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Most therapeutics target inhibition of osteoclast-mediated bone resorption, but more recent attention in early drug discovery has focussed on anabolic targets in osteoblasts or their precursors. Specifically, we seek novel therapeutic strategies to ameliorate the bone loss caused in patients with rickets. It is important that we take a multi-pronged approach to the treatment of children and adolescents with rickets as the disease is multifactorial and multiple factors can contribute to its course. In the context of its chronic sequelae, the diagnosis of rickets may be an indicator of bone marrow abnormalities as well as immunosuppressive disorders. This study reviews the current understanding of the immunological and pathologic mechanisms involved in the development of rickets and highlights new therapeutic options. The rickets complex is a disorder characterized by the depletion of bone mineral by the loss of osteoblasts. Osteoclasts are small cell-like cells that have a unique ability to self-renew and proliferate in cells deficient for osteoclast activity. Bone marrow suppression of bone marrow–derived cells by a variety of cellular products such as lipogenic, inflammatory and glycosylated proteins and secreted factors enhances osteoclasts' ability to survive and proliferate. In addition to the loss of osteoclasts, the bone marrow of children with rickets has been shown to undergo apoptosis, leading to the loss of bone marrow-derived stem cells by bone marrow-specific cytokine-driven signaling [ 7 ]. As many as 1 million children in the US are diagnosed with rickets each year, though this number of cases may be much higher [ 5 ]. Clinical characteristics of the disorder vary greatly, ranging from the onset of the disorder before the age of 1 to a life-long progressive illness in which individuals have no sign of osteoclast activity. The pathophysiology of rickets is complex and involves alterations in cellular activity, bone metabolism, and immunology. The development and prognosis of rickets are similar for young children, older adults and those with chronic or recurrent disease. The disease is primarily considered a consequence of bone marrow deficiency and is most severe in children and adolescents before the age of 10 years. The incidence of rickets in children with cancer is approximately 5-25%, and the rate of recurrence is usually high [ 4 ]. The development and prognosis of rickets differ depending on the age of bone marrow suppression, tumor and age at diagnosis. In children under 10 years of age, the incidence of rickets in first-degree relatives is 4% [ 5 ]. Furthermore, for this age group, recurrence is high. A retrospective study of patients treated for rickets Similar articles:


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