Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Typ-2-Diabetes und Adipositas Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende

Die Highlights vom Kongress des American College of Cardiology 2024

Im April diskutierten die Herz-Kreislauf-Spezialisten aus der ganzen Welt auf dem  Kongress des American College of Cardiology (ACC) u.a. neue Therapieansätze bei akutem Myokardinfarkt, koronarer Herzerkrankung, kardiogenem Schock oder Aortenklappenstenose. In unserem Kongress-Dossier haben wir für Sie Berichte über die „Late-Breaking Trials“ und andere wichtige Studien zusammengestellt. 
Erweiterte Suche
Anmelden
nach oben
Current Oral Health Reports
Erschienen in: Current Oral Health Reports 2/2014

01.06.2014 | Immunology (G Nussbaum, Section Editor)

Immuno-Pathogenesis of Periodontal Disease: Current and Emerging Paradigms

verfasst von: Nasi Huang, Frank C. Gibson III

Erschienen in: Current Oral Health Reports | Ausgabe 2/2014

Einloggen, um Zugang zu erhalten

Abstract

Periodontal disease (PD) is a highly complex disease involving many factors; however, two principal facets central to initiation and progression of the majority of PD are the composition of the microbes in the sub-gingival plaque, and the host immune response to these organisms. Numerous studies point to the complexity of PD, and to the fact that despite innate and adaptive immune activation, and resultant inflammation, our immune response fails to cure disease. Stunning new findings have begun to clarify several complexities of the host-pathogen interaction of PD pointing to key roles for microbial dysbiosis and immune imbalance in the pathogenesis of disease. Furthermore, these investigations have identified novel translational opportunities to intercede in PD treatment. In this review we will highlight a select few recent findings in innate and adaptive immunity, and host pathogen interactions of PD at a micro-environmental level that may have profound impact on PD progression.
Literatur
1.
Benakanakere M, Kinane DF. Innate cellular responses to the periodontal biofilm. Front Oral Biol. 2012;15:41–55.PubMedCrossRef
2.
Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent Jr RL. Microbial complexes in subgingival plaque. J Clin Periodontol. 1998;25:134–44.PubMedCrossRef
3.
Holt SC, Ebersole J, Felton J, Brunsvold M, Kornman KS. Implantation of Bacteroides gingivalis in nonhuman primates initiates progression of periodontitis. Science. 1988;239:55–7.PubMedCrossRef
4.
Kesavalu L, Sathishkumar S, Bakthavatchalu V, et al. Rat model of polymicrobial infection, immunity, and alveolar bone resorption in periodontal disease. Infect Immun. 2007;75:1704–12.PubMedCentralPubMedCrossRef
5.
Polak D, Wilensky A, Shapira L, et al. Mouse model of experimental periodontitis induced by Porphyromonas gingivalis/Fusobacterium nucleatum infection: bone loss and host response. J Clin Periodontol. 2009;36:406–10.PubMedCrossRef
6.
7.
8.•
Colombo AP, Bennet S, Cotton SL, et al. Impact of periodontal therapy on the subgingival microbiota of severe periodontitis: comparison between good responders and individuals with refractory periodontitis using the human oral microbe identification microarray. J Periodontol. 2012;83:1279–87. Use of the human oral microbiome microarray invesitgators identified novel organisms and groups of organisms associated with refractory PD.PubMedCentralPubMedCrossRef
9.
Darveau RP. Periodontitis: a polymicrobial disruption of host homeostasis. Nat Rev Microbiol. 2010;8:481–90.PubMedCrossRef
10.
Hajishengallis G, Liang S, Payne MA, et al. Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement. Cell Host Microbe. 2011;10:497–506.PubMedCentralPubMedCrossRef
11.
12.
Weinberg A, Belton CM, Park Y, Lamont RJ. Role of fimbriae in Porphyromonas gingivalis invasion of gingival epithelial cells. Infect Immun. 1997;65:313–6.PubMedCentralPubMed
13.
Coats SR, Berezow AB, To TT, et al. The lipid A phosphate position determines differential host Toll-like receptor 4 responses to phylogenetically related symbiotic and pathogenic bacteria. Infect Immun. 2011;79:203–10.PubMedCentralPubMedCrossRef
14.
