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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 陳秀熙(Hsiu-Hsi Chen) | |
dc.contributor.author | Ting-Ting Wang | en |
dc.contributor.author | 汪婷婷 | zh_TW |
dc.date.accessioned | 2021-06-13T04:46:55Z | - |
dc.date.available | 2006-08-03 | |
dc.date.copyright | 2006-08-03 | |
dc.date.issued | 2006 | |
dc.date.submitted | 2006-07-17 | |
dc.identifier.citation | Albandar JM, Brunelle JA, Kingman A. Destructive Periodontal Disease in Adults 30 Years of Age and Older in the United States, 1988-1994. J Periodontol 1999; 70: 13-29.
Benveniste R, Bixler D, Conneally PM.Periodontal disease in diabetics. J periodontal 1967;38:271-279. Bergstrom J, Preber H. Tobacco use as a risk factor. J Periodontol 1994; 65: 545-550. Campus G, Salem A, Uzzau S, Baldoni E, Tonolo G. Diabetes and periodontal disease : a case-control study. J Periodontol 2005;76:418-425 Christen AG. Dentistry and the alcoholic patient. Dental Clinics of North America 1983; 27: 341. Cianciola LJ, Park BH, Bruck E, Mosovich L, Genco RJ. Prevalence of periodontal disease in insulin-dependent diabetes mellitus (juvenile diabetes). J Am Dental Asso 1982; 104: 653-660. Chiu YH, Chen LS, Chan CC, Liou DM, Wu SC, Kuo HS, et al. Health information system for community-based multiple screening in Keelung,Taiwan (Keelung Community-Based Integrated Screening No. 3). Int J Med Inform 2006;75:369-383. Chen THH, Chiu YC, Luh DL, et al. Taiwan Community-based Integrated Screening Group. Community-based multiple screening model:design, implementation, and analysis of 42,387 participants. Cancer 2004;100:1734–43 Collin HL, Uusitupa M, Niskanen L, Kontturi-Narhi V, Markkanen H, Koivisto AM, Meurman JH. Periodontal findings in elderly patients with non-insulin dependent diabetes mellitus. J Periodontol 1998;69(9):962-6. Genco RJ. Current view of risk factors for periodontal diseases. J periodontal 1996;67:1041-1049 Gottsegen R. Diabetes mellitus, cardiovascular diseases and alcoholism. In: Periodontal Diseases, eds. Schluger S, Yuodelis R, Page RC, Johnson RH, 2, pp.273-283. Philadelphia: Lea & Febiger. Emrich LJ, Shlossman M, Genco RJ. Periodontal disease in non-insulin-dependent diabetes mellitus. J periodontal 1991;62:`123-131. Farley JR, Fitzsimmons R, Taylor AK, Jorch UM, Lau KH. Direct effects of ethanol on bone resorption and formation in vitro. Archives of Biochemistry and Biophysics 1985; 238: 305-314. Haber J, Wattles J, and Crowley M, et al. Evidence for cigarette smoking as a major risk factor for periodontitis. J Periodontol 1993; 64: 16-23. Hart TC, Kornman KS. Genetic factors in the pathogenesis of periodontitis. Periodontol 2000. 1997; 14:202-215. Holbrook TL, Barret-Conner E. A prospective study of alcohol consumption and bone mineral density. BMJ 1993; 306: 1506-1509. Hove KA, Stallard RE.Diabetes and the periodontal patient. J Peruodontal 1970;41:713-718. Iacono VJ, Singh S, Golub LM, Ramamurthy NS, Kaslick R. In vivo assay of crevicular leukocyte migration. Its development and potential applications. J Periodontol 1985;56(11 Suppl):56-62. Katz J. Elevated blood glucose levels in patients with