The effects of extracting upper second permanent molars.
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Humans↗
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Impacted tooth position: unexpected improvements.
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Adolescent↗
Clinical absence of the first and second permanent molars.
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Adolescent↗
Some further observations on submerging deciduous molars.
34 females and 20 males, all with one or more submerging deciduous molars, were compared with 30 female and 30 male controls. When groups were matched for sex, age and occlusion no conclusive evidence could be found to support the hypothesis that subjects with submerging deciduous molars have different facial proportions. There was a higher prevalence of developmentally absent pre-molar teeth in the submerging group (p less than 0.001). When males and females were compared, no significant differences were found in the number of submerging deciduous molars per patient, the location of those teeth or the number of quadrants involved.
Adolescent↗
Mesial migration and lower third molar tilt.
The angulation of lower third molars is compared in two groups of radiographs of children aged 10.1--13.0 years, one group showing lower second deciduous molars present, the other showing mesial migration of lower first permanent molars and impaction of second premolars following early extraction of lower second deciduous molars. The lower third molar crypts are significantly less tilted in the group where deciduous molars had been removed, the difference between the means of the two groups being 12.5 degrees (p less than 0.001). The findings are discussed in relation to the hypothesis that early mesial migration improves the orientation of third molar crypts by enabling them to develop further forward. There is some evidence that the mean angle of tilt may be reduced by about 20 degrees when mesial migration occurs before third molar crypts begin to form.
Adolescent↗
Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1-deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1.
The primary macrophage growth factor, colony-stimulating factor 1 (CSF-1), is expressed as a secreted glycoprotein or proteoglycan found in the circulation or as a biologically active cell surface glycoprotein (csCSF-1). To investigate the in vivo roles of csCSF-1, we created mice that exclusively express csCSF-1, in a normal tissue-specific and developmental manner, by transgenic expression of csCSF-1 in the CSF-1-deficient osteopetrotic (Csf1(op)/Csf1(op)) background. The gross defects of Csf1(op)/Csf1(op) mice, including growth retardation, failure of tooth eruption, and abnormal male and female reproductive functions were corrected. Macrophage densities in perinatal liver, bladder, sublinguinal salivary gland, kidney cortex, dermis, and synovial membrane were completely restored, whereas only partial or no restoration was achieved in adult liver, adrenal gland, kidney medulla, spleen, peritoneal cavity, and intestine. Residual osteopetrosis, significantly delayed trabecular bone resorption in the subepiphyseal region of the long bone, and incomplete correction of the hematologic abnormalities in the peripheral blood, bone marrow, and spleens of CSF-1-deficient mice were also found in mice exclusively expressing csCSF-1. These data suggest that although csCSF-1 alone is able to normalize several aspects of development in Csf1(op)/Csf1(op) mice, it cannot fully restore in vivo CSF-1 function, which requires the presence of the secreted glycoprotein and/or proteoglycan forms.
Animals↗
Origins of growth factors: NGF and EGF.
This presentation describes the events that led to the sequential discoveries of nerve growth factor (NGF) and epidermal growth factor (EGF). Each was isolated during attempts to understand the biochemical basis for unexpected biological observations. The in vivo stimulation of the growth of specific nerve fibers following the transplantation of a mouse sarcoma into a chick embryo eventually resulted in the finding of NGF, not only in the transplanted tumor but also in snake venom and in the mouse salivary gland. Unexpectedly, treatment of newborn animals with extracts of the mouse salivary gland resulted not only in enhancement of nerve growth but also in precocious eyelid opening and tooth eruption. The latter observations led to the isolation of both EGF and its tyrosine kinase-active receptor.
Animals↗
Treatment of the neonatal rat with epidermal growth factor: differences in time and organ response.
The ability of exogenous mouse epidermal growth factor (EGF) (500 ng/g body weight/day) to retard somatic growth and to alter the timing of integumental maturation was investigated in the newborn rat. The immediate postnatal period (days 0-3) was identified as the critical time for elicitation of EGF effects. Somatic growth retardation produced by EGF persisted through weaning (day 20) and was asymmetric with maximal organ growth retardation present in liver and kidney and with relative sparing of heart and brain. Treatment of newborn rats with EGF on postnatal days 0-3 advanced the mean time of eyelid opening by 146 versus 31 h for tooth eruption. In contrast, EGF delayed opening of the external ear canal by approximately 48 h. EGF-treated pups thus exhibited a rearrangement in the normal sequence of craniofacial development. In summary, these data provide new information on the critical time of EGF response in the rat, the existence of an asymmetric pattern of organ growth retardation following perinatal EGF exposure, and the ability of EGF to retard morphogenesis of the external ear.
Animals↗
Decreased level of epidermal growth factor in milk from diabetic rats.