Nichols FC, Housley WJ, O'Conor CA, Manning T, Wu S, Clark RB. Unique lipids from a common human bacterium represent a new class of Toll-like receptor 2 ligands capable of enhancing autoimmunity. Am J Pathol. 2009;175:2430–8.PubMedCentralPubMedCrossRef
15.
Guo Y, Nguyen KA, Potempa J. Dichotomy of gingipains action as virulence factors: from cleaving substrates with the precision of a surgeon's knife to a meat chopper-like brutal degradation of proteins. Periodontol 2000. 2010;54:15–44.PubMedCentralPubMedCrossRef
16.
Sheets SM, Robles-Price AG, McKenzie RM, Casiano CA, Fletcher HM. Gingipain-dependent interactions with the host are important for survival of Porphyromonas gingivalis. Front Biosci. 2008;13:3215–38.PubMedCentralPubMedCrossRef
17.
Blach A, Franek E, Witula A, et al. The influence of chronic periodontitis on serum TNF-alpha, IL-6 and hs-CRP concentrations, and function of graft and survival of kidney transplant recipients. Clin Transplant. 2009;23:213–9.PubMedCrossRef
18.
Kajita K, Honda T, Amanuma R, et al. Quantitative messenger RNA expression of Toll-like receptors and interferon-alpha1 in gingivitis and periodontitis. Oral Microbiol Immunol. 2007;22:398–402.PubMedCrossRef
19.
Kinane DF, Mooney J, Ebersole JL. Humoral immune response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in periodontal disease. Periodontol 2000. 1999;20:289–340.PubMedCrossRef
20.
Gamonal J, Acevedo A, Bascones A, Jorge O, Silva A. Levels of interleukin-1 beta, -8, and -10 and RANTES in gingival crevicular fluid and cell populations in adult periodontitis patients and the effect of periodontal treatment. J Periodontol. 2000;71:1535–45.PubMedCrossRef
21.
Cekici A, Kantarci A, Hasturk H, Van Dyke TE. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontol 2000. 2014;64:57–80.PubMedCrossRef
22.
Cochran DL. Inflammation and bone loss in periodontal disease. J Periodontol. 2008;79:1569–76.PubMedCrossRef
23.
Yuan H, Gupte R, Zelkha S, Amar S. Receptor activator of nuclear factor kappa B ligand antagonists inhibit tissue inflammation and bone loss in experimental periodontitis. J Clin Periodontol. 2011;38:1029–36.PubMedCrossRef
24.
Tonetti MS, Imboden MA, Gerber L, Lang NP, Laissue J, Mueller C. Localized expression of mRNA for phagocyte-specific chemotactic cytokines in human periodontal infections. Infect Immun. 1994;62:4005–14.PubMedCentralPubMed
25.
Salvi GE, Brown CE, Fujihashi K, et al. Inflammatory mediators of the terminal dentition in adult and early onset periodontitis. J Periodontal Res. 1998;33:212–25.PubMedCrossRef
26.
Taubman MA, Kawai T. Involvement of T-lymphocytes in periodontal disease and in direct and indirect induction of bone resorption. Crit Rev Oral Biol Med. 2001;12:125–35.PubMedCrossRef
27.
Mosmann TR, Cherwinski H, Bond MW, Giedlin MA, Coffman RL. Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins. J Immunol. 1986;136:2348–57.PubMed
28.
Gemmell E, Seymour GJ. Immunoregulatory control of Th1/Th2 cytokine profiles in periodontal disease. Periodontol 2000. 2004;35:21–41.PubMedCrossRef
29.
Ebersole JL, Taubman MA. The protective nature of host responses in periodontal diseases. Periodontol 2000. 1994;5:112–41.PubMedCrossRef
30.
Bannenberg G, Serhan CN. Specialized pro-resolving lipid mediators in the inflammatory response: an update. Biochim Biophys Acta. 1801;2010:1260–73.
31.
Freire MO, Van Dyke TE. Natural resolution of inflammation. Periodontol. 2000;201363:149–64.
32.
Yang R, Chiang N, Oh SF, Serhan CN. Metabolomics-lipidomics of eicosanoids and docosanoids generated by phagocytes. Curr Protoc Immunol. 2011;Chapter 14:Unit 14 26.
33.
Hasturk H, Kantarci A, Goguet-Surmenian E, et al. Resolvin E1 regulates inflammation at the cellular and tissue level and restores tissue homeostasis in vivo. J Immunol. 2007;179:7021–9.PubMedCrossRef
34.
35.
Hasturk H, Kantarci A, Ohira T, et al. RvE1 protects from local inflammation and osteoclast- mediated bone destruction in periodontitis. FASEB J. 2006;20:401–3.PubMed
36.
Nakajima T, Ueki-Maruyama K, Oda T, et al. Regulatory T-cells infiltrate periodontal disease tissues. J Dent Res. 2005;84:639–43.PubMedCrossRef
37.
