Role In New Bone Formation Research Articles

Histologic wound healing in studies using different ridge preservation protocols: A review.

Alveolar ridge preservation (ARP) procedures are designed to lessen dimensional changes in the alveolar ridge after tooth extraction. Wound healing after ridge preservation involves the formation of new vital bone in the former socket, and this vital bone is important in the osseointegration of dental implants. A series of ARP studies have been performed to help clinicians better understand the wound-healing events that occur following tooth extraction and ridge preservation. Different protocols have been examined using various materials and periods of healing time prior to implant placement. The primary aim of these studies was to ascertain the relative percentage of vital bone formation, residual graft material, and connective tissue (CT)/other at the healing site using histomorphometric examination of bone core biopsies obtained during osteotomy preparation. For allografts, the use of demineralized bone alone or in combination with mineralized is associated with more vital bone formation than the use of mineralized allograft alone. For mineralized allografts, the use of cortical versus cancellous bone has only minimal impact on new bone formation. Xenografts from bovine and porcine sources appear to have similar vital bone formation. Longer healing times prior to implant placement are associated with increased vital bone formation and decreased residual graft material. The most stable component in most studies is the percentage of CT/other. The percentage of vital bone and residual graft at ARP sites is dependent on the materials used and the length of healing time prior to obtaining core biopsies. What factors may affect the amount of new bone at the ARP site? At a time point about 4 months after ARP, the type of graft material used for ARP plays a large role in new bone formation. Studies focus on means and standard deviations, but patients often do not "follow the mean." Even if a single ARP protocol is used for all patients, there is great interindividual variability in new bone formation, and there is often variability between sites within a single patient. How long after ARP with an allograft should I wait to place an implant? Longer healing times such as 4-5 months generally provide higher amounts of vital bone formation than shorter healing times like 2-3 months. Differences in vital bone formation between ARP protocols tend to decrease with longer healing time. FDBA that contains demineralized bone, either alone or combined with mineralized FDBA, often provides higher amounts of new bone formation than 100% mineralized allograft, especially at shorter healing periods. Even a year after ARP with an allograft, residual graft material is often still present at the ARP site.

Improved repair of rabbit calvarial defects with hydroxyapatite/chitosan/polycaprolactone composite scaffold-engrafted EPCs and BMSCs.

Endothelial progenitor cells (EPCs) expressing vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) and bone marrow mesenchymal stem cells (BMSCs) expressing endogenous bone morphogenetic protein-2 (BMP-2) play the important role in new bone formation. This study investigated the effects of a porous hydroxyapatite (HA)/chitosan (CS)/polycaprolactone (PCL) composite scaffold-engrafted EPCs and BMSCs on the expression of BMP-2, VEGF, and PDGF in the calvarial defect rabbit model in vivo. It showed that a three-dimensional composite scaffold was successfully constructed by physical interaction with a pore size of 250 μm. The HA/CS/PCL scaffold degraded slowly within 10 weeks and showed non-cytotoxicity. By X-ray, micro-CT examination, and H&E staining, compared with the HA/CS/PCL group, HA/CS/PCL + EPCs, HA/CS/PCL + BMSCs, and HA/CS/PCL + EPCs + BMSCs groups performed a more obvious repair effect, and the dual factor group presented particularly significant improvement on the percentages of bone volume at week 4 and week 8, with evident bone growth. Osteogenesis marker (BMP-2) and vascularization marker (VEGF and PDGF) expression in the dual factor group were much better than those of the HA/CS/PCL control group and single factor groups. Collectively, the HA/CS/PCL composite scaffold-engrafting EPCs and BMSCs is effective to repair calvarial defects by regulating endogenous expression of BMP-2, VEGF, and PDGF. Thus, this study provides important implications for the potential clinical application of biomaterial composite scaffold-engrafted engineering cells.

Down-Regulation of Dkk-1 in Platelets of Patients With Axial Spondyloarthritis.

