Dental caries

The most generally accepted theory as to the cause of dental caries is that certain bacteria in the mouth, in the presence of fermentable sugars, cause the formation of acids which in turn decalcify teeth. Physicians may help reduce the incidence of caries by recommending elimination of refined sugars from the diet, or at least control of the amount consumed.Cleaning the teeth with a well designed tooth brush after each meal will to a certain extent mechanically remove the fermentable sugar and debris from the teeth. One step further in oral hygiene that may be beneficial is to use a dentifrice with 5 per cent dibasic ammonium phosphate and 3 per cent urea to reduce the formation of acid. Anything that will increase salivation will aid in buffering any acids that may be present.A 2 per cent solution of sodium fluoride applied to the thoroughly dried "intact" enamel surface may prevent caries. Sodium fluoride added to drinking water to a concentration of 1 part per million is utilized by the body in formation of an enamel that is particularly resistant to caries.     

Quantitative proteomic analysis of the effect of fluoride on the acquired enamel pellicle

The acquired enamel pellicle (AEP) is a thin film formed by the selective adsorption of salivary proteins onto the enamel surface of teeth. The AEP forms a critical interface between the mineral phase of teeth (hydroxyapatite) and the oral microbial biofilm. This biofilm is the key feature responsible for the development of dental caries. Fluoride on enamel surface is well known to reduce caries by reducing the solubility of enamel to acid. Information on the effects of fluoride on AEP formation is limited. This study aimed to investigate the effects of fluoride treatment on hydroxyapatite on the subsequent formation of AEP. In addition, this study pioneered the use of label-free quantitative proteomics to better understand the composition of AEP proteins. Hydroxyapatite discs were randomly divided in 4 groups (n = 10 per group). Each disc was exposed to distilled water (control) or sodium fluoride solution (1, 2 or 5%) for 2 hours. Discs were then washed and immersed in human saliva for an additional 2 hours. AEP from each disc was collected and subjected to liquid chromatography electrospray ionization mass spectrometry for protein identification, characterization and quantification. A total of 45 proteins were present in all four groups, 12 proteins were exclusively present in the control group and another 19 proteins were only present in the discs treated with 5% sodium fluoride. Relative proteomic quantification was carried out for the 45 proteins observed in all four groups. Notably, the concentration of important salivary proteins, such as statherin and histatin 1, decrease with increasing levels of fluoride. It suggests that these proteins are repulsed when hydroxyapatite surface is coated with fluoride. Our data demonstrated that treatment of hydroxyapatite with fluoride (at high concentration) qualitatively and quantitatively modulates AEP formation, effects which in turn will likely impact the formation of oral biofilms.     

Weaker Dental Enamel Explains Dental Decay

Dental caries continues to be the most prevalent bacteria-mediated non-contagious disease of humankind. Dental professionals assert the disease can be explained by poor oral hygiene and a diet rich in sugars but this does not account for caries free individuals exposed to the same risk factors. In order to test the hypothesis that amount of amelogenin during enamel development can influence caries susceptibility, we generated multiple strains of mice with varying levels of available amelogenin during dental development. Mechanical tests showed that dental enamel developed with less amelogenin is “weaker” while the dental enamel of animals over-expressing amelogenin appears to be more resistant to acid dissolution.     

Aquaporin 5 Interacts with Fluoride and Possibly Protects against Caries

Aquaporins (AQP) are water channel proteins and the genes coding for AQP2, AQP5, and AQP6 are clustered in 12q13. Since AQP5 is expressed in serous acinar cells of salivary glands, we investigated its involvement in caries. DNA samples from 1,383 individuals from six groups were studied. Genotypes of eight single nucleotide polymorphisms covering the aquaporin locus were tested for association with caries experience. Interaction with genes involved in enamel formation was tested. The association between enamel microhardness at baseline, after creation of artificial caries lesion, and after exposure to fluoride and the genetic markers in AQP5 was tested. Finally, AQP5 expression in human whole saliva, after exposure to fluoride in a mammary gland cell line, which is known to express AQP5, and in Wistar rats was also verified. Nominal associations were found between caries experience and markers in the AQP5 locus. Since these associations suggested that AQP5 may be inhibited by levels of fluoride in the drinking water that cause fluorosis, we showed that fluoride levels above optimal levels change AQP5 expression in humans, cell lines, and rats. We have shown that AQP5 is involved in the pathogenesis of caries and likely interacts with fluoride.     

