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===Juvenile Osteoporosis (JO)===
[[Osteoporosis]] in children and adolescents is rare, usually is due to some [[comorbidities]] or [[medications]], secondary [[osteoporosis]]. Surprisingly, no significant causes have been found for rare cases, [[idiopathic]] [[osteoporosis]].
No matter what causes it, juvenile [[osteoporosis]] can be a significant problem because it occurs during the child’s prime [[bone]]-building years. From birth through young adulthood, children steadily accumulate [[bone mass]], which peaks sometime before age 30. The greater their peak [[bone mass]], the lower their risk for [[osteoporosis]] later in life. After people reach their mid thirties, bone mass typically begins to decline—very slowly at first but increasing in their fifties and sixties. Both heredity and [[lifestyle]] choices—especially the amount of [[calcium]] in the diet and the level of [[physical activity]] influence the development of peak [[bone mass]] and the rate at which [[bone]] is lost later in life.
====Secondary Osteoporosis====
*As the primary condition, [[juvenile idiopathic arthritis]] (also known as [[juvenile rheumatoid arthritis]]) provides a good illustration of the possible causes of secondary [[osteoporosis]]. In some cases, the ''[[disease]] process'' itself can cause [[osteoporosis]].
*In other cases, ''[[medication]]'' used to treat the primary disorder may reduce [[bone mass]]. For example, drugs such as [[prednisone]], used to treat severe cases of [[juvenile idiopathic arthritis]], negatively affect [[bone mass]].
*Finally, some ''behaviors'' associated with the primary disorder may lead to [[bone loss]] or reduction in bone formation. For example, a child with juvenile idiopathic arthritis may avoid [[physical activity]], which is necessary for building and maintaining [[bone mass]], because it may aggravate his or her condition or cause pain.<ref name="urlJuvenile Osteoporosis">{{cite web |url=https://www.niams.nih.gov/health_info/bone/Bone_Health/Juvenile/juvenile_osteoporosis.asp |title=Juvenile Osteoporosis |format= |work= |accessdate=}}</ref>
====Idiopathic Juvenile Osteoporosis====
<div style="width: 85%;">
*Idiopathic juvenile [[osteoporosis]] (IJO) is a primary condition with no known cause. It is diagnosed after other causes of juvenile [[osteoporosis]] have been excluded. This rare form of [[osteoporosis]] typically occurs just before the onset of [[puberty]] in previously healthy children. The average age at onset is 7 years, with a range of 1 to 13 years. Most children experience complete recovery of bone.
*The first sign of IJO is usually [[pain]] in the lower back, [[hips]], and [[feet]], often accompanied by difficulty walking. [[Knee]] and [[ankle]] [[pain]] and [[fractures]] of the lower extremities also may occur. Physical malformations include [[kyphosis]], loss of height, a sunken chest, or a limp. These physical malformations are sometimes reversible after IJO has run its course.
*[[X-rays]] of children with IJO often show low [[bone density]], [[fractures]] of weight-bearing [[bones]], and collapsed or misshapen [[vertebrae]]. However, conventional [[X-rays]] may not be able to detect [[osteoporosis]] until significant [[bone mass]] already has been lost. Newer methods such as [[Dual energy X-ray absorptiometry|dual energy x-ray absorptiometry (DXA)]], and quantitative computed tomography (QCT ) allow for earlier and more accurate diagnosis of low [[bone mass]].
