Laboratory efficiency of additive manufacturing for removable denture frameworks: A literature-based review.

The purpose of this literature review was to verify the laboratory efficiency of additive manufacturing (AM) systems for removable partial denture (RPD) frameworks. All available relevant articles in English published from 1990 to 2020 were found by searching online databases and by hand research. A total of 17 articles dealt with the surface roughness, fitness accuracy, and retentive forces of AM frameworks. The surface roughness of AM was inferior to that of casting and milling. Whether conventional cast or AM RPD frameworks had superior fitness accuracy could not be clarified. As compared with casting and AM, milling enabled the fabrication of RPD clasps with comparable or better fitness accuracy. Over time, AM clasps had retentive force values of superior consistency as compared with those of conventional cast clasps. Clasps fabricated by repeated laser sintering and high-speed milling could obtain smoother surfaces and more suitable retention than those of AM clasps.

RAGE, receptor of advanced glycation endoproducts, negatively regulates chondrocytes differentiation.

RAGE, receptor for advanced glycation endoproducts (AGE), has been characterized as an activator of osteoclastgenesis. However, whether RAGE directly regulates chondrocyte proliferation and differentiation is unclear. Here, we show that RAGE has an inhibitory role in chondrocyte differentiation. RAGE expression was observed in chondrocytes from the prehypertrophic to hypertrophic regions. In cultured cells, overexpression of RAGE or dominant-negative-RAGE (DN-RAGE) demonstrated that RAGE inhibited cartilaginous matrix production, while DN-RAGE promoted production. Additionally, RAGE regulated Ihh and Col10a1 negatively but upregulated PTHrP receptor. Ihh promoter analysis and real-time PCR analysis suggested that downregulation of Cdxs was the key for RAGE-induced inhibition of chondrocyte differentiation. Overexpression of the NF-κB inhibitor I-κB-SR inhibited RAGE-induced NF-κB activation, but did not influence inhibition of cartilaginous matrix production by RAGE. The inhibitory action of RAGE was restored by the Rho family GTPases inhibitor Toxin B. Furthermore, inhibitory action on Ihh, Col10a1 and Cdxs was reproduced by constitutively active forms, L63RhoA, L61Rac, and L61Cdc42, but not by I-κB-SR. Cdx1 induced Ihh and Col10a1 expressions and directly interacted with Ihh promoter. Retinoic acid (RA) partially rescued the inhibitory action of RAGE. These data combined suggests that RAGE negatively regulates chondrocyte differentiation at the prehypertrophic stage by modulating NF-κB-independent and Rho family GTPases-dependent mechanisms.