Observations of dental diseases among prehistoric populations of Hungary

The incidence of dental disease among people in developing countries today raises questions about the variation in the oral health of prehistoric populations. Considering these questions, we offer observations describing several types of dental disease which occurred among certain prehistoric populations of Hungary. The dental remains of 162 individuals recovered from seven sites of the Neolithic, Copper, and Bronze Age periods were examined for evidence of caries, hypoplasia, and periodontal disease. Appropriate methods were used to describe and record these dental lesions. The incidence of dental caries was low by comparison to other prehistoric agriculturists except for two forms of root caries: cervical and cemental. These types accounted for 68% of all the carious teeth recorded. Enamel hypoplasia was also lower than expected, occurring on only 4% of the total number of teeth. Periodontal abscesses were rare but other milder forms of periodontal lesions were frequent. Alveolar bone resorption occurred in varying degrees and followed the expected age distribution. The few exceptions were children or adolescents whose crania had other lesions suggesting a mineral metabolic disturbance. The lower incidence of enamel caries is likely due to high fluoride ingestion which also may have influenced the expression of enamel hypoplasia. No clear population trends were seen in dental disease incidence except for cemental caries which were found among Copper and Bronze Age remains.     

Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes may contribute to caries. For the present study, we used DNA samples collected from 1,831 individuals from various population data sets. Single nucleotide polymorphism markers were genotyped in selected genes (ameloblastin, amelogenin, enamelin, tuftelin, and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Associations with caries experience can be detected but they are not necessarily replicated in all population groups and the most expressive results was for a marker in AMELX (p = 0.0007). To help interpret these results, we evaluated if enamel microhardness changes under simulated cariogenic challenges are associated with genetic variations in these same genes. After creating an artificial caries lesion, associations could be seen between genetic variation in TUFT1 (p = 0.006) and TUIP11 (p = 0.0006) with enamel microhardness. Our results suggest that the influence of genetic variation of enamel formation genes may influence the dynamic interactions between the enamel surface and the oral cavity.     

Phase Transformations in a Human Tooth Tissue at the Initial Stage of Caries

The aim of the paper is to study phase transformations in solid tissues of the human teeth during the development of fissure caries by Raman and fluorescence microspectroscopy. The study of the areas with fissure caries confirmed the assumption of the formation of a weak interaction between phosphate apatite enamel and organic acids (products of microorganisms). The experimental results obtained with by Raman microspectroscopy showed the formation of dicalcium phosphate dihydrate - CaHPO₄-2H₂O in the area of mural demineralization of carious fissure. A comparative analysis of structural and spectroscopic data for the intact and carious enamel shows that emergence of a more soluble phase - carbonate-substituted hydroxyapatite - is typical for the initial stage of caries. It is shown that microareas of dental hard tissues in the carious fissure due to an emerging misorientation of apatite crystals have a higher fluorescence yield than the area of the intact enamel. These areas can be easily detected even prior to a deep demineralization (white spot stage) for the case of irreversibly changed organomineral complex and intensive removal of the mineral component.     

