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[The remineralization of enamel lesions by casein phosphopeptide-amorphous calcium fluoride phosphate in vitro].

OBJECTIVE: To evaluate the remineralizing effect on artificial enamel subsurface lesions in vitro by 2% casein phosphopeptide-amorphous calcium fluoride phosphate complexes (CPP-ACFP) solution. METHODS: Twenty-eight enamel blocks were cut from human third molars, in which 2 lesions were prepared from each block. The 28 samples were randomly assigned to the four study groups, in which each group was incubated in remineralization solution for 1, 3, 5, 10 days respectively. After remineralization the samples were sectioned, microradiographied and the mineral content were determined by microdensitometry. RESULTS: The remineralizing solution replaced 9.19%, 14.27%, 29.07%, 38.45% of mineral lost after 1, 3, 5, 10 days respectively (y = 8.9316 x0.6347, R2 = 0.9322; y: remineralizing rate, x: time). Significant differences were found in remineralizing rate between any two groups using One-way Scheffe multiple comparison. CONCLUSIONS: The 2% CPP-ACFP solution could significantly remineralize the artificial enamel subsurface lesion in vitro. The remineralizing rates were increased with the experiment time (within 10 days).

Caseins↗

[Effect of sodium chloride treatment on remineralization of human root dentine caries in vitro].

OBJECTIVE: To investigate the influence of soluble phosphoprotein removal from artificial dentin caries lesions by pretreatment of NaCl on subsequent remineralization. METHODS: Human root dentin samples were demineralized in an acidic gel (pH = 4.4) at 37 degrees C for 48 hours. Samples were pretreated with 0.5 mol/L NaCl solution and 0.5 mol/L disodium EDTA solution respectively. The histomorphologic changes of root caries surface were examined by scannings electronic microscope. Mineral profiles were assessed by means of microradiography. RESULTS: No histomorphologic changes were present on root caries surface after treated with 0.5 mol/L NaCl solution, while many opened dentin tubules were seen after treated with 0.5 mol/L disodium EDTA solution. The remineralization results showed that pretreatment with 0.5 mol/L NaCl solution increased more remineralization than pretreated with 0.5 mol/L disodium EDTA solution. CONCLUSION: 0.5 mol/L NaCl solution has no damage on the root caries surface. The in vitro results suggested that removal of soluble phosphoprotein from dentin lesions is an interesting approach to enhance remineralization.

Dental Caries↗

Odontoblast phosphate and calcium transport in dentinogenesis.

It has been suggested that odontoblasts are instrumental in translocating Ca2+ and inorganic phosphate (Pi) ions during the mineralization of dentin. The aim of this thesis was, therefore, to study the expression of components of the transcellular ion transport system, Na+/Ca2+ exchangers and Na(+)-Pi contransporters, in odontoblastic and osteoblastic cells. Their activity was assayed in osteoblast-like cells and in the recently developed MRPC-1 odontoblast-like cell line. To assess the relationship between ion transport and mineralization, Ca2+ and Pi uptake activities were determined in mineralizing cultures of MRPC-1 cells. Osteoblastic and odontoblastic cells showed an identical expression pattern of Na+/Ca2+ exchanger splice-variants, NCX1.3, NCX1.7 and NCX1.10, derived from the NCX1 gene, while NCX2 was not expressed. The cells showed a high sodium-dependent calcium extrusion activity. Regarding Na(+)-Pi cotransporter expression, Glvr-1, Ram-1 and the two high capacity cotransporters Npt-2a and Npt-2b were found to be expressed in odontoblasts and MRPC-1 cells. Osteoblast-like cells differed from this in expressing the Npt-1 but not the Ram-1 gene but were otherwise identical to the odontoblastic cells. Odontoblast-like cells exhibited almost twice the sodium-dependent Pi uptake activity of osteoblast-like cells. The presence of NaPi-2a and NaPi-2b, gene products of Npt-2a and Npt-2b, was verified in vivo by immunohistochemistry on mouse teeth. Both cotransporters could be detected in fully differentiated, polarized odontoblasts but not in preodontoblasts prior to dentin formation. Both cotransporters were detected in adjacent bone and in ameloblasts. Studying ion uptake in mineralizing MRPC-1 cultures, large changes were detected concomitant with the onset of mineral formation, when phosphate uptake increased by 400% while calcium uptake started to decline. The increase in Pi uptake was found to be due to activation of the NaPi-2a cotransporter. MRPC-1 cells expressed an odontoblast-like phenotype already at the onset of culture, but in order to form mineral a differentiation involving their ion transporters seems necessary. Calculating the theoretical rate of ion transport needed for dentin formation and comparing with data from the studies in this thesis showed that transcellular ion transport is both possible and sufficient to meet the phosphate and calcium demands of dentinogenesis.

