Rickets: Disorders caused by interruption of BONE MINERALIZATION manifesting as OSTEOMALACIA in adults and characteristic deformities in infancy and childhood due to disturbances in normal BONE FORMATION. The mineralization process may be interrupted by disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis, resulting from dietary deficiencies, or acquired, or inherited metabolic, or hormonal disturbances.Familial Hypophosphatemic Rickets: A hereditary disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; renal defects in phosphate reabsorption and vitamin D metabolism; and growth retardation. Autosomal and X-linked dominant and recessive variants have been reported.Hypophosphatemia, Familial: An inherited condition of abnormally low serum levels of PHOSPHATES (below 1 mg/liter) which can occur in a number of genetic diseases with defective reabsorption of inorganic phosphorus by the PROXIMAL RENAL TUBULES. This leads to phosphaturia, HYPOPHOSPHATEMIA, and disturbances of cellular and organ functions such as those in X-LINKED HYPOPHOSPHATEMIC RICKETS; OSTEOMALACIA; and FANCONI SYNDROME.PHEX Phosphate Regulating Neutral Endopeptidase: A membrane-bound metalloendopeptidase that may play a role in the degradation or activation of a variety of PEPTIDE HORMONES and INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS. Genetic mutations that result in loss of function of this protein are a cause of HYPOPHOSPHATEMIC RICKETS, X-LINKED DOMINANT.Osteomalacia: Disorder caused by an interruption of the mineralization of organic bone matrix leading to bone softening, bone pain, and weakness. It is the adult form of rickets resulting from disruption of VITAMIN D; PHOSPHORUS; or CALCIUM homeostasis.Sodium-Phosphate Cotransporter Proteins, Type IIc: A non-electrogenic sodium-dependent phosphate transporter. It is found primarily in apical membranes of PROXIMAL RENAL TUBULES.Hypophosphatemia: A condition of an abnormally low level of PHOSPHATES in the blood.Genetic Diseases, X-Linked: Genetic diseases that are linked to gene mutations on the X CHROMOSOME in humans (X CHROMOSOME, HUMAN) or the X CHROMOSOME in other species. Included here are animal models of human X-linked diseases.Rickets, Hypophosphatemic: A disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; resulting from lack of phosphate reabsorption by the kidneys and possible defects in vitamin D metabolism.Hypercalciuria: Excretion of abnormally high level of CALCIUM in the URINE, greater than 4 mg/kg/day.Hypocalcemia: Reduction of the blood calcium below normal. Manifestations include hyperactive deep tendon reflexes, Chvostek's sign, muscle and abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)Vitamin D Deficiency: A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)Vitamin D: A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.Hydroxycholecalciferols: Hydroxy analogs of vitamin D 3; (CHOLECALCIFEROL); including CALCIFEDIOL; CALCITRIOL; and 24,25-DIHYDROXYVITAMIN D 3.Phosphates: Inorganic salts of phosphoric acid.Phosphorus: A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.Alkaline Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.25-Hydroxyvitamin D 2: 9,10-Secoergosta-5,7,10(19),22-tetraene-3,25-diol. Biologically active metabolite of vitamin D2 which is more active in curing rickets than its parent. The compound is believed to attach to the same receptor as vitamin D2 and 25-hydroxyvitamin D3.Nephrocalcinosis: A condition characterized by calcification of the renal tissue itself. It is usually seen in distal RENAL TUBULAR ACIDOSIS with calcium deposition in the DISTAL KIDNEY TUBULES and the surrounding interstitium. Nephrocalcinosis causes RENAL INSUFFICIENCY.Calcitriol: The physiologically active form of vitamin D. It is formed primarily in the kidney by enzymatic hydroxylation of 25-hydroxycholecalciferol (CALCIFEDIOL). Its production is stimulated by low blood calcium levels and parathyroid hormone. Calcitriol increases intestinal absorption of calcium and phosphorus, and in concert with parathyroid hormone increases bone resorption.Ergocalciferols: Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.25-Hydroxyvitamin D3 1-alpha-Hydroxylase: A mitochondrial cytochrome P450 enzyme that catalyzes the 1-alpha-hydroxylation of 25-hydroxyvitamin D3 (also known as 25-hydroxycholecalciferol) in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP27B1 gene, converts 25-hydroxyvitamin D3 to 1-alpha,25-dihydroxyvitamin D3 which is the active form of VITAMIN D in regulating bone growth and calcium metabolism. This enzyme is also active on plant 25-hydroxyvitamin D2 (ergocalciferol).Cholecalciferol: Derivative of 7-dehydroxycholesterol formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. It differs from ERGOCALCIFEROL in having a single bond between C22 and C23 and lacking a methyl group at C24.Receptors, Calcitriol: Proteins, usually found in the cytoplasm, that specifically bind calcitriol, migrate to the nucleus, and regulate transcription of specific segments