Fluoride induces oxidative damage and SIRT1/autophagy through ROS-mediated JNK signaling

Fluoride is an effective caries prophylactic, but at high doses can also be an environmental health hazard. Acute or chronic exposure to high fluoride doses can result in dental enamel and skeletal and soft tissue fluorosis. Dental fluorosis is manifested as mottled, discolored, porous enamel that is susceptible to dental caries. Fluoride induces cell stress, including endoplasmic reticulum stress and oxidative stress, which leads to impairment of ameloblasts responsible for dental enamel formation. Recently we reported that fluoride activates SIRT1 and autophagy as an adaptive response to protect cells from stress. However, it still remains unclear how SIRT1/autophagy is regulated in dental fluorosis. In this study, we demonstrate that fluoride exposure generates reactive oxygen species (ROS) and the resulting oxidative damage is counteracted by SIRT1/autophagy induction through c-Jun N-terminal kinase (JNK) signaling in ameloblasts. In the mouse-ameloblast-derived cell line LS8, fluoride induced ROS, mitochondrial damage including cytochrome-c release, up-regulation of UCP2, attenuation of ATP synthesis, and H2AX phosphorylation (γH2AX), which is a marker of DNA damage. We evaluated the effects of the ROS inhibitor N-acetylcysteine (NAC) and the JNK inhibitor SP600125 on fluoride-induced SIRT1/autophagy activation. NAC decreased fluoride-induced ROS generation and attenuated JNK and c-Jun phosphorylation. NAC decreased SIRT1 phosphorylation and formation of the autophagy marker LC3II, which resulted in an increase in the apoptosis mediators γH2AX and cleaved/activated caspase-3. SP600125 attenuated fluoride-induced SIRT1 phosphorylation, indicating that fluoride activates SIRT1/autophagy via the ROS-mediated JNK pathway. In enamel organs from rats or mice treated with 50, 100, or 125 ppm fluoride for 6 weeks, cytochrome-c release and the DNA damage markers 8-oxoguanine, p-ATM, and γH2AX were increased compared to those in controls (0 ppm fluoride). These results suggest that fluoride-induced ROS generation causes mitochondrial damage and DNA damage, which may lead to impairment of ameloblast function. To counteract this impairment, SIRT1/autophagy is induced via JNK signaling to protect cells/ameloblasts from fluoride-induced oxidative damage that may cause dental fluorosis.     

Nanotribological characterization of tooth enamel rod affected by surface treatment

Tooth enamel is a hybrid organic–inorganic bionanocomposite comprised predominantly of enamel rods. Understanding the effects of anti-caries treatment on the biomechanical properties of these rods is essential in developing effective caries prevention strategies. Calcium fluoride-like deposits play an important role in caries prevention and their nanotribological properties have a direct effect upon their long-term effectiveness. Accordingly, this study utilizes a variety of techniques, namely nanoindentation, nanoscratch tests, nanowear tests and atomic force microscopy (AFM), to characterize the mechanical and tribological properties of single enamel rods before and after topical fluoride application. The results show that the CaF₂-like deposits formed on the enamel surface following fluoride application increase the coefficient of friction of the enamel rods, but decrease their critical load and nanohardness. As a result, the nanowear depth of the treated enamel surface is around six times higher than that of the native enamel surface under an applied load of 300 μN. Following the removal of the surface deposits, however, the modulus of elasticity and wear depth of the underlying enamel surface are found to be similar to those of the original enamel surface. However, a notable increase in the surface roughness is observed.     

脉冲Nd:YAG激光照射氟斑牙后充填微渗漏的实验研究

目的:观察氟斑牙经脉冲Nd-YAG激光照射后充填微渗漏的发生情况,为相关研究提供参考。方法:选取人体因各种原因而拔除的氟斑牙(重度)30颗,分成A、B两组。A组为Nd:YAG激光消除龋坏组织作为实验组,B组用传统涡轮钻去龋作为对照组。所有牙齿用树脂充填,经冷热循环处理后,再进行微渗漏观察。结果:实验组充填体边缘微渗漏比对照组明显低(P0.01)。结论:脉冲Nd:YAG激光去除氟斑牙坏死组织有助于增强充填物与釉质连接,不增加微渗漏,有助于充填成功。     

Validity of Sealant Retention as Surrogate for Caries Prevention – A Systematic Review

Introduction/Aim

To appraise the clinical literature in determining whether loss of complete sealant retention as surrogate endpoint is directly associated with caries occurrence on sealed teeth as its clinical endpoint and to apply the appraised evidence in testing the null-hypothesis that the retention/caries ratio between different types of sealant materials (resin and glass-ionomer cement) is not statistically significant ( = Prentice criterion for surrogate endpoint validity).

