Iain L C Chapple1, Philippe Bouchard2,3, Maria Grazia Cagetti4, Guglielmo Campus4,5, Maria-Clotilde Carra2,6, Fabio Cocco5, Luigi Nibali7, Philippe Hujoel8, Marja L Laine9, Peter Lingstrom10, David J Manton11, Eduardo Montero12, Nigel Pitts13, Hélène Rangé2,3, Nadine Schlueter14, Wim Teughels15, Svante Twetman16, Cor Van Loveren17, Fridus Van der Weijden9, Alexandre R Vieira18, Andreas G Schulte19. 1. Periodontal Research Group, The University of Birmingham, Birmingham, UK. 2. Department of Periodontology, Service of Odontology, Rothschild Hospital, AP-HP, Paris 7-Denis Diderot University, U.F.R. of Odontology, Paris, France. 3. EA 2496, Paris 5-Descartes University, U.F.R. of Odontology, Paris, France. 4. WHO Collaboration Centre for Epidemiology and Community Dentistry, Milan, Italy. 5. Department of Surgery, Microsurgery and Medicine Sciences, School of Dentistry, Universita degli Studi di Sassari, Sassari, Italy. 6. INSERM, U1018, Villejuif, France. 7. Centre for Oral Clinical Research, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University London (QMUL), London, UK. 8. Public Health Sciences, University of Washington, Seattle, WA, USA. 9. Department of Periodontology, Academic Centre for Dentistry in Amsterdam, Amsterdam, the Netherlands. 10. Department of Cariology, Institute of Odontology, Gothenburg, Sweden. 11. Melbourne Dental School, University of Melbourne, Parkville, Vic., Australia. 12. Faculty of Dentistry, Universidad Complutense de Madrid, Madrid, Spain. 13. Dental Innovation and Translation Centre, Dental Institute, Kings College London, London, UK. 14. Division for Cariology, Department of Operative Dentistry and Periodontology, Center for Dental Medicine, University Medical Center, Albert-Ludwig-University, Freiburg, Germany. 15. Periodontology, K. U. Leuven, Leuven, Belgium. 16. Faculty of Health and Medical Sciences, School of Dentistry, Section of Cariology and Endodontics, University of Copenhagen, Copenhagen, Denmark. 17. Department of Cariology, Academic Centre for Dentistry Amsterdam, Amsterdam, the Netherlands. 18. Oral Biology, University of Pittsburgh, Pittsburgh, PA, USA. 19. Department of Special Care Dentistry, Dental School, Witten/Herdecke University, Witten, Germany.
Abstract
Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self-esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio-economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management. AIM: To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases. METHODS: One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report. RESULTS & CONCLUSIONS: There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor (VDR), Fc gamma receptor IIA (Fc-γRIIA) and Interleukin 10 (IL10) genes. For caries, genes involved in enamel formation (AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics (AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end-products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub-optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases.
Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self-esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio-economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management. AIM: To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases. METHODS: One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report. RESULTS & CONCLUSIONS: There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor (VDR), Fc gamma receptor IIA (Fc-γRIIA) and Interleukin 10 (IL10) genes. For caries, genes involved in enamel formation (AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics (AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end-products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub-optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases.
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