Mini-screw implant-supported pontics for the transitional management of missing permanent maxillary lateral incisors in children and adolescents: a review of currently available evidence.

AIM: To review currently available evidence regarding the use of mini-screw implant (MSI)-supported pontics for the transitional management of missing permanent maxillary lateral incisors in children and adolescents. METHODS: Indexed databases were searched until October 2019. The following inclusion criteria were imposed: (a) children and adolescents with missing permanent maxillary lateral incisor/s; (b) temporary replacement of missing permanent maxillary lateral incisors with MSI-supported pontics; (c) clinical and radiographic assessment of the outcome [MSI stability and/or alveolar bone (ALB) development]; and (d) follow-up after pontic placement. Commentaries, letters to the Editor, reviews, and studies in adult patients and/or patients with systemic/genetic diseases, with no follow-up, and without clinical and radiographic assessment of the outcome were excluded. RESULTS: Six out of 225 initially-identified studies were included. All studies were case-reports/series. A variability was observed among studies-assessed regarding the treatment protocol such as in the MSI dimensions, loading time and pontic retention protocol. Results from the included studies indicate that the MSI-supported pontics remained stable, with no infraocclusion and angular bony defect formation, ALB levels and bone density were maintained, and there was vertical ALB development during the follow-up period which ranged up to 99 months. Reported complications included MSI loss due to mobility, crown repair/replacement due to discoloration, and gingival impingement. CONCLUSIONS: The limited evidence shows that MSI-supported pontics are useful transitional restorations for missing permanent maxillary lateral incisors in children and adolescents; however, further well-designed clinical trials are needed in this regard.

Unilateral coronal synostosis: a histomorphometric study.

OBJECTIVE: This histomorphometric study compared the open and prematurely fused side of the coronal suture in subjects with unilateral coronal synostosis (UCS). METHODS: Sutures and parasutural bone were obtained from seven subjects with nonsyndromic UCS during operative correction at 3 to 24 months of age. Histological and cellular analyses were performed for the affected and open sutures. Specimens were examined by light and polarizing microscopy. Sutural patterns, osseous morphology, calvarial thickness, tartrate-resistant acid phosphatase (TRAP)-positive cells, and marrow spaces were evaluated histomorphologically, qualitatively, and semiquantitatively. Histomorphometry was performed to determine total projected area of marrow space as a percentage of unit area, total number of TRAP-positive cells per specimen, and perisutural cranial thickness. RESULTS: Polarizing microscopy showed that affected sutures were composed of more lamellar bone than the normal sutures. By light microscopy, the clinically fused sutures were 1.7-fold thicker (p <.02), had twofold larger marrow spaces (p <.0006), and contained sixfold more TRAP-positive osteoclasts in marrow spaces near the suture (p <.04) than the normal sutures. Quantitative analysis of the normal sutures revealed that calvarial thickness was greater with age and that there was an inverse correlation between medullary area and age. For the affected sutures, there was also an age-related increase in calvarial thickness. There were also trends for age-related declines in numbers of osteoclasts in both open and affected sides. CONCLUSIONS: These results question the hypothesis that defective osteoclastic activity is pivotal in the pathogenesis of UCS and support the hypothesis that this condition results from abnormally active bony remodeling.

The genetics of human tooth agenesis: new discoveries for understanding dental anomalies.

The important role of genetics has been increasingly recognized in recent years with respect to the understanding of dental anomalies, such as tooth agenesis. The lack of any real insight into the cause of this condition has led us to use a human molecular genetics approach to identify the genes perturbing normal dental development. We are reporting a strategy that can be applied to investigate the underlying cause of human tooth agenesis. Starting with a single large family presenting a clearly recognizable and well-defined form of tooth agenesis, we have identified a defective gene that affects the formation of second premolars and third molars. With the use of "the family study" method, evidence is produced showing that other genetic defects also contribute to the wide range of phenotypic variability of tooth agenesis. Identification of genetic mutations in families with tooth agenesis or other dental anomalies will enable preclinical diagnosis and permit improved orthodontic treatment.

Human NELL-1 expressed in unilateral coronal synostosis.