Methods

Databases searched PubMed/Medline, Directory of Open Access Journals; IndMed, Scielo. Systematic reviews were checked for suitable trials. The search terms: “fiss* AND seal*” and “fissure AND sealant” were used. Article selection criteria were: clinical trial reporting on the retention and caries occurrence of resin and/or glass-ionomer cement (GIC) fissure sealed permanent molar teeth; minimum 24-month follow-up period; systematic review or meta-analysis. Datasets and information were extracted from accepted trials. The principle outcome measure was the ratio of Risk of loss of complete retention to the Risk of caries occurrence per sealant type (RCR). Risk of bias was assessed in trials and sensitivity analysis with regard to potential confounding factors conducted. The null-hypothesis was tested by graphical and statistical methods.

Results

The risk of loss of complete retention of sealant materials was associated with the risk of caries occurrence for resin but not for GIC based sealants. The difference between RCR values of the two sealant types was statistically significant (p<0.05). The null-hypothesis was rejected.

Conclusions

The current clinical evidence suggests that complete retention of pit and fissure sealants may not be a valid surrogate endpoint for caries prevention as its clinical endpoint. Further research is required to corroborate the current results.     

Amounts of Sr and Ca Eluted from Deciduous Enamel to Artificial Saliva Related to Dental Caries

This study was performed to elucidate the relationship between dental caries and the levels of Sr and Ca eluted from enamel, and to examine whether these elements are useful as factors to assess caries risk. The available 103 (Sr) and 108 (Ca) samples were obtained among 111 collected deciduous teeth. The healthy regions of enamel were decalcified in artificial saliva at pH 6.2 and 5.5. The eluted levels of these elements from enamel were determined using atomic absorption spectrophotometry. Sr and Ca levels were not affected by the sex nor tooth type. Sr levels of the caries-experienced tooth (CE) group were 2.6-fold (pH 6.2) and 2.2-fold (pH 5.5) higher than those of the sound tooth (ST) group, respectively. Furthermore, the Sr levels were significantly higher in the teeth with treated than in those with untreated caries. Only at pH 6.2 was a significant difference found in Ca levels between the ST and CE groups. In the ST group, at pH 5.5, both the Sr and Ca levels significantly increased when the children had six or more carious teeth. The Sr and Ca elution levels were significantly inhibited in the teeth receiving fluoride application every 3 or 4 months compared to those that were not. These findings indicate that Sr can be an indicator of the acid resistance of teeth, and a useful factor to assess future caries risk.     

Cessation of Epithelial Bmp Signaling Switches the Differentiation of Crown Epithelia to the Root Lineage in a β-Catenin-Dependent Manner

The differentiation of dental epithelia into enamel-producing ameloblasts or the root epithelial lineage compartmentalizes teeth into crowns and roots. Bmp signaling has been linked to enamel formation, but its role in root epithelial lineage differentiation is unclear. Here we show that cessation of epithelial Bmp signaling by Bmpr1a depletion during the differentiation stage switched differentiation of crown epithelia into the root lineage and led to formation of ectopic cementum-like structures. This phenotype is related to the upregulation of Wnt/β-catenin signaling and epithelial-mesenchymal transition (EMT). Although epithelial β-catenin depletion during the differentiation stage also led to variable enamel defect and precocious/ectopic formation of fragmented root epithelia in some teeth, it did not cause ectopic cementogenesis and inhibited EMT in cultured dental epithelia. Concomitant epithelial β-catenin depletion rescued EMT and ectopic cementogenesis caused by Bmpr1a depletion. These data suggested that Bmp and Wnt/β-catenin pathways interact antagonistically in dental epithelia to regulate the root lineage differentiation and EMT. These findings will aid in the design of new strategies to promote functional differentiation in the regeneration and tissue engineering of teeth and will provide new insights into the dynamic interactions between the Bmp and Wnt/β-catenin pathways during cell fate decisions.     

