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Biomechanical and histological behavior of zirconia implants: an experiment in the rat
Kohal, Ralf J.,Wolkewitz, Martin,Hinze, Marc,Han, Jung-Suk,Bä,chle, Maria,Butz, Frank Blackwell Publishing Ltd 2009 Clinical oral implants research Vol.20 No.4
<P>Abstract</P><P>Objective</P><P>This study aimed at evaluating the integration of zirconia implants in a rat femur model.</P><P>Material and methods</P><P>Zirconia implants with two distinct surface topographies were compared with titanium implants with similar topographies. Titanium and zirconia implants were placed into the femurs of 42 male Sprague–Dawley rats. Four groups of implants were utilized: machined zirconia implants, zirconia implants with a rough surface, machined titanium implants, and titanium implants with an electrochemically roughened surface. After a healing period of 28 days, the load-bearing capacity between the bone and the implant surface was evaluated by a push-in test. Additionally, after a healing period of 14 and 28 days, respectively, bone tissue specimens containing the implants were processed and histologically analyzed.</P><P>Results</P><P>The mean mineralized bone-to-implant contact showed the highest values after 14 and 28 days for the rough surfaces (titanium: 36%/45%; zirconia: 45%/59%). Also, the push-in test showed higher values for the textured implant surfaces, with no statistical significance between titanium (34 N) and zirconia (45.8 N).</P><P>Conclusions</P><P>Within the limits of the animal investigation presented, it was concluded that all tested zirconia and titanium implant surfaces were biocompatible and osseoconductive. The presented surface modification of zirconia implants showed no difference regarding the histological and biomechanical results compared with an established electrochemically modified titanium implant surface.</P>
Lu, Hao,Galeano, Maria C Rondó,n,Ott, Elisabeth,Kaeslin, Geraldine,Kausalya, P Jaya,Kramer, Carina,Ortiz-Brü,chle, Nadina,Hilger, Nadescha,Metzis, Vicki,Hiersche, Milan,Tay, Shang Yew,Tunnin Nature Pub. Co 2017 Nature genetics Vol.49 No.7
<P>Autosomal recessive polycystic kidney disease (ARPKD), usually considered to be a genetically homogeneous disease caused by mutations in PKHD1, has been associated with ciliary dysfunction. Here, we describe mutations in DZIP1L, which encodes DAZ interacting protein 1-like, in patients with ARPKD. We further validated these findings through loss-of-function studies in mice and zebrafish. DZIP1L localizes to centrioles and to the distal ends of basal bodies, and interacts with septin2, a protein implicated in maintenance of the periciliary diffusion barrier at the ciliary transition zone. In agreement with a defect in the diffusion barrier, we found that the ciliary-membrane translocation of the PKD proteins polycystin-1 and polycystin-2 is compromised in DZIP1L-mutant cells. Together, these data provide what is, to our knowledge, the first conclusive evidence that ARPKD is not a homogeneous disorder and further establish DZIP1L as a second gene involved in ARPKD pathogenesis.</P>