Satu Alaluusua

Molar-incisor hypomineralisation

Molar Incisor Hypomineralisation (mih) wordt omschreven als een hypomineralisatie (van systemische oorsprong) van een tot vier blijvende eerste molaren, vaak in combinatie met aangedane incisieven. mih-molaren zijn fragieler en cariesgevoeliger dan gewone molaren. Een kenmerk van mih-molaren is een extreme overgevoeligheid voor koude, warmte en/of lucht. De behandeling van deze molaren kan de behandelaar soms voor klinische problemen stellen. Het aantal gevallen van mih verschilt per land en per geboortejaar en varieren tussen de 3,6% en 25%. De oorzaak van mih is nog niet duidelijk. Wel duidelijk is dat het moet ontstaan in de periode van maturatie van het glazuur, dus tijdens de eerste levensjaren van het kind. Zolang de oorzaken van mih nog niet bekend zijn, is het verstandig om kinderen die in hun eerste levensjaren vaak ziek zijn geweest, kinderen met hypomineralisatie van de 2e melkmolaren en kinderen die op de blijvende incisieven duidelijk begrensde opaciteiten vertonen, tijdens de eerste wisselfase regelmatig te controleren om op tijd eventuele mih te signaleren.

Identification of a nonsense mutation in the PAX9 gene in molar oligodontia.

Development of dentition is controlled by numerous genes, as has been shown by experimental animal studies and mutations that have been identified by genetic studies in man. Here we report a nonsense mutation in the PAX9 gene that is associated with molar tooth agenesis in a Finnish family. The A340T transversion creates a stop codon at lysine 114, and truncates the coded PAX9 protein at the end of the DNA-binding paired-box. All the affected members of the family were heterozygous for the mutation. The tooth agenesis phenotype involves all permanent second and third molars and most of the first molars and resembles the earlier reported phenotype that was also associated with a PAX9 mutation.1 The phenotype is presumably a consequence of haploinsufficiency of PAX9. In another Finnish family with molar tooth agenesis, we could not find similar sequence changes in PAX9.

Best Clinical Practice Guidance for clinicians dealing with children presenting with Molar-Incisor-Hypomineralisation (MIH)

BACKGROUND: The European Academy of Paediatric Dentistry (EAPD) has long recognised the necessity of promoting further research and knowledge regarding the dental defect described as molar-incisor-hypomineralisation (MIH). Following the establishment by EAPD of the defect diagnostic criteria in 2003, the publication of various papers and a whole issue assigned to the defect in the European Archives of Paediatric Dentistry (2008), an Interim Seminar and Workshop on MIH was organized in Helsinki in 2009. RESULT: The outcome of this event is the present consensus paper on the prevalence, diagnosis, aetiology and treatment for children and adolescents presenting with MIH. A clear diagnostic proposal and a treatment decision-making guide are presented together with suggestions on aetiology and guidance forfuture research. CONCLUSION: MIH is an important clinical problem that often concerns both the general dental and specialist paediatric dentists; the present ‘best clinical practice guidance’ aims to further help clinicians dealing with the condition.

Aetiology of Molar-Incisor Hypomineralisation: A systematic review

AIM: This was to review and assess the studies on aetiology of Molar-Incisor Hypomineralisation (MIH) or, as a proxy, of demarcated opacities in permanent first molars and to consider the potential factors involved with findings obtained in animal experiments. METHODS: A systematic search by Medline® online database was performed. Abstracts behind appropriate titles were studied and finally the full articles were evaluated for their strength of evidence in the aetiology of MIH. RESULTS: From a total of 1,142 articles 28 were identified and selected for review. The selected papers covered medical problems in prenatal, perinatal and postnatal period, medication of the child during the first years of life, and exposure to fluoride or environmental toxicants (dioxins and PCBs) in the early childhood. Based on the assessment of the articles it was still not possible to specifically name those factors causing MIH although correlations between several potential factors and MIH were presented. Among the factors suggested and found to cause enamel defects in animal experiments were: high fever, hypoxia, hypocalcaemia, exposure to antibiotics (amoxicillin, a macrolide), and dioxins. CONCLUSION: Despite increased knowledge on the aetiology of MIH insufficient evidence to verify the causative factors exists. Further studies, especially prospective ones, are needed to improve the level and strength of evidence of the role of the present putative factors and to reveal new factors that may be involved. Any combined effect of several factors should be taken into account. Experimental dose/response studies and research on the molecular mechanisms causing the abnormal function of the ameloblasts are also necessary to deepen our knowledge of MIH.

