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At least 1,081 records · Page 60Linked to original sources
PubMed1991

Dynamics of tissue changes found after mechanical loading of the rat incisor. I. A three-dimensional longitudinal study of the morphologic aspects.

A three-dimensional morphometric method was used to evaluate progressive changes in shape and size of recovering dental and periodontal tissues after orthodontic loading. In 35 female rats weighing 212 +/- 4 gm, loads of 19.7 +/- 1.6 gm generated by closed-coil springs were applied for 2 weeks to the shortened lower left incisor. The rats were killed in groups of five at 0, 1, 3, 5, 7, 9, and 10 weeks (groups 0-w to 10-w) after the springs were removed. A group of rats with normal incisors (group C-1) and one with five incisors that had been continually shortened for 10 weeks (group C-2) served as controls for groups 0-w and 10-w, respectively. Width, area, and volume of the tooth and enamel-bordering periodontal ligament (e-PDL) and cementum-bordering PDL (c-PDL) were measured. After 2 weeks of loading (group 0-w), the volume of the compressed e-PDL had decreased by 22%, and the volume of the stretched c-PDL had increased by 72%, suggesting that bone apposition lags behind the rate of tooth movement. During the recovery period, the dental and periodontal parameters tended toward a gradual return to control (C-2) values, although at the end of 10 weeks many still lagged significantly behind the controls. Recovery was slowed by repeated reversals at different sites in the various groups. The ability of the preloaded incisor to adjust to changes in occlusal function was lastingly impaired.

Animals↗
PubMed1995

Etiologic aspects and orthodontic treatment of unilateral localized arrested tooth-development combined with hearing loss.

In this study a case has been presented involving localized, arrested maxillary tooth development, asymmetric maxillary development, and unilateral loss of hearing. No similar case seems to have been described before. The orthodontic treatment comprised extraction of four permanent tooth germs in the maxilla and autotransplantation of mandibular teeth, followed by the use of fixed orthodontic appliances and a one-unit bridge restoration. Etiologic aspects are discussed. It is suggested that a severe attack of mumps that involved massive swelling of the parotid glands immediately after chicken pox and measles at the age of 4 to 5 years, may have resulted in a neurologic reduction of hearing and arrested tooth development. The teeth in which root development in relation to mumps does not appear to have been reported previously, whereas hearing loss after mumps has been reported. In the search for verification of this possible connection, children with arrested tooth development should be examined for reduction of hearing, and children with hearing loss after mumps ought to have their dental development checked.

Bicuspid↗
PubMed1999

Changes in the craniofacial complex from adolescence to midadulthood: a cephalometric study.

The purpose of the present study was to evaluate cephalometrically the craniofacial growth changes and adjustments that occur from late adolescence to midadulthood in persons who had no previous history of orthodontic treatment. Serial lateral cephalograms from 58 subjects from the University of Michigan Elementary and Secondary Growth Study recalled on average in their late 40s were examined. Fifteen of the patients also had cephalograms taken in early adulthood (early 30s). Statistically significant growth changes occurred; mandibular and midfacial lengths as well as posterior and lower anterior facial heights had increased significantly for males and females over both time intervals. The pattern of expression of these changes was different in the two genders: males showed an anterior rotation of the mandible, whereas females demonstrated a posterior rotation of the mandible. Soft tissue changes also were somewhat different between genders. In males, the nose and chin grew downward and forward, with the lips generally moving straight downward. In contrast, females had nasal growth that progressed downward and forward, and there was a slight retrusion of the lips over time. Continued tooth eruption was noted in both genders as well.

Adolescent↗
PubMed1989

Presurgical orthopaedic treatment using hard plates.

Our concept in the treatment of unilateral clefts of lip, alveolus and palate includes early maxillary orthopaedic treatment starting immediately after birth until the end of the first year of life and the surgical closure of the lip at three months and of the soft palate at twelve months. Hard palate and alveolus are closed after three years by secondary osteoplasty in the alveolar region. The appliance is made of hard acrylic resin and is adjusted monthly to allow for growth. It thus encourages passive orthopaedic guidance of maxillary growth. The local compatibility of the plate was excellent and the acceptance by the children created no problems until tooth eruption. Follow-up studies were conducted on twenty children treated in this way until three years of age. After the first year results show a good and harmonious arch alignment without any collapse of the alveolar segments. The cleft narrows and the steepness of the palatal slope flattens. This maxillary development is arrested after suspension of orthopaedic treatment, and a slight collapse of the alveolar segments is observed.

Acrylic Resins↗
PubMed2001

Identification of novel CBFA1/RUNX2 mutations causing cleidocranial dysplasia.

Core binding factor A1 (CBFA1/RUNX2) is a runt-like transcription factor essential for osteoblast differentiation. Haplotype insufficiency causes cleidocranial dysplasia (CCD), a syndrome featuring supernumerary tooth buds, delayed tooth eruption, patent fontanels, Wormian bones, short stature, dysplasia of the clavicles, growth retardation and hypoplasia of the distal phalanges. We identified novel CBFAI/RUNX2 mutations after PCR and direct sequencing of patient leukocyte DNA. In family 1 mother and son are affected by CCD. Both carry the missense mutation R190W (CGG > TGG). This nucleotide change introduced a BsmI restriction site, which was used to independently confirm the mutation. It was absent in healthy members of the family. Family 2, in which father and daughter are affected by CCD, shows a deletion of nucleotide C821. This deletion causes a frameshift mutation with premature stop after the insertion of 18 aberrant amino acids. Healthy family members did not have this mutation. The clavicular dysplasia was more pronounced with the R19OW mutation, while the bone density was markedly reduced in individuals with either mutation, suggesting a previously underemphasized increased risk for osteoporosis in CCD.

Adolescent↗
PubMed2003

Impact of caries experience in the deciduous molars on the emergence of the successors.

The purpose of this study was to evaluate the effect of caries experience in a primary molar (decayed and/or restored vs. extracted) on the timing of emergence of its successor. Data were obtained from a longitudinal epidemiological study in a sample of 4468 Flemish children. Survival analyses with log-logistic distribution were performed to calculate median emergence ages and 95% confidence intervals (CI); caries experience was added as a covariate. The results indicate that the emergence of the maxillary and mandibular premolars was accelerated by 2-8 months when its predecessor had been decayed and or restored but had not been extracted. Premature loss of maxillary primary molars resulted in a significant acceleration of the emergence of the premolars; this was not observed in the mandible. In conclusion, when considering permanent tooth emergence ages, caries experience in the primary dentition should be taken into account.

Child↗
PubMed1999

OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis.

The tumour-necrosis-factor-family molecule osteoprotegerin ligand (OPGL; also known as TRANCE, RANKL and ODF) has been identified as a potential osteoclast differentiation factor and regulator of interactions between T cells and dendritic cells in vitro. Mice with a disrupted opgl gene show severe osteopetrosis and a defect in tooth eruption, and completely lack osteoclasts as a result of an inability of osteoblasts to support osteoclastogenesis. Although dendritic cells appear normal, opgl-deficient mice exhibit defects in early differentiation of T and B lymphocytes. Surprisingly, opgl-deficient mice lack all lymph nodes but have normal splenic structure and Peyer's patches. Thus OPGL is a new regulator of lymph-node organogenesis and lymphocyte development and is an essential osteoclast differentiation factor in vivo.

Animals↗