Obturator prostheses following palatal resection: clinical cases.

Malignant tumours of the upper gum and hard palate account for 1-5% of malignant neoplasms of the oral cavity; two thirds of the lesions which involve these areas are squamous cell carcinomas. Most of these carcinomas are diagnosed late, when they invade the underlying bone. The procedures of choice for removal are: alveolectomy, palatectomy, maxillectomy, which may be total or partial. Surgical reconstruction of the defect may be carried out using a wide range of microvascularized flaps: osteomuscolocutaneous of the internal iliac crest, an osteocutaneous flap of the fibula or scapula, fascia, or osteocutaneous radial flap, or a pedicled flap of temporal muscle. These flaps are supported by single or multiple obturator prostheses. Rehabilitation via palatal obturators is preferred in patients with a poor prognosis or in weak condition. Rehabilitation aims to: restore the separation between the oral and nasal cavities, enable the patient to swallow, maintain or provide mastication, sufficient occlusion and mandibular support, support the soft facial tissues, re-establish speech and restore an aesthetically pleasing smile. Hence, it is crucial to work in close cooperation with the staff who makes the prosthesis and who evaluates the case when the surgery is planned and obtains the necessary gnatological, anatomical and functional information. Thereafter, during the surgical stage, for the immediate obturators, or in the successive days, for the temporary obturators, work is devoted to making the prostheses. In this regard, the Odonto-prostheses Service of the Stomatological Clinic does not follow a rigid protocol but materials and techniques are selected on a personal basis, according to the features of each individual clinical case. Mobile rehabilitative systems are the systems of choice, both of which related to the traditional concepts of retention and stability and systems of self-stabilizing prostheses according to J. Dichamp, albeit modified in materials, limiting, when possible the use of prostheses which are fixed on natural teeth, on appliances or combined.

The acquisition of an insulin-secreting phenotype by HGF-treated rat pancreatic ductal cells (ARIP) is associated with the development of susceptibility to cytokine-induced apoptosis.

The elucidation of mechanisms regulating the regeneration and survival of pancreatic beta cells has fundamental implications in the cell therapy of type 1 diabetes. The present study had the following three aims: 1. to investigate whether pancreatic ductal epithelial cells can be induced to differentiate into insulin-producing cells by exposing them to hepatocyte growth factor (HGF); 2. to characterize some of the molecular events leading to their differentiation toward a beta-cell-like phenotype; 3. to evaluate the susceptibility of newly differentiated insulin-secreting cells to cytokine-induced apoptosis, a mechanism of beta-cell destruction occurring in type 1 diabetes. We demonstrated that HGF-treated rat pancreatic ductal cell line (ARIP) cells acquired the capability to transcribe the insulin gene and translate its counterpart protein. HGF-treated cells also exhibited a glucose-dependent capability to secrete insulin into the cultured medium. Expression analysis of some of the genes regulating pancreatic beta-cell differentiation revealed a time-dependent transcription of neurogenin-3 and Neuro-D in response to HGF. Finally, we determined the susceptibility to proinflammatory cytokine (PTh1)-induced apoptosis by incubating HGF-treated and untreated ARIP cells with a cocktail of interleukin-1 beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). Such treatment induced apoptotic death, as determined by the TUNEL technique, in about 40% of HGF-treated, insulin-secreting ARIP cells, while untreated ARIP cells were resistant to PTh1-induced apoptosis. In conclusion, we showed that HGF promotes the differentiation of ARIP cells into pancreatic beta-cell-like cells, and that the differentiation toward an insulin-secreting phenotype is associated with the appearance of susceptibility to cytokine-induced apoptosis.