Próteses parciais fixas reforçadas por fibras: um estudo clínico retrospectivo preliminar

The aim of this study was to evaluate the clinical performance (retention rate) of fiber-reinforced composite fixed partial dentures (FPDs). Polyethylene fiber (Ribbond®) was used combined with restorative composite during FPDs fabrication. FPDs were placed in thirteen patients in a private clinic. Nineteen FPDs were evaluated. The prosthetic space was filled with only one pontic using extracted teeth (2 cases), acrylic resin teeth (11 cases), or with composite resin (6 cases), combined with Polyethylene fiber. The clinical criterion used was based on retention rate of FPDs. If FPDs were in function in the mouth at the time of examination without previous repair they were classified as Complete Survival (CS) restorations. A classification of Survival with Rebonding (SR) was assigned in the event of an adhesive failure, but after rebonding the FPD still remained under evaluation. Treatment was classified as a Failure (F) if the FPD restoration was lost. The time of evaluation was 41.15 months (±15.13). The FPDs evaluated were retained (CS=94.75%), and no failure was found except for in one situation which required rebonding (SR=5.25%). According to the survival estimation method of Kaplan-Meyer the mean survival time was 42.3 months. At the time of evaluation investigated, polyethylene-reinforced FPDs showed a favorable retention rate in preliminary data.O objetivo deste estudo foi avaliar a performance clínica (percentagem de retenção) de próteses parciais fixas reforçadas por fibras. Fibras de polietileno (Ribbond®) foram usadas em combinação com resina composta durante a confecção das próteses. Os tratamentos foram realizadas em 13 pacientes, em uma clínica privada., sendo que 19 próteses foram reavaliadas. O espaço protético era preenchido com um pôntico usando o próprio dente extraído (2 casos), dentes de acrílico (11 casos) ou confeccionados com resina composta (6 casos), em todas as situações eram empregadas fibras de polietileno. Os critérios clínicos usados foram baseados na percentagem de retenção das próteses parciais fixas. As próteses que estavam em função no momento da avaliação, sem nunca necessitar de qualquer reparo prévio, foram classificadas como sobrevivência completa (SC). A classificação de sobrevivência com nova colagem (SR) foi utilizada para os casos de falha adesiva, com posterior cimentação da peça, a qual permanecia em função. O tratamento era classificado como falha (F) quando a restauração era perdida. O tempo médio de avaliação foi de 41,15 meses (±15,13). Nenhum caso de falha foi detectado, em apenas um caso houve falha adesiva com posterior colagem da peça (SR=5,25%) e em 94.75% dos casos as próteses permaneciam em função.. De acordo com o método de sobrevida de Kaplan-Meyer o tempo médio de sobrevida foi de 42,3 meses. As próteses parciais fixas reforçadas por fibras mostraram uma percentagem de retenção favorável neste estudo preliminar

Overlapping spectra of SMAD4 mutations in juvenile polyposis (JP) and JP-HHT syndrome.

Juvenile polyposis (JP) and hereditary hemorrhagic telangiectasia (HHT) are clinically distinct diseases caused by mutations in SMAD4 and BMPR1A (for JP) and endoglin and ALK1 (for HHT). Recently, a combined syndrome of JP-HHT was described that is also caused by mutations in SMAD4. Although both JP and JP-HHT are caused by SMAD4 mutations, a possible genotype:phenotype correlation was noted as all of the SMAD4 mutations in the JP-HHT patients were clustered in the COOH-terminal MH2 domain of the protein. If valid, this correlation would provide a molecular explanation for the phenotypic differences, as well as a pre-symptomatic diagnostic test to distinguish patients at risk for the overlapping but different clinical features of the disorders. In this study, we collected 19 new JP-HHT patients from which we identified 15 additional SMAD4 mutations. We also reviewed the literature for other reports of JP patients with HHT symptoms with confirmed SMAD4 mutations. Our combined results show that although the SMAD4 mutations in JP-HHT patients do show a tendency to cluster in the MH2 domain, mutations in other parts of the gene also cause the combined syndrome. Thus, any mutation in SMAD4 can cause JP-HHT. Any JP patient with a SMAD4 mutation is, therefore, at risk for the visceral manifestations of HHT and any HHT patient with SMAD4 mutation is at risk for early onset gastrointestinal cancer. In conclusion, a patient who tests positive for any SMAD4 mutation must be considered at risk for the combined syndrome of JP-HHT and monitored accordingly