Polychlorinated dibenzo-p-dioxins and dibenzofurans via mother's milk may cause developmental defects in the child's teeth.

Previous studies have shown developmental dental defects in rhesus macaques and rats experimentally exposed to dioxin. Now it was investigated if dioxin exposure from mothers milk in a normal breast-fed child population correlated with enamel hypomineralization of teeth that mineralize during the first 2 years of life. We studied 102 6-7-year-old Finnish children breast-fed for an average of 10.5 months. Milk samples were collected when the child was 4 weeks old. The concentrations of 17 most toxic polychlorinated dibenzo-p-dioxin and furan congeners were determined. The total exposure to dioxins was calculated from the concentrations in milk and the duration of breast feeding. Hypomineralization of the target teeth was found in 17 children. Both the frequency and severity of the lesions correlated with the total exposure. The results suggest that at the prevailing levels in human milk, dioxin may be an important cause of hypomineralization in the developing teeth of children.

Oral colonization by more than one clonal type of mutans streptococcus in children with nursing-bottle dental caries

By ribotyping the genetic diversity of mutans streptococci in six 1.5-3-yr-old children with nursing-bottle caries and in six caries-free, age-matched children and in their mothers was examined. The proportion of mutans streptococci in the dental plaque of the children and their levels in the saliva of the mothers were also examined. For ribotyping, chromosomal DNA of isolates obtained from the plaque of the children (3-12 isolates per child) and from the saliva of the mothers (4-13 isolates per mother) was digested with restriction endonuclease HindIII. The DNA fragments were hybridized to the plasmid pKK3535 which contains the rRNA operon of the Escherichia coli chromosome. The results showed that children with nursing-bottle caries exposed to frequent consumption of sucrose had a high proportion of mutans streptococci in plaque and four of them were colonized with more than one ribotype, whereas caries-free children had a low proportion of mutans streptococci in plaque and only one of them harboured more than one ribotype. Mothers of children with nursing bottle caries had similar levels and numbers of ribotypes of mutans streptococci in saliva as the mothers of the caries-free children. In both child groups, mothers were probably the main source of infection with mutans streptococci. Thus, children with nursing-bottle caries were not only heavily infected with mutans streptococci but also often colonized with more than one clonal type. In the childs acquisition of such clones, frequent sugar consumption may have an important role.

Developmental dental aberrations after the dioxin accident in Seveso.

Children’s developing teeth may be sensitive to environmental dioxins, and in animal studies developing teeth are one of the most sensitive targets of toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Twenty-five years after the dioxin accident in Seveso, Italy, 48 subjects from the contaminated areas (zones A and B) and in patches lightly contaminated (zone R) were recruited for the examination of dental and oral aberrations. Subjects were randomly invited from those exposed in their childhood and for whom frozen serum samples were available. The subjects were frequency matched with 65 subjects from the surrounding non-ABR zone for age, sex, and education. Concentrations of TCDD in previously analyzed plasma samples (zone ABR subjects only) ranged from 23 to 26,000 ng/kg in serum lipid. Ninety-three percent (25 of 27) of the subjects who had developmental enamel defects had been < 5 years of age at the time of the accident. The prevalence of defects in this age group was 42% (15 of 36) in zone ABR subjects and 26% (10 of 39) in zone non-ABR subjects, correlating with serum TCDD levels (p = 0.016). Hypodontia was seen in 12.5% (6 of 48) and 4.6% (3 of 65) of the zone ABR and non-ABR subjects, respectively, also correlating with serum TCDD level (p = 0.05). In conclusion, developmental dental aberrations were associated with childhood exposure to TCDD. In contrast, dental caries and periodontal disease, both infectious in nature, and oral pigmentation and salivary flow rate were not related to the exposure. The results support our hypothesis that dioxins can interfere with human organogenesis.

