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Overview of rickets in children

Author
Thomas Carpenter, MD
Section Editor
Joseph I Wolfsdorf, MB, BCh
Deputy Editor
Alison G Hoppin, MD

INTRODUCTION

Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused [1]. (See "Epidemiology and etiology of osteomalacia".)

Mineralization defects are classified according to the predominant mineral deficiency. Calcipenic rickets is caused by calcium deficiency, which usually is due to insufficient intake or metabolism of vitamin D, and in some cases insufficient intake or absorption of calcium in the setting of normal vitamin D levels. Phosphopenic rickets usually is caused by renal phosphate wasting. Calcipenic rickets is often but not always associated with low serum calcium levels, while phosphopenic rickets is characterized by low serum levels of phosphorus.

An overview of the pathogenesis, clinical presentation, and the differential diagnosis of rickets is presented here. The etiology and treatment of calcipenic and phosphopenic rickets are discussed separately. (See "Etiology and treatment of calcipenic rickets in children" and "Hereditary hypophosphatemic rickets and tumor-induced osteomalacia".)

PATHOGENESIS

Growth plate thickness is determined by two opposing processes: chondrocyte proliferation and hypertrophy on the one hand, and vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other [1]. Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus [1-3]. In these circumstances, growth plate cartilage accumulates and the growth plate thickens. In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation [4-6] with characteristic expansion of the hypertrophic zone [7]. In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid [8].

These abnormalities alter the overall geometry of the involved skeletal sites, leading to secondary increases in the diameters of the growth plate and metaphysis. These changes may be regarded as an attempt to compensate for decreased bone strength by increased bone size. Nonetheless, bone stability is compromised and, if the underlying condition does not improve, bowing occurs.

            

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Literature review current through: Nov 2016. | This topic last updated: Tue Aug 16 00:00:00 GMT 2016.
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References
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