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Reduced bone mineral density

MedGen UID:
393152
Concept ID:
C2674432
Finding
Synonym: Decreased bone mineral density Z score
 
HPO: HP:0004349

Definition

A reduction of bone mineral density, that is, of the amount of matter per cubic centimeter of bones. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVReduced bone mineral density

Conditions with this feature

Werner syndrome
MedGen UID:
12147
Concept ID:
C0043119
Disease or Syndrome
Werner syndrome is characterized by the premature appearance of features associated with normal aging and cancer predisposition. Individuals with Werner syndrome develop normally until the end of the first decade. The first sign is the lack of a growth spurt during the early teen years. Early findings (usually observed in the 20s) include loss and graying of hair, hoarseness, and scleroderma-like skin changes, followed by bilateral ocular cataracts, type 2 diabetes mellitus, hypogonadism, skin ulcers, and osteoporosis in the 30s. Myocardial infarction and cancer are the most common causes of death; the mean age of death in individuals with Werner syndrome is 54 years.
Pyle metaphyseal dysplasia
MedGen UID:
82704
Concept ID:
C0265294
Disease or Syndrome
Pyle disease is characterized by long bones with wide and expanded trabecular metaphyses, thin cortical bone, and bone fragility. Fractures are common in Pyle disease, and fracture lines usually go through the abnormally wide metaphyses, revealing their fragility (summary by Kiper et al., 2016).
Osteogenesis imperfecta with normal sclerae, dominant form
MedGen UID:
78665
Concept ID:
C0268363
Congenital Abnormality
COL1A1/2 osteogenesis imperfecta (COL1A1/2-OI) is characterized by fractures with minimal or absent trauma, variable dentinogenesis imperfecta (DI), and, in adult years, hearing loss. The clinical features of COL1A1/2-OI represent a continuum ranging from perinatal lethality to individuals with severe skeletal deformities, mobility impairments, and very short stature to nearly asymptomatic individuals with a mild predisposition to fractures, normal dentition, normal stature, and normal life span. Fractures can occur in any bone but are most common in the extremities. DI is characterized by gray or brown teeth that may appear translucent, wear down, and break easily. COL1A1/2-OI has been classified into four types based on clinical presentation and radiographic findings. This classification system can be helpful in providing information about prognosis and management for a given individual. The four more common OI types are now referred to as follows: Classic non-deforming OI with blue sclerae (previously OI type I). Perinatally lethal OI (previously OI type II). Progressively deforming OI (previously OI type III). Common variable OI with normal sclerae (previously OI type IV).
Primrose syndrome
MedGen UID:
162911
Concept ID:
C0796121
Disease or Syndrome
Primrose syndrome is characterized by macrocephaly, hypotonia, developmental delay, intellectual disability with expressive speech delay, behavioral issues, a recognizable facial phenotype, radiographic features, and altered glucose metabolism. Additional features seen in adults: sparse body hair, distal muscle wasting, and contractures. Characteristic craniofacial features include brachycephaly, high anterior hairline, deeply set eyes, ptosis, downslanted palpebral fissures, high palate with torus palatinus, broad jaw, and large ears with small or absent lobes. Radiographic features include calcification of the external ear cartilage, multiple Wormian bones, platybasia, bathrocephaly, slender bones with exaggerated metaphyseal flaring, mild epiphyseal dysplasia, and spondylar dysplasia. Additional features include hearing impairment, ocular anomalies, cryptorchidism, and nonspecific findings on brain MRI.
Osteogenesis imperfecta type 13
MedGen UID:
766801
Concept ID:
C3553887
Disease or Syndrome