Aranha AM, Repeke CE, Garlet TP, et al. Evidence supporting a protective role for th9 and th22 cytokines in human and experimental periapical lesions. J Endod. 2013;39:83–7.PubMedCrossRef
38.
Akdis M, Palomares O, van de Veen W, van Splunter M, Akdis CA. TH17 and TH22 cells: a confusion of antimicrobial response with tissue inflammation versus protection. J Allergy Clin Immunol. 2012;129:1438–49. quiz1450-1431.PubMedCrossRef
39.
Cardoso CR, Garlet GP, Crippa GE, et al. Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease. Oral Microbiol Immunol. 2009;24:1–6.PubMedCrossRef
40.
Garlet GP, Cardoso CR, Mariano FS, et al. Regulatory T cells attenuate experimental periodontitis progression in mice. J Clin Periodontol. 2010;37:591–600.PubMedCrossRef
41.••
Eskan MA, Jotwani R, Abe T, et al. The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss. Nat Immunol. 2012;13:465–73. Linkage of IL-17 to infection-elicited oral bone loss phenotype and defined the role of Del-1 an endogenous inhibitor of neutrophil adherence.PubMedCentralPubMedCrossRef
42.••
Wang L, Wang J, Jin Y, Gao H, Lin X. Oral administration of all-trans retinoic acid suppresses experimental periodontitis by modulating the Th17/Treg imbalance. J Periodontol. 2013. Treatment of mice with all-trans retanoic acid during P. gingivalis infection shifts balance to Treg predominance, reducing cellular infiltration into gingival tissues, and preserved oral bone.
43.
Adibrad M, Deyhimi P, Ganjalikhani Hakemi M, Behfarnia P, Shahabuei M, Rafiee L. Signs of the presence of Th17 cells in chronic periodontal disease. J Periodontal Res. 2012;47:525–31.PubMedCrossRef
44.
Martin M, Katz J, Vogel SN, Michalek SM. Differential induction of endotoxin tolerance by lipopolysaccharides derived from Porphyromonas gingivalis and Escherichia coli. J Immunol. 2001;167:5278–85.PubMedCrossRef
45.
Cohen N, Morisset J, Emilie D. Induction of tolerance by Porphyromonas gingivalis on APCS: a mechanism implicated in periodontal infection. J Dent Res. 2004;83:429–33.PubMedCrossRef
46.
Jotwani R, Palucka AK, Al-Quotub M, et al. Mature dendritic cells infiltrate the T cell-rich region of oral mucosa in chronic periodontitis: in situ, in vivo, and in vitro studies. J Immunol. 2001;167:4693–700.PubMedCentralPubMedCrossRef
47.
Huang CB, Altimova Y, Strange S, Ebersole JL. Polybacterial challenge effects on cytokine/chemokine production by macrophages and dendritic cells. Inflamm Res. 2011;60:119–25.PubMedCentralPubMedCrossRef
48.
Herath TD, Darveau RP, Seneviratne CJ, Wang CY, Wang Y, Jin L. Tetra- and penta-acylated lipid A structures of Porphyromonas gingivalis LPS differentially activate TLR4-mediated NF-kappaB signal transduction cascade and immuno-inflammatory response in human gingival fibroblasts. PLoS One. 2013;8:e58496.PubMedCentralPubMedCrossRef
49.
Nussbaum G, Ben-Adi S, Genzler T, Sela M, Rosen G. Involvement of Toll-like receptors 2 and 4 in the innate immune response to Treponema denticola and its outer sheath components. Infect Immun. 2009;77:3939–47.PubMedCentralPubMedCrossRef
50.
Burns E, Bachrach G, Shapira L, Nussbaum G. Cutting Edge: TLR2 is required for the innate response to Porphyromonas gingivalis: activation leads to bacterial persistence and TLR2 deficiency attenuates induced alveolar bone resorption. J Immunol. 2006;177:8296–300.PubMedCrossRef
51.
Gibson 3rd FC, Genco CA. Porphyromonas gingivalis mediated periodontal disease and atherosclerosis: disparate diseases with commonalities in pathogenesis through TLRs. Curr Pharm Des. 2007;13:3665–75.PubMedCrossRef
52.
Costalonga M, Batas L, Reich BJ. Effects of Toll-like receptor 4 on Porphyromonas gingivalis-induced bone loss in mice. J Periodontal Res. 2009;44:537–42.PubMedCrossRef
53.
Kumar H, Kawai T, Akira S. Toll-like receptors and innate immunity. Biochem Biophys Res Commun. 2009;388:621–5.PubMedCrossRef
54.
Hoebe K, Du X, Georgel P, et al. Identification of Lps2 as a key transducer of MyD88-independent TIR signalling. Nature. 2003;424:743–8.PubMedCrossRef
55.
Burns E, Eliyahu T, Uematsu S, Akira S, Nussbaum G. TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection. J Immunol. 2010;184:1455–62.PubMedCrossRef
