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Dental implants are commonly used to repair missing teeth. The implant surface plays a critical role in promoting osseointegration and implant success. However, little information is available about which implant surface treatment technology best promotes osseointegration and implant stability. The aim of this network meta-analysis was to evaluate the osseointegration and stability of four commonly used dental implants (SLA, SLActive, TiUnite, and Osseotite). The protocol of the current meta-analysis is registered in PROSPERO (International Prospective Register of Systematic Reviews) under the code CRD42020190907 ( https://www.crd.york.ac.uk ). We conducted a systematic review following PRISMA and Cochrane Recommendations. Medline (PubMed), Cochrane Library, Embase, and the Web of Science databases were searched. Only randomized controlled trials were considered. Twelve studies were included in the current network meta-analysis, eleven studies were included concerning the osseointegration effect and five studies were included for stability analysis (four studies were used to assess both stability and osseointegration). Rank possibility shows that the SLActive surface best promoted bone formation at an early healing stage and TiUnite seemed to be the best surface for overall osseointegration. For stability, TiUnite seemed to be the best surface. The present network meta-analysis showed that the SLActive surface has the potential to promote osseointegration at an early stage. The TiUnite surface had the best effect on osseointegration regarding the overall healing period. The TiUnite surface also had the best effect in stability.

While the benefits of direct skeletal attachment of artificial limbs are well recognized, device failure due to infection and insufficient osseointegration remain obstacles to obtaining consistently successful outcomes. Currently, the potential for device failure is assessed by subjective pain, clinical function scores, radiographic evidence of bone atrophy, and the presence of radiolucent lines at the bone-implant interface, and subjective pain and function scores. Our hypothesis is that measurable biological indices might add another objective means to assess trends toward bone and stomal healing. This longitudinal cohort study was undertaken to identify potential serological biomarkers suggestive of bone remodeling and the presence of stomal tissue inflammation. Ten unilateral transfemoral amputee veterans, who were implanted with a percutaneous osseointegrated (OI) skeletal limb docking system, were recruited to participate in this IRB-approved study. Venous blood samples were obtained from before the Stage 1 Surgery up to 1 year following the Stage 2 Surgery. Whole-blood RNA was extracted, sequenced, mapped, and analyzed. Of the significant differentially expressed (DEGs) genes (p<0.05) identified, four genes of interest (IL12B, IL33, COL2A1, and SOST) were validated using qPCR. Enrichment analysis was performed to identify significant (p<0.01) Gene Ontology (GO) terms. Most differentially expressed genes were only detected at PoS1 immediately after the first surgery. Of the significant genes identified, IL12B and IL33 were related to inflammation, and COL2A1 and SOST were associated with bone remodeling. These four genes were identified with greater than 20 log fold-change. Whole-blood RNA-seq data from 10 patients who previously underwent percutaneous osseointegrated lower limb implantation revealed four genes of interest that are known to be involved in inflammation or bone remodeling. If verified in future studies, these genes may serve as markers for predicting optimal bone remodeling and stomal tissue healing following OI device implantation.

Zirconia is one of the most promising implant materials due to its favorable physical, mechanical and biological properties. However, until now, we know little about the mechanism of osseointegration on zirconia. The purpose of this study is to evaluate the effect of Syndecan (Sdc) on osteoblastic cell (MC3T3-E1) adhesion and proliferation onto zirconia materials. The mirror-polished disks 15 mm in diameter and 1.5 mm in thick of commercial pure titanium (CpTi), 3mol% yttria-stabilized tetragonal zirconia polycrystalline (3Y-TZP) and nano-zirconia (NanoZr) are used in this study. MC3T3-E1 cells were seeded onto specimen surfaces and subjected to RNA interference (RNAi) for Syndecan-1, Syndecan-2, Syndecan-3, and Syndecan-4. At 48h post-transfection, the cell morphology, actin cytoskeleton, and focal adhesion were observed using scanning electron microscopy or laser scanning confocal fluorescence microscopy. At 24h and 48h post-transfection, cell counting kit-8 (CCK-8) assay was used to investigate cell proliferation. The cell morphology of MC3T3-E1 cells on CpTi, 3Y-TZP, and NanoZr changed into abnormal shape after gene silencing of Syndecan. Among the Syndecan family, Sdc-2 is responsible for NanoZr-specific morphology regulation, via maintenance of cytoskeletal conformation without affecting cellular attachment. According to CCK-8 assay, Sdc-2 affects the osteoblastic cell proliferation onto NanoZr. Within the limitation of this study, we suggest that Syndecan affects osteoblastic cell adhesion on CpTi, 3Y-TZP, and NanoZr. Sdc-2 might be an important heparin-sensitive cell membrane regulator in osteoblastic cell adhesion, specifically on NanoZr, through the organization of actin cytoskeleton and affects osteoblastic cell proliferation.

