The goal of this article was to illustrate the ease in which virtual surgery and computer-aided design and manufacturing can be used by the craniomaxillofacial surgeon to create tremendously accurate postoperative results and provide confidence with even the most complex three-dimensional bony reconstructions. With advancements in software technology and three-dimensional printing, our ability to plan and execute precise bony reconstruction has become a reality. With this technology, guides can be made to ensure exact bony repositioning or replacement. These guides can help guide cutting of the bone and can act as splints to precisely reposition the bone and direct plate placement. With use of these computer-aided design and manufacturing guides and the addition of guidance technology, the position of the bone can be guaranteed intraoperatively. We review our unique and advanced method in approaching some of these problems and illustrate the application of these techniques in mandibular reconstruction, orthognathic surgery, maxillofacial trauma, and temporomandibular joint reconstruction. This technology continues to evolve, and our indications for its application continue to grow. This article represents only a small portion of the types of cases in which these techniques have already been applied.

Bony defects in the craniomaxillofacial skeleton remain a major and challenging health concern. Surgeons have been trying for centuries to restore functionality and aesthetic appearance using autografts, allografts, and even xenografts without entirely satisfactory results. As a result, physicians, scientists, and engineers have been trying for the past few decades to develop new techniques to improve bone growth and bone healing. In this review, the authors summarize the advantages and limitations of current animal models; describe current materials used as scaffolds, cell-based, and protein-based therapies; and lastly highlight areas for future investigation. The purpose of this review is to highlight the major scaffold-, cell-, and protein-based preclinical tools that are currently being developed to repair cranial defects.

The tear trough and lid/cheek junction are primarily explained by superficial (subcutaneous) anatomical features. Atrophy of skin and fat is the most likely explanation for age-related visibility of these landmarks. "Descent" of this region with age is unlikely (the structures are fixed to bone). Bulging orbital fat accentuates these landmarks. Interventions must extend significantly below the infraorbital rim. Fat or synthetic filler may be best placed in the intraorbicularis plane (tear trough) and in the suborbicularis plane (lid/cheek junction).

Therapeutic, IV.

No abstract

OBJECTIVEProgenitor cells (PCs) contribute to postnatal neovascularization and tissue repair. Here, we explore the mechanism contributing to decreased diabetic circulating PC number and propose a novel treatment to restore circulating PC number, peripheral neovascularization, and tissue healing.RESEARCH DESIGN AND METHODSCutaneous wounds were created on wild-type (C57BL/J6) and diabetic (Leprdb/db) mice. Blood and bone marrow PCs were collected at multiple time points.RESULTSSignificantly delayed wound closure in diabetic animals was associated with diminished circulating PC number (1.9-fold increase vs. 7.6-fold increase in lin−/sca-1+/ckit+ in wild-type mice; P < 0.01), despite adequate numbers of PCs in the bone marrow at baseline (14.4 ± 3.2% lin−/ckit+/sca1+ vs. 13.5 ± 2.8% in wild-type). Normal bone marrow PC mobilization in response to peripheral wounding occurred after a necessary switch in bone marrow stromal cell-derived factor-1α (SDF-1α) expression (40% reduction, P < 0.01). In contrast, a failed switch mechanism in diabetic bone marrow SDF-1α expression (2.8% reduction) resulted in impaired PC mobilization. Restoring the bone marrow SDF-1α switch (54% reduction, P < 0.01) with plerixafor (Mozobil, formerly known as AMD3100) increased circulating diabetic PC numbers (6.8 ± 2.0-fold increase in lin−/ckit+, P < 0.05) and significantly improved diabetic wound closure compared with sham-treated controls (32.9 ± 5.0% vs. 11.9 ± 3% at day 7, P > 0.05; 73.0 ± 6.4% vs. 36.5 ± 7% at day 14, P < 0.05; and 88.0 ± 5.7% vs. 66.7 ± 5% at day 21, P > 0.05, respectively).CONCLUSIONSSuccessful ischemia-induced bone marrow PC mobilization is mediated by a switch in bone marrow SDF-1α levels. In diabetes, this switch fails to occur. Plerixafor represents a potential therapeutic agent for improving ischemia-mediated pathology associated with diabetes by reducing bone marrow SDF-1α, restoring normal PC mobilization and tissue healing.

No abstract

Therapeutic, II.