Here we report a GWAS for "high" gingival crevicular fluid IL-1β expression among 4910 European-American adults and identify association signals in the IL37 locus. rs3811046 at this locus (p = 3.3 × 10<sup>-22</sup>) is associated with severe chronic periodontitis (OR = 1.50; 95% CI = 1.12-2.00), 10-year incident tooth loss (≥3 teeth: RR = 1.33; 95% CI = 1.09-1.62) and aggressive periodontitis (OR = 1.12; 95% CI = 1.01-1.26) in an independent sample of 4927 German/Dutch adults.
IL-1 positive genotypes increase the risk of tooth loss, while no association found between the bleeding on probing (BOP), clinical attachment loss (CAL) and plaque index (PI) with the genotype status.
Age (p=0.0018), absence of IL-1 composite genotype (p=0.0091) and educational status (p=0.0085) were identified as statistically significant risk factors for tooth loss.
Poisson regressions identified mean plaque index during SPT (p<0.0001), irregular attendance of SPT (p<0.0001), age (p<0.0001), initial diagnosis (p=0.0005), IL-1 polymorphism (p=0.0007), smoking (p=0.0053), and sex (p=0.0487) as factors significantly contributing to tooth loss.
The purpose of this study is to assess the role of the interleukin-1 (IL-1) polymorphism on the rate of bone and tooth loss in non-smoking periodontally treated patients during maintenance.
IL-1 positive genotypes increase the risk of tooth loss, while no association found between the bleeding on probing (BOP), clinical attachment loss (CAL) and plaque index (PI) with the genotype status.
Age (p=0.0018), absence of IL-1 composite genotype (p=0.0091) and educational status (p=0.0085) were identified as statistically significant risk factors for tooth loss.
Poisson regressions identified mean plaque index during SPT (p<0.0001), irregular attendance of SPT (p<0.0001), age (p<0.0001), initial diagnosis (p=0.0005), IL-1 polymorphism (p=0.0007), smoking (p=0.0053), and sex (p=0.0487) as factors significantly contributing to tooth loss.
The purpose of this study is to assess the role of the interleukin-1 (IL-1) polymorphism on the rate of bone and tooth loss in non-smoking periodontally treated patients during maintenance.
Mixed-effects models showed that tooth loss was associated with a greater decline in walking speed over time after adjustment for lifestyle-related factors and chronic diseases (p = 0.001 for interaction between time and tooth loss on walking speed decline); however, when further adjusting for inflammation (CRP), the association was attenuated and no longer significant.
Genetic variations in genes known to be associated with EDs that affect only one derivative of the ectoderm (attenuated phenotype) will be grouped as non-syndromic traits of the causative gene (e.g., non-syndromic hypodontia or missing teeth associated with pathogenic variants of EDA "ectodysplasin").
The impact of WNT10A variants on dental development increases with presence of the nonsense c.(321C>A p.(C107*)) variant and the number of missing teeth.
Significant differences in the number of some primary missing teeth (incisor and canine) related to EDA-EDAR genes defects were detected for the first time between XLHED and autosomal recessive HED, suggesting differential local effects of EDA-EDAR genes during odontogenesis.
The significantly smaller tooth crown dimensions recorded in the affected family members show that the effect of the PAX9 mutation is seen not only in the congenitally missing teeth but also in smaller crown size throughout the dentition.