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An important factor in the assessment of caries risk is the presence of specific oral microflora, especially Streptococcus mutans. Some S. mutans strains possess proteins capable of binding collagen, such as the Cnm and Cbm proteins. The aim is to determine the presence of S. mutans strains carrying collagen binding proteins in a group of subjects with severe early childhood caries (S-ECC). S. mutans strains isolated from 15 S-ECC children were analyzed for collagen binding domains (cbd) of the cnm (cbd/cnm) and cbm (cbd/cbm) genes and their ability to bind to collagen. S. mutans strains positive for cbd/cnm or cbd/cbm were only found in 3 subjects with the most severe caries profile, with one subject having both cbd/cnm and cbd/cbm, and the other two with one of each. cnm/cbm-positive S. mutans strains bound to collagen substrate more avidly compared with negative S. mutans strains from each of the three groups. Our findings of an association between the presence of the collagen binding domains of the cnm/cbm genes in plaque S. mutans and the most aggressive form of caries profile in children offer a potential strategy to identify an individual’s risk for caries progression. Our study should be replicated in other settings and communities in longitudinal and longer-term studies. Our data offer a potential tool in the caries risk management and assessment in children.

Objective The objective of this study was to assess the shear bond strength (SBS) of orthodontic brackets bonded to uncut enamel with universal self-etch 1-step adhesive systems. Methods Extracted uncut premolars (n = 160) were randomly divided into 4 groups for treatment with Scotchbond Universal Adhesive (SU), All-Bond Universal (BU), Clearfil Universal Bond (CU) or the control, Adper Scotchbond Multi-Purpose Adhesive. Following bonding of brackets on tooth surfaces, teeth were stored in distilled water for 24 h and 6 months, and brackets were tested for SBS. The adhesive remnant index (ARI) and quantitative percentage of remaining resin (%RR) were recorded. Scanning electron microscopy was used to analyze debonded surfaces qualitatively. SBS and %RR data were analyzed by 2-way ANOVA followed by the Tukey test (α = 0.05). Results At neither time did these universal adhesives achieve satisfactory SBS for orthodontic treatment. The control group had the highest SBS, ARI score and mean %RR (and these differences were significant), while the BU group had the lowest SBS. SBS mean values and ARI scores decreased over time for SU and BU, but remained stable for CU. There was no difference in %RR among the universal adhesives tested. Conclusion None of the universal adhesives used in self-etch mode achieved SBS values (at 24 h and 6 months) that were satisfactory for orthodontic treatment.

Bacteriocins are ribosomally synthesized proteinaceous antibacterial peptides. They selectively interfere with the growth of other bacteria. The production and secretion of bacteriocins confer a distinct ecological advantage to the producer in competing against other bacteria that are present in the same ecological niche. Streptococcus mutans, a significant contributor to the development of dental caries, is one of the most prolific producers of bacteriocins, known as mutacins in S. mutans. In this study, we characterized the locus encoding mutacin B-Ny266, a lantibiotic with a broad spectrum of activity. The chromosomal locus is composed of six predicted operon structures encoding proteins involved in regulation, antimicrobial activity, biosynthesis, modification, transport, and immunity. Mutacin B-Ny266 was purified from semisolid cultures, and two inhibitory peptides, LanA and LanA′, were detected. Both peptides were highly modified. Such modifications include dehydration of serine and threonine and the formation of a C-terminal aminovinyl-cysteine (AviCys) ring. While LanA peptide alone is absolutely required for antimicrobial activity, the presence of LanA′ enhanced the activity of LanA, suggesting that B-Ny266 may function as a two-peptide lantibiotic. The activation of lanAA′ expression is most likely controlled by the conserved two-component system NsrRS, which is activated by LanA peptide but not by LanA′. The chromosomal locus encoding mutacin B-Ny266 was not universally conserved in all sequenced S. mutans genomes. Intriguingly, the genes encoding LanAA′ peptides were restricted to the most invasive serotypes of S. mutans. IMPORTANCE Although dental caries is largely preventable, it remains the most common and costly infectious disease worldwide. Caries is initiated by the presence of dental plaque biofilm that contains Streptococcus mutans, a species extensively characterized by its role in caries development and formation. S. mutans deploys an arsenal of strategies to establish itself within the oral cavity. One of them is the production of bacteriocins that confer a competitive advantage by targeting and killing closely related competitors. In this work, we found that mutacin B-Ny266 is a potent lantibiotic that is effective at killing a wide array of oral streptococci, including nearly all S. mutans strains tested. Lantibiotics produced by oral bacteria could represent a promising strategy to target caries pathogens embedded in dental plaque biofilm.