The role of fluoride and chlorhexidine in preserving hardness and mineralization of enamel and cementum after gamma irradiation

The purpose of this study was to evaluate the effect of 0.05% sodium fluoride and 0.12% chlorhexidine mouthwashes on the micro-hardness of tooth enamel and cementum that was exposed to therapeutic doses of gamma radiation. Sixty extracted human teeth were divided into two groups, one was irradiated, the other was not irradiated. The two groups were further subdivided into three subgroups, which were each treated either with 0.05% sodium fluoride or with 0.12% chlorhexidine; the third subgroup served as a control. After demineralization–remineralization cycling, teeth from the irradiated groups showed a significantly lower micro-hardness when compared to those from the non-irradiated groups. Both in the irradiated and non-irradiated groups, teeth from the control subgroups showed a significantly lower micro-hardness, as compared to teeth treated with sodium fluoride and chlorhexidine. For non-irradiated enamel samples, those treated with chlorhexidine showed a significantly less micro-hardness compared to those treated with sodium fluoride. In contrast, irradiated enamel showed no significant difference in micro-hardness, whatever treatment (chlorhexidine or sodium fluoride) was applied. For cementum, treatment with chlorhexidine resulted in a significantly lower micro-hardness compared to sodium fluoride, both for the irradiated and non-irradiated groups. It is concluded that gamma irradiation with therapeutic doses typically used for head and neck carcinoma treatment has a direct effect in reducing micro-hardness of tooth enamel and cementum. Mouthwash protocols including, for example, application of 0.05% sodium fluoride or 0.12% chlorhexidine three times per day for 6 weeks, can protect enamel and cementum against the reduction in hardness and demineralization caused by gamma irradiation. Sodium fluoride offers more protection compared to chlorhexidine.     

CARCINOMA OF THE CERVIX

Studies by eminent surgeons to reevaluate the place of radical operations in the treatment of carcinoma of the cervix—now that extensive procedures have become less hazardous—apparently have led to confusion in some minds as to choice between surgical and radiation therapy. Pending outcome of the studies, general employment of surgical treatment is unwarranted. Radiation is the treatment of choice in most cases, particularly if the lesion is in an early stage, although radical operation is indicated in certain rare early cases in which delivery of an effective dose of radiation to involved areas is technically difficult. Elsewise it appears at present that operation should be used only in cases of stages III or IV carcinoma—in which results by either means of treatment are poor.One hundred and seven patients were treated with a combination of x-ray and radium irradiation. X-ray was used first to reduce the hazard of implanting the radium. The “five-year arrest” rates were as follows: For 22 patients with stage I lesion, 70 per cent; for 31 with stage II, 55.7 per cent; 33 with stage III, 39.7 per cent; 21 with stage IV, 0. Eighteen patients with diagnosis of carcinoma of the cervix who had had subtotal hysterectomy were treated. The stage of the disease could not be determined. In this group the five-year arrest rate was 52 per cent.     

