A 3D-printed Lateral Skull Base Implant for Repair of Tegmen Defects: A Case Series.

OBJECTIVE: To determine the feasibility of a patient-specific, three-dimensionally (3D)-printed reconstruction plate for repair of lateral skull base defects. STUDY DESIGN: Prospective case series and cadaveric study. SETTING: A university-based, tertiary care hospital. PATIENTS: Three patients with lateral skull base defects and five cadavers. MAIN OUTCOME MEASURE(S): Caliper gauge fit testing was performed in the cadaver temporal bones to determine the fit of the tegmen plate in engaging the tegmen defect. Additionally, three patients underwent standard of care reconstruction of their middle fossa floor using autografts or allografts. Temporary plate insertion during standard operative repair was performed to gauge feasibility and fit. Operative time required for standard grafting compared with placement of the tegmen plate was examined. RESULTS: Real-time, intraoperative placement of the tegmen plate in our patients under 1 minute compared with nearly 60 minutes for standard surgical repair. Tegmen plates covered the defects and locked into place from contour matching without impinging on critical structures. Fit testing revealed flush-fitting plates to the cadaveric temporal bone surface with all gaps less than 500 µm. CONCLUSIONS: Computer modeling and 3D printing can design custom fitted tegmen reconstruction plates for temporal bone defects. Versatility in prefabrication and 3D modeling shows potential in allowing the construct to avoid critical structures and adequately cover defects with high precision to the tegmen surface.

Secondary lymphoid organ fibroblastic reticular cells mediate trans-infection of HIV-1 via CD44-hyaluronan interactions.

Fibroblastic reticular cells (FRCs) are stromal cells in secondary lymphoid organs, the major sites for HIV-1 infection of CD4+ T cells. Although FRCs regulate T cell survival, proliferation, and migration, whether they play any role in HIV-1 spread has not been studied. Here, we show that FRCs enhance HIV-1 spread via trans-infection in which FRCs capture HIV-1 and facilitate infection of T cells that come into contact with FRCs. FRCs mediate trans-infection in both two- and three-dimensional culture systems and in a manner dependent on the virus producer cells. This producer cell dependence, which was also observed for virus spread in secondary lymphoid tissues ex vivo, is accounted for by CD44 incorporated into virus particles and hyaluronan bound to such CD44 molecules. This virus-associated hyaluronan interacts with CD44 expressed on FRCs, thereby promoting virus capture by FRCs. Overall, our results reveal a novel role for FRCs in promoting HIV-1 spread.