Virtual surgical planning and data ownership: Navigating the provider-patient-vendor relationship.

The practice of modern craniomaxillofacial surgery has been defined by emergent technologies allowing for the acquisition, storage, utilization, and transfer of massive amounts of sensitive and identifiable patient data. This alone has thrust providers into an unlikely and unprecedented role as the stewards of vast databases of digital information. This data powers the potent surgical tool of virtual surgical planning, a method by which craniomaxillofacial surgeons plan and simulate procedural outcomes in a digital environment. Further complicating this new terrain is the involvement of third-party contractors-a necessary presence in bringing raw data to bear in the office, virtual space, and operating room. The individual privileges and responsibilities of patients, providers, and vendors towards data are situated within the most recent U.S. court rulings and regulations. This paper offers guidance for overseeing the safe and responsible transfer to third-party contractors, and provides suggestions for negotiating the trinary relationship between physicians, their patients, and the vendors offering this transformative technology.

Mouse genetic background influences the dental phenotype.

Dental enamel covers the crown of the vertebrate tooth and is considered to be the hardest tissue in the body. Enamel develops during secretion of an extracellular matrix by ameloblast cells in the tooth germ, prior to eruption of the tooth into the oral cavity. Secreted enamel proteins direct mineralization patterns during the maturation stage of amelogenesis as the tooth prepares to erupt. The amelogenins are the most abundant enamel proteins and are required for normal enamel development. Phenotypic differences were observed between incisors from individual Amelx (amelogenin) null mice that had a mixed 129xC57BL/6J genetic background and between inbred wild-type (WT) mice with different genetic backgrounds (C57BL/6J, C3H/HeJ, FVB/NJ). We hypothesized that this could be due to modifier genes, as human patients with a mutation in an enamel protein gene causing the enamel defect amelogenesis imperfecta (AI) can also have varied appearance of dentitions within a kindred. Enamel density measurements varied for all WT inbred strains midway during incisor development. Enamel thickness varied between some WT strains, and, unexpectedly, dentin density varied extensively between incisors and molars of all WT and Amelx null strains studied. WTFVB/NJ incisors were more similar to those of Amelx null mice than to those of the other WT strains in terms of incisor height/width ratio and pattern of enamel mineralization. Strain-specific differences led to the conclusion that modifier genes may be implicated in determining both normal development and severity of enamel appearance in AI mouse models and may in future studies be related to phenotypic heterogeneity within human AI kindreds reported in the literature.