Case-control study of early childhood caries in Australia

The aim of this case-control study of 617 children was to investigate early childhood caries (ECC) risk indicators in a non-fluoridated region in Australia. ECC cases were recruited from childcare facilities, public hospitals and private specialist clinics to source children from different socioeconomic backgrounds. Non-ECC controls were recruited from the same childcare facilities. A multinomial logistic modelling approach was used for statistical analysis. The results showed that a large percentage of children tested positive for Streptococcus mutans if their mothers also tested positive. A common risk indicator found in ECC children from childcare facilities and public hospitals was visible plaque (OR 4.1, 95% CI 1.0-15.9, and OR 8.7, 95% CI 2.3-32.9, respectively). Compared to ECC-free controls, the risk indicators specific to childcare cases were enamel hypoplasia (OR 4.2, 95% CI 1.0-18.3), difficulty in cleaning child's teeth (OR 6.6, 95% CI 2.2-19.8), presence of S. mutans (OR 4.8, 95% CI 0.7-32.6), sweetened drinks (OR 4.0, 95% CI 1.2-13.6) and maternal anxiety (OR 5.1, 95% CI 1.1-25.0). Risk indicators specific to public hospital cases were S. mutans presence in child (OR 7.7, 95% CI 1.3-44.6) or mother (OR 8.1, 95% CI 0.9-72.4), ethnicity (OR 5.6, 95% CI 1.4-22.1), and access of mother to pension or health care card (OR 20.5, 95% CI 3.5-119.9). By contrast, a history of chronic ear infections was found to be protective for ECC in childcare children (OR 0.28, 95% CI 0.09-0.82). The biological, socioeconomic and maternal risk indicators demonstrated in the present study can be employed in models of ECC that can be usefully applied for future longitudinal studies.

Tooth fracture risk analysis based on a new finite element dental structure models using micro-CT data

The finite element (FE) analysis is an effective method to study the strength and predict the fracture risk of endodontically-treated teeth. This paper presents a rapid method developed to generate a comprehensive tooth FE model using data retrieved from micro-computed tomography (μCT). With this method, the inhomogeneity of material properties of teeth was included into the model without dividing the tooth model into different regions. The material properties of the tooth were assumed to be related to the mineral density. The fracture risk at different tooth portions was assessed for root canal treatments. The micro-CT images of a tooth were processed by a Matlab software programme and the CT numbers were retrieved. The tooth contours were obtained with thresholding segmentation using Amira. The inner and outer surfaces of the tooth were imported into Solidworks and a three-dimensional (3D) tooth model was constructed. An assembly of the tooth model with the periodontal ligament (PDL) layer and surrounding bone was imported into ABAQUS. The material properties of the tooth were calculated from the retrieved CT numbers via ABAQUS user's subroutines. Three root canal geometries (original and two enlargements) were investigated. The proposed method in this study can generate detailed 3D finite element models of a tooth with different root canal enlargements and filling materials, and would be very useful for the assessment of the fracture risk at different tooth portions after root canal treatments.

Regional chromosomal assignment of human renin gene to 1q12→qter and use in linkage studies in Charcot-Marie-Tooth disease

The gene for renin, previously mapped to human chromosome 1, was further localized to 1q12 → qter using human-mouse somatic cell hybrid DNAs. The renin DNA probe used (λ HR5) could detect a HindIII restriction fragment length polymorphism. When used in studies of 12 informative families, no linkage could be found between the renin and Charcot-Marie-Tooth disease. Furthermore, an association of any renin allele with hypertension was not apparent.

Chromosome I linkage studies in Charcot-Marie-Tooth neuropathy type I

Charcot-Marie-Tooth neuropathy type 1 (CMT1) is an autosomal dominant disorder of peripheral nerve. The gene for CMT1 was originally localized to chromosome 1 by linkage to the Duffy blood group, but it has since been shown that not all CMT1 pedigrees show this linkage. We report here the results of linkage studies using five chromosome 1 markers - Duffy (Fy), antithrombin III (AT3), renin (REN), β-nerve growth factor (NGFB), and salivary amylase (AMY1) - in 16 CMT1 pedigrees. The total lod scores exclude close linkage of CMT1 to any of these markers. However, individual families show probable linkage of CMT1 to Duffy, AT3, and/or AMY1. No linkage was indicated with REN or NGFB. These results indicate that possible location of a CMT1 gene between the AMY1 and AT3 loci at p21 and q23, respectively, on chromosome 1 and support the theory that there is at least one other CMT1 gene.