severe periodontal disease. J Clin Periodontol 2001; 28: 710-712. Katz J, Chaushu G, Sharabi Y. On the association between hypercholesterolemia, cardiovascular disease and severe periodontal disease. J Clin Periodontol 2001;28:865-868. Kuo Y, Chih-Jen C, Ping-Chi H, et al. Detection of putative periodontal pathogens in non-insulin-dependent diabetes mellitus by polymerase chain reaction. J Periodontol Res 2001;36:18-24. Moniz C. Alcohol and bone. British Medical Bulletin 1994; 50: 67-75. Movin S. Relationship between periodontal disease and cirrhosis of the liver in humans. J Clin Periodontol 1981; 8: 450-458. Nelson RG, Shiossman M, Budding LM, et al.Periodontal disease and NIDDM in Pima Indians.Diabetes Care.1990;13:836-840. Novacek G, Plachetzky U, Potzi R, Lentner S, Slavicek R, Gangl A, Ferenci P. Dental and periodontal disease in patients with cirrhosis-role of etiology of liver disease. J Hepatol 1995; 22: 576-582. Rodrigues DC, Taba MJ, Novaes AB, Souza SL, Grisi MF. Effect of non-surgical periodontal therapy on glycemic control in patients with type2 diabetes mellitus. J Periodontol 2003;74:1361-1367. Saito T, Shimazaki Y, Kiyohara Y, Kabo M, Koga T. The severity of intolerance in non-diabetics: the Hisayama study. J Dent Res.2004;83:485-90. Saito T, Shimazaki Y, Kiyohara Y, Kato I, Kabo M, Iida M, Yamashita Y. Relationship between obesity, glucose tolerance, and periodontal disease in Japanese women: the Hisayama study. J Periodontal Res 2005 ;40:346-53. Sara G, Grossi. Treatment of Periodontal Disease and Control of Diabetes: An Assessment of the Evidence and Need for Future Research. Ann Periodontol 2001;6:138-145 Segura-Egea JJ, Jimenez-Pinzon A, Rios-Santos JV, Velasco-Ortega E, Cisneros-Cabello R, Poyato-Ferrera M. High prevalence of apical periodontitis amongst type2 diabetic patients. Int Endod J 2005;38:564-569. Soskolne WA and Klinger A. The relationship between periodontal disease and diabetes: an overview. Ann Periodontol 2000; 6:91-98. Stewart JE, Wager KA, Friedlander AH, Zadeh HH. The effect of periodontal treatment on glycemic control in patients with type2 diabetes mellitus. J Clin periodontol 2001;28:301-310. Safkan-Seppala B, Ainamo J. Periodontal conditions in insulin-dependent diabetes mellitus. J Clin Periodontol 1992; 19: 24-29. Shlossman M, Knowler WC, Pettitt DJ, Genco RJ. Type 2 diabetes mellitus and periodontal disease. J Am Dent Assoc. 1990;121(4):532-6. Taylor GW. Bidirectional Interrelationships Between Diabetes and Periodontal Disease: An Epidemiologic Perspective. Ann Periodontol 2001;6:99-112 Tezal M, Grossi SG, Ho AW, Genco RJ. The effect of alcohol consumption on periodontal disease. J Periodontol 2001;72(2):183-9. Tezal M, Grossi SG, Ho AW, Genco RJ.Alcohol consumption and periodontal disease.The Third National Health and Nutrition Examination Survey.J Clin Periodontol. 