Search

Large‐volume bone defects can result from congenital malformation, trauma, infection, inflammation and cancer. At present, it remains challenging to treat these bone defects with clinically available interventions. Allografts, xenografts and most synthetic materials have no intrinsic osteoinductivity, and so an alternative approach is to functionalize the biomaterial with osteoinductive agents, such as bone morphogenetic protein 2 (BMP2). Because it has been previously demonstrated that human salivary histatin‐1 (Hst1) promotes endothelial cell adhesion, migration and angiogenesis, we examine here whether Hst1 can promote BMP2‐induced bone regeneration. Rats were given subcutaneous implants of absorbable collagen sponge membranes seeded with 0, 50, 200 or 500 μg Hst1 per sample and 0 or 2 μg BMP2 per sample. At 18 days postsurgery, rats were sacrificed, and implanted regional tissue was removed for micro computed tomography (microCT) analyses of new bone (bone volume, trabecular number and trabecular separation). Four samples per group were decalcified and subjected to immunohistochemical staining to analyze osteogenic and angiogenic markers. We observed that Hst1 increased BMP2‐induced new bone formation in a dose‐dependent manner. Co‐administration of 500 μg Hst1 and BMP2 resulted in the highest observed bone volume and trabecular number, the lowest trabecular separation and the highest expression of osteogenic markers and angiogenic markers. Our results suggest that coadministration of Hst1 may enhance BMP2‐induced osteogenesis and angiogenesis, and thus may have potential for development into a treatment for large‐volume bone defects., Sufficient bone tissue is important for aesthetics and musculoskeletal functions. We showed that coadministration of human salivary histatin‐1 enhanced new bone formation (shown by microCT analysis) and angiogenesis (indicated by immunostaining of CD105, as shown by the black arrows) induced by bone morphogenetic protein 2 in a classic ectopic bone induction model using absorbable collagen sponge.

In skeletal muscle, transforming growth factor-β (TGF-β) family growth factors, TGF-β1 and myostatin, are involved in atrophy and muscle wasting disorders. Simultaneous interference with their signalling pathways may improve muscle function; however, little is known about their individual and combined receptor signalling. Here, we show that inhibition of TGF-β signalling by simultaneous muscle-specific knockout of TGF-β type I receptors

Objectives: In order to verify the hypothesis that fibrin glue (FG) is able to seal the area of bone grafting and facilitate bone regeneration. Materials and methods: Twenty-one Sprague–Dawley rats with critical-sized calvarial bone defects were randomly assigned to three groups: (A) co-administrated deproteinized bovine bone (DBB) and autologous bone grafts with FG [fibrin (+)], (B) co-administrated DBB and autologous bone grafts without FG [fibrin (−)], and (C) no graft as control. Four weeks and 8 weeks later, micro-CT analysis and histomorphometric analysis were carried out to evaluate following parameters: bone volume fraction (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th) and trabecular separation (Tb.Sp), percentage of new bone area (Pe.NB), average thickness of bone defect (Th.BD), average thickness of basal bone (Th.BB), and percentage of new bone in center of the skull defect (Pe.NBc). Results: BV/TV, Tb.Th, and Tb.N in fibrin (−) group were significantly higher than that of fibrin (+) group (p = 0.008, 0.000, 0.007, respectively) and control group (p = 0.004, 0.001, and 0.007, respectively) at 8 weeks. Pe.NB in fibrin (−) group (33.67 ± 11.72%) was significantly higher than that of fibrin (+) group (12.33 ± 3.21%) (p = 0.038) and control group (9.66 ± 8.50%) (p = 0.045) at 8 weeks. Pe.NBc in fibrin (−) group (12.05 ± 3.91%) was significantly higher than that of fibrin (+) group (4.79 ± 1.21%) (p = 0.005) and control group (0.00 ± 0.00%) (p = 0.000) at 4 weeks. Conclusions: Administration of both DBB and autograft stimulates calvarial bone defect regeneration, while combination of FG does not additionally accelerate new bone formation. Clinical relevance: The use of fibrin to cement traditional bone graft materials in oral clinical practice requires caution.

This case represents aesthetic restoration by full-contour monolithic zirconia crowns without porcelain veneer via a completely digital workflow. Virtual prostheses were designed following intraora...