Heterogeneity evidence and linkage studies on Charcot-Marie-Tooth disease

Charcot-Marie-Tooth neuropathy type 1 (CMT1) is an autosomal dominant disorder originally localized to chromosome 1 by linkage to the Duffy blood group. Studies have since shown that the disorder may be heterogeneous, as not all families show this linkage. We tested genetic heterogeneity by the HOMOG computer program in 15 CMT1 pedigrees informative for Duffy. We detected no evidence for heterogeneity in this sample, but when we combined results with previously published lod scores, heterogeneity was statistically significant. Twelve of the 15 families studied did not show linkage to Duffy. We found six of these families to be informative for a chromosome 19 marker, apolipoprotein CII(ApoC2). Despite a previous report showing probable linkage of a non-Duffy-linked CMT1 pedigree to two chromosome 19 markers, we did not detect significant linkage of ApoC2 to CMT1 in these families.

Isolation and use of chromosome 1 probes for linkage studies on Charcot-Marie-Tooth disease

Nine probes were isolated from a human chromosome 1 enriched library and mapped to regions of chromosome 1 using somatic cell hybrid lines. One clone, LR67, which mapped 1q12→q23 detected a BglI RFLP. This probe, as well as 4 other known chromosome 1 markers, α-spectrin, Factor XIIIB, DR10 and DR78, were used for linkage studies in 15 Charcot-Marie-Tooth disease (CMT1) families. Close linking of CMT1 to any of the 5 markers was not indicated. Total lod scores excluded linkage of CMT1 to LR67 and to DR10 at 5 cM or less, to DR78 and 10 cM or less, α-spectrin at 15 cM or less and Factor XIIIB at 20 cM or less. Possible linkage, however, was shown between LR67 and CMT1 at a distance of 30 cM. Also linkage at a distance of 5 cM was detected between this probe and α-spectrin.

DNA probes in Charcot-Marie-Tooth neuropathy

Results of Duffy (Fy) linkage confirm genetic heterogeneity in Charcot-Marie-Tooth disease type 1 (CMT1). Of 11 families informative for Fy, four showed probable linkage with CMT1, seven showed probable non-linkage and two showed definite non-linkage. These results suggest that Fy linked CMT1 may be less common than previously thought. These results combined with those of another DNA probe for the antithrombin III gene confirm that there are at least two gene loci for CMT1, termed 1A and 1B.

Consent for third molar tooth extractions in Australia and New Zealand: A review of current practice

Background Informed consent is the legal requirement to educate a patient about a proposed medical treatment or procedure so that he or she can make informed decisions. The purpose of the study was to examine the current practice for obtaining informed consent for third molar tooth extractions (wisdom teeth) by Oral and Maxillofacial Surgeons in Australia and New Zealand. Methods An online survey was sent to 180 consultant Oral and Maxillofacial Surgeons in Australia and New Zealand. Surgeons were asked to answer (yes/no) whether they routinely warned of a specific risk of third molar tooth extraction in their written consent. Results 71 replies were received (39%). The only risks that surgeons agreed should be routinely included in written consent were a general warning of infection (not alveolar osteitis), inferior alveolar nerve damage (temporary and permanent) and lingual nerve damage (temporary and permanent). Conclusions There is significant variability among Australian and New Zealand Oral and Maxillofacial Surgeons regarding risk disclosure for third molar tooth extractions. We aim to improve consistency in consent for third molar extractions by developing an evidence-based consent form.

Estimation of gear tooth deflection by the finite element method

The finite element method (FEM) is used to determine for pitch-point, mid-point and tip loading, the deflection curve of a Image 1 diamentral pitch (DP) standard spur gear tooth corresponding to number of teeth of 14, 21, 26 and 34. In all these cases the deflection of the gear tooth at the point of loading obtained by FEM is in good agreement with the experimental value. The contraflexure in the deflection curve at the point of loading observed experimentally in the cases of pitch-point and mid-point loading, is predicted correctly by the FEM analysis.

Characterisation of the efficacy of endodontic medications using a three-dimensional fluorescent tooth model: An ex vivo study

The purpose of this study was to establish a three-dimensional fluorescent tooth model to investigate bacterial viability against intra-canal medicaments across the thickness and surface of root dentine. Dental microbial biofilms (Enterococcus faecalis and Streptococcus mutans) were established on the external root surface and bacterial kill was monitored over time against intra-canal medicament (Ca(OH)2 ) using fluorescent microscopy in conjunction with BacLight SYTO9 and propidium iodide stains. An Olympus digital camera fitted to SZX16 fluorescent microscope captured images of bacterial cells in biofilms on the external root surface. Viability of biofilm was measured by calculating the total pixel area of green (viable bacteria) and red (non-viable bacteria) for each image using ImageJ® software. All data generated were assessed for normality and then analysed using a Mann-Whitney t-test. The viability of S. mutans biofilm following Ca(OH)2 treatment showed a significant decline compared with the untreated group (P = 0.0418). No significant difference was seen for E. faecalis biofilm between the Ca(OH)2 and untreated groups indicating Ca(OH)2 medicament is ineffective against E. faecalis biofilm. This novel three-dimensional fluorescent biofilm model provides a new clinically relevant tool for testing of medicaments against dental biofilms.