Osteogenesis imperfecta (OI) is a connective tissue disorder characterized by bone fragility and low bone mass. Due to considerable phenotypic variability, Sillence et al. (1979) developed a classification of OI subtypes based on clinical features and disease severity: OI type I, with blue sclerae (166200); perinatal lethal OI type II, also known as congenital OI (166210); OI type III, a progressively deforming form with normal sclerae (259420); and OI type IV, with normal sclerae (166220). Most cases of OI are autosomal dominant with mutations in 1 of the 2 genes that code for type I collagen alpha chains, COL1A1 (120150) and COL1A2 (120160). Martinez-Glez et al. (2012) described osteogenesis imperfecta type XIII, an autosomal recessive form of the disorder characterized by normal teeth, faint blue sclerae, severe growth deficiency, borderline osteoporosis, and an average of 10 to 15 fractures a year affecting both upper and lower limbs and with severe bone deformity.
Cardiofaciocutaneous syndrome 3
MedGen UID:
815336
Concept ID:
C3809006
Disease or Syndrome
Cardiofaciocutaneous (CFC) syndrome is characterized by cardiac abnormalities (pulmonic stenosis and other valve dysplasias, septal defects, hypertrophic cardiomyopathy, rhythm disturbances), distinctive craniofacial appearance, and cutaneous abnormalities (including xerosis, hyperkeratosis, ichthyosis, keratosis pilaris, ulerythema ophryogenes, eczema, pigmented moles, hemangiomas, and palmoplantar hyperkeratosis). The hair is typically sparse, curly, fine or thick, woolly or brittle; eyelashes and eyebrows may be absent or sparse. Nails may be dystrophic or fast growing. Some form of neurologic and/or cognitive delay (ranging from mild to severe) is seen in all affected individuals. Neoplasia, mostly acute lymphoblastic leukemia, has been reported in some individuals.
Seizures-scoliosis-macrocephaly syndrome
MedGen UID:
909039
Concept ID:
C4225248
Disease or Syndrome
Seizures, scoliosis, and macrocephaly/microcephaly syndrome (SSMS) is an autosomal recessive neurodevelopmental disorder characterized by global developmental delay apparent from early infancy, impaired intellectual development, behavioral problems, poor or absent speech, seizures, dysmorphic facial features with macro- or microcephaly, and skeletal abnormalities, including scoliosis and delayed bone age. Other features may include hypotonia, gastrointestinal problems, and exostoses (summary by Gentile et al., 2019).
Osteogenesis imperfecta type 17
MedGen UID:
903845
Concept ID:
C4225301
Disease or Syndrome
Osteogenesis imperfecta (OI) is a group of genetic disorders that mainly affect the bones. The term "osteogenesis imperfecta" means imperfect bone formation. People with this condition have bones that break (fracture) easily, often from mild trauma or with no apparent cause. Multiple fractures are common, and in severe cases, can occur even before birth. Milder cases may involve only a few fractures over a person's lifetime.\n\nThere are at least 19 recognized forms of osteogenesis imperfecta, designated type I through type XIX. Several types are distinguished by their signs and symptoms, although their characteristic features overlap. Increasingly, genetic causes are used to define rarer forms of osteogenesis imperfecta. Type I (also known as classic non-deforming osteogenesis imperfecta with blue sclerae) is the mildest form of osteogenesis imperfecta. Type II (also known as perinatally lethal osteogenesis imperfecta) is the most severe. Other types of this condition, including types III (progressively deforming osteogenesis imperfecta) and IV (common variable osteogenesis imperfecta with normal sclerae), have signs and symptoms that fall somewhere between these two extremes.\n\nOther types of osteogenesis imperfecta are more severe, causing frequent bone fractures that are present at birth and result from little or no trauma. Additional features of these types can include blue sclerae of the eyes, short stature, curvature of the spine (scoliosis), joint deformities (contractures), hearing loss, respiratory problems, and a disorder of tooth development called dentinogenesis imperfecta. Mobility can be reduced in affected individuals, and some may use a walker or wheelchair. The most severe forms of osteogenesis imperfecta, particularly type II, can include an abnormally small, fragile rib cage and underdeveloped lungs. Infants with these abnormalities may have life-threatening problems with breathing and can die shortly after birth.