distal forearm fractures and inheritance of bone mass

Journal of Clinical Densitometry: Assessment of Skeletal Health, vol. 16, no. 1, 79e80, 2013� Copyright 2013 by The International Society for Clinical Densitometry1094-6950/16:79e80/$36.00

Original Article

Distal Forearm Fractures and Inheritance of Bone Mass

Stephen Paul Tuck*

Department of Rheumatology, The James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW,United Kingdom

Low-trauma distal forearm fractures in postmen-opausal women have long been recognized as anindicator of osteoporosis. Indeed, up to 50% ofsuch women have bone density measurements ondual-energy X-ray absorptiometry (DXA) in theosteoporotic range as defined by the World HealthOrganization (1). Similar results are seen in menwith distal forearm fractures, with up to 42% havingT-scores ��2.5 using gender-specific normativedata (2). Furthermore, after a first distal forearmfracture, there is an increased risk of subsequentfractures with hip fractures being increased by 1.4-fold in women and 2.7-fold in men and vertebralfractures by 5.2-fold and 10.7-fold, respectively(3). As reported by Center et al (4) in 1999, thereis also an increase in standardized mortality ratioafter distal forearm fractures, which is particularlyhigh for men and still persists according to morerecent data from both Danish and Canadian cohorts(4,5,6). They are so of considerable importance bothin their own right and as indicators of osteoporosisand increased fracture risk. Therefore, any datathat help us to understand their pathogenesis are tobe welcomed.

In clinic, I am often asked by my patients if theirchildren are at risk? In this journal, Fernandez-Ojeda et al present data that may help to answerthis question. They have demonstrated that thedaughters of women with distal forearm fractureshave lower peak bone mineral density (BMD) thanage- and gender-matched control subjects at the

Received 8/22/2012; Accepted 9/4/2012.*Address correspondence to: Stephen Paul Tuck, BSc,

MBChB, MRCP (Ireland), MD, Department of Rheumatology,The James Cook University Hospital, Marton Road, Middles-brough TS4 3BW, United Kingdom. E-mail: stephen.tuck@stees.nhs.uk

79

hip sites. Daughters of women with distal forearmfractures whose mothers were osteoporotic onDXA scanning also had lower peak lumbar spineBMD. These differences persisted after adjustingfor age, height, and body mass index. This is notsurprising as there is extensive literature to showthat women with a maternal history of fracture orosteoporosis have lower BMD than age-matchedcontrol subjects (7). As far back as 1994, Seemanet al (8) showed that daughters of women with hipfractures have lower BMD compared with a controlpopulation.

The reasons for this could be both genetic andshared environment. Peak bone mass is largely ge-netically determined with genetic epidemiologicalstudies suggesting that the heritable componentmay range between 65% and 92% (9). Recently,quantitative trait locus studies in mice and humanshave identified multiple chromosomal regions thatinfluence bone mass (10e12). Indeed, there arenow many studies implicating a growing numberof genes in the determination of bone density andfracture risk, with the results seeming to vary withboth race and gender. Environmental factors arealso of considerable importance, and these maywell be shared between offspring and their parents.Birth weight and in utero nutrition have been dem-onstrated to be important in determining bone massin both childhood and adulthood (13,14). There arealso good data on the importance of maternal nutri-tion, lifestyle, and 25-hydroxyvitamin D status (15)as well as on physical activity, calcium intake, andchildhood bone mineral content (16). Data fromlong-term follow-up studies from birth to adulthoodsuch as the Newcastle 1000 Families Study (17) at50 yr have demonstrated the importance of adultlife factors on later BMD.

80 Tuck

So the next time that I am asked the question‘‘Are my children at risk?’’ I shall be able to saythat the answer would appear to be yes, and thisincludes daughters of postmenopausal women withlow-trauma distal forearm fractures. The reasonsfor this include genetics and shared environment.All medical and paramedical professionals involvedwith direct patient care need to bear this in mind,and perhaps lifestyle advice and risk assessmentshould be applied to children of patients who sustainosteoporotic fractures.

References1. Earnshaw SA, Caute SA, Worley A, Hosking DJ. 1998

Colles’ fracture of the wrist as an indicator of underlyingosteoporosis in postmenopausal women: a prospectivestudy of bone mineral density and bone turnover rate.Osteoporos Int 8:53e60.

2. Tuck SP, Raj N, Summers GD. 2002 Is distal forearmfracture in men due to osteoporosis? Osteoporos Int 13:630e636.

3. Cuddihy MT, Gabriel SE, Crowson CS, et al. 1999 Forearmfractures as predictors of subsequent osteoporotic fracture.Osteoporos Int 9:469e475.

4. Center JR, Nguyen TV, Schnieder D, et al. 1999 Mortalityafter all major types of osteoporotic fracture in men andwomen: an observational study. Lancet 353:878e882.

5. Morin S, Lix LM, Azimaee M, et al. 2011 Mortality ratesafter incident non-traumatic fractures in older men andwomen. Osteoporos Int 22(9):2439e2448.

6. Kannegaard PN, van der Mark S, Eiken P, Abrahamsen B.2010 Excess mortality in men compared with womenfollowing hip fracture. National analysis of comedications,comorbidity and survival. Age Ageing 39(2):203e209.

Journal of Clinical Densitometry: Assessment of Skeletal Health

7. Keen RW, Hart DJ, Arden NK, et al. 1999 Family history ofappendicular fracture and risk of osteoporosis: a population-based study. Osteoporos Int 10:161e166.

8. Seeman E, Tsalamandris C, Formica C, et al. 1994 Reducedfemoral neck bone density in the daughters of women withhip fractures: the role of low peak density in the pathogen-esis of osteoporosis. J Bone Miner Res 9:739e743.

9. Ngyuen TV, Blangero J, Eisman JA. 2000 Genetic epidemi-ological approaches to the search for osteoporosis genes.J Bone Miner Res 15:392e401.

10. Deng HW, Xu FH, Huang QY, et al. 2002 Awhole-genomelinkage scan suggests several genomic regions potentiallycontaining quantitative trait loci for osteoporosis. J ClinEndocrinol Metab 87:5151e5159.

11. Koller DL, Liu G, Econs MJ, et al. 2001 Genome screen forquantitative trait loci underlying normal variation in femo-ral structure. J Bone Miner Res 16:985e991.

12. Orwoll ES, Belknap JK, Klein RF. 2001 Gender specificityin the genetic determinant of bone mass. J Bone Miner Res16:1962e1971.

13. Baird J, Kurshid MA, Kim M, et al. 2011 Does birthweightpredict bone mass in adulthood? A systematic review andmeta-analysis. Osteoporos Int 22:1323e1334.

14. Harvey NC, Mahon PA, Kim M, et al. 2012 Intrauterinegrowth and postnatal skeletal development: findings fromthe Southampton Women’s Survey. Paediatr Perinat Epide-miol 26:34e44.

15. Goodfellow LR, Earl S, Cooper C, Harvey NC. 2010Maternal diet, behaviour and offspring skeletal health. IntJ Environ Res Public Health 7:1760e1772.

16. Harvey NC, Cole ZA, Crozier SR, et al. 2012 Physi-cal activity, calcium intake and childhood bone mineral:a population-based cross-sectional study. Osteoporos Int23:121e130.

17. Pearce MS, Birrell FN, Francis RM, et al. 2005 Lifecoursestudy of bone health at age 49-51 years: the NewcastleThousand Families Cohort Study. J Epidemiol CommunityHealth 59:475e480.

Volume 16, 2013