Arresting occlusal enamel caries lesions with pit and fissure sealants

The aim of this study was to evaluate the feasibility of pit and fissure sealants and the effectiveness of the two sealant methods applied in every-day practice in public dental health care in Finland. Two sealant methods were evaluated according to their effectiveness in preventing dentin caries and sealant retention. Application time with these sealant methods was compared. The survival rate of sealed first and second molars was followed for nine and 13 year periods, respectively. Caries risk evaluation and observed increased caries risk were the basis for considering sealant application. A questionnaire, sent to all public dental health centers in Finland, monitored the attitudes of the dental profession towards sealant application and explored the current policies used as well as changes noted in the sealant application protocol. DMFT (Decayed, Missing or Filled Teeth) index values collected from the health centers were evaluated. The difference in caries rate between two methods investigated was highly significant. When compared to the glass ionomer sealant method (GIC), the effectiveness of the resin-based method (RB) in preventing dentin caries was 74% and the rate difference 3%. The relative risk for RB-sealed surfaces vs. GIC-sealed surfaces of having detectable dentin caries was 0.3 (95% CI 0.12, 0.57). The retention rate of sealants was higher with RB than GIC (P<0.001). Application of RB sealant material was less time-consuming than application of GIC sealant. Occlusal dentin caries lesions were found in 4% and proximal caries in less than 2% of sealed teeth. The majority of respondents reported application of sealants on a systematic basis along with caries-risk evaluation. Those health centers sealing over suspected or detected enamel caries had lower average DMFT index values (1.0) when compared to DMFT values (1.2) of health centers applying sealants by alternative criteria. It is concluded that the RB sealant method is more effective than the GIC sealant method in preventing dentin caries. Sealant maintenance may increase the costs of a sealant program. Occlusal caries management may be improved if the applied sealant policies are changed towards an interceptive approach i.e. applying the sealants over detected or suspected enamel caries lesions instead of sealing sound teeth in a preventive manner.

Molecular genetics of tooth agenesis

Congenital missing of teeth, tooth agenesis or hypodontia, is one of the most common developmental anomalies in man. The common forms in which one or a few teeth are absent, may cause occlusal or cosmetic harm, while severe forms which are relatively rare always require clinical attention to support and maintain the dental function. Observation of tooth agenesis is also important for diagnosis of malformation syndromes. Some external factors may cause developmental defects and agenesis in dentition. However, the role of inheritance in the etiology of tooth agenesis is well established by twin and family studies. Studies on familial tooth agenesis as well as mouse null mutants have also identified several genetic factors. However, these explain syndromic or rare dominant forms of tooth agenesis, whereas the genes and defects responsible for the majority of cases of tooth agenesis, especially the common and less severe forms, are largely unknown. In this study it was shown, that a dominant nonsense mutation in PAX9 was responsible for severe tooth agenesis (oligodontia) in a Finnish family. In a study of tooth agenesis associated with Wolf-Hirschhorn syndrome, it was shown that severe tooth agenesis was present if the causative deletion in 4p spanned the MSX1 locus. It was concluded that severe tooth agenesis was caused by haploinsufficiency of these transcription factors. A summary of the phenotypes associated with known defects in MSX1 and PAX9 showed that, despite similarities, they were significantly different, suggesting that the genes, in addition to known interactions, also have independent roles during the development of human dentition. The original aim of this work was to identify gene defects that underlie the common incisor and premolar hypodontia. After excluding several candidate genes, a genome-wide search was conducted in seven Finnish families in which this phenotype was inherited in an autosomal dominant manner. A promising locus for second premolar agenesis was identified in chromosome 18 in one family and this finding was supported by results from other families. The results also implied the existence of other loci both for second premolar agenesis and for incisor agenesis. On the other hand the results did not lend support for comprehensive involvement of the most obvious candidate genes in the etiology of incisor and premolar hypodontia. Rather, they suggest remarkable genetic heterogeneity of tooth agenesis. The available evidence suggests that quantitative defects during tooth development predispose to a failure to overcome a developmental threshold and to agenesis. The results of the study increase the understanding of the etiology and heredity of tooth agenesis. Further studies may lead to identification of novel genes that affect the development of teeth.