scholarly journals Bone Deformity due to Rickets and Osteomalacia in Children and Adolescents

Author(s):  
Awadh Saeed Alqahtani ◽  
Hayazi Mohammed Alshehri ◽  
Nazim Faisal Ahmed ◽  
Mohammed Hassan Alatawi ◽  
Wurud Muteb D. Alshammari ◽  
...  

Rickets is a worldwide bone disease that is associated with disorders of calcium and phosphate homeostasis and can lead to short stature and joint deformities. Osteomalacia is a major metabolic bone disease that results from a chronic and severe deficiency of vitamin D or phosphate from any cause after growth has stopped. A deficiency of vitamin D or phosphate leads to defective bone mineralization and generalized or localized vague bone pain in various parts of the skeleton and / or proximal muscle weakness. Rickets and osteomalacia are two different clinical diseases with impaired bone mineralization. Rickets occurs throughout the growing skeleton in infants and children, while osteomalacia occurs in adults after fusion of the growth plates. Rickets and osteomalacia are increasingly common in Saudi Arabia, with vitamin D deficiency being the most common etiological cause. Early skeletal deformities can occur in infants, such as soft, thin skull bones, a condition known as craniotabes. In adults, as a result of demineralization, the bones become less rigid (soft bone) with pathological fractures. The diagnosis of both diseases is based on the medical history and physical examination, radiological characteristics, and biochemical tests. Management depends on the underlying etiology.

2013 ◽  
Author(s):  
Adodra Annika ◽  
Kouklinos Andreas ◽  
Julies Priscilla ◽  
Shaw Mathew ◽  
Jacobs Benjamin

PEDIATRICS ◽  
1993 ◽  
Vol 92 (6) ◽  
pp. 862-864
Author(s):  
YASUSHI NAKO ◽  
NAOBUMI FUKUSHIMA ◽  
TAKESHI TOMOMASA ◽  
KANJI NAGASHIMA ◽  
TAKAYOSHI KUROUME

Hypervitaminosis D is one of the causes of severe hypercalcemia in children. Most cases of hypervitaminosis D during childhood are due to an excessive supplementation of vitamin D by physicians or parents.1,2 To prevent metabolic bone disease of prematurity (rickets of prematurity), formulas designed for premature infants ("premature formulas"), which contain more calcium and vitamin D than standard formulas, are given to premature infants in addition to human milk.1 In some cases, separate vitamin D products are also given to these infants, although requirements for vitamin D and calcium intake in the premature infant and the formerly premature infant have not been fully estimated.1


2016 ◽  
Vol 6 (4) ◽  
pp. 568-590
Author(s):  
Alfredo Walker ◽  
Charis Kepron ◽  
Christopher M. Milroy

Fractures are commonly found in cases regarded as child abuse. The most commonly encountered fractures are to the ribs and the metaphyses. This paper examines the specificity of the classical metaphyseal lesion (CML) and rib fractures as hallmarks of child abuse. Recently, vitamin D deficiency (rickets) has been proposed as an alternative cause for the appearances typically described in CML. The literature in this area is examined. Rib fractures have also been highly associated with child abuse, particularly posterior rib fractures. As well as metabolic bone disease, resuscitation has been examined as a cause of rib fractures in young children. The current literature remains strongly supportive of rib fractures and metaphyseal fractures being indicators of child abuse.


1983 ◽  
Vol 3 (1_suppl) ◽  
pp. 24-26 ◽  
Author(s):  
Francisco Llach

It seems that CAPD may improve some patients with osteomalacia but may be similar to hemodialysis in regard to osteitis fibrosa. However, long-term prospective evaluation of the incidence of bone disease in CAPD patients is necessary before we can determine how CAPD may alter the incidence and expression of renal osteodystrophy. We need more information before we can conclude that CAPD may improve pure osteomalacia. Finally, the data available are insufficient to clarify the role of vitamin D analogues in these patients.


2012 ◽  
Vol 92 (1) ◽  
pp. 131-155 ◽  
Author(s):  
Aline Martin ◽  
Valentin David ◽  
L. Darryl Quarles

Calcium (Ca2+) and phosphate (PO43−) homeostasis are coordinated by systemic and local factors that regulate intestinal absorption, influx and efflux from bone, and kidney excretion and reabsorption of these ions through a complex hormonal network. Traditionally, the parathyroid hormone (PTH)/vitamin D axis provided the conceptual framework to understand mineral metabolism. PTH secreted by the parathyroid gland in response to hypocalcemia functions to maintain serum Ca2+ levels by increasing Ca2+ reabsorption and 1,25-dihydroxyvitamin D [1,25(OH)2D] production by the kidney, enhancing Ca2+ and PO43− intestinal absorption and increasing Ca2+ and PO43− efflux from bone, while maintaining neutral phosphate balance through phosphaturic effects. FGF23 is a recently discovered hormone, predominately produced by osteoblasts/osteocytes, whose major functions are to inhibit renal tubular phosphate reabsorption and suppress circulating 1,25(OH)2D levels by decreasing Cyp27b1-mediated formation and stimulating Cyp24-mediated catabolism of 1,25(OH)2D. FGF23 participates in a new bone/kidney axis that protects the organism from excess vitamin D and coordinates renal PO43− handling with bone mineralization/turnover. Abnormalities of FGF23 production underlie many inherited and acquired disorders of phosphate homeostasis. This review discusses the known and emerging functions of FGF23, its regulation in response to systemic and local signals, as well as the implications of FGF23 in different pathological and physiological contexts.


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