Genetic epidemiology and heritability of AIS: A study of 415 Chinese female patients

Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of quantitative genetic effects, such as heritability, have not been fully evaluated. This genetic epidemiology study examined the sibling recur...

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Published inJournal of orthopaedic research Vol. 30; no. 9; pp. 1464 - 1469
Main Authors Tang, Nelson L.S., Yeung, Hiu-Yan, Hung, Vivian W.Y., Di Liao, Chen, Lam, Tsz-Ping, Yeung, Hau-Man, Lee, Kwong-Man, Ng, Bobby Kin-Wah, Cheng, Jack Chun-Yiu
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.09.2012
Subjects
Adolescent
adolescent idiopathic scoliosis (AIS)
Asian Continental Ancestry Group
Case-Control Studies
Child
China - epidemiology
Female
Genetic Predisposition to Disease
heritability
Humans
Male
Scoliosis - epidemiology
Scoliosis - genetics
sibling recurrent risk
China
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Abstract Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of quantitative genetic effects, such as heritability, have not been fully evaluated. This genetic epidemiology study examined the sibling recurrent risk and heritability of AIS in first‐degree relatives of 415 Chinese female patients, which is up to now the largest cohort. They were first diagnosed by community screening program and compared to 203 age‐matched normal controls. Out of the total 531 sibs of AIS cases, 94 sibs had scoliosis (sibling recurrence risk = 17.7%). The prevalence of AIS among male and female sibs of an index case were 11.5% (95% CI = 7.5–15.5) and 23.0% (95% CI = 18.1–27.9), respectively. Female sibs of an index case had an increased risk of 8.9‐fold (95% CI = 3.2–34.4) for developing AIS. These recurrent risks were significantly higher than the risk in the control group (p < 0.0001). Overall, heritability was estimated to be 87.5 ± 11.1%. The results confirmed the prevailing impression of strong genetic influence on the risk of AIS. Here we provided a large‐scale study for the genetic aggregation estimates in an Asian population for the first time. The finding also positioned AIS among other common disease or complex traits with a high heritability. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1464–1469, 2012
AbstractList Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of quantitative genetic effects, such as heritability, have not been fully evaluated. This genetic epidemiology study examined the sibling recurrent risk and heritability of AIS in first-degree relatives of 415 Chinese female patients, which is up to now the largest cohort. They were first diagnosed by community screening program and compared to 203 age-matched normal controls. Out of the total 531 sibs of AIS cases, 94 sibs had scoliosis (sibling recurrence risk = 17.7%). The prevalence of AIS among male and female sibs of an index case were 11.5% (95% CI = 7.5-15.5) and 23.0% (95% CI = 18.1-27.9), respectively. Female sibs of an index case had an increased risk of 8.9-fold (95% CI = 3.2-34.4) for developing AIS. These recurrent risks were significantly higher than the risk in the control group (p < 0.0001). Overall, heritability was estimated to be 87.5 ± 11.1%. The results confirmed the prevailing impression of strong genetic influence on the risk of AIS. Here we provided a large-scale study for the genetic aggregation estimates in an Asian population for the first time. The finding also positioned AIS among other common disease or complex traits with a high heritability.Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of quantitative genetic effects, such as heritability, have not been fully evaluated. This genetic epidemiology study examined the sibling recurrent risk and heritability of AIS in first-degree relatives of 415 Chinese female patients, which is up to now the largest cohort. They were first diagnosed by community screening program and compared to 203 age-matched normal controls. Out of the total 531 sibs of AIS cases, 94 sibs had scoliosis (sibling recurrence risk = 17.7%). The prevalence of AIS among male and female sibs of an index case were 11.5% (95% CI = 7.5-15.5) and 23.0% (95% CI = 18.1-27.9), respectively. Female sibs of an index case had an increased risk of 8.9-fold (95% CI = 3.2-34.4) for developing AIS. These recurrent risks were significantly higher than the risk in the control group (p < 0.0001). Overall, heritability was estimated to be 87.5 ± 11.1%. The results confirmed the prevailing impression of strong genetic influence on the risk of AIS. Here we provided a large-scale study for the genetic aggregation estimates in an Asian population for the first time. The finding also positioned AIS among other common disease or complex traits with a high heritability.
Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of quantitative genetic effects, such as heritability, have not been fully evaluated. This genetic epidemiology study examined the sibling recurrent risk and heritability of AIS in first‐degree relatives of 415 Chinese female patients, which is up to now the largest cohort. They were first diagnosed by community screening program and compared to 203 age‐matched normal controls. Out of the total 531 sibs of AIS cases, 94 sibs had scoliosis (sibling recurrence risk = 17.7%). The prevalence of AIS among male and female sibs of an index case were 11.5% (95% CI = 7.5–15.5) and 23.0% (95% CI = 18.1–27.9), respectively. Female sibs of an index case had an increased risk of 8.9‐fold (95% CI = 3.2–34.4) for developing AIS. These recurrent risks were significantly higher than the risk in the control group (p < 0.0001). Overall, heritability was estimated to be 87.5 ± 11.1%. The results confirmed the prevailing impression of strong genetic influence on the risk of AIS. Here we provided a large‐scale study for the genetic aggregation estimates in an Asian population for the first time. The finding also positioned AIS among other common disease or complex traits with a high heritability. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1464–1469, 2012
Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of quantitative genetic effects, such as heritability, have not been fully evaluated. This genetic epidemiology study examined the sibling recurrent risk and heritability of AIS in first‐degree relatives of 415 Chinese female patients, which is up to now the largest cohort. They were first diagnosed by community screening program and compared to 203 age‐matched normal controls. Out of the total 531 sibs of AIS cases, 94 sibs had scoliosis (sibling recurrence risk = 17.7%). The prevalence of AIS among male and female sibs of an index case were 11.5% (95% CI = 7.5–15.5) and 23.0% (95% CI = 18.1–27.9), respectively. Female sibs of an index case had an increased risk of 8.9‐fold (95% CI = 3.2–34.4) for developing AIS. These recurrent risks were significantly higher than the risk in the control group ( p  < 0.0001). Overall, heritability was estimated to be 87.5 ± 11.1%. The results confirmed the prevailing impression of strong genetic influence on the risk of AIS. Here we provided a large‐scale study for the genetic aggregation estimates in an Asian population for the first time. The finding also positioned AIS among other common disease or complex traits with a high heritability. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1464–1469, 2012
Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of quantitative genetic effects, such as heritability, have not been fully evaluated. This genetic epidemiology study examined the sibling recurrent risk and heritability of AIS in first-degree relatives of 415 Chinese female patients, which is up to now the largest cohort. They were first diagnosed by community screening program and compared to 203 age-matched normal controls. Out of the total 531 sibs of AIS cases, 94 sibs had scoliosis (sibling recurrence risk = 17.7%). The prevalence of AIS among male and female sibs of an index case were 11.5% (95% CI = 7.5-15.5) and 23.0% (95% CI = 18.1-27.9), respectively. Female sibs of an index case had an increased risk of 8.9-fold (95% CI = 3.2-34.4) for developing AIS. These recurrent risks were significantly higher than the risk in the control group (p < 0.0001). Overall, heritability was estimated to be 87.5 ± 11.1%. The results confirmed the prevailing impression of strong genetic influence on the risk of AIS. Here we provided a large-scale study for the genetic aggregation estimates in an Asian population for the first time. The finding also positioned AIS among other common disease or complex traits with a high heritability.
Author Lam, Tsz-Ping
Di Liao, Chen
Yeung, Hau-Man
Lee, Kwong-Man
Tang, Nelson L.S.
Hung, Vivian W.Y.
Cheng, Jack Chun-Yiu
Ng, Bobby Kin-Wah
Yeung, Hiu-Yan
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  givenname: Vivian W.Y.
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  givenname: Chen
  surname: Di Liao
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  givenname: Bobby Kin-Wah
  surname: Ng
  fullname: Ng, Bobby Kin-Wah
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  givenname: Jack Chun-Yiu
  surname: Cheng
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Nelson L.S. Tang, Hiu-Yan Yeung, and Vivian W.Y. Hung contributed equally to this work.
