Fabricating Ti alloy based dental implants with defined porous scaffold structure is a promising strategy for improving the osteoinduction of implants. In this study, we use Laser Beam Melting (LBM) 3D printing technique to fabricate porous Ti6Al4V dental implant prototypes with three controlled pore sizes (200, 350 and 500 μm). The mechanical stress distribution in the surrounding bone tissue is characterized by photoelastography and associated finite element simulation. Forin-vitrostudies, experiments on implants’ biocompatibility and osteogenic capability are conducted to evaluate the cellular response correlated to the porous structure. As the preliminary results, porous structured implants show a lower stress-shielding to the surrounding bone at the implant neck and a more densed distribution at the bottom site compared to the reference implant. From the cell proliferation tests and the immunofluorescence images, 350 and 500 μm pore sized implants demonstrate a better biocompatibility in terms of cell growth, migration and adhesion. Osteogenic genes expression of the 350 μm group is significantly increased alone with the ALP activity test. All these suggest that a pore size of 350 μm provides an optimal provides an optimal potential for improving the mechanical shielding to the surrounding bones and osteoinduction of the implant itself.

Periodontitis is twice as prevalent in diabetics as in nondiabetics, and type 2 diabetes (T2D)–associated periodontitis is severe in many cases due to the altered and aberrant functions of bone cells in hyperglycemic conditions. Therefore, developing an effective method to halt the disease process, as well as restore and regenerate lost alveolar bone to reserve the natural teeth in diabetics, is critically important. In the current study, we applied a newly discovered adiponectin receptor agonist AdipoRon (APR) in experimental periodontitis in diabetic animal models and demonstrated the underlying molecular mechanisms. We found that when APR systemically quenched the blood sugar level in diet-induced obesity (DIO) diabetic mice, it reduced osteoclast numbers and alveolar bone loss significantly due to APR’s inhibition on osteoclast differentiation shown in our in vitro studies. APR also decreased the production of proinflammatory molecules CC chemokine ligand 2 and interleukin 6 in diseased gingival tissues. On the other hand, APR promoted alveolar bone regeneration through enhancing osteogenic differentiation and decreasing stromal cell–derived factor 1 in the bone marrow that facilitates stem cell migration. Same results were achieved by APR treatment of periodontitis induced in adiponectin (APN) knockout mice, indicating the ability of APR to activate the endogenous APN receptors to exert osteoanabolic effects. In summary, our study supports the notion that APR could be used as an effective multipronged approach to target T2D-associated periodontitis.

Background: Peri-implantitis is a polybacterial infection that can lead to the failure of dental implant rehabilitation. This study aimed to profile the microbiome of the peri-implant plaque and estimate the effect of periodontitis on it among 40 Chinese participants with dental implant prostheses and presenting with varying peri-implant and periodontal health states. Methods: Submucosal plaque samples were collected from four distinct clinical categories based on both their implant and periodontal health status at sampling point. Clinical examinations of dental implant and remaining teeth were carried out. Metagenomic analysis was then performed. Results: The microbiome of the peri-implantitis sites differed from that of healthy implant sites, both taxonomically and functionally. Moreover, the predominant species in peri-implantitis sites were slightly affected by the presence of periodontitis. T. forsythia, P. gingivalis, T. denticola, and P. endodontalis were consistently associated with peri-implantitis and inflammatory clinical parameters regardless of the presence of periodontitis. Prevotella spp. and P. endodontalis showed significant differences in the peri-implantitis cohorts under different periodontal conditions. The most distinguishing function between diseased and healthy implants is related to flagellar assembly, which plays an important role in epithelial cell invasion. Conclusions: The composition of the peri-implant microbiome varied in the diseased and healthy states of implants and is affected by individual periodontal conditions. Based on their correlations with clinical parameters, certain species are associated with disease and healthy implants. Flagellar assembly may play a vital role in the process of peri-implantitis.

Krüppel-like factor 7 (KLF7) is a member of the KLF family of zinc finger transcription factors, and was the first KLF cloned using complementary DNA and polymerase chain reaction (PCR) techniques with human vascular endothelial cells as a template. In addition, KLF7 is known as the ubiquitous Krüppel-like factor, as it is widely expressed in numerous human tissues at low levels. In the present study, the function of KLF7 in migration and epithelial-mesenchymal transition (EMT), which are associated with tumor progression, was investigated in human oral squamous cell carcinoma (OSCC) cells. Genes that were differentially expressed in normal vs. OSCC tissue were identified in the Gene Expression Omnibus database, which identified upregulation of KLF7 in OSCC. The expression and subcellular location of KLF7 was then analyzed using immunohistochemistry. KLF7 expression was measured in three OSCC cell lines, and the two cell lines with the highest (HN13) and lowest (CAL27) KLF7 expression were selected for further analysis. Subsequently, HN13 cells with reduced KLF7 expression (sh-HN13) and CAL27 cells overexpressing KLF7 (OE-CAL27) were constructed. Transwell migration and wound healing assays were then used to analyze the migration of the cells. In addition, mRNA and protein expression levels of the EMT markers E-cadherin, N-cadherin, vimentin and snail were detected using reverse transcription-quantitative PCR and western blotting. KLF7 overexpression in OSCC was validated using tissue immunohistochemistry, which identified moderate to high cytoplasmic staining of KLF7 in OSCC cells. KLF7 knockdown and overexpression altered the migration ability of sh-HN13 and OE-CAL27 cells, which decreased and increased significantly respectively. Expression of E-cadherin, N-cadherin, vimentin and snail was markedly altered in sh-HN13 and OE-CAL27 cells, indicating changes in EMT status. The results of the present study suggest that KLF7 overexpression changes the migratory behavior of OSCC cells, and induces EMT and lymph node metastasis through the expression of snail.