Jörg J Falk Christine S CS Stiesch Meike M Winkel Andreas A

Cells 20200515 5

Human gingival epithelial cells (HGEps) and fibroblasts (HGFs) are the main cell types in peri-implant soft tissue. HGEps are constantly exposed to bacteria, but HGFs are protected by connective tissue as long as the mucosa-implant seal is intact. Streptococcus oralis is one of the commensal bacteria, is highly abundant at healthy implant sites, and might modulate soft tissue cells-as has been described for other streptococci. We have therefore investigated the effects of the S. oralis ...[more]

PMID: 32429151

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Project description:ObjectivesSoft tissue phenotype modification (STPM) could be performed to maintain peri-implant health. Therefore, the aim of the study was to analyze tissue alteration around implants following soft tissue phenotype modification during implant uncovering surgery.Materials and methodsPatients who had STPM (either pouch roll or modified roll technique) during implant second-stage surgery with at least 12-month follow-up were included. Clinical and radiographic parameters including mucosal tissue thickness (MTT), recession (REC), keratinized mucosa width (KMW), probing pocket depth (PPD), marginal bone loss (MBL), emergence profile, and emergence angle were extracted from 2-week, 2-month, and 12-month visits after second-stage surgery.ResultsTwenty-eight patients with 33 implants that fulfilled the inclusion criteria were included. After soft tissue phenotype modification, at 2 weeks, REC was negatively correlated to mean MTT at mid-buccal site (r = - 0.41, p = 0.018) and borderline correlated at mid-lingual site (r = - 0.343, p = 0.051). Stable KMW was maintained from 2 weeks to 12 months with minimal shrinkage rate (3 ~ 14%). MBL change was limited (0.24 ~ 0.47 mm) after STPM. All implants had shallow PPD (≤ 3 mm) with the absence of bleeding on probing. Emergence angle at the mesial side, however, was significantly correlated to surgical techniques, which indicated pouch roll technique would have 6.96 degrees more than modified roll technique (p = 0.024).ConclusionsSoft tissue phenotype modification, either pouch roll or modified roll technique, during uncovering surgery resulted in favorable clinical outcomes. Thin mucosal tissue thickness and pouch roll technique are the factors related to more recession at 2 weeks. Pouch roll technique could influence the restorative design by having a wide emergence angle at the mesial side.Clinical relevanceModified and pouch roll techniques during uncovering surgery were viable methods to yield favorable peri-implant health, while the preciseness of pouch roll technique was required to avoid mucosal recession and inadequate restorative design.

Project description:Oral health is associated with a symbiotic microbial community and host-microbe homeostasis is maintained by the controlled immune response. Various factors can disrupt this homeostasis. Dysbiosis, which is characterized by increased immune response and a shift in the microbiome, contributes the pathogenesis of peri-implantitis. Peri-implant mucosa and commensal bacteria play important roles in the maintenance of host-microbe homeostasis, but little is known about how they interact. We have therefore investigated the early host-microbe interaction between a commensal multispecies biofilm (Streptococcus oralis, Actinomyces naeslundii, Veillonella dispar, Porphyromonas gingivalis) and peri-implant mucosa at 24 and 48 h. Our in vitro peri-implant mucosa-biofilm model contained organotypic oral mucosa, implant material and biofilm. After 24 h, the biofilm induced a modest innate immune response in the peri-implant mucosa by the upregulation of 5 genes related to immune and inflammatory response and the increased secretion of IL-6 and CCL20. This controlled immune response protected tissue integrity and the peri-implant mucosa remained intact. The secreted antibacterial proteins human β-Defensins-1, -2, and CCL20 controlled the overgrowth of the biofilm by reducing its volume - without affecting the live/dead ratio or bacterial distribution. Thus, host-microbe homeostasis was established within the first 24 h. In contrast, host-microbe homeostasis was disrupted after 48 h. The mucosa was damaged and detached from the implant, due to the induced downregulation of cell adhesion related genes. The immune response was enhanced by upregulation of additional genes related to the immune and inflammatory response and increased secretion of IL-1β, TNF-α, and CCL20. Moreover, bacterial distribution was altered, with an increased proportion of V. dispar. The disrupted host-microbe homeostasis could lead to incipient dysbiosis. This deeper understanding of the early host-microbe interaction at the peri-implant site may provide the basis for new strategies to improve the prevention and therapy of peri-implant diseases.

Dataset Information

In Vitro Effects of Streptococcus oralis Biofilm on Peri-Implant Soft Tissue Cells.

Publications

In Vitro Effects of <i>Streptococcus oralis</i> Biofilm on Peri-Implant Soft Tissue Cells.

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