2004;31:484-8. Tervonen T, Knuuttila M. Relation of diabetes control to periodontal pocketing and alveolar bone level. Oral Surgery Oral Med Oral Pathol 1986; 61: 346-349. Tung TH, Chiu YH, Chen LS, Wu HM, Boucher BJ, Chen THH. A population-based study of the association between Areca-nut chewing and Type 2 diabetes mellitus in men (Keelung Community-based Integrated Screening Programme No. 2). Diabetologia 2004;47:1776–81. US Public Health Service, National Institute of Dental Research. Oral Health of United States Adults; National Findings. NIH Publication No 87-2868. Bethesda, MD; NIDR, 1987. Ueta E, Osaki T, Yoneda K, Yamamoto T. Prevalence of diabetes mellitus in odontogenic infections and oral candidiasis: an analysis of neutrophil suppression. J Oral Pathol Med 1993;22(4):168-74. Ver der Velden U. The onset age of periodontal destruction. J Clin Periodontol 1991; 18:380-383. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/33552 | - |
dc.description.abstract | 背景:本研究利用社區牙周指數(community periodontal index, CPI)及附連指數(attachment loss, LA)為工具,於基隆市社區整合式篩檢(Keelung community-based integrated screening, KCIS)針對35-44歲個案進行社區大規模牙周病篩檢。本研究以首次牙周篩檢及參加兩次以上篩檢資料可分別獲得牙周病盛行率及發生率。此外,本研究分別以橫斷性及世代追蹤性研究進行糖尿病與牙周病相關分析。並根據上述所獲得的盛行率、發生率及盛行率池(prevalence pool)進行牙周病平均滯留期(Mean Sojourn Time, MST)估計。
材料與方法:本研究以基隆市社區闔家歡篩檢為主,邀請2003至2005年年齡35-44歲參加民眾牙周病篩檢,同時進行CPI及LA為篩檢方法。每年篩檢執行前,先針對參加的牙醫師進行牙周病相關訓練課程,包括牙周檢查方法、牙周診斷、治療及照護等。參加個案於整合式篩檢除了參與牙周檢查外,並同時進行抽血及問卷訪視。本研究以個案參加第一次篩檢資料為橫斷性研究,除了盛行率外,以單變項及多變項邏輯氏迴歸模式(Logistic regression Model)進行牙周病與糖尿病及其他相關危險因子探討,透過調整其他危險因子後,分析糖尿病與牙周病的相關。另外,本研究利用有參加兩次以上的個案進行發生率分析,並進一步估計牙周病累積發生機率。本研究以卜瓦松迴歸模式進行牙周病發生之危險因子探討。本研究並進一步利用發生率及平均滯留期倒數建構牙周病三階段模式,包括無牙周病、牙周病及缺牙,並估算每階段轉移機率。 結果:本研究共計有8765名個案進入本研究。如果以CPI為診斷標準,取六個Sextants最為嚴重CPI的為代表性,並定義CPI>=3為牙周病個案,整體而言,牙周病盛行率約29%; 如果以附連指數(LA)為診斷,定義LA>=1為牙周個案時,其總盛行率約35%. 以CPI為指標之牙周病盛行率,男性約35.7% 及女性約25.9%,不論於男性或女性其牙周病盛行率皆呈現隨著年齡增加而增加。本研究進行有糖尿病或無糖尿病之兩組,結果有糖尿病族群相對於其無糖尿病個案其高出發生率11.3%,其中男性之糖尿病高於無糖尿病者約11.4% 及女性9%。以嚼食檳榔有無進行牙周病盛行率分析,有嚼食檳榔的個案與無嚼食檳榔個案比較,約高出14.3%。多變項邏輯氏迴歸模式分析,結果顯著相關因子包括年齡 (OR=1.06(95%CI: 1.04-1.07)), 年齡(OR=1.33(CI: 1.17-1.51)), 每天早晚有刷牙習慣相對於無習慣者 (OR=0.70(CI: 0.52-0.95)),有嚼食檳榔鄉對於無嚼食檳榔 (OR=1.29(CI: 1.08-1.54)), 有抽菸習慣者相對於無習慣者 (OR=1.23(CI: 1.07-1.40)),腰圍>=80公分 (OR=1.23(CI: 1.05-1.43)), 以及糖尿病 (OR=1.45(CI: 1.09-1.92))。如果以LA指標為牙周病診斷進行糖尿病與牙周病相關分析,結果呈現邊緣性統計相關。 本研究分別計算出各種背景下之發生率,包括年齡、性別、糖尿病有無及嚼食檳榔有無。整體牙周病發生率約(月份)每千人14.61 (12.75-16.75). 牙周病發生率隨著年齡增加而增加,其中35-39歲牙周病發生率約每千人13.97 (11.76-16.61),40-44歲牙周病發生率約每千人15.81 (12.66-19.74)。以發生率進行1-5年累積發生機率模擬,結果逐年分別為16.08%, 29.58%, 40.90%, 50.40%, and 58.38%。本研究發現有糖尿病個案相對於無糖尿病個案或嚼食檳榔者相對於無嚼食檳榔者,其牙周病累積發生機率皆呈現較高。以卜瓦松模式進行分析,調整其他相關危險因子後,僅嚼食檳榔因素呈現統計顯著相關 (相對危險值=2.13 (95%CI: 1.31-3.46)),顯示糖尿病影響牙周病發生。牙周病發生危險相關因素分析中,調整嚼檳榔習慣後,糖尿病未達統計顯著意義(RR=1.66(95%CI:0.82-3.36))。在牙周病平均滯留期估計方面,本研究利用盛行池(發生率及盛行率)觀念進行估算,整體而言,在牙周病沒有任何積極介入下,牙周病平均滯留期約28.46個月。而在三階段模式中,估計結果顯示一年內由無牙周病轉移至牙周病的機率約15.16% ,另由牙周病轉移至缺牙機率約4.53%。 結論:本研究以盛行世代證明糖尿病與牙周病是有相關的,但若以無牙周病之追蹤世代則未呈現有意義相關,而是檳榔顯示強烈相關,依據所估計平均滯留期建議牙周治療間隔時間為一年。 | zh_TW |
dc.description.abstract | Background: This study was carried out to demonstrate the prevalence and incidence rate of periodontal disease(PD) by community periodontal index (CPI) and attachment loss (LA) and investigated the associations between Type 2 diabetes mellitus and periodontal disease by controlling for possible confounding factors by using community-based survey in Keelung. We also estimated the mean sojourn time (MST) of periodontal disease (PD) by prevalence pool concept.
