Inserción laboral, mercados de trabajo y protección social

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Transmisión de precios en los mercados de maíz y arroz en América Latina

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Impacto económico de un acuerdo parcial de libre comercio entre Colombia y Estados Unidos

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Determinantes económicos del salario mínimo en países pequeños y abiertos: una aplicación para Centroamérica

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Los impactos del ALCA en el MERCOSUR: una revisión analítica de la literatura existente

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Hacia una visión integrada para enfrentar la inestabilidad y el riesgo

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Inserción laboral, mercados de trabajo y protección social

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Hacia una visión integrada para enfrentar la inestabilidad y el riesgo

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Genes expressed in dental enamel development are associated with molar-incisor hypomineralization

Genetic disturbances during dental development influence variation of number and shape of the dentition. In this study, we tested if genetic variation in enamel formation genes is associated with molar-incisor hypomineralization (MIH), also taking into consideration caries experience. DNA samples from 163 cases with MIH and 82 unaffected controls from Turkey, and 71 cases with MIH and 89 unaffected controls from Brazil were studied. Eleven markers in five genes [ameloblastin (AMBN), amelogenin (AMELX), enamelin (ENAM), tuftelin (TUFT1), and tuftelin-interacting protein 11 (TFIP11)] were genotyped by the TaqMan method. Chi-square was used to compare allele and genotype frequencies between cases with MIH and controls. In the Brazilian data, distinct caries experience within the MIH group was also tested for association with genetic variation in enamel formation genes. The ENAM rs3796704 marker was associated with MIH in both populations (Brazil: p = 0.03; OR = 0.28; 95% C.I. = 0.06-1.0; Turkey: p = 1.22e-012; OR = 17.36; 95% C.I. = 5.98-56.78). Associations between TFIP11 (p = 0.02), ENAM (p = 0.00001), and AMELX (p = 0.01) could be seen with caries independent of having MIH or genomic DNA copies of Streptococcus mutans detected by real time PCR in the Brazilian sample. Several genes involved in enamel formation appear to contribute to MIH. © 2013.

Hipomineralización incisivo Y molar: diagnóstico diferencial

Hypomineralized first molar often in combination with hypomineralized incisors (MIH - molar incisor hypomineralization) is a common finding in everyday practice. In this condition, hypomineralized dental enamel is fragile and soft, and it can break easily leading to an exposed dentin, and causing dental sensitivity and progression of caries lesions. The prevalence of MIH range from 3.6 to 25% in North of Europe that consider this condition a public health problem. No conclusive information was reported about the etiologic factors of MIH, however, systemic causes seem to be of importance. Several aetiological factors are mentioned as the cause of this condition and they are frequently associated with complications during pregnancy and childhood diseases during the first three years of life. MIH is frequently misinterpreted as fluorosis, hypoplasia or amelogénesis imperfect, however, this condition presents defined clinical aspects that can distinct it from the other defects.

Study on the origin and nature of the adenomatoid odontogenic tumor by immunohistochemistry

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effect of alendronate on endochondral ossification in mandibular condyles of growing rats

The replacement of the calcified cartilage by bone tissue during the endochondral ossification of the mandibular condyle is dependent of the resorbing activity of osteoclats. After partial resorption, calcified cartilage septa are covered by a primary bone matrix secreted by osteoblasts. Osteoadherin (OSAD) is a small proteoglycan present in bone matrix but absent in cartilage during the endochondral ossification. The aim of this study was to analyze the effect of alendronate, a drug known to inhibit bone resorption by osteoclasts, on the endochondral ossification of the mandibular condyle of young rats, by evaluating the distribution of osteoclasts and the presence of OSAD in the bone matrix deposited. Wistar newborn rats (n = 45) received daily injections of alendronate (n = 27) or sterile saline solution as control (n = 18) from the day of birth until the ages of 4, 14 and 30 days. At the days mentioned, the mandibular condyles were collected and processed for transmission electron microscopy analysis. Specimens were also submitted to tartrate resistant acid phosphatase (TRAP) histochemistry and ultrastructural immunodetection of OSAD. Alendronate treatment did not impede the recruitment and fusion of osteoclasts at the ossification zone during condyle growth, but they presented inactivated phenotype. The trabeculae at the ossification area consisted of cartilage matrix covered by a layer of primary bone matrix that was immunopositive to OSAD at all time points studied. Apparently, alendronate impeded the removal of calcified cartilage and maturation of bone trabeculae in the mandibular ramus, while in controls they occurred normally. These findings highlight for giving attention to the potential side-effects of bisphosphonates administered to young patients once it may represent a risk of disturbing maxillofacial development.

