Site‐Specific Gingival Bleeding on Probing in a Steady‐State Plaque Environment: Influence of Polymorphisms in the Interleukin‐1 Gene Cluster

Background: We previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)‐1A−889 and IL‐1B+3954 in an Arabic population with gingivitis. In a steady state, the proportion of sites with bleeding on probing (BOP) was consistently reduced. The aim of the present s...

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Veröffentlicht in:Journal of periodontology (1970) Jg. 81; H. 1; S. 52 - 61
Hauptverfasser: Müller, Hans‐Peter, Barrieshi‐Nusair, Kefah M.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Chicago, IL American Academy of Periodontology 01.01.2010
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ISSN:0022-3492, 1943-3670, 1943-3670
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Abstract Background: We previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)‐1A−889 and IL‐1B+3954 in an Arabic population with gingivitis. In a steady state, the proportion of sites with bleeding on probing (BOP) was consistently reduced. The aim of the present study is to expand this observation by considering the site level. Methods: Fifty healthy non‐smoking volunteers, 19 to 28 years of age, participated in this study. Clinical examinations included probing depth, BOP, plaque index (PI), and calculus. Examinations were repeated after 2 and 4 weeks, and subjects were advised not to change oral hygiene habits. Polymorphisms in the IL‐1 gene cluster were assessed using a reverse hybridization assay. Results: Twenty‐six subjects (52%) carried alleles 2 at positions IL‐1A−889 and IL‐1B+3954 and were designated genotype positive. In multivariate multilevel models of BOP, bleeding tendency in subjects with positive IL‐1 genotype was only reduced at sites with PI 0 (odds ratio of 0.98, 0.65, and 0.56 at baseline and 2 and 4 weeks, respectively; χ2(3) = 11.946; P = 0.008) or 1 (χ2(3) = 6.027; P = 0.110). A decreased bleeding tendency at certain tooth types in subjects who were IL‐1 positive was largely related to the relative cleanliness of these areas. Random parts of the models revealed very low biserial correlations of 0.13 to 0.15 at the site level, whereas correlations were considerably higher (0.76 to 0.83) at the subject level. Conclusion: Multilevel modeling of site‐specific data yielded new information about the influence of the IL‐1 genotype in plaque‐induced gingivitis.
AbstractList We previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)-1A(-889) and IL-1B(+3954) in an Arabic population with gingivitis. In a steady state, the proportion of sites with bleeding on probing (BOP) was consistently reduced. The aim of the present study is to expand this observation by considering the site level. Fifty healthy non-smoking volunteers, 19 to 28 years of age, participated in this study. Clinical examinations included probing depth, BOP, plaque index (PI), and calculus. Examinations were repeated after 2 and 4 weeks, and subjects were advised not to change oral hygiene habits. Polymorphisms in the IL-1 gene cluster were assessed using a reverse hybridization assay. Twenty-six subjects (52%) carried alleles 2 at positions IL-1A(-889) and IL-1B(+3954) and were designated genotype positive. In multivariate multilevel models of BOP, bleeding tendency in subjects with positive IL-1 genotype was only reduced at sites with PI 0 (odds ratio of 0.98, 0.65, and 0.56 at baseline and 2 and 4 weeks, respectively; chi(2)((3)) = 11.946; P = 0.008) or 1 (chi(2)((3)) = 6.027; P = 0.110). A decreased bleeding tendency at certain tooth types in subjects who were IL-1 positive was largely related to the relative cleanliness of these areas. Random parts of the models revealed very low biserial correlations of 0.13 to 0.15 at the site level, whereas correlations were considerably higher (0.76 to 0.83) at the subject level. Multilevel modeling of site-specific data yielded new information about the influence of the IL-1 genotype in plaque-induced gingivitis.
