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J Mol Endocrinol ; 53(1): T35-44, 2014 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-24711646

RESUMEN

Children with inflammatory diseases usually display abnormal growth patterns as well as delayed puberty. This is a result of several factors related to the disease itself, such as malnutrition, hypercortisolism, and elevated levels of pro-inflammatory cytokines. These factors in combination with glucocorticoid treatment contribute to growth retardation during chronic inflammation by systemically affecting the major regulator of growth, the GH/IGF1 axis. However, recent studies have also shown evidence of a direct effect of these factors at the growth plate level. In conditions of chronic inflammation, pro-inflammatory cytokines are upregulated and released into the circulation. The most abundant of these, tumor necrosis factor α, interleukin 1ß (IL1ß), and IL6, are all known to directly act on growth plate cartilage to induce apoptosis and thereby suppress bone growth. Both clinical and experimental studies have shown that growth retardation can partly be rescued when these cytokines are blocked. Therefore, therapy modulating the local actions of these cytokines may be effective for preventing growth failure in patients with chronic inflammatory disorders. In this review, we report the current knowledge of inflammatory cytokines and their role in regulating bone growth.


Asunto(s)
Desarrollo Óseo/fisiología , Citocinas/fisiología , Placa de Crecimiento/crecimiento & desarrollo , Placa de Crecimiento/fisiología , Mediadores de Inflamación/fisiología , Adolescente , Animales , Desarrollo Óseo/efectos de los fármacos , Enfermedades del Desarrollo Óseo/patología , Enfermedades del Desarrollo Óseo/fisiopatología , Enfermedades del Desarrollo Óseo/prevención & control , Niño , Trastornos de la Nutrición del Niño/patología , Trastornos de la Nutrición del Niño/fisiopatología , Citocinas/antagonistas & inhibidores , Glucocorticoides/efectos adversos , Glucocorticoides/fisiología , Placa de Crecimiento/patología , Humanos , Inflamación/patología , Inflamación/fisiopatología , Inflamación/terapia , Mediadores de Inflamación/antagonistas & inhibidores
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