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Nelson L.S. Tang, Hiu‐Yan Yeung, and Vivian W.Y. Hung contributed equally to this work.
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Kjeldsen MJ, Kyvik KO, Christensen K, et al. 2001. Genetic and environmental factors in epilepsy: a population-based study of 11900 Danish twin pairs. Epilepsy Res 44: 167-178.
Miller NH, Justice CM, Marosy B, et al. 2005. Identification of candidate regions for familial idiopathic scoliosis. Spine (PhilaPa 1976) 30: 1181-1187.
Morocz M, Czibula A, Grozer ZB, et al. 2011. Association study of BMP4, IL6, Leptin, MMP3, and MTNR1B gene promoter polymorphisms and adolescent idiopathic scoliosis. Spine (PhilaPa 1976) 36: E123-E130.
Harney SM, Vilarino-Guell C, Adamopoulos IE, et al. 2008. Fine mapping of the MHC Class III region demonstrates association of AIF1 and rheumatoid arthritis. Rheumatology (Oxford) 47: 1761-1767.
Tang NL, Yeung HY, Lee KM, et al. 2006. A relook into the association of the estrogen receptor [alpha] gene (PvuII, XbaI) and adolescent idiopathic scoliosis: a study of 540 Chinese cases. Spine (PhilaPa 1976) 31: 2463-2468.
Sullivan PF, Kendler KS, Neale MC. 2003. Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies. Arch Gen Psychiatry 60: 1187-1192.
Sharma S, Gao X, Londono D, et al. 2011. Genome-wide association studies of adolescent idiopathic scoliosis suggest candidate susceptibility genes. Hum Mol Genet 20: 1456-1466.
Andersen MO, Thomsen K, Kyvik KO. 2007. Adolescent idiopathic scoliosis in twins: a population-based survey. Spine (PhilaPa 1976) 32: 927-930.
Ahn UM, Ahn NU, Nallamshetty L, et al. 2002. The etiology of adolescent idiopathic scoliosis. Am J Orthop (Belle Mead NJ) 31: 387-395.
Wang J, Yang S, Chen JJ, et al. 2007. Systemic lupus erythematosus: a genetic epidemiology study of 695 patients from China. Arch Dermatol Res 298: 485-491.
Bito LZ, Matheny A, Cruickshanks KJ, et al. 1997. Eye color changes past early childhood. The Louisville Twin Study. Arch Ophthalmol 115: 659-663.
Ashizawa K, Kumakura C, Zhou X, et al. 2005. RUS skeletal maturity of children in Beijing. Ann Hum Biol 32: 316-325.
Riseborough EJ, Wynne-Davies R. 1973. A genetic survey of idiopathic scoliosis in Boston, Massachusetts. J Bone Joint Surg Am 55: 974-982.
Wynne-Davies R. 1968. Familial (idiopathic) scoliosis. A family survey. J Bone Joint Surg Br 50: 24-30.
Burwell RG. 2003. Aetiology of idiopathic scoliosis: current concepts. Pediatr Rehabil 6: 137-170.
Inoue M, Minami S, Nakata Y, et al. 2002. Association between estrogen receptor gene polymorphisms and curve severity of idiopathic scoliosis. Spine (PhilaPa 1976) 27: 2357-2362.
Visscher PM, Hill WG, Wray NR. 2008. Heritability in the genomics era-Concepts and misconceptions. Nat Rev Genet 9: 255-266.
Inoue M, Minami S, Kitahara H, et al. 1998. Idiopathic scoliosis in twins studied by DNA fingerprinting: the incidence and type of scoliosis. J Bone Joint Surg Br 80: 212-217.
Silventoinen K, Magnusson PK, Tynelius P, et al. 2008. Heritability of body size and muscle strength in young adulthood: a study of one million Swedish men. Genet Epidemiol 32: 341-349.
Edery P, Margaritte-Jeannin P, Biot B, et al. 2011. New disease gene location and high genetic heterogeneity in idiopathic scoliosis. Eur J Hum Genet 19: 865-869.
Axenovich TI, Zaidman AM, Zorkoltseva IV, et al. 1999. Segregation analysis of idiopathic scoliosis: demonstration of a major gene effect. Am J Med Genet 86: 389-394.