*There is no established [[medical]] or [[surgical]] therapy for juvenile [[osteoporosis]]. In some cases, no treatment may be needed because the condition usually goes away spontaneously. However, early diagnosis of juvenile [[osteoporosis]] is important so that steps can be taken to protect the child’s [[spine]] and other [[bones]] from [[fracture]] until remission occurs. These steps may include [[physical therapy]], using [[crutches]], avoiding unsafe weight-bearing activities, and other supportive care. A well-balanced diet rich in [[calcium]] and [[vitamin D]] is also important. In severe, long-lasting cases of juvenile [[osteoporosis]], some medications called [[bisphosphonates]], approved by the [[Food and Drug Administration]] for the treatment of [[osteoporosis]] in adults, have been given to children experimentally.
*Most children with IJO experience a complete recovery of [[bone]] tissue. Although growth may be somewhat impaired during the acute phase of the disorder, normal growth resumes—and catch-up growth often occurs—afterward. Unfortunately, in some cases, IJO can result in permanent disability such as [[kyphoscoliosis]] or collapse of the [[rib cage]].<ref name="urlJuvenile Osteoporosis" />
==Causes==
==Causes==
===Life Threatening Causes===
Life-threatening causes include conditions which may result in death or permanent [[disability]] within 24 hours if left untreated. There are no life-threatening causes of [[osteoporosis]], however complications resulting from untreated [[osteoporosis]] are common.
===Common causes===
*[[Aging]]
*[[Alcoholism]]
*[[Calcium deficiency]]
*[[Chronic renal failure]]
*[[Gonadal dysgenesis]]
*[[Hyperparathyroidism]]
*[[Hyperthyroidism]]
*[[Hypophosphatemic rickets]]
*[[Idiopathic]]
*[[Immobility]]
*[[Menopause]]
*[[Mixed connective tissue disease]]
*[[Paget's disease of bone]]
*[[Prednisolone]]
*[[Primary hypoparathyroidism]]
===Less common causes===
{{Columns-list|3|*[[Abderhalden-Kaufmann-Lignac syndrome]]
*[[Acromegaly]]<ref name="pmid22461828">{{cite journal |vauthors=Padova G, Borzì G, Incorvaia L, Siciliano G, Migliorino V, Vetri M, Tita P |title=Prevalence of osteoporosis and vertebral fractures in acromegalic patients |journal=Clin Cases Miner Bone Metab |volume=8 |issue=3 |pages=37–43 |year=2011 |pmid=22461828 |pmc=3279059 |doi= |url=}}</ref>
*[[Acroosteolysis neurogenic]]
*[[Adrenal adenoma]]
*[[Adrenal incidentaloma]]
*[[Adrenocortical carcinoma]]
*[[Albright's hereditary osteodystrophy]]<ref name="pmid19841552">{{cite journal |author=Goswami M, Verma M, Singh A, Grewal H, Kumar G |title=Albright hereditary osteodystrophy: a rare case report |journal=J Indian Soc Pedod Prev Dent |volume=27 |issue=3 |pages=184–8 |year=2009 |pmid=19841552 |doi=10.4103/0970-4388.57101 |url=}}</ref>
*[[Alpha thalassemia]]
*[[Andropause]]<ref name="pmid22400185">{{cite journal |vauthors=Krysiak R, Okopień B |title=[Pathogenesis and clinical presentation of andropause] |language=Polish |journal=Pol. Merkur. Lekarski |volume=32 |issue=187 |pages=70–3 |year=2012 |pmid=22400185 |doi= |url=}}</ref>
*[[Ankylosing spondylitis]]
*[[Aromatase deficiency]]
*[[Boyd-Stearns syndrome]]
*[[Brown-Sequard Syndrome]]<ref name="pmid1431871">{{cite journal |vauthors=Saltzstein RJ, Hardin S, Hastings J |title=Osteoporosis in spinal cord injury: using an index of mobility and its relationship to bone density |journal=J Am Paraplegia Soc |volume=15 |issue=4 |pages=232–4 |year=1992 |pmid=1431871 |doi= |url=}}</ref>