As a potentially bioactive material, the widespread application of nanosized hydroxyapatite (nano-HAP) in the field of bone regeneration has increased the risk of human exposure. However, our understanding of the interaction between nano-HAP and stem cells implicated in bone repair remains incomplete. Here, we characterized the adhesion and cellular internalization of HAP nanoparticles (HANPs) with different sizes (20 nm np20 and 80 nm np80) and highlighted the involved pathway in their uptake using human umbilical cord Wharton's jelly-derived mesenchymal stem cells (hWJ-MSCs). In addition, the effects of HANPs on cell viability, apoptosis response, osteogenic differentiation, and underlying related mechanisms were explored. It was shown that both types of HANPs readily adhered to the cellular membrane and were transported into the cells compared to micro-sized HAP particles (m-HAP; 12 μm). Interestingly, the endocytic routes of np20 and np80 differed, although they exhibited similar kinetics of adhesion and uptake. Our study revealed involvement of clathrin- and caveolin-mediated endocytosis as well as macropinocytosis in the np20 uptake. However, for np80, clathrin-mediated endocytosis and some as-yet-unidentified important uptake routes play central roles in their internalization. HANPs displayed a higher preference to accumulate in the cytoplasm compared to m-HAP, and HANPs were not detected in the nucleolus. Exposure to np20 for 24 h caused a decrease in cell viability, while cells completely recovered with an exposure time of 72 h. Furthermore, HANPs did not influence apoptosis and necrosis of hWJ-MSCs. Strikingly, HANPs enhanced mRNA levels of osteoblast-related genes and stimulated calcium mineral deposition, and this directly correlated with the activation in c-Jun N-terminal kinases and p38 pathways. Our data provide additional insight about the interactions of HANPs with MSCs and suggest their application potential in hard tissue regeneration.

The process in which nanostructured surfaces mediate cell adhesion is not well understood, and may be indirect (via protein adsorption) or direct. We prepared Sr-doped hydroxyapatite (Sr1-HA) 3D nanorods (with interrod spacing of 67.3 ± 3.8, 95.7 ± 4.2, and 136.8 ± 8.7 nm) and 2D nanogranulate patterned coatings on titanium. Employing the coatings under the same surface chemistry and roughness, we investigated the indirect/direct role of Sr1-HA nanotopographies in the regulation of osteoblast adhesion in both serum-free and serum-containing Dulbecco's Modified Eagle/Ham's Medium. The results reveal that the number of adherent cells, cell-secreted anchoring proteins (fibronectin, vitronectin, and collagen), vinculin and focal adhesion kinase (FAK) denoted focal adhesion (FA) contact, and gene expression of vinculin, FAK, and integrin subunits (α2, α5, αv, β1, and β3), undergo significant changes in the inter-nanorod spacing and dimensionality of Sr1-HA nanotopographies in the absence of serum; they are significantly enhanced on the <96 nm spaced nanorods and more pronounced with decreasing interrod spacing. However, they are inhibited on the >96 nm spaced nanorods compared to nanogranulated 2D topography. Although the adsorption of fibronectin and vitronectin from serum are higher on 136.8 ± 8.7 nm spaced nanorod patterned topography than nanogranulated topography, cell adhesion is inhibited on the former compared to the latter in the presence of serum, further suggesting that reduced cell adhesion is independent of protein adsorption. It is clearly indicated that 3D nanotopography can directly modulate cell adhesion by regulating integrins, which subsequently mediate anchoring proteins' secretion and FA formation rather than via protein adsorption.

Background Type II diabetes mellitus (T2DM) is an important risk factor for osseointegration of implants. The aim of this study was to explore key genes of T2DM affecting bone metabolism through bioinformatic analysis of published RNA sequencing data, identify potential biomarkers, and provide a reference for finding the molecular mechanism of abnormal osseointegration caused by T2DM. Methods We identified differentially expressed mRNAs and miRNAs from the Gene Expression Omnibus database using the R package ‘limma’ and analysed the predicted target genes using Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis and Gene Ontology analysis. At the same time, miRNA–mRNA interactions were explored using miRWalk 2.0. Results We constructed an miRNA-gene regulatory network and a protein–protein interaction network. The enrichment pathways of differentially expressed mRNAs included extracellular matrix receptor interactions, protein digestion and absorption, the PI3K-Akt signalling pathway, cytokine–cytokine receptor interactions, chemokine signalling pathways, and haematopoietic cell lineage functions. We analysed the expression of these differentially expressed mRNAs and miRNAs in T2DM rats and normal rats with bone implants and identified Smpd3 , Itga10 , and rno-mir-207 as possible key players in osseointegration in T2DM. Conclusion Smpd3 , Itga10 , and rno-mir-207 are possible biomarkers of osseointegration in T2DM. This study sheds light on the possible molecular mechanism of abnormal osseointegration caused by bone metabolism disorder in T2DM.

