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Periodontal Disease and Cognitive Disorders.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Periodontal Disease and Cognitive Disorders./
作者:	Holmer, Jacob.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2022,
面頁冊數:	85 p.
附註:	Source: Dissertations Abstracts International, Volume: 84-01, Section: B.
Contained By:	Dissertations Abstracts International84-01B.
標題:	Prokaryotes. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29149229
ISBN:	9798835538584

Periodontal Disease and Cognitive Disorders.
Holmer, Jacob.

Periodontal Disease and Cognitive Disorders. - Ann Arbor : ProQuest Dissertations & Theses, 2022 - 85 p.

Source: Dissertations Abstracts International, Volume: 84-01, Section: B.

Thesis (Ph.D.)--Karolinska Institutet (Sweden), 2022.

This item must not be sold to any third party vendors.

Periodontitis and tooth loss have been suggested to be putative aetiological risk factors fordementia and cognitive dysfunction. The identification of new dementia risk factors couldlead to new preventive strategies for dementia. The aim of this thesis was to explore whetherperiodontal disease and tooth loss are associated with cognitive dysfunction, with specialreference to dementia.In paper I, 154 cases from the Karolinska Memory Clinic at Karolinska University Hospitaland 76 cognitively healthy controls from Huddinge municipality were enrolled in a casecontrol study. Cases comprised individuals diagnosed with Alzheimer´s disease (AD), mildcognitive impairment (MCI), or subjective cognitive decline (SCD). All participantsunderwent dental examinations that included panoramic imaging. The primary exposure wasradiologically verified marginal alveolar bone loss (MABL). Generalised MABL was foundto be more prevalent among cases than controls, especially for the AD subgroup. Nobetween-group differences were found for localised MABL. In addition, cases had an overallpoorer oral health status than controls.Paper II explored the subgingival microbiota among AD, MCI and SCD participants andcontrols from paper I. Using 16S rRNA gene sequencing, the compositions of the microbialcommunities were compared across study groups. Only relatively subtle differences wereseen. As signs of periodontitis were more common among the cases than the controls, it wasdifficult to determine whether there would have been actual differences had the periodontitisdistributions been the same. In periodontitis-adjusted models, we demonstrated that thebacterium Prevotella oulorum was present at a higher abundance among cases than controlsand that the bacterium Rothia aeria was less abundant.In paper III, we investigated the dementia incidence in a cohort with or without periodontaldisease at baseline. Data were retrieved from several national registries in Sweden, such asthe Swedish Quality Registry for Caries and Periodontal Diseases and the Swedish DementiaRegistry. During the average eight years of follow-up, the incidence of dementia was shownto be similar in the two groups. No association was evident between periodontal disease anddementia in confounder-adjusted regression models.Paper IV was a cohort study using data from Swedish national registries to investigatewhether tooth loss is associated with the incidence of dementia. Two exposure groups weredefined at the start of the observation period and followed for up to nine years. Severe toothloss (STL) was contrasted with a reference group without the index condition. The dementiaincidence was higher in the group with STL than in the reference group. This finding wasfound to be robust in sensitivity analyses and the confounder-adjusted models.In conclusion, the results in this thesis show the complexity of interactions between dentaldisease and cognitive dysfunction. Among participants with cognitive dysfunction, signs ofgeneralised MABL were more prevalent compared to controls. Differences in the subgingivalmicrobiota were seen, suggesting that cognitive dysfunction was associated with periodontaldisease. In a longitudinal study, periodontal disease was not associated with an increased riskof dementia. In contrast, having severe tooth loss was associated with an increased incidenceof dementia. Thus, severe tooth loss may serve as a marker of dementia risk.

ISBN: 9798835538584Subjects--Topical Terms:

741052
Prokaryotes.

Periodontal Disease and Cognitive Disorders.
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520 $a Periodontitis and tooth loss have been suggested to be putative aetiological risk factors fordementia and cognitive dysfunction. The identification of new dementia risk factors couldlead to new preventive strategies for dementia. The aim of this thesis was to explore whetherperiodontal disease and tooth loss are associated with cognitive dysfunction, with specialreference to dementia.In paper I, 154 cases from the Karolinska Memory Clinic at Karolinska University Hospitaland 76 cognitively healthy controls from Huddinge municipality were enrolled in a casecontrol study. Cases comprised individuals diagnosed with Alzheimer´s disease (AD), mildcognitive impairment (MCI), or subjective cognitive decline (SCD). All participantsunderwent dental examinations that included panoramic imaging. The primary exposure wasradiologically verified marginal alveolar bone loss (MABL). Generalised MABL was foundto be more prevalent among cases than controls, especially for the AD subgroup. Nobetween-group differences were found for localised MABL. In addition, cases had an overallpoorer oral health status than controls.Paper II explored the subgingival microbiota among AD, MCI and SCD participants andcontrols from paper I. Using 16S rRNA gene sequencing, the compositions of the microbialcommunities were compared across study groups. Only relatively subtle differences wereseen. As signs of periodontitis were more common among the cases than the controls, it wasdifficult to determine whether there would have been actual differences had the periodontitisdistributions been the same. In periodontitis-adjusted models, we demonstrated that thebacterium Prevotella oulorum was present at a higher abundance among cases than controlsand that the bacterium Rothia aeria was less abundant.In paper III, we investigated the dementia incidence in a cohort with or without periodontaldisease at baseline. Data were retrieved from several national registries in Sweden, such asthe Swedish Quality Registry for Caries and Periodontal Diseases and the Swedish DementiaRegistry. During the average eight years of follow-up, the incidence of dementia was shownto be similar in the two groups. No association was evident between periodontal disease anddementia in confounder-adjusted regression models.Paper IV was a cohort study using data from Swedish national registries to investigatewhether tooth loss is associated with the incidence of dementia. Two exposure groups weredefined at the start of the observation period and followed for up to nine years. Severe toothloss (STL) was contrasted with a reference group without the index condition. The dementiaincidence was higher in the group with STL than in the reference group. This finding wasfound to be robust in sensitivity analyses and the confounder-adjusted models.In conclusion, the results in this thesis show the complexity of interactions between dentaldisease and cognitive dysfunction. Among participants with cognitive dysfunction, signs ofgeneralised MABL were more prevalent compared to controls. Differences in the subgingivalmicrobiota were seen, suggesting that cognitive dysfunction was associated with periodontaldisease. In a longitudinal study, periodontal disease was not associated with an increased riskof dementia. In contrast, having severe tooth loss was associated with an increased incidenceof dementia. Thus, severe tooth loss may serve as a marker of dementia risk.
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