MSX1 and PAX9 have been associated with tooth agenesis in mice and humans, but interestingly for humans, these genes are associated with specific missing teeth.
Splinted teeth did not show significantly increased risk of tooth loss compared with non-splinted teeth (HR; 95% CI: 1.30; 0.87-1.93); while age (1.07; 1.05-1.09), PPD >6 mm (4.24; 1.26-14.31), bone loss (mean HR was 5.07-15.36 depending on severity), tooth location (posterior versus anterior teeth: HR 2.08; 1.24-3.49) and the number of occlusal contact areas (mean HR was 4.38-17.34 depending on the number of antagonistic contact areas) were associated with tooth loss.
Splinted teeth did not show significantly increased risk of tooth loss compared with non-splinted teeth (HR; 95% CI: 1.30; 0.87-1.93); while age (1.07; 1.05-1.09), PPD >6 mm (4.24; 1.26-14.31), bone loss (mean HR was 5.07-15.36 depending on severity), tooth location (posterior versus anterior teeth: HR 2.08; 1.24-3.49) and the number of occlusal contact areas (mean HR was 4.38-17.34 depending on the number of antagonistic contact areas) were associated with tooth loss.
We investigated 30 traits including "global" [e.g., number of natural teeth (NT) and incident tooth loss], clinically defined (e.g., dental caries via the DMFS index, periodontitis via the CDC/AAP and WW17 classifications), and biologically informed (e.g., subgingival pathogen colonization and "complex" traits).
Splinted teeth did not show significantly increased risk of tooth loss compared with non-splinted teeth (HR; 95% CI: 1.30; 0.87-1.93); while age (1.07; 1.05-1.09), PPD >6 mm (4.24; 1.26-14.31), bone loss (mean HR was 5.07-15.36 depending on severity), tooth location (posterior versus anterior teeth: HR 2.08; 1.24-3.49) and the number of occlusal contact areas (mean HR was 4.38-17.34 depending on the number of antagonistic contact areas) were associated with tooth loss.
Splinted teeth did not show significantly increased risk of tooth loss compared with non-splinted teeth (HR; 95% CI: 1.30; 0.87-1.93); while age (1.07; 1.05-1.09), PPD >6 mm (4.24; 1.26-14.31), bone loss (mean HR was 5.07-15.36 depending on severity), tooth location (posterior versus anterior teeth: HR 2.08; 1.24-3.49) and the number of occlusal contact areas (mean HR was 4.38-17.34 depending on the number of antagonistic contact areas) were associated with tooth loss.
The predictive value of oral health ratings for tooth loss was comparable to that of the CDC/AAP case definition or caries and periodontitis diagnostics.
Risk of tooth loss was significantly increased in active smokers (HR[95% CI]: 4.94[1.91/12.75]), the upper dental arch (1.94[1,16/3.25]), with each mm of residual PPD (1.41[1.29/1.53]), teeth with furcation involvement (FI) (HR 4.00-4.44 for different degrees) and mobility (5.39 [2.06/14.1] for degree III).
Risk of tooth loss was significantly increased in active smokers (HR[95% CI]: 4.94[1.91/12.75]), the upper dental arch (1.94[1,16/3.25]), with each mm of residual PPD (1.41[1.29/1.53]), teeth with furcation involvement (FI) (HR 4.00-4.44 for different degrees) and mobility (5.39 [2.06/14.1] for degree III).
Risk of tooth loss was significantly increased in active smokers (HR[95% CI]: 4.94[1.91/12.75]), the upper dental arch (1.94[1,16/3.25]), with each mm of residual PPD (1.41[1.29/1.53]), teeth with furcation involvement (FI) (HR 4.00-4.44 for different degrees) and mobility (5.39 [2.06/14.1] for degree III).
Risk of tooth loss was significantly increased in active smokers (HR[95% CI]: 4.94[1.91/12.75]), the upper dental arch (1.94[1,16/3.25]), with each mm of residual PPD (1.41[1.29/1.53]), teeth with furcation involvement (FI) (HR 4.00-4.44 for different degrees) and mobility (5.39 [2.06/14.1] for degree III).
Individuals with a c.1072C > T mutation in the EDAR-gene displayed a typical pattern of congenitally missing teeth in the frontal area with functional consequences.
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.
MSX1 and PAX9 have been associated with tooth agenesis in mice and humans, but interestingly for humans, these genes are associated with specific missing teeth.
Multivariate analysis that included age demonstrated that tooth loss is an independent prognostic factor (hazard ratio 1.87, 95% confidence interval 1.22-2.87), in addition to clinical T stage and preoperative serum albumin.
These findings suggest that the loss of teeth causes spatial cognitive impairment in rats and that the underlying mechanism might be associated with a decrease in CBF and an increase in the glutamate level in the hippocampus.
No significant differences in sFRP5 serum levels were found among patients with periodontitis without tooth loss (6.0 [2.5-15.8] ng/ml, median [IQR]) and controls (3.1 [0.0-10.6] ng/ml, median [IQR], p = 0.06).
The anti-Ro/SSA-negative group showed less rheumatoid factor positivity (p<0.001), leucopenia (p=0.003), hyper-gammaglobulinaemia (p<0.001), lower serum β2-microglobulin level (p=0.034), more anti-centromere antibody positivity (p<0.001), higher score in dryness domain of EULAR SS patient-reported index (p=0.048) and more positivity for peripheral nervous system domain in EULAR SS disease activity index and loss of teeth in SS disease damage index (p=0.021 and 0.041, respectively) than patients who were positive for anti-Ro/ SSA antibody.
In this case report we describe a family with c.1972delA, p.Ser658Alafs*31 nonsense variant in AXIN2 where the three confirmed carriers presented with both oligodontia and colorectal adenomatous polyposis; mean number of teeth missing in carriers was 16.5 (range 11-22) and mean number of polyps in carriers was 49 (range 5->100, polyps were predominantly adenomatous).