Rickets and Osteomalacia

Pitt, Michael J.

doi:10.1016/b0-7216-0270-3/50045-1

Cited by 30 publications

(54 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Working long hours indoors can predispose people to developing vitamin D deficiency due to the lack of ultraviolet light on their skins and subsequent lack of formation of the vitamin in the skin. Consequently, calcium and phosphorus are not absorbed and the long bones bend (Pitt 1995). In fact, Hokugo et al (2010) note that in people with osteonecrosis of the mandible there could be an interaction between bisphosphonates and reduced vitamin D. Therefore, this person may have had rickets prior to contracting "phossy jaw".…”

Section: Evidence Of Metabolic Bone Diseasementioning

confidence: 99%

“…The unilateral nature of the new bone formed around the right elbow is less characteristic of scurvy, as is the extensive new bone formation and destruction on the mandible. The endocranial and ectocranial bone changes described above may be also related to vitamin D deficiency (rickets) along with the abnormal bowing of the femora (Pitt 1995:1894, Ortner and Mays 1998, Mays et al 2006. Working long hours indoors can predispose people to developing vitamin D deficiency due to the lack of ultraviolet light on their skins and subsequent lack of formation of the vitamin in the skin.…”

Section: Evidence Of Metabolic Bone Diseasementioning

confidence: 99%

See 1 more Smart Citation

‘Til Poison Phosphorous Brought them Death’: A potentially occupationally-related disease in a post-medieval skeleton from north-east England.

Roberts

Caffell

Filipek-Ogden

et al. 2016

International Journal of Paleopathology

View full text Add to dashboard Cite

Section: Evidence Of Metabolic Bone Diseasementioning

confidence: 99%

Section: Evidence Of Metabolic Bone Diseasementioning

confidence: 99%

‘Til Poison Phosphorous Brought them Death’: A potentially occupationally-related disease in a post-medieval skeleton from north-east England.

Roberts

Caffell

Filipek-Ogden

et al. 2016

International Journal of Paleopathology

View full text Add to dashboard Cite

“…Instead, rickets means an undermineralized skeleton that is primarily caused by deficiency of calcium or phosphorus, of which vitamin D deficiency or genetic disturbances of vitamin D physiology are but a few of the causes (539). The differential diagnosis of the rachitic-appearing fetal and neonatal skeleton encompasses at least 50 different conditions (525), including fetal hypoparathyroidism, skeletal dysplasias (249), metaphyseal chondrodysplasias (525), hypophosphatasias (555,584), type V osteogenesis imperfecta (27), and scurvy (73). Consequently, it is possible that some of these cases of rickets were not due to vitamin D deficiency.…”

Section: Observational Studies and Case Reportsmentioning

confidence: 99%

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

207

188

View full text Add to dashboard Cite

Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

show abstract

“…Exact mechanism of osteosclerosis is unclear and is thought to involve PTH stimulated osteoblastic activity either after treatment or as a counter response to resorption where osteoblasts produce excessive nonhydroxyapatite osteoid [41,42]. Excess accumulation of osteoid appears more opaque than normal bone and results in the classic "rugger-jersey" spine, alternating sclerotic and lucent bands along the inferior and superior endplates of vertebral bodies similar to the stripes on an English rugby shirt [42][43][44] (Figure 12). Osteosclerosis may be the sole manifestation of renal osteodystrophy and may regress postrenal transplantation [36].…”

Section: Radiographic Featuresmentioning

confidence: 99%

Imaging Findings and Evaluation of Metabolic Bone Disease

Patel

Ramanathan

Kuban

et al. 2015

Advances in Radiology

View full text Add to dashboard Cite

Bone is a dynamic organ of the endoskeleton, playing an important role in structural integrity, mineral reservoirs, blood production, coagulation, and immunity. Metabolic bone disease encompasses a broad spectrum of inherited and acquired disorders that disrupt the normal homeostasis of bone formation and resorption. For patients affected by these processes, radiologic imaging plays a central role in diagnosis, monitoring treatment, and risk stratification. Radiologists should be familiar with the diseases, intimately aware of the imaging findings, and possessive of multimodality expertise to wisely guide the best practice of medicine. The purpose of this paper is to review the imaging features and characteristics of the most common types of metabolic bone disease with highlights of clinically relevant information so that readers can better generate appropriate differential diagnoses and recommendations. For this review, a thorough literature search for the most up-to-date information was performed on several key types of metabolic bone disease: osteoporosis, osteomalacia, rickets, scurvy, renal osteodystrophy, hyperparathyroidism, Paget's disease, osteogenesis imperfecta, acromegaly, and osteopetrosis. Although they all affect the bone, these diseases have both shared characteristic features that can be discerned through imaging.

show abstract

Rickets and Osteomalacia

Cited by 30 publications

References 21 publications

‘Til Poison Phosphorous Brought them Death’: A potentially occupationally-related disease in a post-medieval skeleton from north-east England.

‘Til Poison Phosphorous Brought them Death’: A potentially occupationally-related disease in a post-medieval skeleton from north-east England.

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Imaging Findings and Evaluation of Metabolic Bone Disease

Contact Info

Product

Resources

About