CSF-1, RANKL and OPG regulate osteoclastogenesis during murine tooth eruption

During tooth eruption, osteoclast-mediated bone resorption predominates in alveolar bone along the occlusal surface rather than in bone basal to the tooth. CSF-1, RANKL and OPG, regulatory molecules essential for osteoclastogenesis, are expressed during eruption. However, it is unclear if these cytokines exhibit an expression pattern that correlates with sites of osteoclastogenesis in vivo. To address this issue, mouse mandibles, isolated from 1 to 14 days postnatal, were analysed for osteoclast activity using tartrate-resistant acid phosphatase (TRAP) staining as well as colony-stimulating factor-1 (CSF-1), receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG) mRNA expression using in situ hybridisation. Results showed that CSF-1, RANKL and OPG are expressed in a distinct temporal and spatial manner. In the occlusal region, osteoclast activity was maximal at day 5 and correlated with a relative high expression of CSF-1 and RANKL compared to OPG. In basal bone at this time point, osteoclast activity decreased despite persistent CSF-1 expression and was associated with increased expression of OPG compared to RANKL. By day 8, osteoclastogenesis declined and correlated with upregulation of OPG at the occlusal and basal regions, with this effect continuing throughout eruption. These findings suggest that the spatiotemporal pattern and relative abundance of CSF-1, RANKL and OPG during eruption are key determinants of site-specific osteoclast activity in bone surrounding the tooth. Targeting these cytokines to specific regions in alveolar bone may provide a mechanism for regulating osteoclastogenesis in dental disorders associated with altered tooth eruption.     

Possible link between glycolysis and apoptosis induced by sodium fluoride

Fluoride has been used to prevent caries in the dentition, but the possible underlying mechanisms of cytotoxicity induction by this compound are still unclear. Since fluoride is known as an inhibitor of glycolytic enzymes, we investigated the possible connection between NaF-induced apoptosis and glycolysis in human promyelocytic leukemia HL-60 cells. NaF-induced apoptotic cell death is characterized by caspase activation, internucleosomal DNA fragmentation, loss of mitochondrial membrane potential, and production of apoptotic bodies. Higher activation of caspases-3 and -9, as compared with that of caspase-8, suggested the involvement of an extrinsic pathway. Utilization of glucose was nearly halted by NaF, whereas that of glutamine was rather enhanced. NaF enhanced the expression of Bad protein, but not that of Bcl-2 and Bax proteins, and reduced HIF-1alpha mRNA expression. Analysis of these data suggests a possible link between glycolysis and apoptosis.     

Cementum and dentin in hypophosphatasia

Hypophosphatasia (HPP) often leads to premature loss of deciduous teeth, due to disturbed cementum formation. We addressed the question to what extent cementum and dentin are similarly affected. To this end, we compared teeth from children with HPP with those from matched controls and analyzed them microscopically and chemically. It was observed that both acellular and cellular cementum formation was affected. For dentin, however, no differences in mineral content were recorded. To explain the dissimilar effects on cementum and dentin in HPP, we assessed pyrophosphate (an inhibitor of mineralization) and the expression/activity of enzymes related to pyrophosphate metabolism in both the periodontal ligament and the pulp of normal teeth. Expression of nucleotide pyrophosphatase phosphodiesterase 1 (NPP1) in pulp proved to be significantly lower than in the periodontal ligament. Also, the activity of NPP1 was less in pulp, as was the concentration of pyrophosphate. Our findings suggest that mineralization of dentin is less likely to be under the influence of the inhibitory action of pyrophosphate than mineralization of cementum.     

Changes in pituitary and prolactin cells of Wistar rats after two dental fillings with bisphenolic resins

Bisphenol-A (BPA) is used to manufacture dental materials such as sealants, fillings and cements. There is evidence of its estrogenic effects on recipients after the placement of dental sealants. Pituitary and especially prolactin (PRL) cells are targets for estrogens.

Objectives

The aim of this research was to determine if BPA eluted from dental resins can alter the proliferation of pituitary cells and PRL cells in the short, medium and long term in a case-control assay.

Methods

Two dental fillings were inserted in the lower incisors of Wistar rats divided into groups sacrificed after one, three, five and seven months. Immunocytochemical treatment was carried out in order to determine proliferating cell nuclear antigen (PCNA) positive cells, PRL-positive cells, PRL- and PCNA-positive cells.

Results

A significant increase of PCNA-positive cells after one (p < 0.05), three (p < 0.01) and five months (p < 0.01) was recorded. PRL-positive cells showed no statistically significant difference between intervened animals and controls. PRL- and PCNA-positive cells manifested a significant increase after five months (p < 0.05). A significant decrease in proliferating cells was observed after seven months (p < 0.05) for PCNA-positive cells and (p < 0.01) for PRL- and PCNA-positive cells.

Conclusion

Low quantities of BPA eluted during mastication can affect immunocytochemical patterns of pituitary cells, increasing cellular proliferation in the short, medium and long term although PRL cell population remained unaffected after dental fillings.     

Masseter muscle thickness three years after surgical correction of class III dentofacial deformity

Objective

To analyse the effect of integrated orthodontic treatment, orthognathic surgery and orofacial myofunctional therapy on masseter muscle thickness in patients with class III dentofacial deformity three years after orthognathic surgery.

