RESUMO
Osseointegration of dental, craniofacial, and orthopedic implants is critical for their long-term success. Multifunctional surface treatment of implants was found to significantly improve cell adhesion and induce osteogenic differentiation of dental-derived stem cells in vitro. Moreover, local and sustained release of antibiotics via nanolayers from the surface of implants can present unparalleled therapeutic benefits in implant dentistry. Here, we present a layer-by-layer surface treatment of titanium implants capable of incorporating BMP-2-mimicking short peptides and gentamicin to improve their osseointegration and antibacterial features. Additionally, instead of conventional surface treatments, we employed polydopamine coating before layer-by-layer assembly to initiate the formation of the nanolayers on rough titanium surfaces. Cytocompatibility analysis demonstrated that modifying the titanium implant surface with layer-by-layer assembly did not have adverse effects on cellular viability. The implemented nanoscale coating provided sustained release of osteoinductive peptides with an antibacterial drug. The surface-functionalized implants showed successful osteogenic differentiation of periodontal ligament stem cells and antimicrobial activity in vitro and increased osseointegration in a rodent animal model 4 wk postsurgery as compared with untreated implants. Altogether, our in vitro and in vivo studies suggest that this approach can be extended to other dental and orthopedic implants since this surface functionalization showed improved osseointegration and an enhanced success rate.
Assuntos
Implantes Dentários , Osteogênese , Animais , Antibacterianos/farmacologia , Materiais Revestidos Biocompatíveis/farmacologia , Osseointegração , Propriedades de Superfície , TitânioRESUMO
Multiple osteochondromatosis (MO), or EXT1/EXT2-CDG, is an autosomal dominant O-linked glycosylation disorder characterized by the formation of multiple cartilage-capped tumors (osteochondromas). In contrast, solitary osteochondroma (SO) is a non-hereditary condition. EXT1 and EXT2, are tumor suppressor genes that encode glycosyltransferases involved in heparan sulfate elongation. We present the clinical and molecular analysis of 33 unrelated Latin American patients (27 MO and 6 SO). Sixty-three percent of all MO cases presented severe phenotype and two malignant transformations to chondrosarcoma (7%). We found the mutant allele in 78% of MO patients. Ten mutations were novel. The disease-causing mutations remained unknown in 22% of the MO patients and in all SO patients. No second mutational hit was detected in the DNA of the secondary chondrosarcoma from a patient who carried a nonsense EXT1 mutation. Neither EXT1 nor EXT2 protein could be detected in this sample. This is the first Latin American research program on EXT1/EXT2-CDG.
Assuntos
Exostose Múltipla Hereditária/genética , Genômica/métodos , Mutação/genética , N-Acetilglucosaminiltransferases/genética , Estudos de Casos e Controles , Pré-Escolar , Estudos de Coortes , Análise Mutacional de DNA , Feminino , Humanos , América Latina/etnologia , Perda de Heterozigosidade , Masculino , Regiões Promotoras Genéticas , Estados UnidosRESUMO
Multiple osteochondromas is an autosomal dominant skeletal disorder characterized by the formation of multiple cartilage-capped tumours. Two causal genes have been identified, EXT1 and EXT2, which account for 65% and 30% of cases, respectively. We have undertaken a mutation analysis of the EXT1 and EXT2 genes in 39 unrelated Spanish patients, most of them with moderate phenotype, and looked for genotype-phenotype correlations. We found the mutant allele in 37 patients, 29 in EXT1 and 8 in EXT2. Five of the EXT1 mutations were deletions identified by MLPA. Two cases of mosaicism were documented. We detected a lower number of exostoses in patients with missense mutation versus other kinds of mutations. In conclusion, we found a mutation in EXT1 or in EXT2 in 95% of the Spanish patients. Eighteen of the mutations were novel.
Assuntos
Exostose Múltipla Hereditária/genética , Mutação , N-Acetilglucosaminiltransferases/genética , População Branca/genética , Adolescente , Adulto , Criança , Éxons , Estudos de Associação Genética , Humanos , Íntrons , Taxa de Mutação , Linhagem , Espanha , Adulto JovemAssuntos
Anestesia , Tratamento de Emergência , Intubação Intratraqueal , Traqueostomia , Idoso , Humanos , MasculinoRESUMO
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Assuntos
Masculino , Idoso , Humanos , Anestesia , Tratamento de Emergência , Intubação Intratraqueal , TraqueostomiaRESUMO
BACKGROUND: There is confusion in the literature about the potential effect of maternal glucose levels on the fetal heart rate (FHR) cardiotocographic interpretation. STUDY DESIGN: prospective clinical descriptive study. SUBJECTS: 21 pregnant women with diabetes mellitus, 23 women with gestational diabetes and 18 healthy non-diabetic pregnant volunteers (control group). TREATMENT: maternal capillary glucose measurement and objective FHR analysis (Oxford System 8002) pre- and 1 h post-meal. STATISTICAL ANALYSIS: descriptive statistics. Student t-tests and Pearson correlation studies. RESULTS: Maternal capillary glucose levels ranged between 2.7-10.5 mmol/l pre-meal and 4.2 14.8 mmol/l post-meal. The differences between objective FHR parameters pre- and postmeal were not significant in any of the groups of women studied. No correlation was found between prandial glycemic and FHR changes. Women with optimal and suboptimal glycemic control exhibited similar objective FHR parameters pre- and post-meal. Women with gestational diabetes showed similar prandial cardiotocographic changes irrespective of whether they were on insulin therapy or on hypoglycemic diet only. CONCLUSIONS: Objective FHR parameters are unaffected by prandial glycemic changes over a wide range of maternal glucose levels. Timing the non-stress test in relation to the meals seems irrelevant in clinical practice.