Molar-Incisor-Hypomineralisation (MIH) is the term used to depict a condition in which one or more of the permanent molar teeth and usually no less than one incisor tooth is hypomineralised and the prevalence rates vary from 2.4 to 40.2%. The aim of this study was to assess the prevalence and the risk factors of MIH in children in Istanbul, Turkey. A total of 1511 (760 M, 751 F), 8- to 11-year-old children were examined who had their first permanent molar and incisors evaluated using the EAPD criteria for MIH. Hypomineralized molars and incisors were recorded based on developmental defects of enamel index. The potential aetiological factors were retrieved through personal interview and etiological questions were asked to the parents. Statistical analysis was performed with a chi-Square test. MIH was observed in 215 (14.2%; 102 male, 113 female) children. The sample (1511 children) comprised 71 (9.9%) 8 year-olds with MIH and 144 (18.2%) 11 year-olds with MIH. A significant difference was found between 8 (9.9%) and 11-year-old (18.2%) children with MIH (p ≤ 0.001). Complications during the mother's pregnancy, birth prematurity, average breast feeding period, diarrhea frequency, digestive system diseases, asthma, frequent high fever, ear infection, renal failure, rubeola, chickenpox and parotitis were found to be significantly associated with MIH (p < 0.001). There are many events that can cause MIH which we cannot control or predict. Therefore, longitudinal studies with large sample size are needed so as to determine how various likely etiological factors described affect the etiological role.

Molar incisor hypomineralization (MIH) is an enamel condition characterized by lesions ranging in color from white to brown which present rapid caries progression, and mainly affects permanent first molars and incisors. These enamel defects usually occur when there are disturbances during the mineralization or maturation stage of amelogenesis. Both genetic and environmental factors have been suggested to play roles in MIH’s development, but no conclusive risk factors have shown the source of the disease. During head and neck development, the interferon regulatory factor 6 (IRF6) gene is involved in the structure formation of the oral and maxillofacial regions, and the transforming growth factor alpha (TGFA) is an essential cell regulator, acting during proliferation, differentiation, migration and apoptosis. In this present study, it was hypothesized that these genes interact and contribute to predisposition of MIH. Environmental factors affecting children that were 3 years of age or older were also hypothesized to play a role in the disease etiology. Those factors included respiratory issues, malnutrition, food intolerance, infection of any sort and medication intake. A total of 1,065 salivary samples from four different cohorts were obtained, and DNA was extracted from each sample and genotyped for nine different single nucleotide polymorphisms. Association tests and logistic regression implemented in PLINK were used for analyses. A potential interaction betweenTGFArs930655 with all markers tested in the cohort from Turkey was identified. These interactions were not identified in the remaining cohorts. Associations (p<0.05) between the use of medication after three years of age and MIH were also found, suggesting that conditions acquired at the age children start to socialize might contribute to the development of MIH.

Objective: The aim of this in vitro study was to evaluate antimicrobial activities of three different pulp capping materials; Biodentine, mineral trioxide aggregate (MTA) Angelus, and Dycal against Enterococcus faecalis and their durability with time. Materials and Methods: Direct contact test was used for the assessment. Three sets of sealers were mixed and placed on microtiter plate wells: One set was used within 20 min of recommended setting time while others were used after 24-h and 1-week. E. faecalis suspension was placed directly on the materials for 1 h and then transferred to another plate with fresh media. Nine wells of bacteria without the tested cements served as the positive control. One well of the tested cements without bacteria served as the negative control. Bacterial growth was evaluated by a temperature-controlled microplate spectrophotometer for 1-h intervals among 24 h. Data were analyzed using Kruskal–Wallis test. Results: All tested materials showed less bacterial density than the control group. MTA, Biodentine, and Dycal showed significantly higher bacterial density than the control group in freshly mixed samples (P < 0.05). And MTA showed significantly higher antibacterial activity than Dycal (P < 0.05). In 24 h, materials did not show any differences (P > 0.05). MTA and Biodentine samples showed significant differences than Dycal; MTA also showed higher antibacterial activity than control in 1-week samples (P < 0.05). Conclusion: While freshly mixed MTA showed the best antibacterial activity over time, Biodentine had shown similar antibacterial activity to MTA.