56.
Gaddis DE, Michalek SM, Katz J. TLR4 signaling via MyD88 and TRIF differentially shape the CD4+ T cell response to Porphyromonas gingivalis hemagglutinin B. J Immunol. 2011;186:5772–83.PubMedCrossRef
57.
Shaik-Dasthagirisaheb YB, Huang N, Gibson FC, 3rd. Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3. Innate Immun. 2014;20:312–9.
58.
Kabashima H, Yoneda M, Nagata K, Hirofuji T, Maeda K. The presence of chemokine (MCP-1, MIP-1alpha, MIP-1beta, IP-10, RANTES)-positive cells and chemokine receptor (CCR5, CXCR3)-positive cells in inflamed human gingival tissues. Cytokine. 2002;20:70–7.PubMedCrossRef
59.
McWhirter SM, Fitzgerald KA, Rosains J, Rowe DC, Golenbock DT, Maniatis T. IFN-regulatory factor 3-dependent gene expression is defective in Tbk1-deficient mouse embryonic fibroblasts. Proc Natl Acad Sci U S A. 2004;101:233–8.PubMedCentralPubMedCrossRef
60.
Fitzgerald KA, Rowe DC, Barnes BJ, et al. LPS-TLR4 signaling to IRF-3/7 and NF-kappaB involves the toll adapters TRAM and TRIF. J Exp Med. 2003;198:1043–55.PubMedCentralPubMedCrossRef
61.
Decker T, Muller M, Stockinger S. The Yin and Yang of type I interferon activity in bacterial infection. Nat Rev Immunol. 2005;5:675–87.PubMedCrossRef
62.
Prabhu A, Michalowicz BS, Mathur A. Detection of local and systemic cytokines in adult periodontitis. J Periodontol. 1996;67:515–22.PubMedCrossRef
63.
Wright HJ, Matthews JB, Chapple IL, Ling-Mountford N, Cooper PR. Periodontitis associates with a type 1 IFN signature in peripheral blood neutrophils. J Immunol. 2008;181:5775–84.PubMedCrossRef
64.
Gaddis DE, Michalek SM, Katz J. Requirement of TLR4 and CD14 in dendritic cell activation by Hemagglutinin B from Porphyromonas gingivalis. Mol Immunol. 2009;46:2493–504.PubMedCentralPubMedCrossRef
65.
Zhou Q, Amar S. Identification of signaling pathways in macrophage exposed to Porphyromonas gingivalis or to its purified cell wall components. J Immunol. 2007;179:7777–90.PubMedCrossRef
66.•
Nowak M, Kramer B, Haupt M, et al. Activation of invariant NK T cells in periodontitis lesions. J Immunol. 2013;190:2282–91. Specific differences in type 1 NKT cell infiltration into periodontal lesions, as well as ability of cells to differentially respond by producing type 1 IFN may be important difference to the mechanistic progression of aggressive and chronic forms of PD.PubMedCentralPubMedCrossRef
67.
Platt N, Haworth R, Darley L, Gordon S. The many roles of the class A macrophage scavenger receptor. Int Rev Cytol. 2002;212:1–40.PubMedCrossRef
68.
Lin YL, de Villiers WJ, Garvy B, et al. The effect of class A scavenger receptor deficiency in bone. J Biol Chem. 2007;282:4653–60.PubMedCrossRef
69.
Baer MT, Huang N, Gibson 3rd FC. Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF-alpha expression. Oral Microbiol Immunol. 2009;24:456–63.PubMedCentralPubMedCrossRef
70.
Triantafilou M, Gamper FG, Lepper PM, et al. Lipopolysaccharides from atherosclerosis-associated bacteria antagonize TLR4, induce formation of TLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatory responses in human vascular endothelial cells. Cell Microbiol. 2007;9:2030–9.PubMedCrossRef
71.
Elinav E, Strowig T, Henao-Mejia J, Flavell RA. Regulation of the antimicrobial response by NLR proteins. Immunity. 2011;34:665–79.PubMedCrossRef
72.
Wen H, Miao EA, Ting JP. Mechanisms of NOD-like receptor-associated inflammasome activation. Immunity. 2013;39:432–41.PubMedCrossRef
73.
Liu J, Duan J, Wang Y, Ouyang X. Intracellular adhesion molecule-1 is regulated by Porphyromonas gingivalis through nucleotide binding oligomerization domain-containing proteins 1 and 2 molecules in periodontal fibroblasts. J Periodontol. 2014;85:358–68.PubMedCrossRef
74.
75.
Jiao Y, Darzi Y, Tawaratsumida K, et al. Induction of bone loss by pathobiont-mediated Nod1 signaling in the oral cavity. Cell Host Microbe. 2013;13:595–601.PubMedCrossRef
76.
Yuan H, Zelka S, Burkatovskaya M, Gupte R, Leeman SE, Amar S. Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss. Proc Natl Acad Sci U S A. 2013;110:E5059–68.PubMedCrossRef
77.