Introduction Management of mandibular condylar fractures is difficult in children with their inherently dynamic and unstable deciduous and mixed dentitions. We present a variation of the conservative fixed orthodontic approach that was used as an adjunct to aid in the reduction of a bilateral condylar fracture in a pediatric patient. Methods A boy, aged 10 years 9 months, came with clinical signs and symptoms of mandibular fracture after being involved in a motor vehicle accident. A computed tomography scan showed a vertical fracture on the left condylar head, a displaced fracture of the right condylar neck, and a mandibular symphysis fracture. The patient was treated with an orthodontic fixed appliance instead of an arch bar splint, followed by elastic traction to achieve a proper occlusion and condylar remodeling. Follow-up appointments were made 2 weeks and 1, 2, 20, 37, and 49 months after treatment. Results Clinical recovery was observed 2 months after treatment. At the follow-up appointments at 20, 37, and 49 months, jaw function and occlusal relationship remained stable, and no ankylosis was observed. The computed tomography scans showed that the right condyle had remodeled, and the left condyle exhibited a slight curve in the head at 49 months posttreatment. The patient's satisfaction with these treatment results was high. Conclusions Conservative treatment of a mandibular fracture by fixed orthodontic means is a viable treatment option that is relatively straightforward and cost-effective and has a high level of patient acceptance and comfort.

Nitric oxide (NO) is involved in bone remodelling and has been shown to play a role in regulating the rate of orthodontic tooth movement (OTM) in rat models. In humans, however, the role of NO in OTM remains less clear. In this study, NO concentration in gingival crevicular fluid (GCF) was measured in patients undergoing orthodontic treatment. Thirteen male participants (ages 11-18 years) planned for non-extraction fixed orthodontic therapy were recruited. Samples of GCF were collected from each maxillary central incisor and first and second molar immediately before (T0), 1h after (T1), and 3-4 days after (T2) application of light orthodontic forces. The maxillary second molars were not included in the appliance and served as controls. Measureable NO levels were consistently obtained from all sampled sites. Total NO levels showed significantly higher NO levels (p0.05) at T1 at the buccal surfaces of the central incisors when compared to the first and second molars. The results indicate a possible role for NO in OTM at the pressure sites of incisors at early time points. Further studies are required to determine whether NO levels in the periodontal ligament tissues of human teeth during OTM are affected by a force gradient and the magnitude of the applied force.

Aim Caffeine is one of the most widely consumed behaviorally active substances in the world. Although its effects on the central nervous system and bone metabolism have been documented, as yet there is no report on its effect on tissues in the oral cavity. In this study we analyzed the viability of human gingival fibroblasts (HGF) and alkaline phosphatase (ALP) enzyme activity after exposure to different concentrations of caffeine for different exposure time periods. Methods The HGF were cultured with different concentrations of caffeine. Viability of cells exposed to caffeine was analyzed by the 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay to assess mitochondrial dehydrogenase activity. The activity of ALP was analyzed at specific time intervals after caffeine addition. Results Our results showed that caffeine of concentrations

The shape and size of tooth roots are genetically and phylogenetically predetermined. Clinical defects in root formation can manifest in the form of shortened roots caused by either root agenesis or root resorption. We report on a patient who came at age 7 years for space management. In the 2-year period after the initial visit, maxillary arch expansion was performed, followed by serial extractions of all 4 first premolars. A radiograph taken about 18 months after the serial extraction showed that although the crowns of all 4 second premolars had erupted fully into the arch, the roots were only about half of their normal length. With a family history of 1 sibling with a missing second premolar and the symmetrical distribution and pattern of the teeth in the 4 dental quadrants, we speculated that the arrested root development was due most likely to a genetic predisposition. Arrested root development is difficult to predict, but a potential warning sign is a family history of malformed or missing teeth. Proper, adequate, and accurate records continue to remain critical for both medical and legal purposes in the treatment of patients with potential problems in root agenesis.

Craniosynostosis is a relatively common birth defect characterized by the premature fusion of one or more cranial sutures. Examples of craniosynostosis syndromes include Crouzon (CS), Pfeiffer (PS), and Apert (AS) syndrome, with clinical characteristics such as midface hypoplasia, hypertelorism, and in some cases, limb defects. Mutations in Fibroblast Growth Factor Receptor-2 comprise the majority of known mutations in syndromic forms of craniosynostosis. A number of clinical reports of FGFR-associated craniosynostosis patients and mouse mutants have been linked to gastrointestinal tract (GIT) disorders, leading to the hypothesis of a direct link between FGFR-associated craniosynostosis syndromes and GIT malformations. We conducted an investigation to determine GIT symptoms in a sample of FGFR-associated craniosynostosis syndrome patients and a mouse model of CS containing a mutation (W290R) in Fgfr2. We found that, compared to the general population, the incidence of intestinal/bowel malrotation (IM) was present at a higher level in our sample population of patients with FGFR-associated craniosynostosis syndromes. We also showed that the mouse model of CS had an increased incidence of cecal displacement, suggestive of IM. These findings suggest a direct relationship between FGFR-related craniosynostosis syndromes and GIT malformations. Our study may shed further light on the potential widespread impact FGFR mutations on different developmental systems. Based on reports of GIT malformations in children with craniosynostosis syndromes and substantiation with our animal model, GIT malformations should be considered in any child with an FGFR2-associated craniosynostosis syndrome. © 2016 Wiley Periodicals, Inc.

