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Background: The cervical non-carious wedged-shaped lesion is controversial in that its aetiology may involve attrition, erosion, abrasion and stress-corrosion (abfraction). This study examined the histopathology of anterior teeth with cervical wedge-shaped lesions by light and electron microscopy to elucidate their pathogenesis. Methods: Ten undecalcified human teeth with cervical lesions were available for investigation. Patency of the dentine tubules was tested using red dye penetration from the pulp chamber. The morphology of normal and sclerotic dentine adjacent to the cervical wedge-shaped lesions was investigated by scanning electron microscopy. The numbers and diameters of dentinal tubules were measured at different levels beneath the surfaces of the lesions. Results: The gross and microscopic features of the worn teeth were described. Red dye penetration tests showed white tracts of sclerotic tubules contrasted with red tracts of patent tubules. Numbers of tubules per square area and diameters of patent and sclerotic tubules varied at different levels within the dentine due to deposits of intratubular dentine. Conclusions: The cervical wedge is shaped by interactions between acid wear, abrasion and dentinal sclerosis. No histopathological evidence of abfraction was found. Clinical diagnosis, conservation and restoration of non-carious cervical lesions need to take into account the extent of sclerotic dentine beneath wedge-shaped lesions. [ABSTRACT FROM AUTHOR]

Objectives: To compare transmitted forces through ethylene vinyl acetate (EVA) mouthguard material and the same EVA material with gas inclusions in the form of a closed cell foam. Method: EVA mouthguard materials with and without foam gas inclusions and 4 mm thick were impacted with a constant force from an impact pendulum. Various porosity levels in the foam materials were produced by 1%, 5%, and 10% by weight foaming agent. The forces transmitted through the EVA after energy absorption by the test materials were measured with a force sensor and compared. Results: Only minor non-significant differences in transmitted forces through the EVA with and without foam were shown. Conclusions: The inclusion of gas in the form of a closed cell foam in 4 mm thick EVA mouthguard materials did not improve the impact performance of the EVA mouthguard material. [ABSTRACT FROM AUTHOR]

Orthodontic tooth movement may be enhanced by the application of a magnetic field. Bone remodelling necessary for orthodontic tooth movement involves clastic cells, which are tartrate-resistant acid phosphatase (TRAP) positive and which may also be regulated by growth hormone (GH) via its receptor (GHR). The aim of this study was to determine the effect of a static magnetic field (SMF) on orthodontic tooth movement in the rat. Thirty-two male Wistar rats, 9 weeks old, were fitted with an orthodontic appliance directing a mesial force of 30 g on the left maxillary first molar. The appliance incorporated a weight (NM) or a magnet (M). The animals were killed at 1, 3, 7, or 14 days post-appliance insertion, and the maxillae processed to paraffin. Sagittal sections of the first molar were stained with haematoxylin and eosin (H&E), for TRAP activity or immunohistochemically for GHR. The percentage body weight loss/gain, magnetic flux density, tooth movement, width of the periodontal ligament (PDL), length of root resporption lacunae, and hyalinized zone were measured. TRAP and GHR-positive cells along the alveolar bone, root surface, and in the PDL space were counted. The incorporation of a SMF (100-170 Gauss) into an orthodontic appliance did not enhance tooth movement, nor greatly alter the histological appearance of the PDL during tooth movement. However significantly root resorption (P=0.016), increased width of the PDL (P=0.017) and greater TRAP activity (P=0.001) were observed for group M at day 7 on the compression side. At day 14 no differences were observed between the appliance groups. [ABSTRACT FROM AUTHOR]

Adverse effects of corticosteroids on bone metabolism raise concerns as to whether steroid treatment may influence orthodontic movement. This study examined the effect of prednisolone on orthodontic movement using an established rat model. The corticosteroid treated group (N = 6) was administered prednisolone (1 mg/kg) daily, for a 12-day induction period; the control group (N = 6) received equivalent volumes of saline. On day 12, an orthodontic appliance was placed which exerted 30 g of mesial force to the maxillary first molar. Animals were sacrificed on day 24 and tooth movement was measured. Sagittal sections of the molars were stained with haematoxylin and eosin, and for tartrate-resistant acid phosphatase (TRAP) activity. While there were no significant differences in the magnitude of tooth movement between the 2 groups, steroid-treated rats displayed significantly less root resorption on the compression side and fewer TRAP-positive cells within the PDL space on the same side. This suggests steroid treatment suppressed clastic activity.

Glucocorticosteroids are widely used in the treatment of chronic illnesses and have been reported to cause premature obliteration of the pulp space. During the active stages of dentinogenesis, odontoblasts are growth hormone receptor (GHr) positive. The aims of this study were to determine if the glucocorticosteroid, prednisone, affected the rate of dentine deposition and odontoblast expression of GHr in the rat molar. Following subcutaneous injection of 0.05 mg/kg, 1.0 mg/kg or 5.0 mg/kg prednisone for 20 days, immature and mature molars from rats aged 3 and 6 weeks respectively, were examined histologically. Distribution of GHr expression was determined immunohistochemically. No morphological differences were observed in molars from prednisone treated animals. Prednisone did not appear to enhance dentine deposition in immature molars but in mature molars significantly increased dentine deposition on the roof of the pulp chamber at a dosage of 5.0 mg/kg (p < 0.001). In all immature molars, odontoblasts and pulp cells expressed GHr immunoreactivity. In mature molars, odontoblasts and pulpal cells from controls did not show GHr immunoreactivity. However, odontoblasts and pulp cells were GHr immunoreactive in mature molars from animals treated with prednisone.

Female Wistar rats, 3 weeks old, were given sodium fluoride in saline solution (isotonic) by intraperitoneal injection at a dose of either 0, 10 or 20 mg per kg body weight. This treatment was given 9 times over 4.5 days. After fixation by perfusion and demineralization in neutral EDTA, hemi-mandibles were sectioned in a cryostat. Sections were stained for dipeptidyl peptidase II activity, using the specific substrate Lys-Ala-MNA and the coupler Fast Blue B for histochemical localization. Staining indicative of dipeptidyl peptidase II was found in the enamel organ of the incisor, particularly in cells of the stratum intermedium and in both secretory and maturation ameloblasts. This staining was markedly reduced in ameloblasts of rats given either 10 or 20 mg sodium fluoride per kg body weight.

Changes in the surrounding alveolar bone occur during tooth eruption. The microphthalmic (mi/mi) mouse suffers from osteopetrosis and lack of bone resorption; tooth form and eruption were examined in both affected mi/mi mice and unaffected litter-mates to determine the effect of osteopetrosis on tooth development and eruption. Paraffin sections of mandibles from 3, 7, 10, 13, 15 and 20-day-old mice were examined by light microscopy after staining with haematoxylin and eosin and for stable acid phosphatase activity. Mandibles from 15- and 20-day-old mice were examined by scanning electron microscopy. The ultrastructure of odontoblasts was observed in 15-day-old mice. Tooth eruption was significantly reduced in the mi/mi mice; the bone of affected mice increased in area with increasing age and marrow spaces narrowed. There was little bony remodeling in the mi/mi mouse, as indicated by layers of reversal lines. This lack of bone resorption affected tooth eruption and root formation. No abnormalities were detected in odontoblasts, suggesting functional normality, but the wide predentine layer in the mi/mi mouse may indicate an alteration in dentine mineralization.