Axial spondyloarthritis (SpA) is a chronic autoinflammatory disease with new bone formation, which is controlled by Wnt/β-catenin signaling. Dkk-1 is an inhibitor of the Wnt pathway, and in humans, platelets represent a major source of Dkk-1. This study was undertaken to investigate whether levels of Dkk-1 in serum and platelet expression of DKK1 messenger RNA (mRNA) and Dkk-1 protein are affected in patients with axial SpA compared to healthy controls. Forty-one patients with axial SpA and 35 healthy controls were enrolled in the study. Total serum Dkk-1 levels in all patients and healthy controls were measured by quantitative enzyme-linked immunosorbent assay. Platelet DKK1 mRNA was analyzed by quantitative reverse transcriptase-polymerase chain reaction in 20 patients with axial SpA and 20 controls, and Dkk-1 protein levels were measured by immunoblotting in 20 patients with axial SpA and 18 controls. We found a lower concentration of Dkk-1 in the serum from patients with axial SpA compared to the serum from healthy controls (P < 0.0001). Furthermore, the expression of Dkk-1 was significantly reduced both at the transcriptional level (P < 0.04) and at the protein level (P < 0.007) in platelets isolated from the blood of patients with axial SpA. Our preliminary observations suggest that dysfunction of the megakaryocyte/platelet axis might be responsible for reduced serum Dkk-1 levels in patients with axial SpA. Dkk-1 is down-regulated in the platelets of patients with axial SpA, a mechanism that might play a role in new bone formation.

Potential role of myeloid-derived suppressor cells in transition from reaction to repair phase of bone healing process.

Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells with immunosuppressive functions; these cells play a key role in infection, immunization, chronic inflammation, and cancer. Recent studies have reported that immunosuppression plays an important role in the healing process of tissues and that Treg play an important role in fracture healing. MDSCs suppress active T cell proliferation and reduce the severity of arthritis in mice and humans. Together, these findings suggest that MDSCs play a role in bone biotransformation. In the present study, we examined the role of MDSCs in the bone healing process by creating a bone injury at the tibial epiphysis in mice. MDSCs were identified by CD11b and GR1 immunohistochemistry and their role in new bone formation was observed by detection of Runx2 and osteocalcin expression. Significant numbers of MDSCs were observed in transitional areas from the reactionary to repair stages. Interestingly, MDSCs exhibited Runx2 and osteocalcin expression in the transitional area but not in the reactionary area. And at the same area, cllagene-1 and ALP expression level increased in osteoblast progenitor cells. These data is suggesting that MDSCs emerge to suppress inflammation and support new bone formation. Here, we report, for the first time (to our knowledge), the role of MDSCs in the initiation of bone formation. MDSC appeared at the transition from inflammation to bone making and regulates bone healing by suppressing inflammation.

Serum levels of inhibitors of wingless / beta-catenin in patients with ankylosing spondylitis and the relationship with anti-tumour necrosis factor alpha treatments

Aim: The primary aim of the study was to compare the serum levels of Dickkopf-1 (DKK-1) and sclerostin in patients with ankylosing spondylitis (AS) and healthy controls. The secondary aim was to evaluate the effects of anti-tumor necrosis factor alpha (TNF-α) treatments on levels of DKK-1 and sclerostin. The last aim was to evaluate any relationship between DKK-1, sclerostin, and radiologic progression in AS. Material and Method: We included 70 patients with AS (35 anti-TNF-α treated, 35 anti-TNF-α naive) and 31 healthy controls in this study. Serum DKK-1, sclerostin, C reactive protein, and erythrocyte sedimentation rate (ESR) were assessed in patients and healthy controls. The Ankylosing Spondylitis Disease Activity Score (ASDAS), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Metrology Index (BASMI), and Bath Ankylosing Spondylitis Functional Index (BASFI) were calculated for the patients. Radiographs were scored according to the modified Stoke AS Spine Score (mSASSS) by an experienced radiologist who was blinded to the patients’ identity. Results: Patients with AS who were treated with anti-TNF-α agent had higher scores of BASMI and mSASSS compared with the anti-TNF-α naive patients. Serum levels of DKK-1 and sclerostin were significantly lower in patients with AS than in healthy controls. There was a negative correlation between DKK-1 levels with ASDAS and BASMI in patients with AS. There was no correlation between DKK-1 or sclerostin levels with mSASSS. There was a positive correlation between BASMI score with mSASSS in patients with AS. Conclusion: DKK-1 levels in patients with AS were negatively correlated with BASMI, on the other hand, BASMI had a strong positive correlation with mSASSS. Therefore, these findings suggest that lower DKK-1 levels in patients with AS may play a role in new bone formation.

Magnesium doping on TiN coatings affects mesenchymal stem cell differentiation and proliferation positively in a dose-dependent manner.

