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.

The "puffed cheek method" to evaluate mucosal thickness: case series.

OBJECTIVES: Mucosal thickness should be considered in implant treatment planning. Needle probing to measure mucosal thickness is invasive and therefore not used in routine diagnosis. The "puffed cheek" method is an established technique to visualize the vestibule in computed tomography (CT). As CT assesses bone availability, a simultaneous mucosal thickness measurement would be useful. The aim of this study was to evaluate the reliability of mucosal thickness measurement in CT with distended cheeks. MATERIALS AND METHODS: Buccal maxillary mucosa thickness was evaluated at four measurement sites in the incisor and molar area of 11 patients. Each site was evaluated via CT with cheek distension and needle probing. Measurement area was identified with the aid of a thermoplastic splint to localize the exact position by a gutta-percha marker point. The comparison between the two methods was performed by Bland-Altman diagram. RESULTS: The mean clinical thickness was 1.17 mm (±0.31) compared to 1.11 mm (±0.31) in CT evaluation. The mean difference between the two methods was 0.07 mm (±0.40; CI-0.14;0.12, P = 0.88, Krippendorff α = 0.38). According to Bland-Altman diagram the mucosal thickness may diverge by up to 0.9 mm from the radiologic thickness. CONCLUSIONS: The two measurement methods may not be interchangeably used. As additional information to three-dimensional bone analyses, CT may be performed as a pre-operative soft tissue analysis at most implant sites with distended cheeks. Nevertheless, this method yields less valid and reliable results than the gold standard.

Esthetic evaluation of single-tooth implants in the anterior maxilla following autologous bone augmentation.

OBJECTIVES: Autologous bone augmentation to rebuild compromised alveolar ridge contour prior to implant placement allows for favorable three-dimensional implant positioning to achieve optimum implant esthetics. The aim of the present study was to evaluate peri-implant soft tissue conditions around single-tooth implants following bone grafts in the esthetic zone of the maxilla. MATERIALS AND METHODS: Sixty patients underwent autologous bone augmentation of deficient maxillary sites prior to placement of 85 implants in the esthetic zone. In case of multiple implants per patient, one implant was randomly selected. Objective evaluation of 60 single-tooth implants was performed using the Pink-Esthetic-Score (PES) and Papilla Index (PI) and supplemented by subjective patient evaluation, as well as clinical and radiologic examination. RESULTS: Objective ratings of implant esthetics were satisfactory (median PES: 11, median PI: 2) and significantly correlated with high patient satisfaction (mean VAS score: 80%). Both esthetic indices demonstrated respectable levels of inter- as well as intra-observer agreement. Poor implant esthetics (low PES and PI ratings) were significantly associated with increased anatomic crown height, while no influence of horizontal implant-tooth distance could be found. CONCLUSIONS: The present investigation indicates that favorable esthetic results may be achieved in the augmented anterior maxilla. However, bony reconstruction of compromised alveolar ridges does not guarantee optimum implant esthetics.

Prolyl hydroxylase inhibitors increase the production of vascular endothelial growth factor by periodontal fibroblasts.

BACKGROUND AND OBJECTIVE: Pharmacological inhibitors of prolyl hydroxylases (PHDs) can induce a proangiogenic response that favors wound healing and bone regeneration. However, the response of periodontal cells to PHD inhibitors is unknown. MATERIAL AND METHODS: To determine the effects of PHD inhibitors on periodontal cells, we exposed human fibroblasts from the gingiva and the periodontal ligament to dimethyloxallyl glycine, desferrioxamine, l-mimosine and CoCl(2). Viability, proliferation, and protein synthesis were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), [(3)H]thymidine, and [(3)H]leucine incorporation, respectively. The levels of Ki67, hypoxia-inducible factor 1α (HIF-1α), p27, phosphorylated c-Jun N-terminal kinase (JNK) and phosphorylated p38 were determined by immunohistochemistry and western blotting. Vascular endothelial growth factor (VEGF) mRNA levels were measured by quantitative PCR. Protein levels of VEGF and interleukin (IL)-6 were evaluated by immunoassays. RESULTS: We found that PHD inhibitors, while leaving cell viability unchanged, reduced proliferation and protein synthesis. This was paralleled by decreased Ki67 levels and increased p27 levels, suggesting that PHD inhibitors provoke growth arrest. Independently from this response, PHD inhibitors stabilized HIF-1α and increased the production of VEGF. This increase of VEGF was observed in the presence of proinflammatory IL-1 and pharmacological inhibitors of JNK and p38 signaling. Moreover, PHD inhibitors did not modulate expression of IL-6 and the phosphorylation of JNK and p38. CONCLUSION: These results suggest that PHD inhibitors enhance the production of VEGF in periodontal fibroblasts, even in the presence of proinflammatory IL-1. The data further suggest that PHD inhibitors do not provoke a significant proinflammatory or anti-inflammatory response in this in vitro setting.

