ABSTRACT
Hypovitaminosis D, defined by low serum levels of 25(OH)D, is a recognized worldwide public health problem. The most accepted definition considers that deficiency occurs with serum levels fall below 12 ng/ml of 25(OH)D. Long term vitamin D deficiency results in decreased bone mineralization, secondary hyperparathyroidism, increased cortical bone loss (pathogenesis of osteoporosis and hip fractures), differentiation and division of various cell types, muscle strength, diabetes type 2, blood pressure, etc. Twin- and family-based studies indicate that genetic factors influence serum 25(OH)D levels. Genetic studies have shown single-nucleotide polymorphisms (SNPs) are linked to low serum 25(OH)D concentrations through changes in the activity of the enzymes of the 1α,25(OH)2D metabolic pathway. Carriers of high genetic risk scores would need a h igher amount of vitamin D supplementation to achieve adequate serum 25(OH)D concentrations. Clinicians would not need to indicate studies to identify patients with vitamin D insufficiency of genetic origin. They should instruct their patients on their own care, to control the intake of vitamin D and the serum 25(OH)D levels until the latter are adequate. Overall, the literature reveals that the consequences of hypovitaminosis D on bone health are observed in old and infrequently in young subjects. A probable explanation for the latter is: if the rate of bone remodeling allows it, bone tissue has endogenous (genetics, hormones) and exogenous determinants (diet, physical activity) that may compensate the variables of bone health. The consequences of vitamin D deficit on bone health, has not been completely uncovered.
La hipovitaminosis D, definida por bajos niveles séricos de 25(OH)D (<12 ng/ml), es un reconocido problema de salud pública mundial. La deficiencia de vitamina D a largo plazo resulta en una disminución de la mi neralización ósea, hiperparatiroidismo secundario, pérdida de hueso cortical (patogénesis de la osteoporosis y fracturas de cadera), diferenciación y división de varios tipos de células, fuerza muscular, diabetes tipo 2, pres ión arterial, etc. Estudios genéticos han demostrado que algunos "polimorfismos de un solo nucleótido" (SNP) están relacionados con bajas concentraciones séricas de 25(OH)D a través de reducción en la actividad de las enzimas implicadas en la síntesis de 1α,25(OH)2D. Los médicos no necesitan indicar un estudio genético para identificar a la insuficiencia de vitamina D de causa genética. Bastará con instruir a los pacientes sobre su propio cuidado y controlar la ingesta de vitamina D y los niveles séricos de 25(OH)D hasta que estos últimos sean adecuados. En general, la literatura revela que las consecuencias de la hipovitaminosis D sobre la salud ósea se observan en las personas añosas y con poca frecuencia en sujetos jóvenes. Una explicación probable para esta situación es: si la tasa de remodelación ósea lo permite, el tejido óseo tiene factores endógenos (genéticos, hormonales) y exógenos (dieta, actividad física) que pueden compensar las variables de la salud ósea. Las consecuencias del déficit de vitamina D sobre la salud ósea aún no se conocen completamente.
Subject(s)
Humans , Male , Female , Vitamin D Deficiency/genetics , Bone Remodeling/genetics , Parathyroid Hormone/blood , Vitamin D Deficiency/blood , Bone Remodeling/physiology , Polymorphism, Single NucleotideABSTRACT
Abstract Persistent apical periodontitis (AP) is a situation involving an inflammatory and immune response caused mainly by anaerobic polymicrobial infection of the root canal system and the outcome and follow-up of the root canal treatment has been reported as intimately related to host response. The apical periodontitis repair might be associated with genetic polymorphisms. This study aimed to evaluate the association between HIF1A genetic polymorphisms (rs2301113 and rs2057482) with PAP in Brazilian patients. Subjects with at least 1 year of follow-up after root canal therapy (RCT) were recalled. Sixty-four subjects with signs/symptoms of PAP and 84 subjects with root canal-treated teeth exhibiting healthy perirradicular tissues (healed) were included. Genomic DNA was extracted from saliva and used for HIF1A genotyping by real-time PCR. Genotype and allele frequencies were compared by c2 or Fisher's exact tests and odds ratio was implemented, using Epi Info 3.5.2. All tests were performed with an established alpha of 0.05. There was no association between allele and genotype distribution for HIF1As polymorphisms and PAP (p>0.05). The genetic polymorphisms in HIF1A were not associated with persistent apical periodontitis.
Resumo A periodontite apical persistente (PAP) é uma condição que envolve uma resposta inflamatória e imunológica causada principalmente por infecções polimicrobianas de origem anaeróbia no sistema de canais radiculares, tornando o resultado e o acompanhamento do tratamento do canal radicular intimamente relacionados à resposta do hospedeiro. O reparo da periodontite apical pode estar associado a polimorfismos genéticos. Este estudo teve como objetivo avaliar a associação entre os polimorfismos genéticos do HIF1A (rs2301113 e rs2057482) com a PAP em pacientes brasileiros. Indivíduos com pelo menos 1 ano de acompanhamento após o tratamento do canal radicular (TCR) foram agendados para consulta de acompanhamento. Sessenta e quatro indivíduos com sinais/sintomas de PAP e 84 indivíduos com dentes tratados endodonticamente e tecidos perirradiculares saudáveis (cicatrizados) foram incluídos no presente estudo. O DNA genômico foi extraído da saliva e utilizado para a genotipagem do HIF1A por PCR em tempo real. O genótipo e as frequências alélicas foram comparados por teste c2 ou exato de Fisher e odds-ratio foi implementado por meio do software Epi Info 3.5.2. Todos os testes realizados foram estabelecidos com a=0,05. Não houve associação entre alelo e distribuição genotípica para polimorfismos do HIF1A e PAP (p> 0,05). Os polimorfismos genéticos em HIF1A não foram associados à periodontite apical persistente.