In vitro evaluation of cell-surface interactions for hard tissue implants have mostly been done using osteoblasts. However, when an implant is placed in the body, mesenchymal stem cells (MSCs) play a major role in new bone formation. Therefore, using MSCs in cell-surface investigations may provide more reliable information on the prediction of in vivo behavior of implants. In this study, Mg doped TiN coatings ((Ti,Mg)N) were prepared and tested for their effect on MSC differentiation and mineralization. MSCs were isolated from rat bone marrow (rBMSCs) and seeded onto bare Ti, TiN and Mg containing (Ti,Mg)N surfaces. Cell proliferation, osteogenic differentiation (collagen type 1, alkaline phosphatase activity), calcium phosphate deposition (von Kossa staining, Scanning Electron Microscopy) analysis were conducted. Differentiation towards osteoblast lineage was significantly improved with the increment in Mg presence. Collagen type I deposition, mineralization, and the ALP activity were higher on high Mg containing (>10 at% Mg) surfaces but differentiation of rBMSCs were found to be delayed. Mg presence affected rBMSCs proliferation and differentiation positively in a dose-dependent manner. However, high Mg amounts delayed both proliferation and differentiation.

Osteoinduction by Ex Vivo Nonviral Bone Morphogenetic Protein Gene Delivery Is Independent of Cell Type.

Ex vivo nonviral gene delivery of bone inductive factors has the potential to heal bone defects. Due to their inherent role in new bone formation, multipotent stromal cells (MSCs) have been studied as the primary target cell for gene delivery in a preclinical setting. The relative contribution of autocrine and paracrine mechanisms, and the need of osteogenic cells, remains unclear. This study investigates the contribution of MSCs as producer of transgenic bone morphogenetic proteins (BMPs) and to what extent the seeded MSCs participate in actual osteogenesis. Rat-derived MSCs or fibroblasts (FBs) were cotransfected with pBMP-2 and pBMP-6 or pBMP-7 via nucleofection. The bioactivity of BMP products was shown through in vitro osteogenic differentiation assays. To investigate their role in new bone formation, transfected cells were seeded on ceramic scaffolds and implanted subcutaneously in rats. Bone formation was assessed by histomorphometry after 8 weeks. As a proof of principle, we also investigated the suitability of bone marrow-derived mononuclear cells and the stromal vascular fraction isolated from adipose tissue for a one-stage gene delivery strategy. Bone formation was induced in all conditions containing cells overexpressing BMP heterodimers. Constructs seeded with FBs transfected with BMP-2/6 and MSCs transfected with BMP-2/6 showed comparable bone volumes, both significantly higher than controls. Single-stage gene delivery proved possible and resulted in some bone formation. We conclude that bone formation as a result of ex vivo BMP gene delivery can be achieved even without direct osteogenic potential of the transfected cell type, suggesting that transfected cells mainly function as a production facility for osteoinductive proteins. In addition, single-stage transfection and reimplantation of cells appeared feasible, thus facilitating future clinical translation of the method.

Diagnostic utility of histone H3.3 G34W, G34R, and G34V mutant-specific antibodies for giant cell tumors of bone

Giant cell tumors of bone (GCTBs) are characterized by mononuclear stromal cells and osteoclast-like giant cells; up to 95% have H3F3A gene mutation. The RANKL inhibitor denosumab, when used for the treatment of GCTB, leads to histological changes such as new bone formation and giant cell depletion. Here we assessed the diagnostic utility of immunohistochemical staining with the antibodies against histone H3.3 G34W, G34R and G34V mutant proteins for GCTB and other histologically similar bone and joint lesions. H3.3 G34W, G34R and G34V expressions were detected in mononuclear stromal cells in 47/51 (92%), 1/51 (2%) and 3/51 (6%) cases of primary GCTBs, respectively, in a mutually exclusive manner. All recurrent/metastatic GCTBs (n=14), post-denosumab GCTBs (n=8) and secondary malignant GCTBs (n=2) were positive for H3.3 G34W. The immunohistochemical results were essentially correlated with the H3F3A genotype determined by mutation analysis. In post-denosumab GCTBs, H3.3 G34W expression was seen in immature bone-forming cells. H3.3 G34W, G34R and G34V were negative in 121/122 cases of non-GCTB, including chondroblastoma, osteosarcoma, primary aneurysmal bone cyst and other giant cell-rich lesions. The exception was a single case of undifferentiated high-grade pleomorphic sarcoma that was positive for H3.3 G34W, suggesting the possibility of sarcomatous overgrowth of primary malignant GCTB. Therefore, H3.3 G34W/R/V mutant-specific antibodies are useful surrogate markers for the H3F3A genotype and helpful for the diagnosis of GCTB and its variants. The expression of H3.3 G34W mutant protein in post-denosumab GCTB suggests that neoplastic stromal cells may play a role in new bone formation.