Amoxicillin May Cause Molar Incisor Hypomineralization

The etiology of molar incisor hypomineralization (MIH) is unclear. Our hypothesis was that certain antibiotics cause MIH. We examined 141 schoolchildren for MIH and, from their medical files, recorded the use of antibiotics under the age of 4 yrs. MIH was found in 16.3% of children. MIH was more common among those children who had taken, during the first year of life, amoxicillin (OR = 2.06; 95% CI, 1.01–4.17) or the rarely prescribed erythromycin (OR = 4.14; 95% CI, 1.05–16.4), compared with children who had not received treatment. Mouse E18 teeth were cultured for 10 days with/without amoxicillin at concentrations of 100 μg/mL–4 mg/mL. Amoxicillin increased enamel but not dentin thickness. An altered pattern of amelogenesis may have interfered with mineralization. We conclude that the early use of amoxicillin is among the causative factors of MIH.

Salivary Levels of Suspected Periodontal Pathogens in Relation to Periodontal Status and Treatment

The primary ecological niche for suspected periodontal pathogens seems to be the subgingival area, even though periodontal pathogens are also frequently recovered from saliva. The interrelationship of different periodontal conditions and the salivary levels of suspected periodontal pathogens is not known. In the present study, salivary levels of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Campylobacter rectus, and Peptostreptococcus micros were determined by bacterial culture and related to clinical periodontal status in 40 subjects with either advanced, moderate, or initial/no periodontitis. Culture-positive subjects harbored the 5 bacterial species in mean numbers ranging from 2 x 105 to 6 x 107 colony-forming units (CFU)/mL saliva. A. actinomycetemcomitans was found in none and P. gingivalis in one of the subjects with initial periodontitis, whereas both species were found in 33% and 44%, respectively, of the subjects with moderate periodontitis and in 60% and 40%, respectively, of the subjects with advanced periodontitis. The mean numbers of CFU/mL of P. intermedia, C. rectus and P. micros were significantly higher in subjects with advanced periodontitis than in subjects with initial/no periodontitis. Ten patients with advanced periodontitis were treated mechanically and with adjunctive systemic metronidazole, and were re-examined 1 and 6 months after treatment. Periodontal treatment eradicated or significantly reduced the levels of salivary periodontal pathogens for half a year, whereas in untreated subjects, the levels and the detection frequencies generally remained fairly stable. In conclusion, the results showed that the salivary levels of periodontal pathogens reflect the periodontal status of the patient.

Exposure to 2,3,7,8-tetrachlorodibenzo-para-dioxin leads to defective dentin formation and pulpal perforation in rat incisor tooth

A single dose of 1000 micrograms 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg body weight was given to TCDD-resistant (Han/Wistar) young adult male rats. Changes in the skulls and the continuously erupting incisor teeth were evaluated 16 weeks after the administration of TCDD. The skulls of the experimental rats (N = 11) were significantly smaller than those of the control rats (N = 11), and the upper and lower incisor teeth of all experimental rats were significantly thinner than the control rat teeth. The pulps of the lower incisors of all experimental rats were lingually exposed to the oral cavity at their incisal ends. Also in 3 cases the pulps of the upper incisors were exposed, but never in the control rats. Whereas the labial surfaces of the incisors of the control rats were brown, those of the experimental rat teeth appeared greyish and mottled. Histological examination revealed that the pulp chambers in the incisal halves of the affected teeth were larger than normal, at the expense of the thickness of dentin. Towards the incisal tooth ends, odontoblasts gradually lost their polarity and the pulp tissue became necrotic. A dentin zone next to the pulp chambers was irregular. Lingual tapering of the teeth was pronounced, which gave them a mesiodistally flattened appearance. The superficial zone of the otherwise regular enamel was poorly pigmented. In conclusion, a single injection of TCDD was shown to impair normal growth of the skull and incisor tooth formation in rats. The small size of the incisors, their aberrant shape and the defective dentin (and enamel) formation could be mediated by vitamin A metabolism, known to be interfered with by TCDD.