Short-term teriparatide delivery and osseointegration: a clinical feasibility study.

Teriparatide is an anabolic osteoporosis therapeutic agent that can improve healing after fractures and periodontal surgeries. Clinical studies investigating the effects of teriparatide on the osseointegration of titanium implants have not been performed. We conducted an open-label randomized controlled feasibility study and included 24 individuals with edentulous lower jaws. The participants received 2 study implants in the mandible during interforaminal dental implant surgery. They were randomly assigned to receive either 20 µg of teriparatide once daily for 28 days or no treatment. Study implants were retrieved from 23 participants after 9 weeks and were subjected to histomorphometric analyses. Endpoints were new bone-volume-per-tissue-volume (NBV/TV) and new bone-to-implant-contact (NBIC). We report here that median values of NBV/TV in the control and the teriparatide groups were 15.4% vs. 17.6% in the periosteal compartment, 11.3% vs. 16.5% in the cortical compartment, and 7.3% vs. 12.0% in the medullary compartment, respectively. NBIC median values in the control and the teriparatide groups were 3.3% vs. 4.1% in the periosteal compartment, 5.0% vs. 4.4% in the cortical compartment, and 0.3% vs. 1.4% in the medullary compartment, respectively. The results provide the first histological data on the osseointegration of titanium study implants in individuals treated with teriparatide. ClinicalTrials.gov number, NCT00089674.

The response of dental pulp-derived cells to zoledronate depends on the experimental model.

AIM: To investigate whether zoledronate (ZOL) can cause a cytotoxic response in dental pulp-derived cells (DPCs) in vitro. METHODOLOGY: Cell activity was assessed utilizing MTT tests, (3) [H]thymidine, and (3) [H]leucine incorporation assays in human DPCs in response to ZOL. Cell activity assays were also preformed on calcium phosphate-coated plates. Cell death was analysed with annexin V/propidium iodide, trypan blue staining and Western blot analysis. RESULTS: Micromolar concentrations of ZOL were required to decrease the activity of DPCs. The decreased activity of DPCs was associated with the occurrence of apoptosis and necrosis. No adverse effects were observed when DPCs were cultured on calcium phosphate-coated plates with ZOL. CONCLUSION: High concentrations of soluble ZOL were required to cause adverse effects in vitro. These adverse effects are abolished when the bisphosphonate was bound to a mineralized surface. However, the clinical relevance of these results remains to be determined.

Atrophy of the residual alveolar ridge following tooth loss in an historical population.

OBJECTIVES: To study the natural aetiopathology of jaw atrophy after tooth loss, unaltered by prosthetic procedures, an historical population without modern dental treatment was examined. METHODS: Based on the hypothesis that there are predictable changes in shape during jaw-atrophy, frequency and degree of atrophy as well as clinical aspects of bone quality and resorption were determined in the skeletal remains of 263 individuals. The potential association between age and frequency/severity of atrophy was analysed. RESULTS: Atrophy in at least one jaw segment was present in 45.2% of the analysed jaw specimens. The residual ridge underwent a series of changes in shape and height following the pattern of resorption described for modern populations. The severity of these alterations was associated with the age of the individual and the region within the jaw. Atrophy was frequently related to structural degradation of the covering cortical layer. CONCLUSIONS: These findings prove that atrophy of the jaw evidently does occur, displaying similar patterns of resorption in a population without modern prosthetics, where the negative effect of ill-fitting dentures is excluded. The basic information about alterations of shape and the cortical layer covering the residual crest might help to provide a deeper insight into aetiopathological mechanisms of this common oral disease.

Activated platelets increase proliferation and protein synthesis of human dental pulp-derived cells.