Rice TK. 2008. Familial resemblance and heritability. Adv Genet 60: 35-49.
Weinstein SL, Ponseti IV. 1983. Curve progression in idiopathic scoliosis. J Bone Joint Surg Am 65: 447-455.
Gatz M, Reynolds CA, Fratiglioni L, et al. 2006. Role of genes and environments for explaining Alzheimer disease. Arch Gen Psychiatry 63: 168-174.
Takahashi Y, Matsumoto M, Karasugi T, et al. 2011. Replication study of the association between adolescent idiopathic scoliosis and two estrogen receptor genes. J Orthop Res 29: 834-837.
Chan V, Fong GC, Luk KD, et al. 2002. A genetic locus for adolescent idiopathic scoliosis linked to chromosome 19p13.3. Am J Hum Genet 71: 401-406.
Carr AJ. 1990. Adolescent idiopathic scoliosis in identical twins. J Bone Joint Surg Br 72: 1077.
Grjibovski AM, Olsen AO, Magnus P, et al. 2007. Psoriasis in Norwegian twins: contribution of genetic and environmental effects. J Eur Acad Dermatol Venereol 21: 1337-1343.
Justice CM, Miller NH, Marosy B, et al. 2003. Familial idiopathic scoliosis: evidence of an X-linked susceptibility locus. Spine (PhilaPa 1976) 28: 589-594.
Qiu XS, Tang NL, Yeung HY, et al. 2007. Melatonin receptor 1B (MTNR1B) gene polymorphism is associated with the occurrence of adolescent idiopathic scoliosis. Spine (PhilaPa 1976) 32: 1748-1753.
Lee CF, Fong DY, Cheung KM, et al. 2010. Costs of school scoliosis screening: a large, population-based study. Spine 35: 2266-2272.
Weinstein SL. 1989. Adolescent idiopathic scoliosis: prevalence and natural history. Instr Course Lect 38: 115-128.
Lowe TG, Edgar M, Margulies JY, et al. 2000. Etiology of idiopathic scoliosis: current trends in research. J Bone Joint Surg Am 82-A: 1157-1168.
Tu YS, Yin ZQ, Pen HM, et al. 2008. Genetic heritability of a shallow anterior chamber in Chinese families with primary angle closure glaucoma. Ophthalmic Genet 29: 171-176.
Ward K, Ogilvie J, Argyle V, et al. 2010. Polygenic inheritance of adolescent idiopathic scoliosis: a study of extended families in Utah. Am J Med Genet Part A 152A: 1178-1188.
Miller NH. 2002. Genetics of familial idiopathic scoliosis. Clin Orthop Relat Res 401: 60-64.
Salehi LB, Mangino M, De Serio S, et al. 2002. Assignment of a locus for autosomal dominant idiopathic scoliosis (IS) to human chromosome 17p11. Hum Genet 111: 401-404.
Takahashi Y, Matsumoto M, Karasugi T, et al. 2011. Lack of association between adolescent idiopathic scoliosis and previously reported single nucleotide polymorphisms in MATN1, MTNR1B, TPH1, and IGF1 in a Japanese population. J Orthop Res 29: 1055-1058.
Freitag CM. 2007. The genetics of autistic disorders and its clinical relevance: a review of the literature. Mol Psychiatry 12: 2-22.
Miller NH, Schwab DL, Sponseller PD, et al. 2001. Characterization of idiopathic scoliosis in a clinically well-defined population. Clin Orthop Relat Res 392: 349-357.
Cheng JC, Tang NL, Yeung HY, et al. 2007. Genetic association of complex traits: using idiopathic scoliosis as an example. Clin Orthop Relat Res 462: 38-44.
Ogilvie JW, Braun J, Argyle V, et al. 2006. The search for idiopathic scoliosis genes. Spine (PhilaPa 1976) 31: 679-681.
Hyttinen V, Kaprio J, Kinnunen L, et al. 2003. Genetic liability of type 1 diabetes and the onset age among 22,650 young Finnish twin pairs: a nationwide follow-up study. Diabetes 52: 1052-1055.