MiR-29a and Messenger RNA Expression of Bone Turnover Markers in Canonical Wnt Pathway in Patients with Ankylosing Spondylitis.

Recent studies showed that the canonical Wnt pathway and miR-29a play important roles in the pathogenesis of bone formation. We studied the levels of miR-29a and messenger RNA (mRNA) of bone turnover markers in the canonical Wnt pathway in ankylosing spondylitis (AS). The levels of miR-29a and mRNA of bone turnover markers in canonical Wnt pathway from peripheral blood mononuclear cells were determined by real-time quantitative polymerase chain reaction in 38 patients with AS and 32 healthy controls. Correlation analysis was conducted between the levels of miR-29a and mRNA and clinical measurements using Spearman's correlation test. Compared to healthy controls, the levels of miR-29a, Dickkopf (DKK)-1, β-catenin and Runx2 mRNA were significantly higher in AS patients (p < 0.05). In contrast, the levels of Gsk-3β mRNA was significantly lower in AS patients than that in healthy controls (p < 0.05). Gsk-3β mRNA was positively correlated with β-catenin mRNA expression (p < 0.05) and no other correlation was observed between any other markers (p > 0.05). Only DKK-1 mRNA expression was negatively correlated with disease course (p < 0.05) and no other correlation was observed between markers and clinical measurements (p > 0.05). The osteoblastic marker miR-29a and downstream mRNA of canonical Wnt signaling was upregulated in AS, suggesting their possible role in new bone formation in AS.

Controlled-release of tetracycline and lovastatin by poly(D,L-lactide-co-glycolide acid)-chitosan nanoparticles enhances periodontal regeneration in dogs.

Chronic periodontitis is characterized by inflammation of periodontal tissues, leading to bone resorption and tooth loss. The goal of treatment is to regenerate periodontal tissues including bone and cementum lost as a consequence of disease. The local delivery of tetracycline was proven to be effective in controlling localized periodontal infection without apparent side effects. Previous studies suggested that lovastatin has a significant role in new bone formation; however, the local delivery of lovastatin might enhance its therapeutic effects. A number of local delivery devices have been developed recently, including poly(d,l-lactide-co-glycolide acid) (PLGA) nanoparticles. The aim of this study was to develop a local delivery device, PLGA-lovastatin-chitosan-tetracycline nanoparticles, which allows the sequential release of tetracycline and lovastatin to effectively control local infection and promote bone regeneration in periodontitis. The size and microstructure of nanoparticles were examined by transmission electron microscopy, Nanoparticle Size Analyzer, and Fourier transform infrared spectroscopy. The release of tetracycline and lovastatin was quantified using a UV-Vis spectrophotometer. Furthermore, the cytotoxic effect and alkaline phosphatase activity of the nanoparticles in osteoblast cell cultures as well as antibacterial activity against periodontal pathogens were investigated. Finally, the bone regeneration potential of PLGA nanoparticles in three-walled defects in beagle dogs was investigated. The results indicated that PLGA-lovastatin-chitosan-tetracycline nanoparticles showed good biocompatibility, antibacterial activity, and increased alkaline phosphatase activity. The volumetric analysis from micro-CT revealed significantly increased new bone formation in defects filled with nanoparticles in dogs. This novel local delivery device might be useful as an adjunctive treatment in periodontal regenerative therapy.

Evaluation of bone formation guided by DNA/protamine complex with FGF‐2 in an adult rat calvarial defect model

DNA/protamine complex paste (D/P) and D/P complex paste with Fibroblast Growth Factor-2 (FGF-2) (D/P-FGF) were prepared to investigate their new bone formation abilities using an ∼40-week-old rat calvarial defect model. It was found that D/P could release FGF-2 proportionally in an in vitro experiment with an enzyme-linked immunosorbent assay. It was also found that aging adversely affected self-bone healing of rats by comparison with the results in a previous study using 10-week-old rats. Microcomputed tomography and histopathological examinations showed that new bone formation abilities of D/P and D/P-FGF were superior to that of the control (sham operation). Control, D/P and D/P-FGF showed newly formed bone areas of 6.7, 58.3, and 67.0%, respectively, 3 months after the operation. Moreover, it was found that FGF-2 could support the osteoanagenesis ability of D/P. It was considered that FGF-2 could play an important role in new bone formation at early stages because it induced the genes such as collagen I, CBFA, OSX, and OPN, which are initiated first in the process of osteogenesis. Therefore, D/P-FGF will be a useful injectable biomaterial with biodegradable properties for the repair of bone defects in the elderly.