Methods: Study population was based on participants in routine KCIS program who were 35-44 years from 2003 to 2005. The CPI and LA were used as screening tool to assess the status of PD. The courses focused on periodontal examination, diagnosis and basic treatment were carried out before the activity of Keelung Community-based Integrated Screening (KCIS) every year. The bioassay and questionnaire information were simultaneously collected by KCIS. To assess the effect of Type 2 DM on PD, a prospective cohort free of PD was designed for the investigation of the effect of Type 2 DM on PD. The univariate and multiple logistic regressions were performed to identify significant factors responsible for occurrence of PD. We used cumulative density method to calculate cumulative risk for developing PD based on incidence rate. Poisson regression model was further used to identify significant factors responsible for occurrence of incident PD. We applied prevalence pool concept based on prevalent cases at first survey and incidence cases after following up the cohort free of PD. The natural history of periodontal disease was proposed by three-state model for progression from free of PD, PD, and severest or tooth loss. Results: The total of eligible 8765 attendants participated this KCIS multiple screening. The overall rate of PD defined by taking the severest one of CPI greater than 3 in different sextants in individual level was 29%. Similar findings were also noted for PD defined by loss attachment (LA>=1). The overall prevalence rate of loss attachment was 35%. The prevalence rates of severe CPI of male and female were 35.7% and 25.9% respectively. The prevalence rate increased with advancing age. The prevalence rate of PD in type2 diabetes was higher than that in non-diabetes by 11.3%, with 11.4% for male and 9% for female. The prevalence rate of PD in subjects with betel quids chewing was statistically higher than that in subjects without betel quids chewing by 14.3%. Multivariate logistic regression including significant indicated age (OR=1.06(CI: 1.04-1.07)), gender (OR=1.33(CI: 1.17-1.51)), twice brush-teeth per day (OR=0.70(CI: 0.52-0.95)), betel quid chewing (OR=1.29(CI: 1.08-1.54)), cigarette Smoking (OR=1.23(CI: 1.07-1.40)), Waist (OR=1.23(CI: 1.05-1.43)), and Type 2 DM (OR=1.45(CI: 1.09-1.92)). The association between Type 2 DM and PD defined by LA was borderline significant. The overall incidence of PD and specific incidence by age, gender, presence of Type 2 DM, and betel quids chewing. The incidence rate (in month) in the overall group was 14.61 (12.75-16.75) per 1000. The incidence rate (per 1000) increased with age, with 13.97 (11.76-16.61) per 1000 for subjects aged 35-39 years and 15.81 (12.66-19.74) per 1000 for subjects aged 40-44 years. The risks for PD for the overall group were 16.08%, 29.58%, 40.90%, 50.40%, and 58.38% at 1, 2, 3, 4 and 5 year of follow-up. Those diagnosed as T2DM or with the habit of betel quids chewing had higher risk for developing PD than those without Type 2 DM or the habit of betel quids chewing. After adjusting for significant factors obtained from univariate analysis, only betel quids chewing (relative risk=2.13 (CI: 1.31-3.46)) was statistically