Surgical correction of unilateral coronal synostosis offers a unique opportunity to examine the molecular differences between an abnormal and a normal cranial suture. We isolated and identified a cDNA fragment whose expression was up-regulated in the premature fusing and fused coronal sutures, as compared with normal coronal sutures. The nucleotide sequence of the full-length cDNA of this gene, human NELL-1, has approximately 61% homology with the chicken Nel gene. Both chicken Nel and human NELL-1 are comprised of six epidermal growth factor-like repeats. The human NELL-1 messages were localized primarily in the mesenchymal cells and osteoblasts at the osteogenic front, along the parasutural bone margins, and within the condensing mesenchymal cells of newly formed bone in sites of premature sutural fusion. Human multiorgan tissue mRNA blot showed that NELL-1 was specifically expressed in fetal brain but not in fetal kidney, liver, or lung. We also showed that Nell-1 was expressed in rat calvarial osteoprogenitor cells and was largely absent in rat tibiae and fibroblast cell cultures. In conclusion, our data suggest that the NELL-1 gene is preferentially expressed in cranial intramembranous bone and neural tissue (both of neural crest cell origin) and is up-regulated during unilateral premature closure of the coronal suture. The precise role of this gene is unknown.

Haploinsufficiency of MSX1: a mechanism for selective tooth agenesis.

Previously, we found that the cause of autosomal dominant selective tooth agenesis in one family is a missense mutation resulting in an arginine-to-proline substitution in the homeodomain of MSX1. To determine whether the tooth agenesis phenotype may result from haploinsufficiency or a dominant-negative mechanism, we have performed biochemical and functional analyses of the mutant protein Msx1(R31P). We show that Msx1(R31P) has perturbed structure and reduced thermostability compared with wild-type Msx1. As a consequence, the biochemical activities of Msx1(R31P) are severely impaired, since it exhibits little or no ability to interact with DNA or other protein factors or to function in transcriptional repression. We also show that Msx1(R31P) is inactive in vivo, since it does not display the activities of wild-type Msx1 in assays of ectopic expression in the limb. Furthermore, Msx1(R31P) does not antagonize the activity of wild-type Msx1 in any of these assays. Because Msx1(R31P) appears to be inactive and does not affect the action of wild-type Msx1, we propose that the phenotype of affected individuals with selective tooth agenesis is due to haploinsufficiency.

A human MSX1 homeodomain missense mutation causes selective tooth agenesis.

We demonstrate that a mutation in the homeobox gene, MSX1, causes a common developmental anomaly, familial tooth agenesis. Genetic linkage analyses in a family with autosomal dominant agenesis of second premolars and third molars identified a locus on chromosome 4p, where the MSX1 gene resides. Sequence analyses demonstrated an Arg31Pro missense mutation in the homeodomain of MSX1 in all affected family members. Arg 31 is a highly conserved homeodomain residue that interacts with the ribose phosphate backbone of target DNA. We propose that the Arg31 Pro mutatrion comprises MSX1 interactions, and suggest that MSX1 functions are critical for normal development of specific human teeth.

Evaluation of cervical spine abnormalities on cephalometric radiographs.

Cephalometric radiographs, a key element of orthodontic diagnosis, contain useful information related to the cervical spine often neglected by orthodontists and medical specialists. This article reviews cervical spine anatomy in a manner that will enable the clinician to trace the cervical spine accurately and detect cervical spine abnormalities. Examples of syndromic, nonsyndromic, and idiopathic anomalies of the cervical spine are presented and their significance discussed. Cephalometric radiographs can be used by clinicians as a potential resource for screening for pathologic abnormalities of the cervical spine and potentially averting some pathologic complications.

[Morphometric studies on the fetal development of the human mandible]. / Morphometrische Untersuchungen zur Fetalentwicklung der menschlichen Mandibula.

Serial sections of eleven human mandibles of embryos and fetuses ranging in size from 18 mm CRL to 66 mm CRL were computer-graphically reconstructed. The extension of the Meckel cartilage and the mandibular bony structures were morphometrically studied. In emphasis the study encompassed measurements portraying length, width, dorsal opening angle, and the position of the mental foramen. In addition five mandibles of human embryos and fetuses with a size range between 30 and 50 mm CRL were radiographically examined. Results showed that in the younger specimens between 21 and 29 CRL size development of the structures of the mandible and the development of overall fetal body size take place independently from each other. During further development a change in the form of the mandible from a wide V over an acute V to a more rounded U form was observed.