Experimental diabetes was induced in rats with streptozocin before mating, and the influence of diabetes on epidermal growth factor (EGF) in milk and on other milk components was studied. Throughout the lactation period, a significant decrease was found both in the production of milk and in the concentration of EGF in milk from untreated diabetic rats compared with an insulin-treated diabetic group and a control group. Thus, the total output of EGF in milk from diabetic rats was considerably decreased. The concentrations of total protein and haptocorrin, a cobalamin (vitamin B12)-binding protein, and the content of fat, however, were unaltered by diabetes. Therefore, the decrease in milk EGF seemed to be selective compared with total protein in milk. The pups of diabetic dams had reduced body weights within 1 wk of lactation and reduced body lengths on d 16 of lactation compared with control pups. Furthermore, the time of eyelid opening was delayed, but no difference in the time of tooth eruption was observed. Insulin-treatment of diabetic rats restored the milk volume and the EGF concentration to values comparable to those of the controls. Pups of the insulin-treated diabetic dams were comparable to the pups of the controls. These results indicate that insulin deficiency in lactating rats causes a decrease in the lactational performance and in the EGF content of milk.
Animals↗
Granulocyte-macrophage colony-stimulating factor corrects macrophage deficiencies, but not osteopetrosis, in the colony-stimulating factor-1-deficient op/op mouse.
The op mutation in the mouse is in the coding region of the colony-stimulating factor-1 (CSF-1) gene, prevents formation of biologically active factor, and, thus, results in generalized macrophage deficiency and, in osteopetrosis, secondary to deficiency of osteoclasts. Although a few macrophages and osteoclasts are present in these mutants, it was not clear whether the inability of endogenous granulocyte-macrophage CSF (GM-CSF) to compensate for the absence of CSF-1 was due to the limitations of biological activity of this molecule or to its inability to reach respective target populations. In this study, we examined whether sc GM-CSF in large doses (20-40 micrograms/mouse.day) for 3 weeks would correct some or all of the deficiencies observed in mutant mice. All organ macrophage populations tested (liver, spleen, thymus, marrow, pleural, and peritoneal cavity) were significantly increased, reaching levels exceeding those observed in normal mice. Restoration of peritoneal and pleural macrophage populations by sc GM-CSF is of particular interest, because it was not previously observed in op/op mice treated with sc CSF-1. In contrast, there was no indication of increased bone resorption, no appearance of osteoclasts, and no tooth eruption in response to GM-CSF treatment. These data suggest that GM-CSF is able to compensate for the absence of CSF-1 during macrophage formation, but is unable to play a similar role in osteoclast differentiation.
Animals↗
Rescue of the osteopetrotic defect in op/op mice by osteoblast-specific targeting of soluble colony-stimulating factor-1.
Soluble colony-stimulating factor-1 (sCSF-1) and membrane bound CSF-1 are synthesized by osteoblasts and stromal cells. However, the precise role of each form in osteoclastogenesis is unclear. In the op/op mouse, absence of osteoblast-derived CSF-1 leads to decreased osteoclasts and osteopetrosis. To determine whether sCSF-1 gene replacement can cure the osteopetrotic defect, we took advantage of the osteoblast specificity of the osteocalcin promoter to selectively express sCSF-1 in the bone of op/op mice. Transgenic mice harboring the human sCSF-1 cDNA under the control of the osteocalcin promoter were generated and cross-bred with heterozygous op/wt mice to establish op/op mutants expressing the transgene (op/opT). The op/op genotype and transgene expression were confirmed by PCR and Southern blot analysis, respectively. High levels of human sCSF-1 protein were selectively expressed in bone. At 2(1/2) wk, op/opT mice showed normal growth and tooth eruption. Femurs removed at 5 and 14 wk were analyzed by peripheral quantitative computed tomography and histomorphometry. The abnormal bone mineral density, cancellous bone volume, and growth plate width observed in op/op mice was completely reversed in op/opT mice by 5 wk, and this effect persisted at 14 wk, with measurements comparable with wt/wt mice at each time point. Correction of the skeletal abnormalities in the 5-wk-old op/opT mice correlated with a marked increase in the total osteoclast number, and their number per millimeter of bone surface compared with that of op/op mutants. Osteoclast number was maintained at 14 wk in op/opT mice and morphologically resembled wt/wt osteoclasts. These results indicate that sCSF-1 is sufficient to drive normal osteoclast development and that the osteocalcin promoter provides an efficient tool for delivery of exogenous genes to the bone. Moreover, targeting sCSF-1 to osteoblasts in the bone microenvironment may be a potentially useful therapeutic modality for treating bone disorders.
Acid Phosphatase↗
Mice lacking tartrate-resistant acid phosphatase (Acp 5) have disrupted endochondral ossification and mild osteopetrosis.
Mature osteoclasts specifically express the purple, band 5 isozyme (Acp 5) of tartrate-resistant acid phosphatase, a binuclear metalloenzyme that can generate reactive oxygen species. The function of Acp 5 was investigated by targeted disruption of the gene in mice. Animals homozygous for the null Acp 5 allele had progressive foreshortening and deformity of the long bones and axial skeleton but apparently normal tooth eruption and skull plate development, indicating a rôle for Acp 5 in endochondral ossification. Histomorphometry and mineralization density analysis of backscattered electron imaging revealed widened and disorganized epiphyseal growth plates with delayed mineralization of cartilage in 6- to 8-week-old mutant mice. The membrane bones of the skull showed increased density at all ages examined, indicating defective osteoclastic bone turnover. Increased mineralization density was observed in the long bones of older animals which showed modelling deformities at their extremities: heterozygotes and homozygous Acp 5 mutant mice had tissue that was more mineralized and occupied a greater proportion of the bone in all regions. Thus the findings reflect a mild osteopetrosis due to an intrinsic defect of osteoclastic modelling activity that was confirmed in the resorption pit assay in vitro. We conclude that this bifunctional metalloprotein of the osteoclast is required for normal mineralization of cartilage in developing bones; it also maintains integrity and turnover of the adult skeleton by a critical contribution to bone matrix resorption.