*[[Chromosome 1, deletion q21 q25]]
*[[Chronic acidosis]]
*[[Chronic Hepatitis]]
*[[Chronic Liver Disease]]
*[[Chronic obstructive pulmonary disease]]
*[[Copper deficiency]]<ref name="pmid22025246">{{cite journal |vauthors=Nojiri H, Saita Y, Morikawa D, Kobayashi K, Tsuda C, Miyazaki T, Saito M, Marumo K, Yonezawa I, Kaneko K, Shirasawa T, Shimizu T |title=Cytoplasmic superoxide causes bone fragility owing to low-turnover osteoporosis and impaired collagen cross-linking |journal=J. Bone Miner. Res. |volume=26 |issue=11 |pages=2682–94 |year=2011 |pmid=22025246 |doi=10.1002/jbmr.489 |url=}}</ref>
*[[Crohn's disease]]
*[[Cushing's disease]]
*[[Cushing's syndrome]]<ref name="pmid22450549">{{cite journal |vauthors=Lekva T, Ueland T, Bøyum H, Evang JA, Godang K, Bollerslev J |title=TXNIP is highly regulated in bone biopsies from patients with endogenous Cushing's syndrome and related to bone turnover |journal=Eur. J. Endocrinol. |volume=166 |issue=6 |pages=1039–48 |year=2012 |pmid=22450549 |doi=10.1530/EJE-11-1082 |url=}}</ref>
*[[Cyproterone]]<ref name="pmid12877306">{{cite journal |vauthors=Grasswick LJ, Bradford JM |title=Osteoporosis associated with the treatment of paraphilias: a clinical review of seven case reports |journal=J. Forensic Sci. |volume=48 |issue=4 |pages=849–55 |year=2003 |pmid=12877306 |doi= |url=}}</ref><ref name="pmid11469484">{{cite journal |vauthors=Vasireddy S, Swinson DR |title=Male osteoporosis associated with longterm cyproterone treatment |journal=J. Rheumatol. |volume=28 |issue=7 |pages=1702–3 |year=2001 |pmid=11469484 |doi= |url=}}</ref>
*[[Cystathionine beta-synthase deficiency]]
*[[Cystic Fibrosis]]
*[[Depression]]<ref name="pmid17112423">{{cite journal |vauthors=Gold DT, Solimeo S |title=Osteoporosis and depression: a historical perspective |journal=Curr Osteoporos Rep |volume=4 |issue=4 |pages=134–9 |year=2006 |pmid=17112423 |doi= |url=}}</ref>
*[[Diamond-Blackfan anemia]]
*[[Dibasic aminoaciduria 2]]
*[[Dyskeratosis Congenita|Dyskeratosis Congenital]]<ref name="pmid18028256">{{cite journal |vauthors=Pignolo RJ, Suda RK, McMillan EA, Shen J, Lee SH, Choi Y, Wright AC, Johnson FB |title=Defects in telomere maintenance molecules impair osteoblast differentiation and promote osteoporosis |journal=Aging Cell |volume=7 |issue=1 |pages=23–31 |year=2008 |pmid=18028256 |pmc=2394673 |doi=10.1111/j.1474-9726.2007.00350.x |url=}}</ref>
*[[Eccentrochondrodysplasia]]
*[[Ehlers-Danlos syndrome]]- progeroid form
*[[Ethanol]]
*Excessive [[Dieting]]
*[[Exemestane]]
*[[Fabry's disease]]
*[[Fanconi-Albertini-Zellweger syndrome]]
*[[Fanconi-ichthyosis-dysmorphism]]
*[[Female athlete triad]]
*[[Flunisolide]]
*[[Fluticasone]] (aerosol)
*[[Functioning pancreatic endocrine tumor]]
*[[Galactorrhoea]]-[[Hyperprolactinaemia]]
*[[Generalized mastocytosis]]<ref name="pmid9129284">{{cite journal |author=Delsignore JL, Dvoretsky PM, Hicks DG, O'Keefe RJ, Rosier RN |title=Mastocytosis presenting as a skeletal disorder |journal=Iowa Orthop J |volume=16 |issue= |pages=126–34 |year=1996 |pmid=9129284 |pmc=2378151 |doi= |url=}}</ref>
*[[Geroderma osteodysplastica]]<ref name="pmid17014644">{{cite journal |author=Boente Mdel C, Asial RA, Winik BC |title=Geroderma osteodysplastica. Report of a new family |journal=Pediatr Dermatol |volume=23 |issue=5 |pages=467–72 |year=2006 |pmid=17014644 |doi=10.1111/j.1525-1470.2006.00285.x |url=}}</ref>
*[[Glycerol kinase]] deficiency