associated with the development of PD. The effect of T2DM on occurrence of PD was not statistically significant after controlling for betel quids chewing. The application of prevalence pool equation yielded 28.46 months of MST in chronic state for PD patients without appropriate intervention. The risk for having PD and for tooth missing during one-year period was 15.16% and 4.53% respectively. Conclusions: We demonstrated a positive association between early-detected T2DM and PD based on a large population-based and community-oriented program targeted at habitant aged 35-44 years. However, the effect of Type 2 DM on newly discovered PD didn’t show significant finding. Instead, incidence rate was higher for those with the habit of betel quids chewing. This suggests the influence of Type 2 DM may be predominated by the impact of betel quids chewing. The MST estimated in the current study suggests one-year as an appropriate inter-examination interval for PD. | en |
dc.description.provenance | Made available in DSpace on 2021-06-13T04:46:55Z (GMT). No. of bitstreams: 1 ntu-95-P93846001-1.pdf: 621490 bytes, checksum: 1c10396b6f72f4554ddb488a1e6c3da4 (MD5) Previous issue date: 2006 | en |
dc.description.tableofcontents | 第一章 緒論 1
一、 研究背景 1 二、 研究目的 3 第二章 牙周病與糖尿病及其他相關危險因子文獻探討 4 一、年齡(Age) 8 二、性別(Gender) 9 三、社經地位(Socioeconomic Status) 9 四、抽菸(smoking) 9 五、飲酒 9 六、 肥胖 10 七、先天性缺陷或疾病 12 八、家族聚集(Familial aggregation) 12 第三章 材料與方法 13 一、 研究族群 13 二、 研究設計 14 三、 社區篩檢資料收集 16 四、 牙周病測量及分類 16 五、 分析方法 17 第四章結果 21 一、基本發現 21 二、盛行率及發生率 23 三、盛行世代危險因子探討 24 第五章討論 56 一、研究主要發現 56 二、研究方法及設計新穎 56 三、過去研究比較 57 四、因果關係 58 五、牙周病平均停留期間 59 六、牙周病造成糖尿病 59 七、研究限制 59 第六章結論 64 參考文獻 65 圖表目錄 表1、2003-2005年社區闔家歡篩檢牙周篩檢年齡分布情形 31 表2、社區牙周病篩檢參加及未參加之及年齡分布 32 表3、社區牙周病篩檢參加及未參加牙周病篩檢之教育程度分佈情形 33 表4、社區牙周病篩檢牙周指數(CPI)檢查結果 34 表5、社區牙周病篩檢之附連喪失(Loss Attachment, LA)檢查結果 35 表6、社區牙周病篩檢性別及各年齡層牙周病(CPI>=3)盛行率 36 表7、社區牙周病篩檢性別及各年齡層牙周病(LA>=1)盛行率 37 表8、社區牙周病篩檢性別及各年齡層糖尿病與非糖尿病牙周病盛行率 38 表9、社區牙周病篩檢性別及各年齡層有無嚼檳榔習慣者其牙周病盛行率 39 表10、探討性別與糖尿病、嚼食檳榔之牙周病發生率 40 表11、社區牙周病篩檢牙周病(CPI≥3)與相關危險因子之分析 41 表12、社區牙周病篩檢附連喪失(LA≥1)與相關危險因子分析 42 表13、社區牙周病篩檢牙周病(CPI 0-4)與相關危險因子分析 43 表14、社區牙周病篩檢牙周病(LA 0-4)與相關危險因子分析 44 表15、社區牙周病篩檢對牙周病(CPI>=3)發生之相關危險因子分析(logistic單變項) 45 表16、探討糖尿病及相關危險因子對牙周病(CPI>=3)發生之分析(logistic多變項) 46 表17、探討高血糖及相關危險因子對牙周病(CPI>=3)發生之分析(logistic多變項) 47 表18、社區牙周病篩檢對牙周病(CPI>=3)發生之相關危險因子分析(單變項) 48 表19、探討性別、糖尿病及嚼食檳榔之牙周疾病期間分析 49 表20、性別、糖尿病有無、嚼食檳榔有無之牙周病或缺牙之疾病轉移機率 50 表21、以性別及牙周病有無之糖尿病發生率分析 60 表22、糖尿病發生之相關危險因子單變項分析 61 表23、參加一次及參加二次以上之年齡層比較 62 表24、參加一次及參加二次以上之教育程度比較 63 | |
dc.language.iso | zh-TW | |
dc.title | 糖尿病與牙周病相關危險因子探討 | zh_TW |
dc.title | Elucidating the Effect of Type2 Diabetes on Periodontal Disease | en |
dc.type | Thesis | |
dc.date.schoolyear | 94-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 許銘能(Ming-Nong Shiu),嚴明芳(Ming-Fang Yeu),張淑惠(Shu -Hui chang),鄭錦暉 | |
dc.subject.keyword | 第二型糖尿病,牙周病,社區整合式篩檢,社區牙周病指數,附連指數, | zh_TW |
dc.subject.keyword | Type 2 Diabetes,Periodontal Disease,Community-based integrated screening, | en |
dc.relation.page | 125 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2006-07-18 | |
dc.contributor.author-college | 公共衛生學院 | zh_TW |
dc.contributor.author-dept | 預防醫學研究所 | zh_TW |
顯示於系所單位: | 流行病學與預防醫學研究所 |
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