Objective:Since its first description, the A strain of mice have been utilized extensively as models to study the processes involved in clefting of the midfacial region. Of the A substrains, the A/WySn has a spontaneous rate of clefting of the lip of about 20% to 30%. The A/WySn mouse model was utilized in this study to analyze and compare the phenotypic and molecular changes in the midfacial region of embryos with and without cleft.Results:Scanning electron microscopy and skeletal and cartilage preparations of newborn A/WySn pups showed the presence of bilateral and unilateral clefts of the lips and the disruption of the skeletal and cartilaginous components of the mice with clefts of the lip. The expression of the msx1 homeobox gene was analyzed by whole mount in situ hybridization of A/WySn embryos at different stages of midfacial development. The results showed that there was misregulation of the expression of the msx1 gene in embryos with cleft, with a persistence of expression in the distal growing tips of the midfacial processes and in areas that have fused in normal embryos without cleft.Conclusions:Although the genetic defect in A/WySn mice is not known, a possible candidate gene has been mapped to a corresponding human chromosome carrying retinoic acid receptor α, and there exists a possibility that msx1 is in the same genetic pathway affected by the mutation of the gene in A/WySn.

Defects of the head and neck region account for a substantial portion of all human birth disorders. The high incidence of malformations in this region may be attributed in part to the intricate means by which the facial region is assembled during embryonic development. The starting constituent for the majority of skeletal and connective tissues in the face is a pluripotent population of cells, the cranial neural crest (CNC) cells. This population of cells exhibit remarkable migratory abilities and diversity of potential cell types. This review draws on extensive research that has been done in the field, focusing specifically on findings generated in the last decade on cell behavior and the gene regulatory networks of migratory CNC cells. In the later part of this review, the importance of the CNC cells in the overall development of the craniofacial region will be illustrated with a discussion of a craniofacial birth defect, the Treacher Collins syndrome. The next decade will most likely herald in an era of greater understanding of the integrative molecular networks at different stages of the development of the CNC cells. Such new information is essential towards a better understanding the etiology and pathogenesis of the many craniofacial birth defects and will ultimately lead to new therapeutic modalities.

Mutations in Fibroblastic Growth Factor Receptors (FGFR) have been associated with human craniosynostotic birth defects like Crouzon syndrome. Several anecdotes and case reports have indicated higher incidence of gastrointestinal tract disorders in FGFR-associated craniosynostotic birth defects. Our objective was to characterize esophageal defects in a mouse model of human Crouzon syndrome, with a mutation in codon 290 of FGFR2.Dissected esophagi of Fgfr2(W290R) postnatal heterozygous (HET) and wild-type mice were analyzed by histological staining, immunohistochemically with cell proliferation marker, and functionally by strain gauge measures of electrically evoked contractile force.The esophagi of HETs were noticeably smaller but with wider lumen than those of wild-type littermates. The HET esophagi showed a decrease in proliferation and an increase in expression of Sonic Hedgehog as compared to wild-type esophagi. Histological investigations revealed reduced amounts and disorganization of collagen in muscle layers. Functional analysis revealed altered contractile properties in HET with reduced peak amplitude and prolonged duration of evoked contractile force response and lower stimulation threshold.The defects observed in the esophagus of the mutant may explain some of the clinical symptoms observed in humans, for example, recurrent vomiting, gastroesophageal reflux, and esophageal strictures. Taken together, our results provide evidence for the importance of Fibroblastic Growth Factor signaling in the growth and patterning of the esophagus, providing a possible scientific basis for the gastrointestinal tract clinical findings in craniosynostotic patients. Furthermore, the findings also provide a sound scientific rationale for any changes in the clinical management of gastrointestinal tract problems in patients with craniosynostotic defects.