Animals↗

Age of attainment of mineralization stages of the permanent dentition.

The ages at which the maxillary and mandibular teeth of 121 boys and 111 girls reached 14 mineralization stages were determined from serial cephalograms at the Burlington Growth Centre. The present data are more comprehensive than any previously available and can be applied to chronological age determinations in juveniles of indefinite age, and of specimens in anthropological and forensic investigations. The sexes differed in the age at which they attained the stages of mineralization, with the canines demonstrating the greatest difference. In each sex, the ages at identical stages were similar for the corresponding teeth in the maxilla and mandible. Variability in age was greater among the males, especially for the first premolars, and increased with age, except for the third molars. Variability in age of third molar mineralization was greater in females and diminished among both sexes at late stages of root formation.

Adolescent↗

[The effect of dentin phosphoprotein on inducing mineralization].

OBJECTIVE: To investigate the effect of dentin phosphoprotein (DPP) in inducing dentinal mineralization. METHODS: Human DPP was combined with EAH-Sepharose 4B beads and its function of inducing mineralization was studied in mineralization system in-vitro. The mineral formed on the surface of the beads was analyzed by scanning electron microscopy (SEM) and the structure was analyzed by X-ray diffraction and plasma emission spectrum. RESULTS: There was mineral formed on the beads with combined DPP and the mineral was calcium phosphates whose ratio of calcium to phosphate was 1.33. The diffractogram of the formed mineral was more similar to hydroxyapatite than to other calcium phosphates. CONCLUSION: When tightly combined with certain support substance, human DPP can induce mineralization.

Calcium Phosphates↗

Proteoglycans in predentin: the last 15 micrometers before mineralization.

Small leucine-rich proteoglycans (SLRPs) regulate extracellular matrix organization. In order to investigate the distribution and potential functions of decorin, biglycan (BGN), and fibromodulin (3 SLRPs, potentially related to dentinogenesis), we performed light and electron immunochemistry on teeth from rats, and on wild-type and biglycan knockout mice (BGN KO). Immunohistochemical data demonstrate that chondroitin sulfate/dermatan sulfate (CS/DS) and keratan sulfate (KS) distributions displayed reverse gradients in predentin. The decrease of CS/DS labeling from the proximal to the distal predentin contrasted with the sharp decorin increase observed in the distal predentin near the predentin/dentin transition, an effect possibly attributable to the deglycosylation action of stromelysin-1. In contrast, BGN concentration was apparently constant throughout the whole predentin. Additional immunolabelings showed, for the first time, the presence of fibromodulin in predentin. Compared with the wild-type mouse, the mean diameter of collagen fibrils in the BGN KO was smaller in the proximal predentin but larger in the central and distal predentin, the metadentin was broader, and the dentin mineralization appeared altered and heterogeneous. Altogether, our data suggest an important role for BGN in dentin formation and mineralization.

Animals↗

Gene expression, signal transduction and tissue-specific biomineralization during mammalian tooth development.

Tooth development provides a paradigm for intrinsic molecular controls for cell- and extracellular matrix (ECM)-mediated biomineralization. The intent of this review is to evaluate the sequential timing and positional information prerequisite for tissue-specific biomineralization. Recent investigations suggest that 1,25-dihydroxyvitamin D3 functions to up-regulate VDR (vitamin D receptor) that in turn could induce structural gene products, including calcium-binding proteins and several ECM proteins (e.g., enamelins, amelogenins, dentine sialoglycoproteins (DSP) and dentine phosphoproteins (DPP)), resulting in dentine and enamel formation. Inhibition of regulatory gene products and/or their receptors likely results in hypoplastic and/or hypomineralized ECM as a direct consequence of down-regulated (1) transcription and/or translation of structural and regulatory genes, (2) posttranslational modifications, (3) and/or decreased calcium transport to the forming dentine and enamel matrices. Advances in serumless in vitro culture methodology; computer-assisted access to nucleic acid sequences for probes to define when, where, and how many specific regulatory and structural gene products are expressed; antisense oligodeoxynucleotides to inhibit specific translation; and microtechniques to analyze biomineralization all provide additional avenues to investigate tissue-specific biomineralization.