Lawrence JS, Martins CL, Drake GL. 1987. A family survey of lupus erythematosus. 1. Heritability. J Rheumatol 14: 913-921.
Falconer DS. 1965. The inheritance of liability to certain diseases, estimated from the incidence among relatives. Ann Hum Genet 29: 51-76.
Luk KD, Lee CF, Cheung KM, et al. 2010. Clinical effectiveness of school screening for adolescent idiopathic scoliosis: a large population-based retrospective cohort study. Spine (PhilaPa 1976) 35: 1607-1614.
Kesling KL, Reinker KA. 1997. Scoliosis in twins. A meta-analysis of the literature and report of six cases. Spine (PhilaPa 1976) 22: 2009-2014; discussion 2015.
1987; 14
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2001; 44
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2007; 12
2002; 27
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2001; 392
2003; 6
2010; 152A
2008; 29
2007; 298
2011; 20
2008; 47
1983; 65
2000; 82‐A
2005; 30
2007; 80
2002; 401
2005; 32
2003; 28
2002; 71
1968; 50
2003; 60
1989; 38
2007; 21
2011; 29
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References_xml – reference: Luk KD, Lee CF, Cheung KM, et al. 2010. Clinical effectiveness of school screening for adolescent idiopathic scoliosis: a large population-based retrospective cohort study. Spine (PhilaPa 1976) 35: 1607-1614.
– reference: Wynne-Davies R. 1968. Familial (idiopathic) scoliosis. A family survey. J Bone Joint Surg Br 50: 24-30.
– reference: Kesling KL, Reinker KA. 1997. Scoliosis in twins. A meta-analysis of the literature and report of six cases. Spine (PhilaPa 1976) 22: 2009-2014; discussion 2015.
– reference: Edery P, Margaritte-Jeannin P, Biot B, et al. 2011. New disease gene location and high genetic heterogeneity in idiopathic scoliosis. Eur J Hum Genet 19: 865-869.
– reference: Sullivan PF, Kendler KS, Neale MC. 2003. Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies. Arch Gen Psychiatry 60: 1187-1192.
– reference: Tang NL, Yeung HY, Lee KM, et al. 2006. A relook into the association of the estrogen receptor [alpha] gene (PvuII, XbaI) and adolescent idiopathic scoliosis: a study of 540 Chinese cases. Spine (PhilaPa 1976) 31: 2463-2468.
– reference: Lawrence JS, Martins CL, Drake GL. 1987. A family survey of lupus erythematosus. 1. Heritability. J Rheumatol 14: 913-921.
– reference: Burwell RG. 2003. Aetiology of idiopathic scoliosis: current concepts. Pediatr Rehabil 6: 137-170.
– reference: Visscher PM, Hill WG, Wray NR. 2008. Heritability in the genomics era-Concepts and misconceptions. Nat Rev Genet 9: 255-266.
– reference: Chan V, Fong GC, Luk KD, et al. 2002. A genetic locus for adolescent idiopathic scoliosis linked to chromosome 19p13.3. Am J Hum Genet 71: 401-406.
– reference: Grjibovski AM, Olsen AO, Magnus P, et al. 2007. Psoriasis in Norwegian twins: contribution of genetic and environmental effects. J Eur Acad Dermatol Venereol 21: 1337-1343.
– reference: Axenovich TI, Zaidman AM, Zorkoltseva IV, et al. 1999. Segregation analysis of idiopathic scoliosis: demonstration of a major gene effect. Am J Med Genet 86: 389-394.
– reference: Falconer DS. 1965. The inheritance of liability to certain diseases, estimated from the incidence among relatives. Ann Hum Genet 29: 51-76.
– reference: Rice TK. 2008. Familial resemblance and heritability. Adv Genet 60: 35-49.
– reference: Ward K, Ogilvie J, Argyle V, et al. 2010. Polygenic inheritance of adolescent idiopathic scoliosis: a study of extended families in Utah. Am J Med Genet Part A 152A: 1178-1188.
– reference: Takahashi Y, Matsumoto M, Karasugi T, et al. 2011. Replication study of the association between adolescent idiopathic scoliosis and two estrogen receptor genes. J Orthop Res 29: 834-837.