AIM: To evaluate the impact of activated platelets on the mitogenic expansion of human dental pulp-derived cells (DPC) in vitro. METHODOLOGY: The effect of supernatants released from activated platelets (PRS) and the corresponding platelet membranes (MEM) on proliferation and protein synthesis of DPC was evaluated. The contributions of the phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) pathways to the response of DPC were assessed using kinase inhibitors. Also examined was whether the presence of calcium hydroxide or the inflammatory mediators tumour necrosis factor alpha, interleukin-1, interleukin-6 and lipopolysaccharide of Escherichia coli modulated the expansion of DPC. RESULTS: Physiologic concentrations of PRS and MEM stimulated proliferation and protein synthesis by 18.4-fold (P < 0.01) and 2.9-fold (P < 0.01), respectively. This mitogenic expansion was paralleled by activation of AKT and the MAP kinases extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. Inhibitor studies revealed that the mitogenic response of DPC involved PI3K/AKT, JNK and p38 signalling (P < 0.05). Calcium hydroxide and inflammatory factors did not significantly modulate the mitogenic response of DPC to PRS and MEM. CONCLUSION: Supernatants released from activated platelets and the corresponding platelet membranes stimulated DPC proliferation and protein synthesis involving PI3K/AKT and MAPK signalling. These findings may serve as a basis for preclinical studies that address the role of activated platelets in dental pulp repair.

Is zoledronate toxic to human periodontal fibroblasts?

Exposed necrotic alveolar bone is a hallmark of bisphosphonate-related osteonecrosis of the jaw. However, it is unknown whether zoledronate causes soft-tissue damage via adverse actions toward periodontal fibroblasts. We therefore examined whether zoledronate causes a cytotoxic response in fibroblasts isolated from the gingiva and the periodontal ligament. We report that micromolar concentrations of zoledronate and serum-free conditions decreased cell activity, as measured by assays for formazan formation, proliferation, and protein synthesis. Under these conditions, periodontal fibroblasts underwent apoptosis and necrosis, as indicated by cleavage of PARP and membrane disruption, respectively. However, these adverse effects of zoledronate were mitigated by the presence of serum. Moreover, zoledronate bound to calcium phosphate failed to reduce cell activity. Analysis of these data suggests that the cytotoxic responses of periodontal fibroblasts require high concentrations of zoledronate and depend on the in vitro experimental conditions. Whether these findings translate into soft-tissue damage will require further investigation.

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.

Periodontal histomorphometry and status of aged sheep subjected to ovariectomy, malnutrition and glucocorticoid application.

OBJECTIVE: Ageing, hypogonadism, malnutrition, and the application of glucocorticoids have adverse effects on skeletal homeostasis. Herein we determined to which extent the periodontium undergoes catabolic changes under these conditions in a sheep model. METHODS: Six old sheep with a mean age of 7.5+/-1.0 years were subjected to ovariectomy, calcium/vitamin D-restricted diet, and intramuscular administration of approximately 2g methylprednisolone. Six adult sheep with a mean age of 3.8+/-0.9 years remained untreated and served as controls. First and second premolars of both jaws were subjected to histological analysis. The distances from the gingival margin (GM) and from the alveolar bone crest (ABC) to the cemento-enamel junction (CEJ) were determined. Periodontal attachment was given as the ratio between the dimension of the periodontal ligament and the alveolar bone. Clinical data were collected by counting the number of teeth missing, teeth with gingival recession, and teeth with a probing depth > 4 mm. RESULTS: We report that distance between GM and CEJ (2.1+/-1.7 mm and 6.6+/-2.6mm maxilla; -0.4+/-1.4 mm and 3.2+/-1.5 mm mandible), and between ABC and CEJ (-3.4+/-1.3mm and 1.8+/-2.7 mm maxilla; -3.5+/-1.1mm and -0.1+/-1.4mm mandible) are significantly lower in test than in control animals. In line with these findings, periodontal attachment was 67% in the maxilla and 86% in the mandible of the test group and almost completely preserved in the control group. Clinical evaluation showed that the overall number of teeth with recessions was significantly higher in the test compared to the control group (4.9+/-2.4 and 2.3+/-3.6), but not the number of teeth missing and teeth with a probing depth>4mm. CONCLUSIONS: Together these findings suggest that in sheep, the cumulating effects of ageing, hypogonadism, malnutrition and glucocorticoid application can cause substantial catabolic changes of the periodontium.

Trabecular bone structures in the edentulous diastema of osteoporotic sheep.