Few three-dimensional (3-D) models exist to study the cellular aspects and molecular regulation of orthodontic tooth movement (OTM). The aim of this study was to develop a 3-D in vitro model to study mechanical loading of human periodontal ligament (PDL) fibroblasts (hPDLF). hPDLF were seeded within collagen gels to form a PDLF analogue. Characterisation of the seeded collagen gels revealed that the gels supported cell proliferation, viability and the emergence of a possible contractile phenotype, replicating the constrained condition of the human PDL in vivo. We next developed a 3-D model that incorporated a seeded collagen gel interlocked mechanically at two ends to movable end plates. The movable end plates allowed for static tensile or compressive loading of the hPDLF-seeded collagen gels. Preliminary testings showed that this 3-D model mimicked PDL strains similar to those observed during OTM. Our 3-D model of OTM therefore offers promise for use as a model system in future studies to improve our understanding of the effects of OTM on PDLF.

Introduction Rapid palatal expanders (RPEs) have attachments cemented to the teeth and a screw that covers the palate. Because of their position and relative size, RPEs can affect speech. Our objective was to assess speech perturbation and adaptation related to RPE appliances over time. Methods RPEs were planned for the treatment of 22 patients in the orthodontic clinic at the University of Toronto in Canada. Speech recordings were made at 6 time points: before RPE placement, after placement, during expansion, during retention, after removal, and 4 weeks after removal. The speech recordings consisted of 35 sentences, from which 3 sentences were chosen for analysis. Speech acceptability was assessed perceptually by 10 listeners who rated each sentence on an equal-appearing interval scale. The vowel formants for /i/ and the fricative spectra for /s/ and /∫/ were measured with speech analysis software. Repeated-measures analysis of variance with post-hoc paired t tests was used for statistical analysis. Results When the appliance was placed, speech acceptability deteriorated. Over time, the ratings improved and returned to baseline when the appliance was removed. For the vowel /i/, the first formant increased, and the second formant decreased in frequency, indicating centralization of the vowel. The formants returned to the pretreatment levels during treatment. For the fricatives (/s/ and /∫/), low-to-high frequency ratios indicated that the fricatives were distorted when the appliance was placed. The ratios returned to baseline levels once the appliance was removed. The results for the spectral moments indicated that spectral mean decreased and skewness became more positive. Repeated-measures analysis of variance showed significant effects for time for all acoustic measures. Conclusions Speech was altered and distorted when the appliance was first placed. The patients’ speech gradually improved over time and returned to baseline once the appliance was removed. The results from the study will be useful for pretreatment counseling of patients and their families.

Dentinogenesis imperfecta (DGI) and dentin dysplasia (DD) are allelic disorders that primarily affect the formation of tooth dentin. Both conditions are autosomal-dominant and can be caused by mutations in the dentin sialophosphoprotein gene ( DSPP, 4q21.3). We recruited 23 members of a four-generation kindred, including ten persons with dentin defects, and tested the hypothesis that these defects are linked to DSPP. The primary dentition showed amber discoloration, pulp obliteration, and severe attrition. The secondary dentition showed either pulp obliteration with bulbous crowns and gray discoloration or thistle-tube pulp configurations, normal crowns, and mild gray discoloration. Haplotype analyses showed no recombination between three 4q21-q24 markers and the disease locus. Mutational analyses identified no coding or intron junction sequence variations associated with affection status in DMP1, MEPE, or the DSP portion of DSPP. The defects in the permanent dentition were typically mild and consistent with a diagnosis of DD-II, but some dental features associated with DGI-II were also present. We conclude that DD-II and DGI-II are milder and more severe forms, respectively, of the same disease.

Distraction osteogenesis (DO) has been used recently to correct maxillary hypoplasia with predictable and stable results. In patients with clefts of the secondary palate, DO can also be used to aid in vertical alveolus augmentation and rapid orthodontic tooth movement. If an osteotomized dental arch can be transported to a new position without complications, it would reduce or eliminate the need for a secondary bone graft to the cleft alveolus in cleft patients and help prevent dentoalveolar defects by approximating the native alveolar bone and gingiva. Mobilizing a segment in the dentoalveolar region also results in the creation of new bone and attached gingiva. This report shows that the application of DO for skeletal expansion and rapid movement of tooth-bone segments should receive more careful consideration in the treatment of patients with clefts of the palate.

Excessive blood loss is one of the major complications of orthognathic surgery. Numerous strategies, including hypotensive anesthetic techniques and blood transfusion, have been developed to deal with the blood loss. Blood for transfusions can be obtained from banked blood or from autologous donation. In this study, the authors looked at 2 groups of patients who had bimaxillary orthognathic surgery. One group included patients who had autodonated blood (group 1) and who were operated on between 1991 and 1993, and the other patients did not autodonate and were operated on between 1998 and 2000 (group 2). It was found that fewer than 50% of patients in group 1 were transfused, and none of the group 2 patients were. A protocol to lessen blood loss that should obviate the need for blood transfusion is proposed. It is concluded that blood transfusion should no longer be a consideration during routine bimaxillary orthognathic surgery.