of DNA with the participation of D receptor interacting proteins (called DRIP). Vitamin D is converted in the liver and kidney to calcitriol and ultimately acts through these receptors.Fanconi Syndrome: A hereditary or acquired form of generalized dysfunction of the PROXIMAL KIDNEY TUBULE without primary involvement of the KIDNEY GLOMERULUS. It is usually characterized by the tubular wasting of nutrients and salts (GLUCOSE; AMINO ACIDS; PHOSPHATES; and BICARBONATES) resulting in HYPOKALEMIA; ACIDOSIS; HYPERCALCIURIA; and PROTEINURIA.Cod Liver Oil: Oil obtained from fresh livers of the cod family, Gadidae. It is a source of VITAMIN A and VITAMIN D.Microradiography: Production of a radiographic image of a small or very thin object on fine-grained photographic film under conditions which permit subsequent microscopic examination or enlargement of the radiograph at linear magnifications of up to several hundred and with a resolution approaching the resolving power of the photographic emulsion (about 1000 lines per millimeter).Infant Nutrition Disorders: Disorders caused by nutritional imbalance, either overnutrition or undernutrition, occurring in infants ages 1 month to 24 months.Lions: Large, chiefly nocturnal mammals of the cat family FELIDAE, species Panthera leo. They are found in Africa and southern Asia.Calcification, Physiologic: Process by which organic tissue becomes hardened by the physiologic deposit of calcium salts.Fibroblast Growth Factors: A family of small polypeptide growth factors that share several common features including a strong affinity for HEPARIN, and a central barrel-shaped core region of 140 amino acids that is highly homologous between family members. Although originally studied as proteins that stimulate the growth of fibroblasts this distinction is no longer a requirement for membership in the fibroblast growth factor family.Genu Valgum: An inward slant of the thigh in which the knees are close together and the ankles far apart. Genu valgum can develop due to skeletal and joint dysplasias (e.g., OSTEOARTHRITIS; HURLER SYNDROME); and malnutrition (e.g., RICKETS; FLUORIDE POISONING).Sunlight: Irradiation directly from the sun.Cystinosis: A metabolic disease characterized by the defective transport of CYSTINE across the lysosomal membrane due to mutation of a membrane protein cystinosin. This results in cystine accumulation and crystallization in the cells causing widespread tissue damage. In the KIDNEY, nephropathic cystinosis is a common cause of RENAL FANCONI SYNDROME.Dihydroxycholecalciferols: Cholecalciferols substituted with two hydroxy groups in any position.Electronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Food Dispensers, Automatic: Mechanical food dispensing machines.Editorial Policies: The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.Authorship: The profession of writing. Also the identity of the writer as the creator of a literary production.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Postal Service: The functions and activities carried out by the U.S. Postal Service, foreign postal services, and private postal services such as Federal Express.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Forehead: The part of the face above the eyes.Skin Pigmentation: Coloration of the skin.Ultraviolet Rays: That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.Hyperparathyroidism: A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.Parathyroid Glands: Two pairs of small oval-shaped glands located in the front and the base of the NECK and adjacent to the two lobes of THYROID GLAND. They secrete PARATHYROID HORMONE that regulates the balance of CALCIUM; PHOSPHORUS; and MAGNESIUM in the body.Hypoparathyroidism: A condition caused by a deficiency of PARATHYROID HORMONE (or PTH). It is characterized by HYPOCALCEMIA and hyperphosphatemia. Hypocalcemia leads to TETANY. The acquired form is due to removal or injuries to the PARATHYROID GLANDS. The congenital form is due to mutations of genes, such as TBX1; (see DIGEORGE SYNDROME); CASR encoding CALCIUM-SENSING RECEPTOR; or PTH encoding parathyroid hormone.Hyperparathyroidism, Primary: A condition of abnormally elevated output of PARATHYROID HORMONE due to parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. It is characterized by the combination of HYPERCALCEMIA, phosphaturia, elevated renal 1,25-DIHYDROXYVITAMIN D3 synthesis, and increased BONE RESORPTION.Organizations, Nonprofit: Organizations which are not operated for a profit and may be supported by endowments or private contributions.Food: Any substances taken in by the body that provide nourishment.Voluntary Health Agencies: Non-profit organizations concerned with various aspects of health, e.g., education, promotion, treatment, services, etc.Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake.Food Habits: Acquired or learned food preferences.Foundations: Organizations established by endowments with provision for future maintenance.Eating: The consumption of edible substances.
