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At least 163 records · Page 9Linked to original sources
PubMed1999

Malformation in the primary and permanent dentitions following trauma prior to tooth eruption: a case report.

Dento-facial injuries that occur prior to the eruption of teeth in the primary dentition are rare, but can result in damage to the primary dentition. We report a rare case where an injury to the anterior maxilla and mandible of an infant prior to primary tooth eruption resulted in hypoplasia, displacement and impaction of the primary dentition and damage to a developing permanent tooth.

Child, Preschool↗
PubMed1980

Tooth eruption: evidence for the central role of the dental follicle.

The roles of the gubernaculum dentis, root formation, tooth crown and dental follicle in prefunctional eruption of a mandibular premolar have been studied in nine beagle dogs by radiographic and histologic evaluations of the effects of surgical ablation or removal of these structures on tooth eruption. The dental follicle was the only one of these structures required for the coordinated enlargement of the eruption pathway and formation of bone in the base of the bony crypt, the radiographic and histologic hallmarks of tooth eruption. These data, together with the topographic relationships of the dental follicle to areas of localized bone resorption and formation, are interpreted to mean that the dental follicle may influence, if not coordinate, these processes in tooth eruption.

Alveolar Process↗
PubMed1998

Parathyroid hormone-related protein is required for tooth eruption.

Parathyroid hormone (PTH)-related protein (PTHrP)-knockout mice die at birth with a chondrodystrophic phenotype characterized by premature chondrocyte differentiation and accelerated bone formation, whereas overexpression of PTHrP in the chondrocytes of transgenic mice produces a delay in chondrocyte maturation and endochondral ossification. Replacement of PTHrP expression in the chondrocytes of PTHrP-knockout mice using a procollagen II-driven transgene results in the correction of the lethal skeletal abnormalities and generates animals that are effectively PTHrP-null in all sites other than cartilage. These rescued PTHrP-knockout mice survive to at least 6 months of age but are small in stature and display a number of developmental defects, including cranial chondrodystrophy and a failure of tooth eruption. Teeth appear to develop normally but become trapped by the surrounding bone and undergo progressive impaction. Localization of PTHrP mRNA during normal tooth development by in situ hybridization reveals increasing levels of expression in the enamel epithelium before the formation of the eruption pathway. The type I PTH/PTHrP receptor is expressed in both the adjacent dental mesenchyme and in the alveolar bone. The replacement of PTHrP expression in the enamel epithelium with a keratin 14-driven transgene corrects the defect in bone resorption and restores the normal program of tooth eruption. PTHrP therefore represents an essential signal in the formation of the eruption pathway.

Animals↗
PubMed2003

Growth hormone receptor and insulin-like growth factor-I immunoreactivity in osteoclast-like cells during tooth eruption in the toothless (osteopetrotic) rat following treatment with colony-stimulating factor-1.

In the toothless (tl/tl) osteopetrotic rat, teeth form but fail to erupt. Treatment of tl/tl rats with colony-stimulating factor-1 (CSF-1) activates bone resorption by osteoclasts, permits tooth eruption, and up-regulates the immunoreactivity of bone marrow mononuclear cells to growth hormone receptor (GHr) and insulin-like growth factor (IGF)-I. This study examined the distribution of tartrate-resistant acid phosphatase (TRAP) and immunoreactivity for GHr and IGF-I in osteoclast-like cells located on the alveolar bone margin, adjacent to the lower first molar crown, in 14-day-old normal and tl/tl rats, following treatment with CSF-1. Osteoclast-like cells demonstrated a positive reaction for TRAP, GHr, and IGF-I in all groups. However, in tl/tl tissue, osteoclast-like cells were generally negative for GHr. There was no significant difference in the total number of TRAP-, GHr-, and IGF-I-positive osteoclast-like cells on the adjacent bone margin in normal, normal treated with CSF-1, and tl/tl rats. CSF-1 treatment of the tl/tl rat significantly increased the total number of osteoclast-like cells, which were positive for TRAP (p < 0.001), GHr (p < 0.05) and IGF-I (p < 0.01).

Acid Phosphatase↗
PubMed1984

[Oral epithelium during tooth eruption in the rat: a scanning electron microscopic study].

The evolution of the ultrastructural aspect of the oral epithelium during the pre- and posteruptive periods of rat molars was investigated using a scanning electron microscope. The eruption is preceded by a rupture of the superficial layers of the oral epithelium with a desquamation following concentrical circles. As the tooth erupts, the epithelial attachment is generated from ameloblasts.

Aging↗
PubMed1992

Granule proteins of the dental follicle and stellate reticulum inhibit tooth eruption and eyelid opening in postnatal rats.

Electron-dense granules within cells of the dental follicle and stellate reticulum of rat mandibular molars can be isolated; their major components are 167 and 200 kDa proteins. Injecting these granule proteins into postnatal rats results in a delay of incisor eruption and eyelid separation. These inhibitory effects were most pronounced with the 167 kDa protein (a delay of 3 days in incisor eruption and of 2 days in eyelid opening) and were opposite to the stimulatory effects of epidermal growth factor. Thus, these granules may play an inhibitory part in tooth eruption.

Animals↗
PubMed1997

Restoration of disturbed tooth eruption in osteopetrotic (op/op) mice by injection of macrophage colony-stimulating factor.

Osteopetrotic (op/op) mice show severe osteosclerosis caused by an inherited deficiency of osteoclast and resultant failure of tooth eruption, which can be cured by the injection of macrophage colony-stimulating factor (M-CSF). The present study revealed that consecutive injections of M-CSF in these mutant mice brought about a recovery of bone resorption resulting in the resumption of growth of tooth root and periodontal ligament. Bone resorption at the inner surface of bony crypts was noted on the 5th day after the start of M-CSF injections. This activity was reduced with the progress of root and periodontal ligament formation, being confined to the basal and crestal portion of bony crypts by the 15th day of the experiment. Second molars emerged into the oral cavity on the 15th day, but no eruption of first molars was observed until the 20th day. Throughout the experiment, first molars exhibited appreciable root deformity, which was less severe in second molars. Delayed eruption of first molars was thought to be related to the severity of the disturbance of root formation.

Age Factors↗