Environmental and Heritable Factors in the Etiology of Oral Diseases—A Population-based Study of Swedish Twins

Mucci, Lorelei A.; Björkman, Lars; Douglass, Chester W.; Pedersen, Nancy L.

doi:10.1177/154405910508400904

Cited by 61 publications

(84 citation statements)

References 22 publications

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“…Because of a relatively low prevalence of AgP in the general population, it is very difficult to identify enough affected twins to provide sufficient statistical power to test the concordance of this disease phenotype. Nevertheless, because of strong familial aggregation, rapid progression and early onset of disease, it is clear that genetic factors play a large role in the disease susceptibility of AgP ( Figure 3) (21,22). Thus, the earlier periodontitis manifests itself, the greater the role of genetic factors, which is similar to other complex inflammatory diseases.…”

Section: Figure 2 a Generic Multi-causality Model For Periodontitismentioning

confidence: 80%

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What is the Contribution of Genetics to Periodontal Risk?

Loos

Papantonopoulos

Jepsen

et al. 2015

Dental Clinics of North America

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This review addresses the multi-causal etiology of periodontitis, in which genetic factors play a role. The various proposed causes for periodontitis always play a role simultaneously, but the relative contribution of each of these, varies from case to case. In young individuals often with aggressive periodontitis (AgP) a stronger contribution from genetic factors is apparent, while in older individuals often with chronic periodontitis (CP), the relative contribution of the established subgingival biofilms (environmental factors) and life style factors (e.g. smoking, stress, diet), play a more dominant role in the phenotype of the disease.Nevertheless always some genetic susceptibility is present, for CP estimated at 25%.Periodontitis is therefore a complex disease, i.e. it behaves in a nonlinear fashion. Actually the disease progression rate fluctuates, where the disease sometimes moves into an aberrant state of host response and then swings back into a resolving state; in between, a settlement zone is present where essentially no differences are found for immunological parameters between cases with periodontitis and healthy controls. The genotype determines part of this fluctuation and the extent of it. The disease is polygenic, i.e. multiple genetic variants in multiple genes determine the phenotype, but there are individual and ethnic differences in the genes involved. We are still at the early stage to have identified the involved genes, in comparisons to other chronic diseases, we need to count on it that at least 100 causative genes across various global populations exist in AgP and CP. To date, the genetic variations firmly and repeatedly associated with periodontitis in some populations are found within the following genes: ANRIL, COX2, IL1, IL10, DEFB1, while many proposed periodontitis candidate genes have not been firmly proven or replicated. 3 KeypointsPeriodontitis is a multi-causal disease, with each of the causal factors playing a role but the relative contribution of these vary form case to case.The disease behaves in a nonlinear fashion, with periods of aberrant host response to periods within an active disease resolving state.To date only a few of the multitude of possible genetic factors for periodontitis are identified. Outline

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Section: Figure 2 a Generic Multi-causality Model For Periodontitismentioning

confidence: 80%

“…It is generally accepted that genetic factors play an important role in the disease susceptibility of AgP ( Figure 3) (13,21,22). (9,13).…”

Section: Figure 2 a Generic Multi-causality Model For Periodontitismentioning

confidence: 99%

What is the Contribution of Genetics to Periodontal Risk?

Loos

Papantonopoulos

Jepsen

et al. 2015

Dental Clinics of North America

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“…mandibular right first molar loss, presence of untreated lesions, number of affected occlusal surfaces, depth of dentinal lesions, preference for sugars, presence of specific microbial species) and varies from 26% to 64% (Nibali et al 2017). The magnitude of a genetic contribution to overall periodontitis susceptibility (measured clinically or selfreported) has been estimated as 33-50% (Michalowicz et al 1991, Michalowicz et al 2000, Mucci et al 2005. The increase in odds for individual genetic variants based on robust association studies on periodontal diseases and caries is estimated to be up to 50% (Nibali et al 2017).…”

Section: Inherited and Acquired Risk Factors For Dental Caries And Pementioning

confidence: 99%

Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases

Chapple

Bouchard

Cagetti

et al. 2017

J Clinic Periodontology

388

369

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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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“…In addition, a number of analyses of the SALT cohort have been published (e.g., Bulik et al, 2006;Cameron et al, 2002;Crowe, et al, in press;Gatz et al, 2006;Kato et al, 2006aKato et al, , 2006bKendler, et al, 2006;Mackintosh, et al, 2006;Michaelsson et al, 2005;Mucci, et al, 2005;Rasgon et al, 2005;Soldani, et al, 2005;Svensson, et al, 2004;Wirdefeldt, et al, 2004). As these studies have been described elsewhere, we focus here on a new initiative involving the SALT cohort, establishing a biobank.…”

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confidence: 99%