The aim of this clinical case series is to present a diagnosis and different treatment methods of patients in different ages with amelogenesis imperfecta (AI) as well as further treatments during a 3-6 years follow-up period. A number of 31 patients (16 female, 15 male with a mean age of 10.77 ± 2.65 years) with AI have been examined for the study group between 2007 and 2010 years. A detailed anamnesis was recorded, followed by a clinical and radiological assessment of oral health. The types of AI classified for each patient according to clinical and radiographic evaluation. The main complaints of patients, presence of dental caries and dental anomalies were noted. Necessary treatments had been planned for the individual cases of AI. A number of 19 patients had hypoplastic (HP) form, and 10 patients showed hypomaturation (HM) form of AI, while one patient showed hypocalcified form of AI and one patient had HM-HP form with taurodontism. Main complaints were chiefly related to dissatisfactory esthetics and dental sensitivity. Caries prevalence index was 93.5%. Mean decayed, missing, filling permanent teeth (DMF) and DMF surface (DMFS) were found as 2.74 ± 1.71 and 6.23 ± 3.99; df (decayed, filling primary teeth) and dfs (decayed, filling primary teeth surface) were found as 3.12 ± 2.85 and 5.24 ± 4.97, respectively. All patients received individual clinical care, including preventive, restorative, and prosthetic treatments. Patients have scheduled for regular follow-up in every 3 months. Composite restorations were used as the most common treatment (25 patients, 80.6%). The treatment plan should be based on patient's age, type of defects and individual needs of the patients. Necessary treatment plan is essential, not only due to functional and aesthetic reasons, but also for the positive psychological impact on young patients.

Amelogenesis imperfecta (AI) is a genetic disease affecting tooth enamel formation. AI can be an isolated entity or a phenotype of syndromes. To date, more than 10 genes have been associated with various forms of AI. We have identified 2 unrelated Turkish families with hypoplastic AI and performed mutational analysis. Whole-exome sequencing identified 2 novel heterozygous nonsense mutations in the ENAM gene (c.454G>T p.Glu152* in family 1, c.358C>T p.Gln120* in family 2) in the probands. Affected individuals were heterozygous for the mutation in each family. Segregation analysis within each family revealed individuals with incomplete penetrance or extremely mild enamel phenotype, in spite of having the same mutation with the other affected individuals. We believe that these findings will broaden our understanding of the clinical phenotype of AI caused by ENAM mutations.

Mutations in Dentin Sialophosphoprotein (DSPP) are known to cause, in order of increasing severity, dentin dysplasia type-II (DD-II), dentinogenesis imperfecta type-II (DGI-II), and dentinogenesis imperfecta type-III (DGI-III). DSPP mutations fall into two groups: a 5′-group that affects protein targeting and a 3′-group that shifts translation into the −1 reading frame. Using whole-exome sequence (WES) analyses and Single Molecule Real-Time (SMRT) sequencing, we identified disease-causing DSPP mutations in 12 families. Three of the mutations are novel: c.53T>C/p.(Val18Ala); c.3461delG/p.(Ser1154Metfs*160); and c.3700delA/p.(Ser1234Alafs*80). We propose genetic analysis start with WES analysis of proband DNA to identify mutations in COL1A1 and COL1A2 causing dominant forms of osteogenesis imperfecta, 5′-DSPP mutations, and 3′-DSPP frameshifts near the margins of the DSPP repeat region, and SMRT sequencing when the disease-causing mutation is not identified. After reviewing the literature and incorporating new information showing distinct differences in the cell pathology observed between knockin mice with 5′-Dspp or 3′-Dspp mutations, we propose a modified Shields Classification based upon the causative mutation rather than phenotypic severity such that patients identified with 5′-DSPP defects be diagnosed as DGI-III, while those with 3′-DSPP defects be diagnosed as DGI-II.