*[[Gnathodiaphyseal dysplasia]]<ref name="pmid11547842">{{cite journal |vauthors=Riminucci M, Collins MT, Corsi A, Boyde A, Murphey MD, Wientroub S, Kuznetsov SA, Cherman N, Robey PG, Bianco P |title=Gnathodiaphyseal dysplasia: a syndrome of fibro-osseous lesions of jawbones, bone fragility, and long bone bowing |journal=J. Bone Miner. Res. |volume=16 |issue=9 |pages=1710–8 |year=2001 |pmid=11547842 |doi=10.1359/jbmr.2001.16.9.1710 |url=}}</ref>
*[[Haemochromatosis]]
*[[Hajdu-Cheney syndrome]]<ref name="pmid22570971">{{cite journal |author=Nozaki T, Ihara K, Makimura M, Kinjo T, Hara T |title=A girl with Hajdu-Cheney syndrome and premature ovarian failure |journal=J. Pediatr. Endocrinol. Metab. |volume=25 |issue=1-2 |pages=171–3 |year=2012 |pmid=22570971 |doi= |url=}}</ref>
*[[Hashimoto's Thyroiditis]]
*[[Hemoglobin H disease]]
*[[Heparin]]
*[[Homocystinuria]]
*[[Hutchinson Gilford Syndrome]]<ref name="pmid16838330">{{cite journal |vauthors=Hennekam RC |title=Hutchinson-Gilford progeria syndrome: review of the phenotype |journal=Am. J. Med. Genet. A |volume=140 |issue=23 |pages=2603–24 |year=2006 |pmid=16838330 |doi=10.1002/ajmg.a.31346 |url=}}</ref>
*[[Hyper IgE syndrome]] / [[Job syndrome]]
*[[Hyperadrenalism]]
*[[Hyperglycerolemia]] - infantile form
*Hyperostosis corticalis deformans juvenilis
*[[Hypertrichotic osteochondrodysplasia]]
*[[Hypogonadotropic hypogonadism]] -- [[Syndactyly]]
*[[Hyperprolactinemia]]
*[[Infantile sialic acid storage disorder]]
*Iridogoniodysgenesis and skeletal anomalies
*[[Isotretinoin]]
*Kaler-Garrity-Stern syndrome<ref name="pmid1415349">{{cite journal |vauthors=Kaler SG, Garrity AM, Stern HJ, Rosenbaum KN, Orrison BM, Marini JC, Bernardini I, Saal HM |title=New autosomal recessive syndrome of sparse hair, osteopenia, and mental retardation in Mennonite sisters |journal=Am. J. Med. Genet. |volume=43 |issue=6 |pages=983–8 |year=1992 |pmid=1415349 |doi=10.1002/ajmg.1320430615 |url=}}</ref>
*[[Kallmann syndrome]]
*[[Klinefelter syndrome]]<ref name="pmid21214887">{{cite journal |vauthors=Ferlin A, Schipilliti M, Foresta C |title=Bone density and risk of osteoporosis in Klinefelter syndrome |journal=Acta Paediatr. |volume=100 |issue=6 |pages=878–84 |year=2011 |pmid=21214887 |doi=10.1111/j.1651-2227.2010.02138.x |url=}}</ref>
*[[Kidney disease]]
*[[Lactotroph adenoma]]
*Larsen syndrome, recessive type<ref name="pmid9237505">{{cite journal |vauthors=Kurtoglu S, Dundar M, Hallaç IK, Uzüm K, Okumuş Y, Oktem T |title=Polycystic kidney disease, biliary dysgenesis in a patient with Larsen's syndrome |journal=Clin. Genet. |volume=51 |issue=6 |pages=408–11 |year=1997 |pmid=9237505 |doi= |url=}}</ref>
*[[Leukemia]]
*[[Lobstein disease]]
*[[Lymphoma]]
*[[Lysinuric protein intolerance]]
*[[Maldigestion]]
*Marie-Bamberg syndrome
*[[Menkes Disease]]<ref name="pmid15876739">{{cite journal| author=Tanaka H| title=[Systemic bone diseases; clues for the pathogenetic mechanism of osteoporosis]. | journal=Clin Calcium | year= 2005 | volume= 15 | issue= 5 | pages= 776-82 | pmid=15876739 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15876739  }}</ref>
*[[Menopause]]
*Metaphyseal chondrodysplasia Spahr type
*[[Metaphyseal dysplasia Pyle type]]
*[[Methylmalonic acidemia]]
*[[Morquio syndrome]]
*[[Nodulosis-arthropathy-osteolysis syndrome]]<ref name="pmid19653001">{{cite journal |vauthors=Gok F, Crettol LM, Alanay Y, Hacihamdioglu B, Kocaoglu M, Bonafe L, Ozen S |title=Clinical and radiographic findings in two brothers affected with a novel mutation in matrix metalloproteinase 2 gene |journal=Eur. J. Pediatr. |volume=169 |issue=3 |pages=363–7 |year=2010 |pmid=19653001 |doi=10.1007/s00431-009-1028-7 |url=}}</ref>