Background: We previously reported a high prevalence of a combination of alleles 2 at positions interleukin ( IL)‐1A −889 and IL‐1B +3954 in an Arabic population with gingivitis. In a steady state, the proportion of sites with bleeding on probing (BOP) was consistently reduced. The aim of the present study is to expand this observation by considering the site level. Methods: Fifty healthy non‐smoking volunteers, 19 to 28 years of age, participated in this study. Clinical examinations included probing depth, BOP, plaque index (PI), and calculus. Examinations were repeated after 2 and 4 weeks, and subjects were advised not to change oral hygiene habits. Polymorphisms in the IL‐1 gene cluster were assessed using a reverse hybridization assay. Results: Twenty‐six subjects (52%) carried alleles 2 at positions IL‐1A −889 and IL‐1B +3954 and were designated genotype positive. In multivariate multilevel models of BOP, bleeding tendency in subjects with positive IL‐1 genotype was only reduced at sites with PI 0 (odds ratio of 0.98, 0.65, and 0.56 at baseline and 2 and 4 weeks, respectively; χ 2 (3) = 11.946; P = 0.008) or 1 (χ 2 (3) = 6.027; P = 0.110). A decreased bleeding tendency at certain tooth types in subjects who were IL‐1 positive was largely related to the relative cleanliness of these areas. Random parts of the models revealed very low biserial correlations of 0.13 to 0.15 at the site level, whereas correlations were considerably higher (0.76 to 0.83) at the subject level. Conclusion: Multilevel modeling of site‐specific data yielded new information about the influence of the IL‐1 genotype in plaque‐induced gingivitis.
Background: We previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)‐1A−889 and IL‐1B+3954 in an Arabic population with gingivitis. In a steady state, the proportion of sites with bleeding on probing (BOP) was consistently reduced. The aim of the present study is to expand this observation by considering the site level. Methods: Fifty healthy non‐smoking volunteers, 19 to 28 years of age, participated in this study. Clinical examinations included probing depth, BOP, plaque index (PI), and calculus. Examinations were repeated after 2 and 4 weeks, and subjects were advised not to change oral hygiene habits. Polymorphisms in the IL‐1 gene cluster were assessed using a reverse hybridization assay. Results: Twenty‐six subjects (52%) carried alleles 2 at positions IL‐1A−889 and IL‐1B+3954 and were designated genotype positive. In multivariate multilevel models of BOP, bleeding tendency in subjects with positive IL‐1 genotype was only reduced at sites with PI 0 (odds ratio of 0.98, 0.65, and 0.56 at baseline and 2 and 4 weeks, respectively; χ2(3) = 11.946; P = 0.008) or 1 (χ2(3) = 6.027; P = 0.110). A decreased bleeding tendency at certain tooth types in subjects who were IL‐1 positive was largely related to the relative cleanliness of these areas. Random parts of the models revealed very low biserial correlations of 0.13 to 0.15 at the site level, whereas correlations were considerably higher (0.76 to 0.83) at the subject level. Conclusion: Multilevel modeling of site‐specific data yielded new information about the influence of the IL‐1 genotype in plaque‐induced gingivitis.
We previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)-1A(-889) and IL-1B(+3954) in an Arabic population with gingivitis. In a steady state, the proportion of sites with bleeding on probing (BOP) was consistently reduced. The aim of the present study is to expand this observation by considering the site level.BACKGROUNDWe previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)-1A(-889) and IL-1B(+3954) in an Arabic population with gingivitis. In a steady state, the proportion of sites with bleeding on probing (BOP) was consistently reduced. The aim of the present study is to expand this observation by considering the site level.Fifty healthy non-smoking volunteers, 19 to 28 years of age, participated in this study. Clinical examinations included probing depth, BOP, plaque index (PI), and calculus. Examinations were repeated after 2 and 4 weeks, and subjects were advised not to change oral hygiene habits. Polymorphisms in the IL-1 gene cluster were assessed using a reverse hybridization assay.METHODSFifty healthy non-smoking volunteers, 19 to 28 years of age, participated in this study. Clinical examinations included probing depth, BOP, plaque index (PI), and calculus. Examinations were repeated after 2 and 4 weeks, and subjects were advised not to change oral hygiene habits. Polymorphisms in the IL-1 gene cluster were assessed using a reverse hybridization assay.Twenty-six subjects (52%) carried alleles 2 at positions IL-1A(-889) and IL-1B(+3954) and were designated genotype positive. In multivariate multilevel models of BOP, bleeding tendency in subjects with positive IL-1 genotype was only reduced at sites with PI 0 (odds ratio of 0.98, 0.65, and 0.56 at baseline and 2 and 4 weeks, respectively; chi(2)((3)) = 11.946; P = 0.008) or 1 (chi(2)((3)) = 6.027; P = 0.110). A decreased bleeding tendency at certain tooth types in subjects who were IL-1 positive was largely related to the relative cleanliness of these areas. Random parts of the models revealed very low biserial correlations of 0.13 to 0.15 at the site level, whereas correlations were considerably higher (0.76 to 0.83) at the subject level.RESULTSTwenty-six subjects (52%) carried alleles 2 at positions IL-1A(-889) and IL-1B(+3954) and were designated genotype positive. In multivariate multilevel models of BOP, bleeding tendency in subjects with positive IL-1 genotype was only reduced at sites with PI 0 (odds ratio of 0.98, 0.65, and 0.56 at baseline and 2 and 4 weeks, respectively; chi(2)((3)) = 11.946; P = 0.008) or 1 (chi(2)((3)) = 6.027; P = 0.110). A decreased bleeding tendency at certain tooth types in subjects who were IL-1 positive was largely related to the relative cleanliness of these areas. Random parts of the models revealed very low biserial correlations of 0.13 to 0.15 at the site level, whereas correlations were considerably higher (0.76 to 0.83) at the subject level.Multilevel modeling of site-specific data yielded new information about the influence of the IL-1 genotype in plaque-induced gingivitis.CONCLUSIONMultilevel modeling of site-specific data yielded new information about the influence of the IL-1 genotype in plaque-induced gingivitis.
Author Müller, Hans‐Peter
Barrieshi‐Nusair, Kefah M.
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crossref_primary_10_1111_jcpe_12118
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Issue 1
Keywords genetic
interleukin-1
Stomatology
Dental disease
Dental plaque
Dentistry
Multivariate analysis
Gingivitis
Hemorrhage
Steady state
Periodontal disease
Gene
Interleukin 1
Environment
Genetics
Gingiva
Polymorphism
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Snippet Background: We previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)‐1A−889 and IL‐1B+3954 in an Arabic population...
Background: We previously reported a high prevalence of a combination of alleles 2 at positions interleukin ( IL)‐1A −889 and IL‐1B +3954 in an Arabic...
We previously reported a high prevalence of a combination of alleles 2 at positions interleukin (IL)-1A(-889) and IL-1B(+3954) in an Arabic population with...
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StartPage 52
SubjectTerms Adult
Arabs - genetics
Biological and medical sciences
Dental plaque
Dental Plaque - physiopathology
Facial bones, jaws, teeth, parodontium: diseases, semeiology
Female
Genetic Predisposition to Disease
Gingival Hemorrhage - etiology
Gingival Hemorrhage - genetics
gingivitis
Gingivitis - complications
Gingivitis - genetics
Humans
Interleukin-1alpha - genetics
Interleukin-1beta - genetics
interleukin‐1
Male
Medical sciences
Multilevel Analysis
multivariate analysis
Non tumoral diseases
Otorhinolaryngology. Stomatology
Periodontal Index
Polymorphism, Genetic
Reference Values
Young Adult
Title Site‐Specific Gingival Bleeding on Probing in a Steady‐State Plaque Environment: Influence of Polymorphisms in the Interleukin‐1 Gene Cluster
URI https://onlinelibrary.wiley.com/doi/abs/10.1902%2Fjop.2009.090315
https://www.ncbi.nlm.nih.gov/pubmed/20059417
https://www.proquest.com/docview/733882269
Volume 81
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