Animals↗

Judgement criteria for molar incisor hypomineralisation (MIH) in epidemiologic studies: a summary of the European meeting on MIH held in Athens, 2003.

AIM: This paper reviews the proceedings and conclusions of a meeting of experts concerned with the problem of hypomineralised incisors and molars (MIH). The aims of this meeting were to establish criteria for the judgement of MIH, to select representative cases and to discuss how the name of the condition was best described as hypomineralised, or hypomaturated, first permanent molars. CONCLUSION: There was not complete agreement as to the correct diagnosis and aetiology of the condition. A suggested list of definitions of the judgement criteria to be used in diagnosing Molar Incisor Hypomineralisation (MIH) for prevalence studies was agreed upon.

Child↗

Molar incisor hypomineralisation (MIH).

REVIEW: Molar Incisor Hypomineralisation (MIH) is defined as a hypomineralisation of systemic origin of one to four permanent first molars frequently associated with affected incisors. MIH molars are fragile and caries can develop very easily in those molars. Although MIH molars are well known by paediatric dentists and their occurrence is related in severe cases to major clinical problems, only limited data of the size of the problem are available. The prevalence of MIH ranges in the literature from about 3.6 to 25% and seems to differ in certain regions and birth cohorts. Unfortunately more complete comparable valid data are lacking at the moment. It seems that several aetiological factors can cause the enamel defects and that their occurrence is child related. CONCLUSION: For children with repeated illnesses in the first years after birth and children with opacities on erupted molars or incisors it seems useful to increase the frequency of dental check-ups during the period of erupting first permanent molars.

Child↗

Molar incisor hypomineralisation: restorative management.

AIM: The methods for the restoration of permanent molars and incisors affected by Molar Incisor Hypomineralisation are reviewed. The special problems associated with restoring these teeth, such as sensitivity, occlusion and aesthetics are discussed. The various options for restoration are outlined and recommendations made as to the appropriate types of restoration.

Child↗

Prevalence of enamel mineralisation disturbances in an area with 1-1.2 ppm F in drinking water. Review and summary of a report published in Sweden in 1981.

AIM: This was to study the prevalence of dental fluorosis in a Swedish city (Uppsala) with natural 1-1.2 ppm F in drinking water. It was also to compare the prevalence of idiopathic enamel disturbances (Morbus S) in children born in Uppsala with the prevalence in children who had moved in to Uppsala at an age when the Uppsala water could not have influenced the development of Morbus S. METHODS: Children born in 1970 and 1967 in Uppsala (Sweden) on even days (n=840) were invited to the study. All children not born in Uppsala were included (n=475), 24 children refused to take part and 45 were sick or had moved. Four examination teams performed the examinations after calibration against a "gold standard". Dental fluorosis was determined by the criteria of Dean [1934], idiopathic white spots according to Nevitt et al. [1963] and Morbus S was diagnosed according to Forsman [1979]. RESULTS: Children born in Uppsala had a higher prevalence and severity of fluorosis compared with those not born in Uppsala. It was found that 40 out of the 715 children born in Uppsala had enamel disturbances according to criteria for Morbus S and the corresponding figures for children not born in Uppsala were 33 out of 486. CONCLUSION: The specific enamel hypomineralisations type Morbus S cannot be connected to intake of fluoride.

Child↗

Molar incisor hypomineralisation in a group of children and adolescents living in Dresden (Germany).

AIM: This was to determine the prevalence of Molar Incisor Hypomineralisation (MIH) and to evaluate possible causes of these enamel defects. METHODS: The study group consisted of 2,408 10-17 year old children born during 1985-1992 and living in Dresden (Germany). Enamel defects were recorded using the modified DDE index. Children with enamel defects and their parents were invited for a re-examination to record the medical history of the children during the first 3 years of life; these children were matched by age with other children with apparently normal first molars (control group). RESULTS: 135 (5.6%) of the children had demarcated opacities in at least one first molar, i.e. MIH. A significantly higher prevalence of MIH was seen in children born between 1989 and 1991 compared with those born before and after that period (p<0.01). The number of children returning for the medical history questionnaire was low, 31 out of 135 responded (test group). Although there were no significant differences between the test and control groups in terms of peri and neonatal complications or other health problems, the low return precluded any definitive interpretation. CONCLUSION: The overall prevalence of MIH in this study was low by comparison with other previous epidemiological reports.

Adolescent↗