Dental health of elderly confederate veterans: evidence from the Texas State Cemetery

Analysis of the skeletal remains of 50 Confederate veterans provided a unique opportunity to explore the dental health of a geriatric sample. These men, who died between 1907-1932, had an average age at death of 76.7 years. Ninety percent were institutionalized at the Confederate Home for Men (Austin, TX) prior to their deaths. This elderly sample was assessed in terms of caries, antemortem tooth loss (AMTL), abscesses, and linear enamel hypoplasias. On a per tooth basis, the AMTL rate was 57.2%. Of 39 dentate men, 33 (84.6%) had dental caries, and 24.4% (121 of 496) of teeth were carious. Ten (25.0%) of the dentate men had hypoplastic teeth. At least one abscess was seen in 14 (28%) of 50 individuals. Results from this geriatric institutionalized sample are compared to contemporaneous historical samples. Disparities in dental health among these groups may be due to differences in average age at death, and these comparisons allow a better understanding of dental changes that occur with age. The sample is also compared to modern elderly samples: modern groups have higher caries rates, possibly because they retained more teeth. This finding may be due in part to diets in the United States becoming increasingly cariogenic over time. In addition, dental care has moved from the reactive practices seen in the nineteenth and early twentieth centuries (such as tooth extractions) to modern proactive solutions dedicated to preserving and restoring teeth (such as tooth brushing, fluoride treatments, and dental fillings).     

NONPOLIOVIRUSES AND PARALYTIC DISEASE

A number of nonpolioviruses have been implicated as the probable etiologic agents of paralytic illness clinically resembling poliomyelitis, including certain immunotypes of Coxsackie group A, Coxsackie group B, and ECHO viruses, and the viruses of mumps, herpes simplex and arthropod-borne encephalitides. A number of well documented cases provide evidence that some of these viruses may on occasion be the causative agents of severe, even fatal, myelitis, bulbomyelitis or encephalomyelitis, but they have been associated much more frequently with cases of “poliomyelitis” in which there has been slight to moderate paresis. In the aggregate, various “nonpolioviruses” have been encountered in approximately 10 per cent of the patients with clinical poliomyelitis studied, but it is uncertain how many of these cases may represent coincidental infections not causally related to the current illness.     

Fat Metabolism in the West African Oil Palm (Elaeis Guineensis): PART I. FATTY ACID FORMATION IN THE MATURING KERNEL

Using a column chromatographic technique for the estimationand identification of fatty acids, a study has been made offat formation in developing Oil Palm kernels from 10 weeks afterpollination to full maturity (20 weeks), during which time thefat content may increase a hundredfold. Nuts from three differenttrees have been analysed and differences between these in ratesof maturation (as indicated by appearance of the endosperm)can be directly correlated with changes in character of theoil present. Amounts of reducing sugars, sucrose, and starch in the developingendosperm have also been followed, but these carbohydrates arepresent throughout in low concentration, and it is assumed thattranslocation from the rest of the plant to the developing kernelmust account for the major part of storage material. The mature kernel contains in its fat an unusual mixture ofeight different saturated fatty acids. The major such componentis lauric acid (46·1 to 49·5 per cent.) and thereare present two common unsaturated acids, oleic (15·7to 16·5 per cent.) and linoleic acid (0·7 to 3·1per cent.). At the earliest stage examined (10 weeks after pollination)all these acids are.present but in altered proportions, unsaturatedacids forming a larger fraction (36·5 to 81·2per cent., according to the tree investigated), and lauric acid(1·4 to 8·5 per cent.) a smaller. The results suggest that young kernels contain a small quantityof a largely unsaturated ‘protoplasmic’ fat, andthat at a certain stage in development some physiological changein the tissue results in the formation, in large quantities,of a new, highly saturated storage fat. No fatty acid interconversionscould be demonstrated although there is some suggestion thatoleic acid behaves anomalously. There is evidence that free fatty acids are not accumulatedprior to esterification.     

MALIGNANT TUMORS OF CHILDHOOD

In the past 20 years, cancer in the age group, 0-14 years has become the second leading cause of death by disease. At some ages, notably between 5 and 14, it may be the leading cause of death by disease.Leukemia is the most frequent form of cancer in childhood, and tumors of the brain are in second place.An attempt should be made to categorize more accurately tumors stated in reports as “miscellaneous,” since in the reports analyzed herein, 15.8 per cent of all malignant lesions were so classified.