\n\nThe milder forms of osteogenesis imperfecta, including type I, are characterized by bone fractures during childhood and adolescence that often result from minor trauma, such as falling while learning to walk. Fractures occur less frequently in adulthood. People with mild forms of the condition typically have a blue or grey tint to the part of the eye that is usually white (the sclera), and about half develop hearing loss in adulthood. Unlike more severely affected individuals, people with type I are usually of normal or near normal height.
Bone marrow failure syndrome 3
MedGen UID:
934711
Concept ID:
C4310744
Disease or Syndrome
Bone marrow failure syndrome-3 is an autosomal recessive disorder characterized by onset of pancytopenia in early childhood. Patients may have additional variable nonspecific somatic abnormalities, including poor growth, microcephaly, and skin anomalies (summary by Tummala et al., 2016). BMFS3 has a distinct phenotype and may include features that overlap with Shwachman-Diamond syndrome (SDS1; 260400), such as pancreatic insufficiency and short stature, and with dyskeratosis congenita (see, e.g., DKCA1, 127550), such as dental and hair abnormalities and shortened telomeres. In addition, some patients may have joint and skeletal abnormalities, impaired development, and retinal dysplasia (summary by D'Amours et al., 2018). For a discussion of genetic heterogeneity of BMFS, see BMFS1 (614675).
Cole-Carpenter syndrome 1
MedGen UID:
1374755
Concept ID:
C4317154
Disease or Syndrome
Cole-Carpenter syndrome is characterized by bone fragility, craniosynostosis, ocular proptosis, hydrocephalus, and distinctive facial features (Cole and Carpenter, 1987). Genetic Heterogeneity of Cole-Carpenter Syndrome Cole-Carpenter syndrome-2 (CLCRP2; 616294) is caused by mutation in the SEC24D gene (607186).
Spondyloepimetaphyseal dysplasia, di rocco type
MedGen UID:
1646454
Concept ID:
C4693799
Disease or Syndrome
Spondyloepimetaphyseal dysplasia of the Di Rocco type (SEMDDR) is characterized by short stature, joint pain, and genu varum, as well as SEMD involving primarily the hips but also affecting the wrists, hands, knees, and ankles. Patients also exhibit variable degrees of metaphyseal and spine involvement (Di Rocco et al., 2018).
Spondyloepiphyseal dysplasia, kondo-fu type
MedGen UID:
1683128
Concept ID:
C5193071
Disease or Syndrome
The Kondo-Fu type of spondyloepiphyseal dysplasia (SEDKF) is characterized by severely retarded growth and skeletal anomalies, including spondyloepiphyseal dysplasia with associated kyphosis and reduced bone mineral density. Elevated levels of blood lysosomal enzymes have also been observed (Kondo et al., 2018).
Rajab interstitial lung disease with brain calcifications 1
MedGen UID:
1750003
Concept ID:
C5436276
Disease or Syndrome
Rajab interstitial lung disease with brain calcifications-1 (RILCBC1) is an autosomal recessive multisystem disorder with a highly variable phenotype. Most patients present in infancy or early childhood with poor growth and interstitial lung disease, which may lead to death. Some may also have liver, skeletal, and renal abnormalities, and most have intracranial calcifications on brain imaging. Some may have early impaired motor development, but most have normal cognitive development (summary by Xu et al., 2018). Genetic Heterogeneity of Rajab Interstitial Lung Disease with Brain Calcifications Also see Rajab interstitial disease with brain calcifications-2 (RILDBC2; 619013), caused by mutation in the FARSA gene (602918).
Combined osteogenesis imperfecta and Ehlers-Danlos syndrome 1
MedGen UID:
1763836
Concept ID:
C5436842
Disease or Syndrome
