Simulation of postoperative occlusion and direction in autotransplantation of teeth: application of computer-aided design and digital surgical templates.

Autotransplantation of teeth requires optimisation of both occlusion and direction to ensure minimal injury to the dental crown and the alveolar bone. We describe a method that could simulate postoperative occlusion and direction of the donor tooth by using CAD and digital surgical templates, and evaluate the postoperative effect in five patients who had teeth autotransplanted. Computed tomographic data were imported into ProPlan CMF 3.0 software, the donor tooth was simulated to replace the recipient site according to the position of the occlusion and alveolar bone, and a digital template was designed to guide preparation of the socket. A computer-aided, rapid prototyped, tooth was used to match the socket and, finally, an occlusal template was designed to ensure that the donor tooth was in the simulated position. We compared the position of the tooth in the simulation with its postoperative position using ProPlan CMF 3.0 software. In this way it was possible to simulate and guide the donor tooth accurately to the recipient site. At six-month follow up all teeth had survived successfully. Given the efficiency and precision of placement and the success, we conclude that CAD can successfully help to simulate occlusion and direction in autotransplantation of teeth while simplifying the procedure.

Transdifferentiation of neoplastic cells.

Transdifferentiation is a process in which a stable cell's phenotype changes to that of a distinctly different cell type. It occurs during certain physiological processes and leads to transition of tumor cell phenotypes. The latter process includes neoplastic epithelial-epithelial transition, neoplastic epithelial-mesenchymal transition, neoplastic mesenchymal-epithelial transition and transition between non-neural and neural neoplastic cell. This phonomenon is exemplified in some origin-debated tumors, such as carcinosarcoma, pleomorphic adenoma, synovial sarcoma, Ewing's/pPNET, and malignant fibrohistiocytoma. We propose that differentiation disturbance of cancer cells should include not only undifferentiation and dedifferentiation, but also transdifferentiation as well. Tumor cell transdifferentiation may be influenced or determined by cellular genetic instabilities, proliferation and apoptosis, as well as by extracellular matrix and growth factors.

Transdifferentiation in neoplastic development and its pathological implication.

Transdifferentiation is a process in which a cell committed to a particular specialization changes to another quite distinct type. It occurs during embryological development and some pathological processes, and causes the tumor cells to express a phenotype different from that of their normal progenitors. Neoplastic transdifferentiation involves pathogenesis of cancer subtype, transition between neoplastic epithelia and neuroendocrine cell, transition between neoplastic epithelia and mesenchyme, as well as transition between non-neuroectodermal and neuroectodermal cells. We propose that differentiation disturbance of cancer cells should include not only lower-, un-, or de-differentiation, but also transdifferentiation. Tumor cell transdifferentiation results from genetic instabilities. In some type of neoplastic transition, the initiation may be induced by extracellular matrix and growth factors.

The establishment of two cell lines from a mouse uterine cervical carcinoma (U14) and their metastatic phenotype changes.

This paper studies the heterogeneity of metastatic potential of murine cervical carcinoma (U14). Two cell lines, P11-90 and L10-90, were established from a pulmonary metastatic substrain (U14AP11) and a lymphatic metastatic substrain (U14AL10), which were selected from U14 in vivo after 11 and 10 passages, respectively. The biologic differences between the two cell lines are as follows. (1) The cells of the P11-90 line grow more rapidly compared with the L10-90 line. From the 40th passage the medium pH was different. (2) The median number of chromosomes in P11-90 and L10-90 was 72 and 64, respectively; the rates of gap aberration were 88% and 78%, respectively. (3) The number of T lymphocytes and T helper lymphocytes in the peripheral blood from hosts with P11-90 were higher than that of hosts transplanted with L10-90, but the number of B lymphocytes in the latter was larger than that in the former. (4) The metastatic potential of each cell line partially decreased compared to the relative tumor substrain, but their organ preference still remained and the transplant locations, axillary or footpad, had a prominent influence on their metastatic behavior. To observe the effects of metastatic target organs on the metastatic phenotypes of tumor cells, as well as to explore a method for the establishment and maintenance of the metastatic organ preference of tumor cells, conditioned medium (CM) from pulmonary or lymphatic node diploid cells was added to the culture medium of P11-90 and L10-90. Two sublines, P + P11-90 and Ln + L10-90, were thus established. Using stereological methods we found that the majority of P + P11-90 cells became larger and their nuclei also increased in size compared with their parental lines, but the majority of Ln + L10-90 cells became smaller in size, though the nuclei were enlarged. The pulmonary metastatic rate and lymphatic metastatic rate of P + P11-90, as well as the lymphatic metastatic rate of Ln + L10-90, were restored dramatically. The results suggest that by taking advantage of the interaction between tumor cells and the CM of host cells the metastatic potential of tumor cell lines can be maintained in vitro. Our work may offer an experimental model for the manipulation of metastasis of cell lines coming from the same parent strain but with different metastatic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)