The edentulous ovine diastema represents a suitable region for implantological research. Due to distinctive embryonic origin and mechanical loading, the edentulous diastema may respond differently to osteoporosis than tooth-bearing areas. To test this assumption, we subjected geriatric sheep to ovariectomy, calcium-/vitamin-D-restricted diet, and methylprednisolone administration. Adult control sheep remained untreated. Structural parameters and bone mineral density were determined by microcomputed tomography and conventional computed tomography, respectively. We report that the trabecular microstructure in the diastema was preserved from catabolic changes. In contrast, the premolar maxillary region of osteoporotic sheep had diminished trabecular bone mineral density, with the corresponding structural deteriorations. These results suggest that maxillary trabecular bone of the edentulous diastema does not respond to catabolic changes which occur in the tooth-bearing area in osteoporosis. Our findings imply that regional anatomic domains must be considered in the planning of pre-clinical studies, taking osteoporotic changes into account.

Effects of platelet-derived growth factor isoforms on plasminogen activation by periodontal ligament and gingival fibroblasts.

BACKGROUND AND OBJECTIVE: Platelet-derived growth factor isoforms and components of the plasminogen activator system are expressed at higher levels during periodontal regeneration. Recombinant platelet-derived growth factor-BB is approved for the treatment of periodontal defects. In the present study we investigated the effect of platelet-derived growth factor isoforms on the plasminogen activator system in periodontal fibroblasts. MATERIAL AND METHODS: Human periodontal ligament fibroblasts and gingival fibroblasts were exposed to platelet-derived growth factor isoforms. Changes in urokinase-type plasminogen activator, tissue-type plasminogen activator, plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 transcript levels by platelet-derived growth factor-BB were monitored with a quantitative reverse transcription-polymerase chain reaction. Urokinase-type plasminogen activator and plasminogen activator inhibitor-1 protein levels were assessed by immunoassays. The effects of platelet-derived growth factor-BB on mitogen-activated protein kinase and phosphoinositol-3 kinase/Akt signaling were investigated by western blot and inhibitor studies. Casein zymography and kinetic assays revealed the size and activity, respectively, of the plasminogen activators. RESULTS: We found that incubation of periodontal ligament fibroblasts and gingival fibroblasts with platelet-derived growth factor-BB resulted in enhanced levels of urokinase-type plasminogen activator and plasminogen activator inhibitor-1 transcripts, but not of tissue-type plasminogen activator and plasminogen activator inhibitor-2. Platelet-derived growth factor-BB also increased urokinase-type plasminogen activator and plasminogen activator inhibitor-1 release into the culture medium. Phosphorylation of extracellular signal-regulated kinase, p38, c-Jun N-terminal kinase and Akt was observed in fibroblasts of both origin. Inhibition of phosphoinositol-3 kinase signaling abrogated the platelet-derived growth factor-BB effect on plasminogen activator inhibitor-1 production. Casein zymography revealed enzymatic activity of the urokinase-type plasminogen activator in cell-conditioned media and lysates of periodontal ligament fibroblasts and gingival fibroblasts. Exposure of gingival fibroblasts, but not of periodontal ligament fibroblasts, to platelet-derived growth factor isoforms moderately increased total plasminogen activation in the medium. CONCLUSION: These findings suggest that periodontal ligament fibroblasts attempt to maintain an equilibrium of the plasminogen activator system in the presence of platelet-derived growth factor isoforms.

Comparison of the validity of three dental methods for the estimation of age at death.

The aim of the present study was to compare the accuracy, precision, and bias of two macroscopic and one histological age at death estimation methods on human teeth. The sample was comprised of 67 permanent teeth, obtained from 37 individuals aged 20-91 years. Age was predicted according to the methods proposed by Lamendin et al. (LAM), Bang and Ramm (BR), and the quantification of tooth cementum annulations (TCA). TCA was found to be most accurate in all age groups. Its mean absolute error of the estimated age was about half as high as the mean absolute error for both LAM and BR. BR achieved approximately the same mean absolute error as TCA for old adults only. LAM displayed the highest precision in the young and the old age group whereas TCA was more precise in the middle age group. TCA was found to be the most precise method when the precision was calculated for all ages. Considering the bias, all methods displayed a tendency to overestimate age in young and to underestimate it in old specimens. The exception to this rule was TCA, which provided unbiased estimates for young adults. The higher accuracy and precision recommends favouring TCA over LAM and BR, provided that the required know-how and equipment are available.

The chronology of third molar mineralization in the Austrian population--a contribution to forensic age estimation.

