Frequency distribution of TMJ internal derangement by gender, age and genotypes of ANKH polymorphisms in the sample of the study (n = 55).

a<p>results based on univariate logistic regression statistics.</p>b<p>results based on multivariate logistic regression statistics when excluding genotypes of ANKH-OR polymorphisms.</p>c<p>results based on multivariate logistic regression statistics when excluding genotypes of ANKH-TR polymorphisms.</p>d<p>mean ± standard deviation (years of age).</p>e<p>each additional 10 years of age.</p

Patient flowchart.

<p>BPs = Bisphosphonates; EMR = Electronic Medical Records. </p

Pre-operative arthroscopic view of the right TMJ from an ANKH-OR homozygote (Genotype 2/2) with closed lock.

<p>The white strip at the right portion of the view indicated fibrous tissues adhering the joint (arrow).</p

Results of ANKH mRNA expression in the TMJ and sequence traces of ANKH polymorphic sites.

<p>(A) Assessment of ANKH mRNA expression in RT-PCR. The sizes of the molecular weight markers (MW) are displayed on the left. Sizes are given in base pairs (bp). (B to G) Sequence traces of identified polymorphic sites on the ANKH gene in the human sample of the study. (B) Genotype 1/1 of ANKH-OR. (C) Genotype 1/2 of ANKH-OR. (D) Genotype 2/2 of ANKH-OR. (E) Genotype 7/7 of ANKH-TR. (F) Genotype 7/8 of ANKH-TR. (G) Genotype 8/8 of ANKH-TR.</p

Receiver operating characteristic curves of risk indices in predicting the incidence of OMJ.

<p>Areas under the curve are 0.683 (95% confidence interval, 0.607 to 0.760) for the solid curve among oral BPs users and 0.718 (0.648 to 0.789) for the dashed curve in all patients.</p

Additional file 2: Figure S2. of Effects of Usag-1 and Bmp7 deficiencies on murine tooth morphogenesis

Malocclusion observed in Usag-1−/− (C57BL/6) mice and Usag-1−/− Bmp7+/− (F2 generation) mice. (A) Normal occlusion. A Usag-1−/− female mouse in the C57BL/6 background at 3 months after birth. These data were added in the analysis of the lower incisors. Scale bar: 1 mm. (B) Normal occlusion. A Usag-1−/−Bmp7+/− male mouse in the F2 generation at 4 months after birth. These data were added in the analysis of the lower incisors. (C) Malocclusion. A Usag-1−/− female mouse in C57BL/6 background at 3 months after birth. The mouse was excluded from the analysis of the lower incisors. (D) Malocclusion. A Usag-1−/−Bmp7+/− female mouse in the F2 generation at 4 months after birth. The mouse was excluded from the analysis of the lower incisors. (TIF 14671 kb

Additional file 1: Figure S1. of Effects of Usag-1 and Bmp7 deficiencies on murine tooth morphogenesis

X-gal staining in mandibular molars of Usag-1+/− (C57BL/6) mice at E14 and E15. Tissue sections from mandibular molars of Usag-1+/− (C57BL/6) mice at E14 and E15 were stained with X-gal. Scale bar: 100 μm. (A, B) Sagittal sections. (C) Coronal sections. (B, C) Usag-1 was expressed (blue) in a small portion of epithelia, except for the enamel knot and the mesenchyme near the tooth germ. (TIF 16106 kb

Characteristics of male participants by masticatory performance.

<p>Continuous variables are presented as medians (interquartile range).</p><p>Categorical variables are presented as numbers (%).</p

Masticatory performance and risk of diabetes.

<p>OR  =  odds ratio; CI  =  confidence interval; ref  =  reference.</p><p>Multivariate ORs for diabetes were adjusted for age (40–49, 50–64 or 65–74), body mass index (<18.5, 18.5–24.9, 25.0–29.9 or ≥30.0), family history of diabetes (no or yes), current smoking (no or yes), current alcohol drinking (no or yes), physical activity (slight, moderate, or strenuous), caloric restriction (no, yes at subject discretion, or yes due to medical diagnosis), rate of eating (slow, intermediate, or fast) and periodontal status (no pathological pockets (score 0, 1 and 2), periodontal pockets (score 3 and 4), or edentulous).</p

USAG-1 antagonises BMP-7 in maxillary supernumerary incisors formation.

<p>Sagittal sections of E15 (A–D) embryos and frontal sections of mice on the day of birth (E–H). (A’–H’) Higher magnification of the boxed regions in (A–H). USAG-1^+/+/BMP-7^+/+, (A, A’, E, E’); USAG-1^−/−/BMP-7^+/+, (B, B’, F, F’); USAG-1^+/+/BMP-7^−/−, (C, C’, G, G’) and USAG-1^−/−/BMP-7^−/− (D, D’, H, H’). The area of rudimentary incisor was measured in transverse sections of USAG-1^+/+/BMP-7^+/+ (white bars), USAG-1^−/−/BMP-7^+/+ (right grey bars), USAG-1^+/+/BMP-7^−/− (dark grey bars) and USAG-1^−/−/BMP-7^−/− (black bars) mice (n = 5) in E15 (I) and P0 (J). At E15, the area of the maxillary deciduous incisor was identified in wild type as well as all mutant mice in the labial border of the epithelial invagination. The size of rudimentary incisor is similar except USAG-1^+/+/BMP-7^−/− at E15 (A, A’, B, B’, C, C’, D, D’ and I).Rudimentary tooth primordia in USAG-1^−/−/BMP-7^−/− and USAG-1^+/+/BMP-7^+/+ regressed and its size became smaller at birth, whereas the teeth in USAG-1^−/−/BMP-7^+/+ continued to develop and enamel organ was formed (E, E’, F, F’, H, H’ and J).</p