*[[Oncogenic osteomalacia]]
*[[Oophorectomy]] - bilateral
*[[Orchidectomy]]
*[[Osteochondrodysplatic dwarfism -- deafness -- retinitis pigmentosa]]<ref name="pmid2783003">{{cite journal |author=Khaldi F, Bennaceur B, Gharbi HA |title=[Familial osteochondrodysplatic dwarfism associated with deafness and tapeto-retinal heredo-degeneration] |language=French |journal=Arch. Fr. Pediatr. |volume=46 |issue=6 |pages=429–32 |year=1989 |pmid=2783003 |doi= |url=}}</ref>
*[[Osteogenesis imperfecta]]
*Osteoporosis -- macrocephaly -- mental retardation -- blindness<ref name="pmid7265806">{{cite journal |vauthors=Heide T |title=[A syndrome of osteogenesis imperfecta, macrocephaly, wormian bones, frontal bossing, brachytelephalangy, hyperextensible joints, congenital blindness and oligophrenia in 3 sibs (author's transl)] |language=German |journal=Klin Padiatr |volume=193 |issue=4 |pages=334–40 |year=1981 |pmid=7265806 |doi=10.1055/s-2008-1034490 |url=}}</ref>
*[[Osteoporosis -- oculocutaneous -- hypopigmentation syndrome]]<ref name="pmid8721572">{{cite journal |vauthors=Hernández A, Nazará Z, Reynoso MC, Sarralde A, Bobadilla L, Fragoso R |title=Generalized osteoporosis in a patient with oculocutaneous hypopigmentation syndrome (OOCHS), without cerebral defects. A new syndrome? |journal=Clin. Genet. |volume=49 |issue=1 |pages=46–8 |year=1996 |pmid=8721572 |doi= |url=}}</ref>
*Osteoporosis-pseudoglioma syndrome<ref name="pmid8659519">{{cite journal |vauthors=Gong Y, Vikkula M, Boon L, Liu J, Beighton P, Ramesar R, Peltonen L, Somer H, Hirose T, Dallapiccola B, De Paepe A, Swoboda W, Zabel B, Superti-Furga A, Steinmann B, Brunner HG, Jans A, Boles RG, Adkins W, van den Boogaard MJ, Olsen BR, Warman ML |title=Osteoporosis-pseudoglioma syndrome, a disorder affecting skeletal strength and vision, is assigned to chromosome region 11q12-13 |journal=Am. J. Hum. Genet. |volume=59 |issue=1 |pages=146–51 |year=1996 |pmid=8659519 |pmc=1915094 |doi= |url=}}</ref>
* [[Otospondylomegaepiphyseal dysplasia]]
* [[Ovarian insufficiency due to FSH resistance]]
* [[Ovarian insufficiency, familial]]
* [[Pelizaeus-Merzbacher disease, recessive, acute infantile]]
* [[Pergolide]]
* Pena Shokeir syndrome
* Peroxisomal bifunctional enzyme deficiency
* Pointer syndrome<ref name="pmid9028464">{{cite journal |vauthors=Huq AH, Braverman RM, Greenberg F, Bacino CA, Rimoin DL, Lachman RS, Levin ML |title=The Pointer syndrome: a new syndrome with skeletal abnormalities, camptodactyly, facial anomalies, and feeding difficulties |journal=Am. J. Med. Genet. |volume=68 |issue=2 |pages=225–30 |year=1997 |pmid=9028464 |doi= |url=}}</ref>
* [[Postgastrectomy]]
* [[Prader-Willi syndrome]]
* [[Pregnancy]]<ref name="pmid22708337">{{cite journal |vauthors=Dytfeld J, Horst-Sikorska W |title=Pregnancy associated osteoporosis--a case report |journal=Ginekol. Pol. |volume=83 |issue=5 |pages=377–9 |year=2012 |pmid=22708337 |doi= |url=}}</ref>
* [[Premature aging]]
* [[Primary biliary cirrhosis]]
* [[Primary hypoparathyroidism]]
* [[Prolidase deficiency]]
* [[Protein deficiency]]
* Pseudoprogeria syndrome
* [[Reflex sympathetic dystrophy syndrome]]
* [[Renal osteodystrophy]]
* [[Sakati syndrome]]
* [[Sarcoidosis]]
* Schwartz-Jampel Syndrome