– reference: Morocz M, Czibula A, Grozer ZB, et al. 2011. Association study of BMP4, IL6, Leptin, MMP3, and MTNR1B gene promoter polymorphisms and adolescent idiopathic scoliosis. Spine (PhilaPa 1976) 36: E123-E130.
– reference: Cheng JC, Tang NL, Yeung HY, et al. 2007. Genetic association of complex traits: using idiopathic scoliosis as an example. Clin Orthop Relat Res 462: 38-44.
– reference: Lee CF, Fong DY, Cheung KM, et al. 2010. Costs of school scoliosis screening: a large, population-based study. Spine 35: 2266-2272.
– reference: Andersen MO, Thomsen K, Kyvik KO. 2007. Adolescent idiopathic scoliosis in twins: a population-based survey. Spine (PhilaPa 1976) 32: 927-930.
– reference: Wang J, Yang S, Chen JJ, et al. 2007. Systemic lupus erythematosus: a genetic epidemiology study of 695 patients from China. Arch Dermatol Res 298: 485-491.
– reference: Carr AJ. 1990. Adolescent idiopathic scoliosis in identical twins. J Bone Joint Surg Br 72: 1077.
– reference: Miller NH, Justice CM, Marosy B, et al. 2005. Identification of candidate regions for familial idiopathic scoliosis. Spine (PhilaPa 1976) 30: 1181-1187.
– reference: Miller NH. 2002. Genetics of familial idiopathic scoliosis. Clin Orthop Relat Res 401: 60-64.
– reference: Freitag CM. 2007. The genetics of autistic disorders and its clinical relevance: a review of the literature. Mol Psychiatry 12: 2-22.
– reference: Hyttinen V, Kaprio J, Kinnunen L, et al. 2003. Genetic liability of type 1 diabetes and the onset age among 22,650 young Finnish twin pairs: a nationwide follow-up study. Diabetes 52: 1052-1055.
– reference: Riseborough EJ, Wynne-Davies R. 1973. A genetic survey of idiopathic scoliosis in Boston, Massachusetts. J Bone Joint Surg Am 55: 974-982.
– reference: Inoue M, Minami S, Nakata Y, et al. 2002. Association between estrogen receptor gene polymorphisms and curve severity of idiopathic scoliosis. Spine (PhilaPa 1976) 27: 2357-2362.
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– reference: Gatz M, Reynolds CA, Fratiglioni L, et al. 2006. Role of genes and environments for explaining Alzheimer disease. Arch Gen Psychiatry 63: 168-174.
– reference: Weinstein SL. 1989. Adolescent idiopathic scoliosis: prevalence and natural history. Instr Course Lect 38: 115-128.
– reference: Bito LZ, Matheny A, Cruickshanks KJ, et al. 1997. Eye color changes past early childhood. The Louisville Twin Study. Arch Ophthalmol 115: 659-663.
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– reference: Inoue M, Minami S, Kitahara H, et al. 1998. Idiopathic scoliosis in twins studied by DNA fingerprinting: the incidence and type of scoliosis. J Bone Joint Surg Br 80: 212-217.
– reference: Ashizawa K, Kumakura C, Zhou X, et al. 2005. RUS skeletal maturity of children in Beijing. Ann Hum Biol 32: 316-325.
– reference: Weinstein SL, Ponseti IV. 1983. Curve progression in idiopathic scoliosis. J Bone Joint Surg Am 65: 447-455.
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Snippet Recent familial segregation studies supported a multifactorial genetic model for the etiology of adolescent idiopathic scoliosis (AIS). However, the extent of...
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SubjectTerms Adolescent
adolescent idiopathic scoliosis (AIS)
Asian Continental Ancestry Group
Case-Control Studies
Child
China - epidemiology
Female
Genetic Predisposition to Disease
heritability
Humans
Male
Scoliosis - epidemiology
Scoliosis - genetics
sibling recurrent risk
Title Genetic epidemiology and heritability of AIS: A study of 415 Chinese female patients
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https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjor.22090
https://www.ncbi.nlm.nih.gov/pubmed/22362628
https://www.proquest.com/docview/1039208384
Volume 30
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