Mariano Sanz1, David Beighton2, Michael A Curtis3, Jaime A Cury4, Irene Dige5, Henrik Dommisch6, Roger Ellwood7, Rodrigo A Giacaman8, David Herrera1, Mark C Herzberg9, Eija Könönen10, Philip D Marsh11, Joerg Meyle12, Alex Mira13, Ana Molina1, Andrea Mombelli14, Marc Quirynen15, Eric C Reynolds16, Lior Shapira17, Egija Zaura18. 1. ETEP (Etiolgy and Therapy of Periodontal Diseases) Research Group, University Complutense, Madrid, Spain. 2. King's College London School of Medical Education, London, UK. 3. Microbiology, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. 4. Piracicaba Dental School, UNICAM, Piracicaba, SP, Brazil. 5. Department of Dentistry and Oral Health, Faculty of Health, Aarhus Universitet, Aarhus C, Denmark. 6. Charite, Berlin, Germany. 7. Manchester University, Manchester, UK. 8. Oral Rehabilitation, University of Talca, Talca, Chile. 9. University of Minnesota School of Dentistry, Minneapolis, MN, USA. 10. Periodontology, University of Turku, Turku, Finland. 11. Department of Oral Biology, School of Dentistry, University of Leeds, Leeds, UK. 12. Periodontology, University of Giessen, Giessen, Germany. 13. Centre for Advanced Research in Public Health, FISABIO Foundation, Valencia, Spain. 14. Periodontology, University of Geneva, Geneva, Switzerland. 15. Katholieke Universiteit Leuven, Leuven, Belgium. 16. Oral Health Cooperative Research Centre, Melbourne Dental School, The University of Melbourne, Melbourne, Australia. 17. Periodontology, Hebrew University and Hadassah Medical Center, Jerusalem, Israel. 18. Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), Amsterdam, The Netherlands.
Abstract
BACKGROUND AND AIMS: The scope of this working group was to review (1) ecological interactions at the dental biofilm in health and disease, (2) the role of microbial communities in the pathogenesis of periodontitis and caries, and (3) the innate host response in caries and periodontal diseases. RESULTS AND CONCLUSIONS: A health-associated biofilm includes genera such as Neisseria, Streptococcus, Actinomyces, Veillonella and Granulicatella. Microorganisms associated with both caries and periodontal diseases are metabolically highly specialized and organized as multispecies microbial biofilms. Progression of these diseases involves multiple microbial interactions driven by different stressors. In caries, the exposure of dental biofilms to dietary sugars and their fermentation to organic acids results in increasing proportions of acidogenic and aciduric species. In gingivitis, plaque accumulation at the gingival margin leads to inflammation and increasing proportions of proteolytic and often obligately anaerobic species. The natural mucosal barriers and saliva are the main innate defence mechanisms against soft tissue bacterial invasion. Similarly, enamel and dentin are important hard tissue barriers to the caries process. Given that the present state of knowledge suggests that the aetiologies of caries and periodontal diseases are mutually independent, the elements of innate immunity that appear to contribute to resistance to both are somewhat coincidental.
BACKGROUND AND AIMS: The scope of this working group was to review (1) ecological interactions at the dental biofilm in health and disease, (2) the role of microbial communities in the pathogenesis of periodontitis and caries, and (3) the innate host response in caries and periodontal diseases. RESULTS AND CONCLUSIONS: A health-associated biofilm includes genera such as Neisseria, Streptococcus, Actinomyces, Veillonella and Granulicatella. Microorganisms associated with both caries and periodontal diseases are metabolically highly specialized and organized as multispecies microbial biofilms. Progression of these diseases involves multiple microbial interactions driven by different stressors. In caries, the exposure of dental biofilms to dietary sugars and their fermentation to organic acids results in increasing proportions of acidogenic and aciduric species. In gingivitis, plaque accumulation at the gingival margin leads to inflammation and increasing proportions of proteolytic and often obligately anaerobic species. The natural mucosal barriers and saliva are the main innate defence mechanisms against soft tissue bacterial invasion. Similarly, enamel and dentin are important hard tissue barriers to the caries process. Given that the present state of knowledge suggests that the aetiologies of caries and periodontal diseases are mutually independent, the elements of innate immunity that appear to contribute to resistance to both are somewhat coincidental.
Authors: J T Marchesan; K M Byrd; K Moss; J S Preisser; T Morelli; A F Zandona; Y Jiao; J Beck Journal: J Dent Res Date: 2020-04-22 Impact factor: 6.116
Authors: Ting Sang; Zhou Ye; Nicholas G Fischer; Erik P Skoe; Constanza Echeverría; Jun Wu; Conrado Aparicio Journal: Colloids Surf B Biointerfaces Date: 2020-03-03 Impact factor: 5.268