Combined osteogenesis imperfecta and Ehlers-Danlos syndrome-1 (OIEDS1) is an autosomal dominant generalized connective tissue disorder characterized by features of both osteogenesis imperfecta (bone fragility, long bone fractures, blue sclerae) and Ehlers-Danlos syndrome (joint hyperextensibility, soft and hyperextensible skin, abnormal wound healing, easy bruising, vascular fragility) (summary by Cabral et al., 2007; Malfait et al., 2013). Genetic Heterogeneity of Combined Osteogenesis Imperfecta and Ehlers-Danlos Syndrome Also see OIEDS2 (619120), caused by mutation in the COL1A2 gene (120160) on chromosome 7q21.
Marbach-Rustad progeroid syndrome
MedGen UID:
1784907
Concept ID:
C5543388
Disease or Syndrome
Marbach-Rustad progeroid syndrome (MARUPS) is characterized by progeroid appearance with little subcutaneous fat and triangular facies, growth retardation with short stature, hypoplastic mandible crowded with unerupted supernumerary teeth, and cerebellar intention tremor. Psychomotor development is normal. Although features are reminiscent of Hutchinson-Gilford progeria syndrome (HGPS; 176670), MARUPS is less severe, with a relatively good prognosis. Two patients have been reported (Marbach et al., 2019).
Osteootohepatoenteric syndrome
MedGen UID:
1785846
Concept ID:
C5543557
Disease or Syndrome
Osteootohepatoenteric syndrome (OOHE) is characterized by a variable combination of bone fragility, hearing loss, cholestasis, and congenital diarrhea. Some patients also display mild developmental delay and intellectual disability (Esteve et al., 2018).
Short stature, Dauber-Argente type
MedGen UID:
1794178
Concept ID:
C5561968
Disease or Syndrome
Short stature of the Dauber-Argente type (SSDA) is characterized by progressive postnatal growth failure, moderate microcephaly, thin long bones, and mildly decreased bone density. Patients have elevated circulating levels of total IGF1 (147440) due to impaired proteolysis of IGFBP3 (146732) and IGFBP5 (146734), resulting in reduced free IGF1 (Dauber et al., 2016).
Osteogenesis imperfecta, IIA 22
MedGen UID:
1801631
Concept ID:
C5676943
Disease or Syndrome
Osteogenesis imperfecta comprises a group of connective tissue disorders characterized clinically by bone fragility, low bone mass, and increased susceptibility to fractures. Osteogenesis imperfecta type XXII (OI22) is a severe recessive form of the disease (Dubail et al., 2020).
Congenital disorder of glycosylation, type IIy
MedGen UID:
1824067
Concept ID:
C5774294
Disease or Syndrome
Congenital disorder of glycosylation type IIy (CDG2Y) is an autosomal recessive multisystemic congenital disorder characterized by poor overall growth and global developmental delay with impaired intellectual development. Other features may include hypotonia, seizures, brain imaging abnormalities, dysmorphic features, and various skeletal defects. Laboratory studies show a subtle type II glycosylation defect of serum transferrin (Tambe et al., 2020). For a general discussion of CDGs, see CDG1A (212065).
Neurodevelopmental disorder with dysmorphic facies and ischiopubic hypoplasia
MedGen UID:
1824071
Concept ID:
C5774298
Disease or Syndrome
Neurodevelopmental disorder with dysmorphic facies and ischiopubic hypoplasia (NEDFIH) is an autosomal recessive disorder characterized by these features and moderate to severe global developmental delay. Affected individuals show episodic regression during periods of stress, including seizures or infection, the latter of which may be associated with lymphopenia. Brain imaging shows diminished white matter volume, enlarged ventricles, and thin corpus callosum (Muffels et al., 2023).
Joint contractures, osteochondromas, and B-cell lymphoma
MedGen UID:
1824078
Concept ID:
C5774305
Disease or Syndrome
Joint contractures, osteochondromas, and B-cell lymphoma (JCOSL) is an autosomal recessive systemic disorder characterized by the development of painless fixed contractures of the joints in early childhood. There is evidence of abnormal chondrocyte homeostasis, resulting in contractures, osteopenia, and the development of osteochondromas. Laboratory studies show abnormal levels and function of B- and T-cell subsets, and patients can develop B-cell lymphomas or malignancies. Despite the abnormalities in immunologic cells, immunodeficiency is not a feature of the disease, suggesting that it can be classified as a 'primary immune regulatory disorder' (Sharma et al., 2022).