* [[Sickle cell anemia]]<ref name="pmid22662000">{{cite journal |vauthors=Elshal MF, Bernawi AE, Al-Ghamdy MA, Jalal JA |title=The association of bone mineral density and parathyroid hormone with serum magnesium in adult patients with sickle-cell anaemia |journal=Arch Med Sci |volume=8 |issue=2 |pages=270–6 |year=2012 |pmid=22662000 |pmc=3361039 |doi=10.5114/aoms.2012.28554 |url=}}</ref>
* [[Shprintzen-Golberg craniosynostosis]]
* [[Singleton-Merten syndrome]]<ref name="pmid175395">{{cite journal |vauthors=Gay BB, Kuhn JP |title=A syndrome of widened medullary cavities of bone, aortic calcification, abnormal dentition, and muscular weakness (the Singleton-Merten syndrome) |journal=Radiology |volume=118 |issue=2 |pages=389–95 |year=1976 |pmid=175395 |doi=10.1148/118.2.389 |url=}}</ref>
* Snyder-Robinson syndrome<ref name="pmid19206178">{{cite journal |vauthors=Becerra-Solano LE, Butler J, Castañeda-Cisneros G, McCloskey DE, Wang X, Pegg AE, Schwartz CE, Sánchez-Corona J, García-Ortiz JE |title=A missense mutation, p.V132G, in the X-linked spermine synthase gene (SMS) causes Snyder-Robinson syndrome |journal=Am. J. Med. Genet. A |volume=149A |issue=3 |pages=328–35 |year=2009 |pmid=19206178 |pmc=2653108 |doi=10.1002/ajmg.a.32641 |url=}}</ref>
* Spinocerebellar ataxia -- dysmorphism
* Sponastrime dysplasia<ref name="pmid2771481">{{cite journal |author=Lachman RS, Stoss H, Spranger J |title=Sponastrime dysplasia. A radiologic-pathologic correlation |journal=Pediatr Radiol |volume=19 |issue=6-7 |pages=417–24 |year=1989 |pmid=2771481 |doi= |url=}}</ref>
* Spondyloepimetaphyseal dysplasia with multiple dislocations
* Spondylometaphyseal dysplasia with dentinogenesis imperfecta
* Spondylo-ocular syndrome<ref name="pmid12719077">{{cite journal |vauthors=Rudolph G, Kalpadakis P, Bettecken T, Lichtner P, Haritoglou C, Hergersberg M, Meitinger T, Schmidt H |title=Spondylo-ocular syndrome: a new entity with crystalline lens malformation, cataract, retinal detachment, osteoporosis, and platyspondyly |journal=Am. J. Ophthalmol. |volume=135 |issue=5 |pages=681–7 |year=2003 |pmid=12719077 |doi= |url=}}</ref>
* [[Storm syndrome]]
* [[Sub clinical hypothyroidism]]
* Systemic infantile hyalinosis
* Thick skull syndrome
* Torg osteolysis syndrome<ref name="pmid20720557">{{cite journal |vauthors=Jeong SY, Kim BY, Kim HJ, Yang JA, Kim OH |title=A novel homozygous MMP2 mutation in a patient with Torg-Winchester syndrome |journal=J. Hum. Genet. |volume=55 |issue=11 |pages=764–6 |year=2010 |pmid=20720557 |doi=10.1038/jhg.2010.102 |url=}}</ref>
* [[Tricho-hepato-enteric syndrome]]
* [[Tuberous sclerosis]]
* [[Turner's syndrome]]
* [[Ulcerative colitis]]
* [[Underweight]]
* [[Urban rogers meyer syndrome]]
* [[Waldenstrom's macroglobulinemia]]
* [[Werner syndrome]]
* White Phosphorus poisoning
* [[Wilson's Disease]]
* [[Winchester syndrome]]
* [[Wolcott-Rallison syndrome]]<ref name="pmid10932183">{{cite journal |vauthors=Delépine M, Nicolino M, Barrett T, Golamaully M, Lathrop GM, Julier C |title=EIF2AK3, encoding translation initiation factor 2-alpha kinase 3, is mutated in patients with Wolcott-Rallison syndrome |journal=Nat. Genet. |volume=25 |issue=4 |pages=406–9 |year=2000 |pmid=10932183 |doi=10.1038/78085 |url=}}</ref>
* Wolman syndrome
* [[Xylosylprotein 4-beta-galactosyltransferase]] (XGPT) deficiency
* [[Zero gravity]]
}}
===Causes by organ system===
===Life threatening causes===
===Life threatening causes===
===Common causes and less common causes===
===Common causes and less common causes===

