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Three-dimensional (3D) printing is based on additive technology in which layers of materials are gradually placed to create 3D objects. The world of 3D printing is a rapidly evolving field in the medical industry as well as in most sectors of our lives. In this report we present current technological possibilities for 3D printing in the surgical field. There are different 3D printing modalities and much confusion among clinicians regarding the differences between them. Three-dimensional printing technologies can be classified based on the basic material used: solid, liquid, and powder. We describe the main printing methods from each modality and present their advantages while focusing on their applications in different fields of surgery, starting from 3D printing of models for preoperative planning up to patient-specific implants (PSI). We present the workflow of 3D printing for the different applications and our experience in 3D printing surgical guides as well as PSI. We include examples of 3D planning as well as clinical and radiological imaging of cases. Three-dimensional printing of models for preoperative planning enhances the 3D perception of the planned operation and allows for preadaptation of surgical instruments, thus shortening operation duration and improving precision. Three-dimensional printed PSI allow for accurate reconstruction of anatomic relations as well as efficiently restoring function. The application of PSI is expanding rapidly, and we will see many more innovative treatment modalities in the near future based on this technology.

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The amelogenins comprise 90% of the developing extracellular enamel matrix proteins and play a major role in the biomineralization and structural organization of enamel. Amelogenins were also detected, in smaller amounts, in postnatal calcifying mesenchymal tissues, and in several nonmineralizing tissues including brain. Low molecular mass amelogenin isoforms were suggested to have signaling activity; to produce ectopically chondrogenic and osteogenic‐like tissue and to affect mouse tooth germ differentiation in vitro. Recently, some amelogenin isoforms were found to bind to the cell surface receptors; LAMP‐1, LAMP‐2 and CD63, and subsequently localize to the perinuclear region of the cell. The recombinant amelogenin protein (rHAM+) alone brought about regeneration of the tooth supporting tissues: cementum, periodontal ligament and alveolar bone, in the dog model, through recruitment of progenitor cells and mesenchymal stem cells.We show that amelogenin is expressed in various tissues of the developing mouse embryonic cranio‐facial complex such as brain, eye, ganglia, peripheral nerve trunks, cartilage and bone, and is already expressed at E10.5 in the brain and eye, long before the initiation of tooth formation. Amelogenin protein expression was detected in the tooth germ (dental lamina) already at E13.5, much earlier than previously reported (E19). Application of amelogenin (rHAM+) beads together with DiI, on E13.5 and E14.5 embryonic mandibular mesenchyme and on embryonic tooth germ, revealed recruitment of mesenchymal cells. The present results indicate that amelogenin has an important role in many tissues of the cranio‐facial complex during mouse embryonic development and differentiation, and might be a multifunctional protein. J. Exp. Zool. (Mol. Dev. Evol.) 312B:445–457, 2009. © 2008 Wiley‐Liss, Inc.

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The tuftelin protein isoforms undergo post-translation modifications, and are ubiquitously expressed in various tissues in embryos, adults, and tumors. Developmental and pathological studies suggested an apparent correlation between oxygen deprivation and tuftelin expression. The aim of the study was therefore to investigate the effect of a pathological insult (hypoxia) and a physiological growth factor (NGF), which antagonistically regulate HIF1 expression, on tuftelin expression using the neuronal PC12 cell model. In the present study, we first demonstrated the expression of tuftelin in PC12 cells, providing an experimental system to investigate the pathophysiological role of tuftelin. Furthermore, we demonstrated the induction of tuftelin during hypoxia by oxygen deprivation and during chemical hypoxia by cobalt chloride. Down-regulation of HIF1α mRNA blocked hypoxia-induced HIF1α expression, and reduced by 89% hypoxia-induced tuftelin expression. In mice, intraperitoneal injection of cobalt chloride significantly induced tuftelin mRNA and protein expression in the brain. During NGF-mediated PC12 differentiation, tuftelin expression was significantly induced in correlation with neurite outgrowth. This induction was partially blocked by K252a, a selective antagonist of the NGF receptor TrkA, indicating the involvement of the TrkA-signaling pathways in tuftelin induction by NGF. Revealing the physiological role of tuftelin will clarify mechanisms related to the "hypoxic genome," and NGF-induced neurotrophic and angiogenic effects.

Frontal sinus fractures account for 2% to 15% of maxillofacial injuries. Up to 66% to 87% of the patients with frontal sinus fractures experience associated facial fractures. The majority of classifications used today categorize frontal sinus fractures depending on the integrity of the anterior table, posterior table, and the nasofrontal outflow. A retrospective study was performed, which included 24 patients diagnosed with frontal sinus fractures. Treatment in all patients consisted of open reduction and bone fixation. We analyzed population variables, injury etiology, fracture site, associated craniofacial injuries, surgical technique employed, handling of the nasofrontal duct, and postoperative complications. The most frequent etiology was falling accidents. Fifty-eight percent of the fractures involved both the anterior and posterior tables. Sixty-six percent experienced associated facial fractures. Fifty percent of frontal sinus fractures were treated by open reduction internal fixation as the only treatment, 33.3% underwent sinus obliteration, and 16.6% were treated with cranialization. Frontal sinus fractures resulting from high-energy impact exhibited additional facial bone fractures in 100% of the cases, whereas fractures following low-energy impact showed involvement of additional facial fractures in only 27% of the cases. In this report, we suggest a modification to the anteroposterior classification of frontal sinus fractures. In addition to the involvement of the anterior and posterior walls and the degree of dislocation, high and low energy impact can direct us to the involvement of additional facial fractures and influence the surgical strategy.

ADO offers marked vertical ridge augmentation with simultaneous soft tissue expansion and stable results. ADO diminishes the need for autogenous bone graft, thus sparing donor-site morbidity. ADO of the deficient posterior mandibular alveolar ridge is useful in moderate to severe bony deficiencies and allows for adequate bone formation, which allows implant insertion.