Professional guidelines

PubMed

Li D, Gao Z, Li Q, Liu X, Liu H
Front Endocrinol (Lausanne) 2023;14:1135181. Epub 2023 May 5 doi: 10.3389/fendo.2023.1135181. PMID: 37214253Free PMC Article
Giustina A, Bouillon R, Dawson-Hughes B, Ebeling PR, Lazaretti-Castro M, Lips P, Marcocci C, Bilezikian JP
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LeBlanc KE, Muncie HL Jr, LeBlanc LL
Am Fam Physician 2014 Jun 15;89(12):945-51. PMID: 25162161

Recent clinical studies

Etiology

Li D, Gao Z, Li Q, Liu X, Liu H
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Hou W, Chen S, Zhu C, Gu Y, Zhu L, Zhou Z
Front Endocrinol (Lausanne) 2023;14:1074574. Epub 2023 Feb 3 doi: 10.3389/fendo.2023.1074574. PMID: 36817605Free PMC Article
Jun L, Robinson M, Geetha T, Broderick TL, Babu JR
Int J Mol Sci 2023 Feb 3;24(3) doi: 10.3390/ijms24032973. PMID: 36769296Free PMC Article
Berman NK, Honig S, Cronstein BN, Pillinger MH
Osteoporos Int 2022 Jun;33(6):1235-1241. Epub 2022 Jan 4 doi: 10.1007/s00198-021-05972-w. PMID: 34981132
Vierucci F, Saggese G, Cimaz R
Curr Opin Rheumatol 2017 Sep;29(5):535-546. doi: 10.1097/BOR.0000000000000423. PMID: 28582319

Diagnosis

Dai Z, Xu W, Ding R, Peng X, Shen X, Song J, Du P, Wang Z, Liu Y
Front Public Health 2023;11:1151837. Epub 2023 May 26 doi: 10.3389/fpubh.2023.1151837. PMID: 37304119Free PMC Article
Rochira V
Andrology 2020 Nov;8(6):1539-1550. Epub 2020 Jun 17 doi: 10.1111/andr.12827. PMID: 32469467
He J, Xu S, Zhang B, Xiao C, Chen Z, Si F, Fu J, Lin X, Zheng G, Yu G, Chen J
Aging (Albany NY) 2020 May 11;12(9):8583-8604. doi: 10.18632/aging.103168. PMID: 32392181Free PMC Article
Bover J, Ureña-Torres P, Torregrosa JV, Rodríguez-García M, Castro-Alonso C, Górriz JL, Laiz Alonso AM, Cigarrán S, Benito S, López-Báez V, Lloret Cora MJ, daSilva I, Cannata-Andía J
Nefrologia (Engl Ed) 2018 Sep-Oct;38(5):476-490. Epub 2018 Apr 24 doi: 10.1016/j.nefro.2017.12.006. PMID: 29703451
Vierucci F, Saggese G, Cimaz R
Curr Opin Rheumatol 2017 Sep;29(5):535-546. doi: 10.1097/BOR.0000000000000423. PMID: 28582319

Therapy

Dai Z, Xu W, Ding R, Peng X, Shen X, Song J, Du P, Wang Z, Liu Y
Front Public Health 2023;11:1151837. Epub 2023 May 26 doi: 10.3389/fpubh.2023.1151837. PMID: 37304119Free PMC Article
Giustina A, Bouillon R, Dawson-Hughes B, Ebeling PR, Lazaretti-Castro M, Lips P, Marcocci C, Bilezikian JP
Endocrine 2023 Jan;79(1):31-44. Epub 2022 Oct 26 doi: 10.1007/s12020-022-03208-3. PMID: 36287374Free PMC Article
Berman NK, Honig S, Cronstein BN, Pillinger MH
Osteoporos Int 2022 Jun;33(6):1235-1241. Epub 2022 Jan 4 doi: 10.1007/s00198-021-05972-w. PMID: 34981132
Bover J, Ureña-Torres P, Torregrosa JV, Rodríguez-García M, Castro-Alonso C, Górriz JL, Laiz Alonso AM, Cigarrán S, Benito S, López-Báez V, Lloret Cora MJ, daSilva I, Cannata-Andía J
Nefrologia (Engl Ed) 2018 Sep-Oct;38(5):476-490. Epub 2018 Apr 24 doi: 10.1016/j.nefro.2017.12.006. PMID: 29703451
Vierucci F, Saggese G, Cimaz R
Curr Opin Rheumatol 2017 Sep;29(5):535-546. doi: 10.1097/BOR.0000000000000423. PMID: 28582319