THU0262 Sclerostin does not predict radiographic progression in patients on anti-tnf therapy – new results from the european ankylosing spondylitis (AS) infliximab cohort (EASIC)

BackgroundAnti-TNF therapy has been shown to be clinically efficacious in patients with ankylosing spondylitis (AS) but there is no evidence that it inhibits new bone formation. Biomarkers of increased bone...

Translocation of autogenous bone particles to improve peri-implant osteogenesis

During the placement of titanium implants into bone, particles are loosened and translocated as a result of the inherent roughness of the surface. Such bone particles have been shown to play a significant role in new bone formation. Therefore, the aim of the present study was to establish a new regenerative procedure, which can be implemented immediately during surgery, to provide implants with additional autogenous bone particles. Thereafter, we investigated the effect of such 'bone-coated' implants on the healing response. In our model, dental screw-type implants were placed in the iliac crests of goats, following three approaches: (a) implants were placed, then removed while retaining bone debris on the surface, and subsequently placed into freshly prepared holes; (b) new implants were installed in the donor sites from group 1; and (c) control implants were inserted according to the standard protocol. After 3 weeks, microcomputed tomography and histomorphometerical analyses on bone-implant contact (BIC) and bone area (BA) were performed. The results showed that the retained bone debris in group 1 was viable bone-like tissue when cultured in vitro. In vivo histological results showed a significantly higher BIC for the 'bone-coated' (43.42 ± 11.29%) compared to the control (28.15 ± 11.86%) implants. Also, adjacent to the implants a significantly higher BA was found for 'bone-coated' implants (39.51 ± 11.17%) compared to the controls (31.92 ± 10.25%). Notably, no detrimental effects were noticed for the 'donor-site' positions. In conclusion, the transported autogenous bone particles accelerated peri-implant osteogenesis. Clinical studies are needed to evaluate the potential of this procedure in clinical practice.

An inflammation-responsive transcription factor in the pathophysiology of osteoarthritis

A number of risk factors including biomechanical stress on the articular cartilage imposed by joint overloading due to obesity, repetitive damage of the joint tissues by injury of the menisci and ligaments, and abnormal joint alignment play a significant role in the onset of osteoarthritis (OA). Genetic predisposition can also lead to the formation of defective cartilage matrix because of abnormal gene expression in the cartilage-specific cells. Another important biochemical event in OA is the consequence of inflammation. It has been shown that synovial inflammation triggers the synthesis of biological stimuli such as cytokines and growth factors which subsequently reach the chondrocyte cells of the articular cartilage activating inflammatory events in the chondrocytes leading to cartilage destruction. In addition to cartilage degradation, hypertrophy of the subchondral bone and osteophyte formation at the joint margins also takes place in OA. Both processes involve abnormal expression of a number of genes including matrix metalloproteinases (MMPs) for cartilage degradation and those associated with bone formation during osteophyte development. To address how diverse groups of genes are activated in OA chondrocyte, we have studied their induction mechanism. We present evidence for abundant expression of an inflammation-responsive transcription factor, SAF-1, in moderate to severely damaged OA cartilage tissues. In contrast, cells in normal cartilage matrix contain very low level of SAF-1 protein. SAF-1 is identified as a major regulator of increased synthesis of MMP-1 and -9 and pro-angiogenic factor, vascular endothelial growth factor (VEGF). While VEGF by stimulating angiogenesis plays a key role in new bone formation in osteophyte, increase of MMP-1 and -9 is instrumental for cartilage erosion in the pathogenesis of OA. Increased expression in degenerated cartilage matrix and in the osteophytes indicate for a key regulatory role of SAF-1 in directing catabolic matrix degrading and anabolic matrix regenerating activities.