Revision as of 19:58, 21 August 2017


For Osteoporosis click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Osteoporosis Resident Survival Guide Microchapters
Overview
Classification
Causes
FIRE
Diagnosis
Treatment
Do's
Don'ts

Overview

Osteoporosis was first discovered by John Hunter, British surgeon, in 1800's. Osteoporosis divided to primary and secondary diseases, upon classification based on disease origin. While, it becomes divided to osteopenia, osteoporosis, and severe osteoporosis, upon classification based on disease severity. The pathophysiology of osteoporosis basically involves an imbalance between bone resorption and bone formation. Major factors that contribute to the development of osteoporosis include estrogen deficit and aging. The main pathway, through which these factors might lead to osteoporosis is reactive oxygen species (ROS) damage to osteocytes. Decreasing the capability of autophagy in osteocytes is another important issue; which make them vulnerable to oxidative stresses. Genes involved in the pathogenesis of osteoporosis are many genes that majorly can categorized in four main groups, include the osteoblast regulatory genes, osteoclast regulatory genes, bone matrix elements genes, and hormone/receptor genes. Osteoporosis must be differentiated from other diseases that cause decreasing in bone mineral density (BMD), such as idiopathic transient osteoporosis of hip, osteomalacia, scurvy, osteogenesis imperfecta, multiple myeloma, homocystinuria, and hypermetabolic resorptive osteoporosis. Osteoporosis is a major health problem involving 43.9% (43.4 million) of male and female population in the United States. White females and African-American males have the highest frequency among the other races. Risk factors for osteoporosis disease are of two types, including non-modifiable and modifiable (potentially) factors. Non-modifiable risk factors are age, sex, menopause, and family history. Modifiable (potentially) factors are smoking, alcohol consumption, immobility, glucocorticoid abuse, and proton pump inhibitor (PPI). Today, risk of fracture due to osteoporosis is threatening one out of two postmenopausal women and also one out of five older men. The 10-year risk for any osteoporosis-related fractures in 65-year-old white woman with no other risk factor is 9.3%. Upon the guidelines of USPSTF, all women ≥ 65 years old along with women < 65 years old with high risk of fracture are target of screening for osteoporosis; but there is not any recommendation to screen men for the disease. There are two major methods, that is suggested to use for screening osteoporosis, include dual energy x-ray absorptiometry (DXA) of both hip and lumbar spine bones, and quantitative ultrasonography of the calcaneus. If left untreated, most of patients with osteoporosis may progress to develop fracture. With appropriate and timely usage of medications along with calcium and/or vitamin D supplementation, the outcome of osteoporosis is usually good. The mainstays of treatment in primary osteoporosis disease are based on in lifestyle modifications. Most of the time in high risk patients and people with past history of osteoporotic fracture, medical therapy is necessary. Bisphosphonates are the first line treatment for osteoporosis disease. Raloxifene is the second line treatment of osteoporosis in postmenopausal women, for both treatment and prevention. Denosumab is a human monoclonal antibody designed to inhibit RANKL (RANK ligand), a protein that acts as the primary signal for bone removal. It is used to treat Osteoporosis in elder men and postmenopausal women. Teriparatide and Abaloparatide are human recombinant parathyroid hormones used to treat postmenopausal woman with osteoporosis at high risk of fracture or to increase bone mass in men with osteoporosis.

