Oral rehabilitation of tooth agenesis frequently starts in paediatric dentistry. A retrospective analysis of 625 patients.

AIM: As oral rehabilitation of tooth agenesis usually begins at a very young age, it is important to plan the therapy in advance in order to prepare the patient for the final treatment after the end of skeletal and dental growth. The diverse patterns of tooth agenesis require interdisciplinary oral rehabilitation adapted to individual factors like patient's age, number of missing teeth, and alveolar-bone development. The aim of the present high volume single-center study was to provide an overview of the management of patients with tooth agenesis, in terms of treatment approaches, associations, and long-term implant survival, over a period of 30 years. METHODS: Descriptive analyses were performed to analyse treatment approaches and and how they reated to severity of agenesis as well as patients' gender and age. Kaplan-Meier survival curves and log-rank-tests were used to investigate implant survival over time. CONCLUSION: Treatment starts usually in childhood or adolescence; orthodontic therapy was the most common treatment. All treatment options showed similar high survival rates. External bone augmentation might be a risk-factor for implant loss.

Caries frequency and distribution in an early medieval Avar population from Austria.

OBJECTIVE: The aim of this study was to determine frequency and distribution of dental caries in an early medieval Avar population from Central Europe, namely Vienna. METHODS: The evaluation of caries was carried out in an anthropological sample consisting of the remains of 136 individuals and included 2215 permanent teeth. Age and sex estimations were based on dental development and on skeletal ageing methods. The presence of dental caries was determined according to clinical aspects using a dental probe. RESULTS: The frequency of ante mortem tooth loss in the sample was 23.8%; the total caries frequency was calculated as 14.9%. The highest caries rate was recorded in the second mandibular molar (34.6%). The most affected tooth surface was found to be the root with 12.7%, followed by the approximal surface with 8.6%, but only 7.7% of the occlusal surfaces were affected by caries. CONCLUSION: This study revealed that Avars suffered from higher caries rates than most other medieval European populations, but experienced a similar dental caries distribution. Attrition of the occlusal surface resulting from a diet containing abrasive particles with accompanying posteruptive tooth movement is considered the major factor causing this premodern caries pattern.

Dental pulp fibroblasts contain target cells for lysophosphatidic Acid.

Lysophosphatidic acid (LPA) is a locally produced bioactive phospholipid which is involved in tissue repair. The objective of this study was to determine whether dental pulp tissue also responds to the phospholipid. Effects of LPA on proliferation, differentiation, and mitogen-activated protein kinase (MAPK) signaling of dental pulp fibroblasts (DPF) were examined in vitro. We report that DPF express LPA receptors LPA1, LPA2, and LPA3 and respond to the ligand with increased mitogenic activity. Involvement of extracellular signal-regulated kinase, p38 MAPK, and c-Jun NH(2)-terminal kinase in LPA signaling could be demonstrated by use of specific inhibitors and detection of the phosphorylation status of the kinases. An increased mitogenic activity paralleled a decreased number of alkaline-phosphatase-positive cells and expression levels of dentin sialophosphoprotein and osteocalcin. Together, these results suggest that dental pulp fibroblasts can respond to LPA, a process that may play a role in pulp tissue repair.

S-nitroso albumin enhances bone formation in a rabbit calvaria model.

Nitric oxide (NO) is a mediator involved in bone regeneration. We therefore examined the effect of the novel NO donor, S-nitroso human serum albumin (S-NO-HSA) on bone formation in a rabbit calvaria augmentation model. Circular grooves (8 mm diameter, two per animal) were created by a trephine drill in the cortical bone of 40 rabbits and titanium caps were placed on the rabbit calvaria bone filled with a collagen sponge soaked with either 100 µL S-NO-HSA (5%, 20%) or human albumin (5%, 20%). After 4 weeks the titanium hemispheres were subjected to histological and histomorphometric analysis. Bone formation and the volume of the residual collagen sponge were evaluated. S-NO-HSA treatment groups had a significantly higher volume of newly formed bone underneath the titanium hemispheres compared to the albumin control groups (5%: 15.5 ± 4.0% versus 10.6 ± 2.9%; P < 0.05; 20%: 14.0 ± 4.6% versus 6.0 ± 3.8%; P < 0.01). The volume of residual collagen sponge was also significantly lower in the S-NO-HSA groups compared to the control groups (5%: 0.4 ± 0.5% versus 2.6 ± 2.4%; P < 0.05 and 20%: 1.5 ± 2.7% versus 13.0 ± 18.7%; P < 0.01). This study demonstrates for the first time that S-NO-HSA promotes bone formation by slow NO release. Additionally, S-NO-HSA increases collagen sponge degradation.

Proliferation of dental pulp fibroblasts in response to thrombin involves mitogen-activated protein kinase signalling.

AIM: To examine the involvement of mitogen-activated protein kinases (MAPK) signalling on thrombin-stimulated human dental pulp fibroblasts (DPF). METHODOLOGY: Dental pulp fibroblasts were isolated from dental pulp connective tissue of third molars and expanded in vitro. Expression of thrombin receptors was analysed by RT-PCR, and cell proliferation was measured by 3[H]-thymidine incorporation assay. Phosphorylation levels of MAPK were determined by Western blot analysis, and alkaline phosphatase activity was measured to serve as a marker for odontogenic differentiation. Statistical analysis was performed by Student's t-test. RESULTS: Dental pulp fibroblasts express the thrombin receptors protease-activated receptor-1 (PAR-1), PAR-3 and PAR-4. Measurement of 3[H]-thymidine incorporation revealed a dose-dependent increase of DNA synthesis in response to thrombin treatment. The thrombin-induced mitogenic activity was decreased by the extracellular signal-regulated protein kinase (ERK) signalling inhibitor PD98059 (P < 0.05), and by SB203580 (P < 0.05), a p38 MAPK inhibitor. Western blot analysis demonstrated increased phosphorylation of ERK in DPF following stimulation with thrombin, while p38 MAPK and c-Jun NH2-terminal kinase (JNK) were not activated. Alkaline phosphatase activity of DPF remained unchanged upon incubation with thrombin. CONCLUSIONS: These results suggest that signalling via MAPK mediates the mitogenic activity of thrombin on DPF and may thus play a role during the early stages of pulp repair.