We examined alveolar bone samples in the area of on-bone fixation of a free gingival graft performed during surgery in patients aged 37-55 years with a diagnosis of secondary partial adentia of the upper and lower jaws. Six months after fixation of the graft in the alveolar bone, foci of neoosteogenesis were found in the contact zone. They were characterized by the appearance of appositional lines, cords of basophilic osteoblasts, and growing osteons. An immunohistochemical study revealed an increase in the number of CD44 + , CD29 + , and osteocalcin+ cells in the layer of the outer circumferential lamellae, primary osteons, and the lining of the Haversian canals. TGF-β1 + cells were located in the intertrabecular reticular tissue and wall of microvessels. The results indicate activation of mesenchymal stem cells in the area of localization of the graft and differentiating osteoblasts. The observed osteoinductive effect of free gingival graft is associated with its participation in reorganization in MSC and induction of morphogenetic molecules.

Successful dental and orthopedic implants require the establishment of an intimate association with bone tissue; however, the mechanistic explanation of how biological systems accomplish osseointegration is still incomplete. We sought to identify critical gene networks involved in osseointegration by exploring the implant failure model under vitamin D deficiency. Adult male Sprague-Dawley rats were exposed to control or vitamin D-deficient diet prior to the osteotomy surgery in the femur bone and the placement of T-shaped Ti4Al6V implant. Two weeks after the osteotomy and implant placement, tissue formed at the osteotomy site or in the hollow chamber of T-shaped implant was harvested and total RNA was evaluated by whole genome microarray analyses. Two-way ANOVA of microarray data identified 103 genes that were significantly (>2 fold) modulated by the implant placement and vitamin D deficiency. Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses assigned the highest z-score to the circadian rhythm pathway including neuronal PAS domain 2 (NPAS2), and period homolog 2 (Per2). NPAS2 and Aryl hydrocarbon receptor nuclear translocator-like (ARNTL/Bmal 1) were upregulated around implant and diminished by vitamin D deficiency, whereas the expression pattern of Per2 was complementary. Hierarchical cluster analysis further revealed that NPAS2 was in a group predominantly composed of cartilage extracellular matrix (ECM) genes. Whereas the expression of bone ECM genes around implant was not significantly affected by vitamin D deficiency, cartilage ECM genes were modulated by the presence of the implant and vitamin D status. In a proof-of-concept in vitro study, the expression of cartilage type II and X collagens was found upregulated when mouse mesenchymal stem cells were cultured on implant disk with 1,25D supplementation. This study suggests that the circadian rhythm system and cartilage extracellular matrix may be involved in the establishment of osseointegration under vitamin D regulation.

Bone generation occurs around titanium implants; however, its underlying mechanisms are unknown. We hypothesized that molecular determinants distinct from those undertaking normal bone healing regulate osseointegration. Using differential display-polymerase chain-reaction in the male rat model, we isolated 3 genes that are differentially expressed in bone healing with implants, but not in osteotomy healing. A homology search indicated that these 3 genes are apolipoprotein E, prolyl 4-hydroxylase α-subunit, and an unknown transcript. Differential expression of these genes was remarkable during early healing stages up to week 2, and accelerated with rough acid-etched surfaces compared with machined surfaces. The differential expression was confirmed in the female rats, with enhanced expression for the acid-etched surfaces. The osseointegration-unfavorable condition created by gonadal estrogen deficiency reduced the level of differential expression. This study provides evidence that selected gene transcripts are induced by titanium implants under regulatory control strongly associated with the nature of osseointegration.

Objective Dental implants consist in the treatment of choice to replace tooth loss. The knowledge that implant loss tends to cluster in subsets of individuals may indicate that host immuneinflammatory response is influenced by genetic factors. In fact, genetic polymorphisms influence the osseointegration process. The objective of this study was investigate the possible relationship between C-799T polymorphism in matrix metalloproteinase 8 (MMP-8) gene and early implant failure in nonsmoker patients. Methods and materials Subjects were divided into two groups: control group (100 patients with one or more healthy implants) and test group (80 patients that had suffered one or more early implant failures). Genomic DNA from oral mucosa was amplified by PCR and analyzed by restriction endonucleases. The significance of the differences in observed frequencies of polymorphisms was assessed by Chi-square. Results Statistical analysis shows that in the MMP-8 gene, the T allele in 76.25% in the test group and the T/T genotype, 63.75% in the same group, may predispose to early loss of implants osseointegrated. Conclusion These results suggest that polymorphism in the promoter region of MMP-8 gene is associated with early implant failure. This polymorphism can be a genetic marker to risk of implant loss. Clinical relevance The determination of this genetic pattern in osseointegration would enable the identification of individuals at higher risk to loss implant. Thus, genetic markers will be identified, contributing to an appropriate preoperative selection and preparation of strategies for prevention and therapy individualized to modulate the genetic markers and increase the success rate of treatments.