Prognosis

Dai Z, Xu W, Ding R, Peng X, Shen X, Song J, Du P, Wang Z, Liu Y
Front Public Health 2023;11:1151837. Epub 2023 May 26 doi: 10.3389/fpubh.2023.1151837. PMID: 37304119Free PMC Article
Rochira V
Andrology 2020 Nov;8(6):1539-1550. Epub 2020 Jun 17 doi: 10.1111/andr.12827. PMID: 32469467
Bover J, Ureña-Torres P, Torregrosa JV, Rodríguez-García M, Castro-Alonso C, Górriz JL, Laiz Alonso AM, Cigarrán S, Benito S, López-Báez V, Lloret Cora MJ, daSilva I, Cannata-Andía J
Nefrologia (Engl Ed) 2018 Sep-Oct;38(5):476-490. Epub 2018 Apr 24 doi: 10.1016/j.nefro.2017.12.006. PMID: 29703451
Vierucci F, Saggese G, Cimaz R
Curr Opin Rheumatol 2017 Sep;29(5):535-546. doi: 10.1097/BOR.0000000000000423. PMID: 28582319
Adams LA, Anstee QM, Tilg H, Targher G
Gut 2017 Jun;66(6):1138-1153. Epub 2017 Mar 17 doi: 10.1136/gutjnl-2017-313884. PMID: 28314735

Clinical prediction guides

Dai Z, Xu W, Ding R, Peng X, Shen X, Song J, Du P, Wang Z, Liu Y
Front Public Health 2023;11:1151837. Epub 2023 May 26 doi: 10.3389/fpubh.2023.1151837. PMID: 37304119Free PMC Article
Hou W, Chen S, Zhu C, Gu Y, Zhu L, Zhou Z
Front Endocrinol (Lausanne) 2023;14:1074574. Epub 2023 Feb 3 doi: 10.3389/fendo.2023.1074574. PMID: 36817605Free PMC Article
Afarideh M, Sartori-Valinotti JC, Tollefson MM
JAMA Dermatol 2021 Dec 1;157(12):1437-1446. doi: 10.1001/jamadermatol.2021.4143. PMID: 34705034Free PMC Article
He J, Xu S, Zhang B, Xiao C, Chen Z, Si F, Fu J, Lin X, Zheng G, Yu G, Chen J
Aging (Albany NY) 2020 May 11;12(9):8583-8604. doi: 10.18632/aging.103168. PMID: 32392181Free PMC Article
Bover J, Ureña-Torres P, Torregrosa JV, Rodríguez-García M, Castro-Alonso C, Górriz JL, Laiz Alonso AM, Cigarrán S, Benito S, López-Báez V, Lloret Cora MJ, daSilva I, Cannata-Andía J
Nefrologia (Engl Ed) 2018 Sep-Oct;38(5):476-490. Epub 2018 Apr 24 doi: 10.1016/j.nefro.2017.12.006. PMID: 29703451

Recent systematic reviews

Loxton P, Narayan K, Munns CF, Craig ME
Diabetes Care 2021 Aug;44(8):1898-1905. Epub 2021 Jul 20 doi: 10.2337/dc20-3128. PMID: 34285100Free PMC Article
Singh NK, Jha RH, Gargeshwari A, Kumar P
Eur Arch Otorhinolaryngol 2018 Jan;275(1):1-10. Epub 2017 Oct 17 doi: 10.1007/s00405-017-4768-4. PMID: 29043479
Salman-Monte TC, Torrente-Segarra V, Vega-Vidal AL, Corzo P, Castro-Dominguez F, Ojeda F, Carbonell-Abelló J
Autoimmun Rev 2017 Nov;16(11):1155-1159. Epub 2017 Sep 9 doi: 10.1016/j.autrev.2017.09.011. PMID: 28899800
Lucato P, Trevisan C, Stubbs B, Zanforlini BM, Solmi M, Luchini C, Girotti G, Pizzato S, Manzato E, Sergi G, Giannini S, Fusaro M, Veronese N
Osteoporos Int 2016 Nov;27(11):3155-3164. Epub 2016 Jun 11 doi: 10.1007/s00198-016-3658-8. PMID: 27289533
Amorim T, Wyon M, Maia J, Machado JC, Marques F, Metsios GS, Flouris AD, Koutedakis Y
Sports Med 2015 Feb;45(2):257-68. doi: 10.1007/s40279-014-0268-5. PMID: 25281333

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