Skeletal muscle fibrosis and regeneration are modulated by transforming growth factor β (TGF-β) superfamily. Amongst them, TGF-β1 is a highly potent pro-fibrotic factor, while TGF-β3 has been implicated to reduce scar formation and collagen production in skin and vocal mucosa. However, little is known about the individual and combined short- and long-term effects of TGF-β1 and TGF-β3 on collagen expression in myoblasts and myotubes. Here we show that in C2C12 myoblasts TGF-β1 and/or TGF-β3 increased mRNA expression of Ctgf and Fgf-2 persistently after 3 h and of Col1A1 after 24 h, while TGF-β1+TGF-β3 mitigated these effects after 48 h incubation. Gene expression of Tgf-β1 was enhanced by TGF-β1 and/or TGF-β3 after 24 h and 48 h. However, Tgfbr1 mRNA expression was reduced at 48 h. After 48 h incubation with TGF-β1 and/or TGF-β3, Col3A1 and Col4A1 mRNA expression levels were decreased. Myoblasts produced collagen after three days incubation with TGF-β1 and/or TGF-β3 in a dose independent manner. Collagen deposition was doubled when myoblasts differentiated into myotubes and TGF-β1 and/or TGF-β3 did not stimulate collagen production any further. TGF-β type I receptor (TGFBR1) inhibitor, LY364947, suppressed TGF-βs-induced collagen production. Collagen I expression was higher in myotubes than in myoblasts. TGF-β1 and/or TGF-β3 inhibited myotube differentiation which was antagonized by LY364947. These results indicate that both C2C12 myoblasts and myotubes produce collagen. Whereas TGF-β1 and TGF-β3 individually and simultaneously stimulate collagen production in C2C12 differentiating myoblasts, in myotubes these effects are less prominent. In muscle cells, TGF-β3 is ineffective to antagonize TGF-β1-induced collagen production.

Cell‐based bone tissue engineering techniques utilize both osteogenic cells and biomedical materials, and have emerged as a promising approach for large‐volume bone repair. The success of such techniques is highly dependent on cell adhesion, spreading, and osteogenic activities. In this study, we investigated the effect of co‐administration of all‐trans retinoic acid (ATRA) and human salivary peptide histatin‐1 (Hst1) on the spreading and osteogenic activities of pre‐osteoblasts on bio‐inert glass surfaces. Pre‐osteoblasts (MC3T3‐E1 cell line) were seeded onto bio‐inert glass slides in the presence and absence of ATRA and Hst1. Cell spreading was scored by measuring surface areas of cellular filopodia and lamellipodia using a point‐counting method. The distribution of fluorogenic Hst1 within osteogenic cells was also analyzed. Furthermore, specific inhibitors of retinoic acid receptors α, β, and γ, such as ER‐50891, LE‐135, and MM‐11253, were added to identify the involvement of these receptors. Cell metabolic activity, DNA content, and alkaline phosphatase (ALP) activity were assessed to monitor their effects on osteogenic activities. Short‐term (2 h) co‐administration of 10 μm ATRA and Hst1 to pre‐osteoblasts resulted in significantly higher spreading of pre‐osteoblasts compared to ATRA or Hst1 alone. ER‐50891 and LE‐135 both nullified these effects of ATRA. Co‐administration of ATRA and Hst1 was associated with significantly higher metabolic activity, DNA content, and ALP activity than either ATRA or Hst1 alone. In conclusion, co‐administration of Hst1 with ATRA additively stimulated the spreading and osteogenicity of pre‐osteoblasts on bio‐inert glass surfaces in vitro., Adhesion and spreading of osteogenic cells are indispensable for initiation of bone regeneration. We showed that the co‐administration of all‐trans retinoic acid (ATRA) and human salary histatin‐1 (Hst1) resulted in significantly enhanced spreading, metabolic activity, proliferation (DNA content), and osteogenic differentiation (alkaline phosphatase activity) of pre‐osteoblasts on bio‐inert surfaces, thus bearing a promising application potential in bone tissue engineering.

The amount of enamel wear on the antagonist occlusal surfaces caused by self-glazed zirconia crowns was compared with that caused by contralateral natural teeth. Thirteen self-glazed zirconia crowns were placed in situ. The impressions of self-glazed zirconia crowns, their antagonists and the control teeth were taken and scanned at baseline and 6-month follow-up. The patients were divided into two groups, the self-glazed crowns in one group were subjected to a large amount of grinding with well polishing (LaP group, n = 7), while the other group required a little amount of grinding with well polishing (LiP group, n = 6). Statistics were analysed by two-sided paired Student’s t-tests to a significance level of p