Madrigal AG, Barth K, Papadopoulos G, Genco CA. Pathogen-mediated proteolysis of the cell death regulator RIPK1 and the host defense modulator RIPK2 in human aortic endothelial cells. PLoS Pathog. 2012;8:e1002723.PubMedCentralPubMedCrossRef
78.
Attstrom R, Laurel AB, Lahsson U, Sjoholm A. Complement factors in gingival crevice material from healthy and inflamed gingiva in humans. J Periodontal Res. 1975;10:19–27.PubMedCrossRef
79.
Hajishengallis G, Abe T, Maekawa T, Hajishengallis E, Lambris JD. Role of complement in host-microbe homeostasis of the periodontium. Semin Immunol. 2013;25:65–72.
80.
Liang S, Krauss JL, Domon H, et al. The C5a receptor impairs IL-12-dependent clearance of Porphyromonas gingivalis and is required for induction of periodontal bone loss. J Immunol. 2011;186:869–77.PubMedCentralPubMedCrossRef
81.
Abe T, Hosur KB, Hajishengallis E, et al. Local complement-targeted intervention in periodontitis: proof-of-concept using a C5a receptor (CD88) antagonist. J Immunol. 2012;189:5442–8.PubMedCentralPubMedCrossRef
82.
Haffajee AD, Socransky SS, Taubman MA, Sioson J, Smith DJ. Patterns of antibody response in subjects with periodontitis. Oral Microbiol Immunol. 1995;10:129–37.PubMedCrossRef
83.
Gibson FC, Savelli J, Van Dyke TE, Genco CA. Gingipain-specific IgG in the sera of patients with periodontal disease is necessary for opsonophagocytosis of Porphyromonas gingivalis. J Periodontol. 2005;76:1629–36.PubMedCrossRef
84.
Whitney C, Ant J, Moncla B, Johnson B, Page RC, Engel D. Serum immunoglobulin G antibody to Porphyromonas gingivalis in rapidly progressive periodontitis: titer, avidity, and subclass distribution. Infect Immun. 1992;60:2194–200.PubMedCentralPubMed
85.
86.
Charon J, Toto PD, Gargiulo AW. Activated macrophages in human periodontitis. J Periodontol. 1981;52:328–35.PubMedCrossRef
87.
88.
Sima C, Glogauer M. Macrophage subsets and osteoimmunology: tuning of the immunological recognition and effector systems that maintain alveolar bone. Periodontol 2000. 2013;63:80–101.PubMedCrossRef
89.
Okada H, Murakami S. Cytokine expression in periodontal health and disease. Crit Rev Oral Biol Med. 1998;9:248–66.PubMedCrossRef
90.
Gordon S, Taylor PR. Monocyte and macrophage heterogeneity. Nat Rev Immunol. 2005;5:953–64.PubMedCrossRef
91.
92.
93.
Martinez FO, Helming L, Gordon S. Alternative activation of macrophages: an immunologic functional perspective. Annu Rev Immunol. 2009;27:451–83.PubMedCrossRef
94.
Mantovani A, Sica A, Sozzani S, Allavena P, Vecchi A, Locati M. The chemokine system in diverse forms of macrophage activation and polarization. Trends Immunol. 2004;25:677–86.PubMedCrossRef
95.
Martinez FO, Sica A, Mantovani A, Locati M. Macrophage activation and polarization. Front Biosci. 2008;13:453–61.PubMedCrossRef
96.
Benoit M, Desnues B, Mege JL. Macrophage polarization in bacterial infections. J Immunol. 2008;181:3733–9.PubMedCrossRef
97.
Papadopoulos G, Weinberg EO, Massari P, et al. Macrophage-specific TLR2 signaling mediates pathogen-induced TNF-dependent inflammatory oral bone loss. J Immunol. 2013;190:1148–57.PubMedCentralPubMedCrossRef
98.
Chapple CC, Srivastava M, Hunter N. Failure of macrophage activation in destructive periodontal disease. J Pathol. 1998;186:281–6.PubMedCrossRef
99.
Topoll HH, Zwadlo G, Lange DE, Sorg C. Phenotypic dynamics of macrophage subpopulations during human experimental gingivitis. J Periodontal Res. 1989;24:106–12.PubMedCrossRef
100.
Yamamoto M, Kawabata K, Fujihashi K, et al. Absence of exogenous interleukin-4-induced apoptosis of gingival macrophages may contribute to chronic inflammation in periodontal diseases. Am J Pathol. 1996;148:331–9.PubMedCentralPubMed
101.
Pradeep AR, Roopa Y, Swati PP. Interleukin-4, a T-helper 2 cell cytokine, is associated with the remission of periodontal disease. J Periodontal Res. 2008;43:712–6.PubMedCrossRef
Metadaten
Titel
Immuno-Pathogenesis of Periodontal Disease: Current and Emerging Paradigms
verfasst von
Nasi Huang
Frank C. Gibson III
Publikationsdatum
01.06.2014
Verlag
Springer International Publishing
Erschienen in
Current Oral Health Reports / Ausgabe 2/2014
Elektronische ISSN: 2196-3002
DOI
https://doi.org/10.1007/s40496-014-0017-8

