Thyroid function during catch-up growth: A focus on the growth plate

Abstract

Thyroid hormone (TH) has long been recognised as a potent regulator of skeletal maturation at the growth plate. The action of TH interfaces not only with major regulatory pathways governing proliferation and differentiation of chondrocytes at the growth plate but also with mechanisms controlling the extracellular matrix surrounding these cells. In addition, TH contributes to regulation of catch-up growth in children with other endocrine disorders, such as those with GH deficiency who are receiving rhGH treatment. Hypothyroidism in childhood is almost invariably associated with growth failure. Usually, after T4 replacement therapy is initiated, specific growth abnormalities resolve and a period of catch-up growth ensues. Some authors have shown that incomplete catch-up growth often occurs in children in whom T4 replacement therapy was initiated after a long period of untreated hypothyroidism or during pubertal development. Recent data seem to support the hypothesis that catch-up growth is caused by delayed growth plate senescence. The failure of complete catch-up growth that occurs in some patients for whom treatment is delayed may therefore result from the fact that their hypothyroidism has a greater impact on their rate of growth than it does on the rate of senescence at their growth plate, producing a smaller clonal population of proliferative zone chondrocytes and resulting in less efficient growth. The acceleration of growth plate senescence by oestrogen, resulting in an earlier exhaustion of the proliferative potential of growth plate chondrocytes, may also play an important role in incomplete growth catch-up in these children.