Osteoimmunological mechanisms involved in orthodontically and bacterially induced periodontal stressJ Orofac Orthop

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Authors
A. Konermann, W. Götz, D. Wohlleber, P. Knolle, J. Deschner, A. Jäger
Year
2012
DOI
10.1007/s00056-012-0102-3
Subject
Oral Surgery / Orthodontics

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Text

430 J Orofac Orthop 2012 · No. 6 © Springer-Verlag

Journal of Orofacial Orthopedics

Fortschritte der Kieferorthopädie Original article

J Orofac Orthop 2012; 73:430-439

DOI 10.1007/s00056-012-0102-3

Osteoimmunological mechanisms involved in orthodontically and bacterially induced periodontal stress

Osteoimmunologische Mechanismen bei orthodontisch sowie bakteriell induziertem parodontalem Stress

Abstract

Background and objective. Orthodontic tooth movement is known to cause sterile inflammation of the periodontal ligament (PDL). It may also be accompanied by pathological effects of external apical root resorption, with interindividual differences in the incidence and extent of resorption. An involvement of autoimmunological mechanisms is currently under discussion. This study aimed to improve our understanding of similarities between the inflammatory mechanisms underlying the pathophysiology of periodontitis and root resorption.

Materials and methods. Human PDL cells were stimulated with interleukin (IL)-1β/IL-17A/IFN-γ, or left non-stimulated. Their potential for phagocytosis was then evaluated by incubation with dextran or E. coli or S. aureus particles, followed by flow cytometric and immunohistochemical analysis. Real-time polymerase chain reaction (PCR) was used to analyze receptor activator of NFκB ligand (RANKL) and osteoprotegerin (OPG) expression in PDL cells. Verification was obtained in vivo by studying IL-17A, RANKL, and OPG expression in biopsies of inflamed periodontal tissues and in biopsies of rat maxillae with mechanically induced root resorption. Statistical analysis included Wilcoxon's rank sum test to analyze gene expression data and one-way ANOVA in conjunction with Tukey's post hoc test to analyze flow cytometric data.

Results. PDL cells phagocytosed foreign particles under both inflammatory and non-inflammatory conditions. Furthermore, IL17A significantly downregulated RANKL expression while significantly upregulating OPG expression in PDL cells. These immunomodulatory cytokines were also demonstrable in both inflammatorily altered periodontal tissues and root resorption lacunae, while the incidence of IL-7A was strikingly variable in resorption areas.

Conclusion. PDL cells were demonstrated to effect phagocytosis and to express immunomodulatory molecules, which proves

Zusammenfassung

Hintergrund und Zielsetzung. Im Parodontalligament (PDL) manifestiert sich aufgrund orthodontischer Zahnbewegungen eine sterile Entzündung. Die externe apikale Wurzelresorption ist eine potenzielle pathologische Begleiterscheinung orthodontischer Zahnbewegungen mit interindividuellen Unterschieden bezüglich Inzidenz und Ausmaß der Resorptionsprozesse, wobei die Beteiligung autoimmunologischer Aspekte diskutiert wird.

Ziel dieser Studie war es, eine mögliche Korrelation der zugrunde liegenden inflammatorischen Mechanismen bei der Pathophysiologie von Parodontitis und Wurzelresorptionen genauer zu untersuchen.

Material und Methoden. Humane PDL-Zellen wurden mit

IL(Interleukin)-1β, IL-17A, IFN(Interferon)g vorstimuliert oder unstimuliert belassen. Zur Analyse ihrer Phagozytosefähigkeit wurden die PDL-Zellen anschließend mit Dextran, E. coli oder S. aureus inkubiert und durchflusszytometrisch sowie immunzytochemisch untersucht. Die Analyse der Expression von RANKL und OPG in PDL-Zellen erfolgte mittels Real-time-PCR. Die In-vivo-Expression von IL-17A, RANKL („receptor activator of NF-κB ligand“) und

OPG (Osteoprotegerin) wurde an Biopsien entzündeter parodontaler Gewebe sowie an Biopsien von Rattenoberkiefern mit mechanisch induzierten Wurzelresorptionen untersucht. Die statistische Auswertung erfolgte mit dem Wilcoxon Rangsummentest für die Genexpressionsanalysen und mit one-way ANOVA und Tukey Post-hoc-Test für die durchflusszytometrischen Analysen.

Ergebnisse. PDL-Zellen phagozytierten Fremdpartikel unter entzündlichen und entzündungsfreien Bedingungen. Weiterhin wurde die Expression von RANKL in PDL-Zellen durch IL-17A signifikant herunterreguliert, OPG hingegen gleichzeitig signifikant hochreguliert. Diese immunmodulatorischen Zytokine waren auch in vivo im entzündlich veränderten Parodont sowie in Wurzelresorptionslakunen nachweisbar mit auffälliger Variabilität bezüglich der Inzidenz von IL-17A in Wurzelresorptionsarealen.

Anna Konermann1, Werner Götz1, Dirk Wohlleber2, Percy Knolle2, James Deschner3, Andreas Jäger1 1 Policlinic of Orthodontics, University of Bonn, Germany 2 Institute of Experimental Immunology, University of Bonn, Germany 3 Experimental Dental, Oral and Maxillary Medicine, University of

Bonn, Germany

Received: March 7, 2012; accepted: May 14, 2012; published online: September 21, 2012

This study was presented as a lecture at the 84th Annual Meeting of the German Orthodontic Society, winning the award for best junior-scientist presentation in basic orthodontic research. 431J Orofac Orthop 2012 · No. 6 © Springer-Verlag

Konermann A et al. Osteoimmunology of periodontal inflammations their capability of participating in periodontal osteoimmunological processes. The development of root resorption and periodontitis appears to be governed by similar pathophysiological mechanisms.

Keywords

Root resorption · Sterile inflammation · Bacterial inflammation · Periodontal ligament · Periodontal ligament cells

Introduction

Alterations of the periodontal ligament (PDL) during orthodontic tooth movement have been proposed to reflect an inflammatory reaction [19]. PDL compressed by experimentally induced tooth movement has been demonstrated to harbor cells expressing major histocompatibility complex (MHC) class

II, thus, exhibiting a typical feature of antigen-presenting cells, and cells expressing CD40 as well as its ligand CD40L [1, 19].

Periodontal inflammation of this type is associated with the pathological phenomenon of external apical root resorption.

Multiple factors, including the aggressiveness of host-specific cells promoting resorption, impact the incidence and extent of this clinical finding, which is characterized by large interindividual differences [3].