  • For a more complete review of nutritional rickets and its management, please refer to the recent publication in Endocrinology and Metabolism Clinics of North America on the topic. (aappublications.org)
  • The seminal discovery that sunlight was important in the prevention of nutritional rickets was made in 1890 by Theobald A. Palm, a medical missionary who contrasted the prevalence of rickets in northern European urban areas with similar areas in Japan and other tropical countries. (mdpi.com)
  • 10 This expert consensus statement was supported by studies of breastfed infants in the United States, Norway, and China and suggested that infants who ingest 100 or 200 IU of supplemental vitamin D daily were less likely to develop rickets. (aafp.org)
  • Carvalho and colleagues, 1 in their article entitled, "Severe Nutritional Deficiencies in Toddlers Resulting From Health Food Milk Alternatives," describe 1 case of vitamin D-deficient rickets and 1 case of kwashiorkor associated with the misuse of milk alternatives during weaning. (aappublications.org)
  • At presentation with failure-to-thrive at age six months, radiographs revealed severe rickets and serum 25(OH)D was 8 ng/mL (Nl, 30-100), yet low ALP activity 55 U/L (Nl, 124-341), normal Ca 9.3 mg/dL (Nl, 8.5-10.1) and Pi 6.4 mg/dL (Nl, 3.5-7.0), and low-normal parathyroid hormone 21 pg/mL (Nl, 14-72) were instead consistent with HPP. (wustl.edu)
  • A disorder of vitamin D metabolism resulting in severe rickets, hypocalcemia and secondary hyperparathyroidism. (abcam.com)
  • Rickets in the Middle East: role of environment and genetic predisposition. (cdc.gov)
  • We chose a molecular genetic approach to understand the changes that characterize the final phase of adult eclosion, studying the behavior in wild-type Drosophila and in rickets ( rk ) mutants that do not complete the post-ecdysial expansion behaviors. (biologists.org)
  • Genetic forms of rickets, including vitamin D-dependent rickets, are much less common. (medlineplus.gov)
  • Each type of vitamin D-dependent rickets has a different genetic cause: VDDR1A is caused by CYP27B1 gene mutations, VDDR1B is caused by CYP2R1 gene mutations, and VDDR2A is caused by VDR gene mutations. (medlineplus.gov)
  • In early history, humans lived at latitudes where greater daily exposure of their bodies to sunlight produced adequate levels of vitamin D. When we migrated toward higher latitudes, where the proper wavelength of light is absent for half the year, childhood rickets became common because vitamin D is necessary to absorb calcium and for the proper formation of bone. (survivalblog.com)
  • A female who survives childhood rickets may reach maturity with a deformed pelvis that makes it impossible to deliver a baby naturally. (survivalblog.com)
  • Although we found no additional cases of rickets or kwashiorkor associated with use of milk alternatives, we did identify 5 additional cases of vitamin D-deficient rickets and 3 additional cases of protein energy malnutrition. (aappublications.org)
  • Because the newly discovered substance was the fourth vitamin identified, it was called vitamin D. The 1928 Nobel Prize in Chemistry was awarded to Adolf Windaus, who discovered the steroid 7-dehydrocholesterol, the precursor of vitamin D. Prior to the fortification of milk products with vitamin D, rickets was a major public health problem. (wikipedia.org)
  • In the United States, milk has been fortified with 10 micrograms (400 IU) of vitamin D per quart since the 1930s, leading to a dramatic decline in the number of rickets cases. (wikipedia.org)
  • Experiments using the rk mutants give a novel insight into the complex regulatory pathway that controls wing expansion programs in insects and suggest a physiological role for a glycoprotein hormone receptor in insects. (biologists.org)
  • Interestingly, ionic phosphate species not only provide a fundamental building block of biological mineral, but rather exhibit several diverse roles in mediating mineral formation in the physiological milieu. (rsc.org)
  • Vitamin D has a crucial role in improving physiological function in both skeletal and extraskeletal tissues (1,2). (who.int)
  • Healing rickets can show up on an x-ray as what looks like a fracture, which immediately casts suspicion on the parents. (mercola.com)
  • Beyond the Abstract - Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression, by Sandra Karlsson, et al. (urotoday.com)
  • In this review, we focus on elucidating the complex roles of phosphate ions and molecules within human biomineralisation pathways, primarily referring to the nucleation and crystallisation of bone mineral. (rsc.org)

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