Tyrosine derived polycarbonate membrane is useful for guided bone regeneration in rabbit mandibular defects

Standardized bilateral through-and-through defects (12x6 mm) were created extraorally in the mandibular angle of 18 New Zealand White rabbits. Animals were divided in to three groups (n=6) according to the intended healing time. On the left side, defects were covered with a poly(desaminotyrosyl-tyrosine-ethyl ester carbonate) (PDTE carbonate) membrane wrapped around the inferior border of the mandible and fixed with bioabsorbable sutures. On the right side, the defects were filled with a mesh made of bioactive glass 13-93 and 3 wt% chitosan. The defects were covered with the same membranes. Periosteal flap was sutured over the membrane. Radiographically, bone ingrowth was seen in all specimens at 12 weeks postoperatively. At 24 weeks, completely ossified area remained approximately at the same level as at 12 weeks, but the non-ossified area decreased to almost zero. However, the bioactive glass mesh did not improve the results. Nevertheless, enveloping the defect with PDTE carbonate membrane seemed to play a crucial role in new bone formation. Based on these results, we conclude that tyrosine polycarbonate is a promising new material for guided bone regeneration.

Condyle-fossa modifications and muscle interactions during Herbst treatment, Part 2. Results and conclusions

Herbst appliances were activated progressively in growing nonhuman primates, and the results were compared with primate and human controls. The methods and materials of this research are explained in Part 1 of this study. The results are discussed here in Part 2. All experimental subjects developed large super Class I malocclusions, the result of many factors including posterior movement of the maxilla and the maxillary teeth, an increased horizontal component of condylar growth, and anterior displacement of the mandible and the mandibular teeth. The growth modification measured in the glenoid fossa was in an inferior and anterior direction. Restriction of the downward and backward growth of the fossa observed in the control subjects might additionally contribute to the overall super Class I malocclusion. Clinically, these combined effects could be significant at the fossa. The restriction of local temporal bone (fossa) growth cannot be observed clinically; thus, these results might also clarify some Class II correction effects that cannot be explained with functional appliances. Differences in the area and maximum thickness of new bone formation in the glenoid fossa and in condylar growth were statistically significant. The bony changes in the condyle and the glenoid fossa were correlated with decreased postural electromyographic activity during the experimental period. Results from permanently implanted electromyographic sensors demonstrated that lateral pterygoid muscle hyperactivity was not associated with condyle-glenoid fossa growth modification with functional appliances, and that other factors, such as reciprocal stretch forces and subsequent transduction along the fibrocartilage between the displaced condyle and fossa, might play a more significant role in new bone formation. These results support the growth relativity concept.

Inhibition of gap junction intercellular communication by extremely low-frequency electromagnetic fields in osteoblast-like models is dependent on cell differentiation.

Electromagnetic fields have been used to augment the healing of fractures because of its ability to increase new bone formation. The mechanism of how electromagnetic fields can promote new bone formation is unknown, although the interaction of electromagnetic fields with components of the plasma membrane of cells has been hypothesized to occur in bone cells. Gap junctions occur among bone forming cells, the osteoblasts, and have been hypothesized to play a role in new bone formation. Thus it was investigated whether extremely low-frequency (ELF) magnetic fields alter gap junction intercellular communication in the pre-osteoblastic model, MC3T3-E1, and the well-differentiated osteoblastic model, ROS 17/2.8. ELF magnetic field exposure systems were designed to be used for an inverted microscope stage and for a tissue culture incubator. Using these systems, it was found that magnetic fields over a frequency range from 30 to 120 Hz and field intensities up to 12.5 G dose dependently decreased gap junction intercellular communication in MC3T3-E1 cells during their proliferative phase of development. The total amount of connexin 43 protein and the distribution of connexin 43 gap junction protein between cytoplasmic and plasma membrane pools were unaltered by treatment with ELF magnetic fields. Cytosolic calcium ([Ca(2+)](i)) which can inhibit gap junction communication, was not altered by magnetic field exposure. Identical exposure conditions did not affect gap junction communication in the ROS 17/2.8 cell line and when MC3T3-E1 cells were more differentiated. Thus ELF magnetic fields may affect only less differentiated or pre-osteoblasts and not fully differentiated osteoblasts. Consequently, electromagnetic fields may aid in the repair of bone by effects exerted only on osteoprogenitor or pre-osteoblasts.

Hydrolysis and phase transition of alpha-tricalcium phosphate

Increasing attention has been paid in recent years to alpha-tricalcium phosphate (α-TCP), which is used as the main constituent of calcium phosphate bioactive bone cements and biphasic calcium phosphate ceramics. Its hydrolysis and conversion into apatite phase may play an important role in new bone formation in vivo. In this experiment, α-TCP powder was made and immersed in deionized water. The morphology change and phase composition were analysed before and after immersion. Based on the results of hydrolysis, a formula for the converted apatite-TCP phase containing lattice water was put forward and a partial structural model along the hydroxyl column was proposed.