Design

A longitudinal study was conducted on 13 patients with class III dentofacial deformities, denoted here as group P1 (before surgery) and group P3 (same patients 3 years to 3 years and 8 months after surgery). Fifteen individuals with no changes in facial morphology or dental occlusion were assigned to the control group (CG). Masseter muscle ultrasonography was performed in the resting and biting situations in the three groups. Data were analysed statistically by a mixed-effects linear model considering a level of significance of P < 0.05.

Results

Significantly higher values (P < 0.01) of masseter muscle thickness (cm) were detected in group P3 (right rest: 0.82 ± 0.16, left rest: 0.87 ± 0.21, right bite: 1 ± 0.22, left bite: 1.04 ± 0.28) compared to group P1 (right rest: 0.63 ± 0.19, left rest: 0.64 ± 0.15, right bite: 0.87 ± 0.16, left bite: 0.88 ± 0.14). Between P3 and CG (right rest: 1.02 ± 0.19, left rest: 1 ± 0.19, right bite: 1.18 ± 0.22, left bite: 1.16 ± 0.22) there was a significant difference on the right side of the muscle (P < 0.05) in both situations and on the left side at rest.

Conclusion

The proposed treatment resulted in improved masseter muscle thickness in patients with class III dentofacial deformity.     

Biomechanics of the mandible and growth extension

Background and objective

One way of determining the direction of growth of the mandible is to consider the temporomandibular joint and movement of the mandible as a four-joint gear system, regarding growth then as an extension of the gear system. Our aim was to examine any correlations between the type of biomechanical growth extension and change in the maxilomandibular relation after Class?II therapy.

Subjects and methods

A total of 130?lateral cephalograms??before and after orthodontic treatment??were available from 65?adolescent class?II patients with open bite or deep bite. The two lateral cephalograms from each patient were superimposed on the occlusal plane. Cephalometric values and the vertical base point deviation were determined from biomechanical analyses, together with three distances and three angles.

Results

No correlation between the cephalometric data and distances or angles were observed. Although there were no significant differences in the distances, we did note significant differences in all three angles (p?Conclusion If gear system extension during growth is considered, this can be interpreted as meaning that the occlusal plane of those patients with an initially open bite dropped during treatment, but that it rose in patients with an initially deep bite.     

Occlusal alterations in unilateral coronal craniosynostosis

There are few studies on maxillomandibular skeletal alterations. Twenty-one patients with unilateral coronal craniosynostosis were analysed and compared with controls. Landmarks analysed were: sella-nasion-point A and B angles, point A-nasion-point B angle, interincisal angle, angle of superior incisor axis on the sella-nasion plane, lower incisor to mandibular plane angle, Frankfort mandibular plane angle, zygomatic-frontal suture (Z), point on the most concave part of pyramidal apophysis of the upper maxilla (Mx), antegonial incisure (AG), upper (UMT) and lower (LMT) molar teeth. Differences were significant for class II dentoskeletal occlusion (p < 0.0001), mandibular hyperdivergence (p < 0.0001), lingualization of superior incisor (p < 0.005), deviation of inferior interincisal contralateral line to the synostosis (p < 0.0001) in the plagiocephalic population. Compared with contralateral counterpoints, Z (p < 0.05), Mx (p < 0.005) and UMT (p < 0.0005) on the affected side were closer to the midline; AG (p < 0.0005) and LMT (p < 0.05) were further from it. On the frontal plane, Z, Mx, UMT, LMT and AG on the affected side were higher. Vertical and transversal contraction of the jaw of the synostotic side and laterodeviation of the mandibular interincisal line of the contralateral synostotic were clear. The altered position of the glenoid cavity, anteriorized in unilateral coronal craniosynostosis, could be the cause of mandibular dentoskeletal asymmetry.     

Global oral health inequalities in incidence and outcomes for oral cancer: causes and solutions

The mouth and oropharynx are among the ten most common sites affected by cancer worldwide, but global incidence varies widely. Five-year survival rates exceed 50% in only the best treatment centers. Causes are predominantly lifestyle-related: Tobacco, areca nut, alcohol, poor diet, viral infections, and pollution are all important etiological factors. Oral cancer is a disease of the poor and dispossessed, and reducing social inequalities requires national policies co-ordinated with wider health and social initiatives - the common risk factor approach: control of the environment; safe water; adequate food; public and professional education about early signs and symptoms; early diagnosis and intervention; evidence-based treatments appropriate to available resources; and thoughtful rehabilitation and palliative care. Reductions in inequalities, both within and between countries, are more likely to accrue from the application of existing knowledge in a whole-of-society approach. Basic research aimed at determining individual predisposition and acquired genetic determinants of carcinogenesis and tumor progression, thus allowing for targeted therapies, should be pursued opportunistically.     

Acanthomatous ameloblastoma of anterior maxilla

The unusual case of acanthomatous ameloblastoma occurring in maxillary left anterior region in a 13-year-old female child is presented with chief complaint of swelling in the upper left anterior region since one year and spacing between maxillary left central incisor and canine. Microscopic examination of surgically excised specimen revealed solid epithelial cell nests with peripheral palisading ameloblastic cells and the central squamous cell assemblage that was consistent with the findings of acanthomatous ameloblastoma type. Acanthomatous ameloblastoma is the extremely rare variant. The present report discusses issues related to the incidence of such formations in the target tissues.