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.

Bone repair and regeneration is a dynamic process that involves a complex interplay between the (1) ground substance, (2) cells, and (3) milieu. While each constituent is integral to the final product, it is often helpful to consider each component individually. Therefore, we created a two-part review to examine scaffolds and cells' roles in bone tissue engineering. In Part I, we review the myriad of materials use for in vivo bone engineering. In Part II, we discuss the variety cell types (e.g., osteocytes, osteoblasts, osteoclasts, chondrocytes, mesenchymal stem cells, and vasculogenic cells) that are seeded upon or recruited to these scaffolds. In Part III, we discuss the optimization of the microenvironment. The biochemical processes and sequence of events that guide matrix production, cellular activation, and ossification are vital to developing successful bone tissue engineering strategies and are thus succinctly reviewed herein.

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Therapeutic, III.

We have measured peak plasma concentrations of lignocaine and bupivacaine after dual injection peribulbar block and investigated the influence of adrenaline and hyaluronidase. Twenty-four patients were allocated randomly to one of four groups: (I) local anaesthetic alone (lignocaine 10 mg ml-1-bupivacaine 3.75 mg ml-1); (II) local anaesthetic with adrenaline (5 micrograms ml-1); (III) local anaesthetic with hyaluronidase (75 iu ml-1); or (IV) local anaesthetic with adrenaline and hyaluronidase. Venous plasma concentrations of lignocaine and bupivacaine were measured in 24 patients using gas liquid chromatography before and at 5, 10, 15, 20, 25, 30, 45, 60, 90, 120, 180, 300 and 540 min after completion of the peribulbar injections. Main outcome measures were analysed using two-way analysis of variance. All patients, with one exception, received 10 ml of the local anaesthetic mixture. Overall peak plasma concentrations varied from 230 to 1910 micrograms ml-1 for lignocaine and from 160 to 1090 micrograms ml-1 for bupivacaine. Adrenaline significantly reduced peak plasma concentrations of lignocaine to 57% (P = 0.001) and bupivacaine to 61% (P = 0.004) compared with the nonadrenaline groups. Hyaluronidase had no significant effect on peak plasma concentrations of lignocaine and bupivacaine, which were 90% (P = 0.34) and 100% (P = 0.84) of the non-hyaluronidase groups. The area under the plasma concentration-time curves to 300 min (AUC300) behaved similarly. There was a reduction in AUC300 for lignocaine (P = 0.005) and bupivacaine (P = 0.011) in the adrenaline groups compared with the non-adrenaline groups, in contrast with no significant effects of hyaluronidase on AUC300 for lignocaine (P = 0.14) or bupivacaine (P = 0.53) compared with the non-hyaluronidase groups.

There is insufficient evidence to recommend supplementation of critically ill patients with selenium or ebselen. Trials are required which overcome the defects of the reviewed studies, particularly inadequate size and methodology. This review will be updated when four ongoing trials are completed.

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Unfortunately, many conditions at the core of plastic surgery remain outside the realm of plastic surgery in the opinion of the surveyed public.