Weitere Artikel der Ausgabe 2/2014

Current Oral Health Reports 2/2014 Zur Ausgabe

Immunology (G Nussbaum, Section Editor)

Cytokine Networks Regulating Inflammation and Immune Defense in the Oral Cavity

Oral Cancer (A Le, Section Editor)

Salivary Biomarkers for Detection of Oral Squamous Cell Carcinoma: Current State and Recent Advances

Immunology (G Nussbaum, Section Editor)

The Role of Distinct T Cell Subsets in Periodontitis—Studies from Humans and Rodent Models

Immunology (G Nussbaum, Section Editor)

Neutrophil Dysfunction and Host Susceptibility to Periodontal Inflammation: Current State of Knowledge

Neu im Fachgebiet Zahnmedizin

Darf man die Behandlung eines Neonazis ablehnen?

08.05.2024 Gesellschaft Nachrichten

In einer Leseranfrage in der Zeitschrift Journal of the American Academy of Dermatology möchte ein anonymer Dermatologe bzw. eine anonyme Dermatologin wissen, ob er oder sie einen Patienten behandeln muss, der eine rassistische Tätowierung trägt.

Ein Drittel der jungen Ärztinnen und Ärzte erwägt abzuwandern

07.05.2024 Klinik aktuell Nachrichten

Extreme Arbeitsverdichtung und kaum Supervision: Dr. Andrea Martini, Sprecherin des Bündnisses Junge Ärztinnen und Ärzte (BJÄ) über den Frust des ärztlichen Nachwuchses und die Vorteile des Rucksack-Modells.

Endlich: Zi zeigt, mit welchen PVS Praxen zufrieden sind

IT für Ärzte Nachrichten

Darauf haben viele Praxen gewartet: Das Zi hat eine Liste von Praxisverwaltungssystemen veröffentlicht, die von Nutzern positiv bewertet werden. Eine gute Grundlage für wechselwillige Ärztinnen und Psychotherapeuten.

Parodontalbehandlung verbessert Prognose bei Katheterablation

19.04.2024 Vorhofflimmern Nachrichten

Werden Personen mit Vorhofflimmern in der Blanking-Periode nach einer Katheterablation gegen eine bestehende Parodontitis behandelt, verbessert dies die Erfolgsaussichten. Dafür sprechen die Resultate einer prospektiven Untersuchung.

Newsletter

Bestellen Sie unseren kostenlosen Newsletter Update Zahnmedizin und bleiben Sie gut informiert – ganz bequem per eMail.

Newsletter bestellen
Bildnachweise