Classification

Osteoporosis may be classified into several subtypes based on disease origin, and disease severity.

 
 
 
 
 
 
 
 
 
 
 
 
 
 
Osteoporosis classifications
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Based on
Disease severity
 
 
 
 
 
 
 
 
 
 
 
Based on
Disease etiology
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
T-score measurement
 
 
 
 
 
 
 
 
 
 
 
Bone loss due to other diseases?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
-1>T-score>-2.5
 
 
T-score≤-2.5
 
 
T-score≤-2.5
plus
history of fracture
 
 
 
No
 
 
 
Yes
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Osteopenia
 
 
Osteoporosis
 
 
Severe osteoporosis
 
 
 
Primary osteoporosis
 
 
 
Secondary osteoporosis
 
 


Juvenile Osteoporosis (JO)

Osteoporosis in children and adolescents is rare, usually is due to some comorbidities or medications, secondary osteoporosis. Surprisingly, no significant causes have been found for rare cases, idiopathic osteoporosis.

No matter what causes it, juvenile osteoporosis can be a significant problem because it occurs during the child’s prime bone-building years. From birth through young adulthood, children steadily accumulate bone mass, which peaks sometime before age 30. The greater their peak bone mass, the lower their risk for osteoporosis later in life. After people reach their mid thirties, bone mass typically begins to decline—very slowly at first but increasing in their fifties and sixties. Both heredity and lifestyle choices—especially the amount of calcium in the diet and the level of physical activity influence the development of peak bone mass and the rate at which bone is lost later in life.

Secondary Osteoporosis

Idiopathic Juvenile Osteoporosis

  • Idiopathic juvenile osteoporosis (IJO) is a primary condition with no known cause. It is diagnosed after other causes of juvenile osteoporosis have been excluded. This rare form of osteoporosis typically occurs just before the onset of puberty in previously healthy children. The average age at onset is 7 years, with a range of 1 to 13 years. Most children experience complete recovery of bone.
  • The first sign of IJO is usually pain in the lower back, hips, and feet, often accompanied by difficulty walking. Knee and ankle pain and fractures of the lower extremities also may occur. Physical malformations include kyphosis, loss of height, a sunken chest, or a limp. These physical malformations are sometimes reversible after IJO has run its course.
  • There is no established medical or surgical therapy for juvenile osteoporosis. In some cases, no treatment may be needed because the condition usually goes away spontaneously. However, early diagnosis of juvenile osteoporosis is important so that steps can be taken to protect the child’s spine and other bones from fracture until remission occurs. These steps may include physical therapy, using crutches, avoiding unsafe weight-bearing activities, and other supportive care. A well-balanced diet rich in calcium and vitamin D is also important. In severe, long-lasting cases of juvenile osteoporosis, some medications called bisphosphonates, approved by the Food and Drug Administration for the treatment of osteoporosis in adults, have been given to children experimentally.
  • Most children with IJO experience a complete recovery of bone tissue. Although growth may be somewhat impaired during the acute phase of the disorder, normal growth resumes—and catch-up growth often occurs—afterward. Unfortunately, in some cases, IJO can result in permanent disability such as kyphoscoliosis or collapse of the rib cage.[1]

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of osteoporosis, however complications resulting from untreated osteoporosis are common.

Common causes

Less common causes

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Causes by organ system

Life threatening causes

Common causes and less common causes

FIRE: Focused Initial Rapid Evaluation

Diagnosis

Treatment

Do's

Dont's

References

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