Additive manufacturing technologies in the oral implant clinic: A review of current applications and progress.

Additive manufacturing (AM) technologies can enable the direct fabrication of customized physical objects with complex shapes, based on computer-aided design models. This technology is changing the digital manufacturing industry and has become a subject of considerable interest in digital implant dentistry. Personalized dentistry implant treatments for individual patients can be achieved through Additive manufacturing. Herein, we review the applications of Additive manufacturing technologies in oral implantology, including implant surgery, and implant and restoration products, such as surgical guides for implantation, custom titanium meshes for bone augmentation, personalized or non-personalized dental implants, custom trays, implant casts, and implant-support frameworks, among others. In addition, this review also focuses on Additive manufacturing technologies commonly used in oral implantology. Stereolithography, digital light processing, and fused deposition modeling are often used to construct surgical guides and implant casts, whereas direct metal laser sintering, selective laser melting, and electron beam melting can be applied to fabricate dental implants, personalized titanium meshes, and denture frameworks. Moreover, it is sometimes required to combine Additive manufacturing technology with milling and other cutting and finishing techniques to ensure that the product is suitable for its final application.

Construction of a Localized and Long-Acting CCN2 Delivery System on Percutaneous Ti Implant Surfaces for Enhanced Soft-Tissue Integration.

Soft-tissue integration (STI) plays an essential role in the long-term success of percutaneous Ti implants since it acts as a biological barrier that protects the soft and hard tissue around implants. Surface modification of Ti implants with drug-release properties to achieve soft-tissue regeneration has been proven to be effective in STI. However, the short-acting effect caused by the uncontrolled drug release of the topical delivery system limits long-term STI enhancement. Herein, a long-acting protein delivery system for Ti implants that involved micro-arc oxidation of Ti surfaces (MAO-Ti) and localized immobilization of cellular communication network factor 2 (CCN2) bearing mesoporous silica nanoparticles (MSNs) on MAO-Ti was prepared, namely, CCN2@MSNs-Ti. The CCN2 release study of CCN2@MSNs-Ti demonstrated a sustained-release profile for 21 days, which was able to maintain long-term stable STI. In addition, in vitro cell behavior evaluation results indicated that CCN2@MSNs-Ti could promote the STI-related biological response of human dermal fibroblasts via the FAK-MAPK pathway. More importantly, the system could effectively enhance STI after 4 weeks and proinflammatory factors in the soft tissue decreased significantly in a rat model of implantation. These results denote that CCN2@MSNs-Ti showed an appealing application prospect for enhanced STI around transcutaneous Ti implants, which would ultimately result in an increased success rate of percutaneous Ti implants.

Asperuloside Prevents Peri-Implantitis via Suppression of NF-κB and ERK1/2 on Rats.

Peri-implantitis is characterized by inflammatory cell infiltration and hyperactivation of the osteoclasts surrounding dental implants which can result in bone resorption and ultimately implant failure. Therefore, coordinating the activity of inflammatory response and bone-resorbing osteoclasts is crucial for the prevention of peri-implantitis. Asperuloside (ASP), an iridoid glycoside, has significant anti-inflammatory activities, suggesting the great potential in attenuating peri-implantitis bone resorption. A ligature-induced peri-implantitis model in the maxilla of rats was established, and the effects of ASP on preventing peri-implantitis were evaluated after four weeks of ligation using micro-CT and histological staining. RT-PCR, western blotting, tartrate-resistant acid phosphatase (TRAP), and immunofluorescent staining were conducted on osteoclasts to confirm the mechanisms of ASP on osteoclastogenesis. The results show that ASP could lead to attenuation of alveolar bone resorption in peri-implantitis by inhibiting osteoclast formation and decreasing pro-inflammatory cytokine levels in vivo. Furthermore, ASP could inhibit osteoclastogenesis by downregulating expression levels of transcription factors nuclear factor of activated T-cell (NFATc1) via restraining the activations of nuclear factor kappa beta (NF-κB) and the phosphorylation of extracellular signal-related kinase 1/2 (ERK1/2). In conclusion, ASP could significantly attenuate bone resorption in peri-implantitis via inhibition of osteoclastogenesis by suppressing NF-κB and ERK1/2 signaling pathways activations.