Acid Phosphatase↗
Determination of age in monkeys (Macaca irus) on the basis of dental development.
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Age Determination by Teeth↗
The influence of alveolar bone grafting on the orthodontic and prosthodontic treatment of patients with cleft lip and palate.
The introduction of mixed dentition bone grafting of alveolar clefts means that the alveolar process can be fully restored, permitting adjacent teeth to migrate or be orthodontically moved into the grafted bone. Thus a complete dental arch can be obtained without prosthodontics in the great majority of patients. In addition, oral-nasal fistulae are closed, mucosal recesses eliminated (facilitating oral hygiene) and the long-term periodontal health of the teeth adjacent to the former cleft is improved. Alveolar bone grafting with subsequent orthodontic treatment, together with advances in dental materials, have contributed substantially to the care of patients with alveolar clefts, reducing the need for prosthodontic procedures and allowing completion of the dental treatment at an earlier age.
Alveolar Ridge Augmentation↗
Dens evaginatus on the labial surface of a central incisor: a case report.
A 7-year-old girl in the mixed dentition phase presented with abnormal morphology of the upper right central incisor. The diagnosis was a dens evaginatus, an anomaly of odontogenesis of unknown aetiology. This article describes the management of this anomaly and discusses the importance of maintaining space in the developing dentition. The aetiology and natural history of dens evaginatus are also considered.
Child↗
The aetiology of gingival recession.
Gingival recession affects a large proportion of the adult population. This paper discusses the aetiology and mechanisms behind the formation of gingival recession, and considers the relevance of gingival recession to both orthodontics and restorative dentistry. It is followed by a second paper on the management of gingival recession.
Adult↗
Overeruption--another challenge?
UNLABELLED: Awareness of the occlusal changes following individual tooth loss may be increasingly important when planning treatment for patients who are likely to retain a relatively intact dentition throughout life. Some evidence exists to support dentists who are considering prevention or treatment of overeruption. This paper explores the literature available on the changes in the prevalence of tooth loss, the prevalence and presentation of overeruption, its relevance to dental restoration and the prevention and treatment of overeruption. CLINICAL RELEVANCE: This article reviews the prevalence and consequence of overeruption in posterior teeth.
Dental Occlusion↗
Nuclear localization of type I parathyroid hormone/parathyroid hormone-related protein receptors in deer antler osteoclasts: evidence for parathyroid hormone-related protein and receptor activator of NF-kappaB-dependent effects on osteoclast formation in regenerating mammalian bone.
Parathyroid hormone-related protein (PTHrP) is not required for osteoclastogenesis during embryonic development; however, after birth it has been shown to regulate osteoclast formation during tooth eruption. Our study explores the hypothesis that PTHrP also may regulate osteoclast differentiation in the regenerating skeletal tissues of deer antlers, bones capable of complete regeneration. Osteoclast-like multinucleated cells (MNCs) formed spontaneously in micromass cultures derived from antler cartilage and these cells had the phenotypic characteristics of osteoclasts. PTHrP and receptor activator of NF-kappaB ligand (RANKL) stimulated antler osteoclast formation although the effect of RANKL was less marked than that of PTHrP. The addition of osteoprotegerin (OPG) only partially decreased (by approximately 65%) the number of osteoclasts in PTHrP-treated cultures. To determine whether PTHrP also potentially could have direct effects on antler osteoclasts, we studied, by confocal microscopy, the expression of the type I PTH/PTHrP receptor (PTH1R) in MNCs cultured on glass and found the receptor protein to have a nuclear localization. In situ hybridization showed that antler MNCs also expressed PTH1R and PTHrP messenger RNAs (mRNAs). PTHrP was immunolocalized in MNCs cultured on glass but was undetectable in cells resorbing a dentine substrate. In tissue sections of antler cartilage, PTHrP and PTH1R were expressed in vitronectin receptor-positive (VNR+) osteoclast-like cells localized in the perivascular stroma. Thus, these data show that PTHrP plays a role in the regulation of osteoclast differentiation in regenerating skeletal tissues and that PTHrP can have effects on osteoclastogenesis that are independent of RANKL synthesis. Ours is the first study to describe the expression of the type I PTH/PTHrP receptor in mammalian osteoclasts at a protein and mRNA level, which indicates that PTHrP also may have a direct effect on osteoclasts. This also is the first study to show a nuclear localization of the PTHIR in cells of the osteoclast lineage, although the functional significance of this observation has yet to be established.
Animals↗