The aim of the present study was to determine the chronology of third molar mineralization and to establish Austrian reference data. Therefore, a cross-sectional study was undertaken by evaluating 610 panoramic radiographs in order to assess the mineralization status of the mandibular third molars of Austrian male and female individuals (275 males and 335 females) between the ages of 12 and 24. The evaluation was carried out using the eight grade scheme of Demirjian et al. (1973). Mean ages, standard deviations, standard errors and percentile distributions are presented for each stage of development. Significant differences between the left and right mandibular third molars were not found. Males reach the developmental stages earlier than females, statistically significant differences were noted in stages E and F. Both mandibular third molars were observed in the majority of the individuals of the Austrian sample (477 individuals, 78.2%). For medicolegal purposes the likelihood of whether an Austrian individual is older than 18 years or not was determined.

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.

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.

Dental CT: imaging technique, anatomy, and pathologic conditions of the jaws.

In addition to conventional imaging methods, dental CT has become an established method for anatomic imaging of the jaws prior to dental implant placement. More recently, this high-resolution imaging technique has gained importance in diagnosing dental-associated diseases of the mandible and maxilla. Since most radiologists have had little experience in these areas, many of the CT findings remain undescribed. The objective of this review article is to present the technique of dental CT, to illustrate the typical appearance of jaw anatomy and dental-related diseases of the jaws with dental CT, and to show where it can serve as an addition to conventional imaging methods in dental radiology.

Platelet-released supernatants stimulate formation of osteoclast-like cells through a prostaglandin/RANKL-dependent mechanism.

Platelets are activated at fracture sites or upon the insertion of implants as a consequence of vascular disruption and secrete the contents of their granules into the developing hematoma. The regeneration of injured tissue requires bone remodeling and the resorbing activity of osteoclasts. To test our hypothesis that platelets can stimulate osteoclastogenesis, we examined the effects of supernatants released from thrombin-activated platelets on osteoclast-like cell formation in murine bone marrow cultures. Histochemical analysis indicated the presence of bone-resorbing, tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Transcripts that are characteristically expressed in native osteoclasts were increased in these cultures, as determined by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis. The inhibition of both cyclooxygenases with indomethacin, as well as the addition of the cyclooxygenase-2 (COX-2)-selective antagonist, NS398, completely blocked osteoclast-like cell formation and decreased endogenous prostaglandin E(2) production. Platelet-released supernatants stimulated the expression of receptor activator of NF-kappaB ligand (RANKL), whereas mRNA levels of osteoprotegerin (OPG) were decreased. The formation of osteoclast-like cells was prevented by recombinant OPG. Our results suggest that COX-2 activity is necessary for osteoclast-like cell formation in response to platelet-released supernatants, and that endogenously produced prostaglandin E(2) can, in turn, increase the RANKL:OPG ratio, indicating that platelets can contribute to bone remodeling by stimulation of osteoclastogenesis.

Short epithetic implants for orthodontic anchorage in the paramedian region of the palate. A clinical study.

Orthodontic movement of teeth often requires maximum anchorage, so that additional resistance must be added to teeth to avoid reaction to reciprocal forces. Thus, use of endosseous implants may be a valuable alternative for ensuring stable intraoral anchorage. This study was designed to evaluate the efficacy of short epithetic implants for orthodontic anchorage in the paramedian region of the palate. Twenty-one patients (15 female, 6 male; mean age 25.8+/-9.9 yrs, min 12.7, max. 48.1) were included in this study. Following adequate preoperative planning, an implant system with reduced length, which had already been used for anchorage of epitheses, was placed in the paramedian region avoiding the anterior palatine suture. After a mean period of 4 months with unloaded healing, the implants were subjected to direct or indirect orthodontic loading. Despite varying bone quality and varying vertical bone volume in this region, adequate primary stability was achieved for all of the implants. No implant was lost during the healing period. Three out of the 21 implants placed were considered as failures. Two implants loosened shortly after the start of orthodontic loading. One of these was lost at a later stage due to peri-implant inflammation, while the other one was left in place during the 9-month follow-up period because no inflammation developed and this implant is still indirectly included in the orthodontic treatment. Another implant loosening was observed after 8.5 months following direct loading with 8 N. This implant was also lost due to peri-implant inflammation. The time-related survival probability was 84.8% after 22.9 months. As yet, 4 implants have been removed due to completion of orthodontic treatment. The results of this study indicate that short epithetic implants are suitable to achieve maximum anchorage in the paramedian region of the hard palate in orthodontic treatment.