Bone Structure, Growth, and Hormonal Regulation

Chesney, Russell W.

doi:10.1016/b978-1-4377-0755-7.00694-1

Cited by 4 publications

(5 citation statements)

References 11 publications

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“…The rachitic child, therefore, has biochemical features of hypocalcemia, hypophosphatemia, increased alkaline phosphatase, hypocalciuria, and hyperphosphaturia (17). These biochemical abnormalities are reversed by the administration of calcitriol, either directly or via vitamin D administration, and become associated with bone healing as the extracellular calcium and phosphate levels return to normal and hydroxyapatite is deposited on osteoid tissue (18).…”

Section: Discussionmentioning

confidence: 99%

Rickets: Historical, Epidemiological, Pathophysiological, and Pathological Perspectives

Walker

Demellawy

Dávila

2017

Academic Forensic Pathology

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Rickets was a common metabolic disease of bone a century ago in Europe, North America, and East Asia (mainly due to vitamin D deficiency) but was largely eradicated in growing children by use of cod liver oil and the introduction of vitamin D fortification of milk in the 1930s in the United States. Vitamin D deficiency (VDD) remains the most common form of metabolic bone disease that is entirely preventable and treatable. Historically, rickets has appeared in sporadic epidemics and, despite the introduction of numerous preventive strategies, VDD has remained a global health problem amongst children. Moreover, developed countries such as Canada, Australia, the United Kingdom, and the United States have not been exempt from this. The radiological and histological features of rickets are both distinctive and characteristic and they reflect the underlying pathophysiological issue of decreased mineralization of bone as a result of VDD. The radiological features include 1) metaphyseal cupping and fraying, 2) poor mineralization of epiphyseal centers, 3) irregular and widened epiphyseal plates, 4) increased distance between the end of shaft and epiphyseal center, 5) cortical spurs at right angles to the metaphysis, 6) coarse trabeculation, and 7) periosteal reactions. Fractures may also be evident. The histological features of rickets reflect the failure of cartilage to mineralize and undergo resorption. This results in 1) disordered proliferation of chondrocytes in the hypertrophic zone secondary to a lack of apoptosis, 2) loss of the columnar arrangement of chondrocytes that results in thickening and disorganization of the hypertrophic zone, 3) tongue-like projections of cartilage that extend into the spongiosa, 4) irregularity of the limit between the proliferative and hypertrophic zones, and 5) penetration of blood vessels into the hypertrophic zone. The case of a premature 3-month-old female infant, born in the winter months in the arctic region of Canada who died from a lobar pneumonia with an incidental finding of radiological and pathological evidence of rickets, is presented. The case is used to review the entity of rickets from historical, pathophysiological, radiological, and histological perspectives.

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Section: Discussionmentioning

confidence: 99%

Rickets: Historical, Epidemiological, Pathophysiological, and Pathological Perspectives

Walker

Demellawy

Dávila

2017

Academic Forensic Pathology

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“…Additionally, the prone physical examination used in the current study was limited to 4 palpatory assessments that Vertebral BMD is determined by a complex relationship between genetic, chemical, and biomechanical factors. 34,35 had previously demonstrated interexaminer reliability in preliminary studies. 26,27 In a clinical setting, physicians use a wider variety of somatic dysfunction assessments with the patient in multiple positions, such as seated or supine.…”

Section: Limitationsmentioning

confidence: 94%

Association of Low Back Pain, Somatic Dysfunction, and Lumbar Bone Mineral Density: Reproducibility of Findings

Snider

Johnson²,

Degenhardt³

et al. 2014

Journal of Osteopathic Medicine

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“…History should focus to identify the risk factors, assess the symptoms of vitamin D deficiency and health consequences. 12,13,14,15 Table 3 shows the physical signs that can be elicited in children and adults Measurement of plasma concentration of calcium, phosphate, intact PTH and alkaline phosphatase can identify deficiency and also help in determining the etiology. Table 4 illustrates typical biochemical profile of vitamin D deficiency.…”

Section: Suganthan Nmentioning

confidence: 99%

The Sunshine Vitamin

Suganthan

2016

Jaffna Med. J.

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Vitamin D deficiency is the most common nutritional deficiency worldwide, characterized by serum 25(OH)D < 50 nmol/L. It is usually caused by sun avoidance, using sun protection, inadequate dietary and supplementary vitamin D intake, malabsorption syndrome and usage of medications. Most of the patients are asymptomatic; severe and prolonged vitamin deficiency causes rickets and growth retardation in children and osteomalacia, osteopenia and osteoporosis in adults. Vitamin D deficiency and insufficiency are treated with supplementary vitamin D and sensible sunlight exposure.

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Bone Structure, Growth, and Hormonal Regulation

Cited by 4 publications

References 11 publications

Rickets: Historical, Epidemiological, Pathophysiological, and Pathological Perspectives

Rickets: Historical, Epidemiological, Pathophysiological, and Pathological Perspectives

Association of Low Back Pain, Somatic Dysfunction, and Lumbar Bone Mineral Density: Reproducibility of Findings

The Sunshine Vitamin

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