Osteogenesi imperfetta e Dentinogenesi imperfetta Tipo I: correlazioni cliniche e istologiche

Osteogenesis imperffecta (OI) is a heterogeneous group of heritable connetive tissue diseases, quantity and/or qualitative defect in type 1 collagen syntesis; sometimes and in some types it can be associated to dentinogenesis imperfecta (DI), a hereditary disorder in dentin formation that comprises a group of autosomal dominant genetic conditions characterized by abnormal dentine structure affecting either the primary or both the primary and secondary dentitions. Aim: the aim of this study was to assess the correlation between OI and DI from both a clinical and histological point of view, clarifying the structural and ultrastructural changes. Eighteen children (&-15 years aged) with diagnosis of OI were examined for dental alterations referable to DI; for each patient, the OI type (I, III, IV) was recorded. Extracted or normally exfolied teeth were subjected to a histological examination.Results: a total of eleven patients had abnormal discolourations referable to DI: five patients were affected by OI type I, three by OI III, and three patients by OI type IV. The discolourations, yellow/brown or oplaescent grey, could not be related to the different types of OI. Histological exam of primary teeth showed severe pathological change in dentin, structured into four diffeent layers. A collagen defect due to odontoblast dysfunction was theorized to be on the base of the histological changes. Conclusions: there is no correlation between the type of OI and the type of discolouration. The underlying dentinal defect seems to be related to an odontoblast dysfunction.

Prenatal sonographic diagnosis of skeletal dysplasias

OBJECTIVE: To assess the types and numbers of cases, gestational age at specific prenatal diagnosis and diagnostic accuracy of the diagnosis of skeletal dysplasias in a prenatal population from a single tertiary center. METHODS: This was a retrospective database review of type, prenatal and definitive postnatal diagnoses and gestational age at specific prenatal diagnosis of all cases of skeletal dysplasias from a mixed referral and screening population between 1985 and 2007. Prenatal diagnoses were grouped into 'correct ultrasound diagnosis' (complete concordance with postnatal pediatric or pathological findings) or 'partially correct ultrasound diagnosis' (skeletal dysplasias found postnatally to be a different one from that diagnosed prenatally). RESULTS: We included 178 fetuses in this study, of which 176 had a prenatal ultrasound diagnosis of 'skeletal dysplasia'. In 160 cases the prenatal diagnosis of a skeletal dysplasia was confirmed; two cases with skeletal dysplasias identified postnatally had not been diagnosed prenatally, giving 162 fetuses with skeletal dysplasias in total. There were 23 different classifiable types of skeletal dysplasia. The specific diagnoses based on prenatal ultrasound examination alone were correct in 110/162 (67.9%) cases and partially correct in 50/162 (30.9%) cases, (160/162 overall, 98.8%). In 16 cases, skeletal dysplasia was diagnosed prenatally, but was not confirmed postnatally (n = 12 false positives) or the case was lost to follow-up (n = 4). The following skeletal dysplasias were recorded: thanatophoric dysplasia (35 diagnosed correctly prenatally of 40 overall), osteogenesis imperfecta (lethal and non-lethal, 31/35), short-rib dysplasias (5/10), chondroectodermal dysplasia Ellis-van Creveld (4/9), achondroplasia (7/9), achondrogenesis (7/8), campomelic dysplasia (6/8), asphyxiating thoracic dysplasia Jeune (3/7), hypochondrogenesis (1/6), diastrophic dysplasia (2/5), chondrodysplasia punctata (2/2), hypophosphatasia (0/2) as well as a further 7/21 cases with rare or unclassifiable skeletal dysplasias. CONCLUSION: Prenatal diagnosis of skeletal dysplasias can present a considerable diagnostic challenge. However, a meticulous sonographic examination yields high overall detection. In the two most common disorders, thanatophoric dysplasia and osteogenesis imperfecta (25% and 22% of all cases, respectively), typical sonomorphology accounts for the high rates of completely correct prenatal diagnosis (88% and 89%, respectively) at the first diagnostic examination.

Familial occurrence and heritable connective tissue disorders in cervical artery dissection

OBJECTIVE In a large series of patients with cervical artery dissection (CeAD), a major cause of ischemic stroke in young and middle-aged adults, we aimed to examine frequencies and correlates of family history of CeAD and of inherited connective tissue disorders. METHODS We combined data from 2 large international multicenter cohorts of consecutive patients with CeAD in 23 neurologic departments participating in the CADISP-plus consortium, following a standardized protocol. Frequency of reported family history of CeAD and of inherited connective tissue disorders was assessed. Putative risk factors, baseline features, and 3-month outcome were compared between groups. RESULTS Among 1,934 consecutive patients with CeAD, 20 patients (1.0%, 95% confidence interval: 0.6%-1.5%) from 17 families (0.9%, 0.5%-1.3%) had a family history of CeAD. Family history of CeAD was significantly more frequent in patients with carotid location of the dissection and elevated cholesterol levels. Two patients without a family history of CeAD had vascular Ehlers-Danlos syndrome with a mutation in COL3A1. This diagnosis was suspected in 2 additional patients, but COL3A1 sequencing was negative. Two patients were diagnosed with classic and hypermobile Ehlers-Danlos syndrome, one patient with Marfan syndrome, and one with osteogenesis imperfecta, based on clinical criteria only. CONCLUSIONS In this largest series of patients with CeAD to date, family history of symptomatic CeAD was rare and inherited connective tissue disorders seemed exceptional. This finding supports the notion that CeAD is a multifactorial disease in the vast majority of cases.