LETTER TO THE EDITOR

Another perspective on the cause of metaphyseal fractures

Marvin Miller

Received: 13 December 2007 /Accepted: 5 January 2008 /Published online: 12 February 2008# Springer-Verlag 2008

Sir,I read with interest the article by O’Connell and Donoghue[1] that describes three newborn infants with classicmetaphyseal fractures (CMLs) following cesarean delivery.All of the CMLs were diagnosed radiographically or byclinical features on day 2 of life. Two of the infants were inthe breech presentation, and in the third case the mother hadpoorly controlled gestational diabetes. While the authorsattribute these fractures to twisting and pulling of theextremities during delivery, and possibly to large size (allthree infants weighed >3.45 kg), there are many suchinfants born in a similar fashion who never show anyevidence of bone fractures. The critical issue is whetherthese three infants may be predisposed to having lowernewborn bone strength, and I would suggest that fetalimmobilization is likely the common thread to understandingsuch a predisposition in these three infants.

Application of the Utah paradigm to the in uterodevelopment of fetal bone strength would suggest thatbone loading through fetal movement is critical to therealization of normal bone strength at the time of birth [2].Situations that diminish fetal movement will decrease bonestrength and include the following: cephalopelvic dispro-portion, malpresentation (including breech presentation),twin pregnancy, prematurity, oligohydramnios, large maternalfibroids, and maternal use of medications that can causedecreased fetal movement [3, 4]. Since two of the threeinfants were in the breech presentation, it is likely that they

may have been confined and moved less than normal whilein utero.

It is known that infants of diabetic mothers have a lowerbone mineral content at birth compared to controls as aresult of increased bone resorption [5, 6]. It is also knownthat infants of diabetic mothers have decreased cyclicmovements compared to normal controls, and this relativefetal immobilization would explain the osteoclast-mediatedosteopenia in infants of diabetic mothers [7].

Case reports such as those in the article by O’Connelland Donoghue support the existence of a transient brittlebone state from fetal immobilization that can lead to thesame types of fractures as seen in child abuse [1, 8]. CMLsassociated with physical therapy in the treatment of clubfeethave also been described in this journal, and it has alsobeen noted that some of these cases were also associatedwith fetal immobilization [9, 10]. The idea of decreasedfetal bone loading leading to decreased bone strength has ascientific foundation based on experimental observationsand is in accord with contemporary thinking of bonephysiology [2, 8, 11, 12].

The authors imply that CMLs are specific for abuseunless there is a prior history of accidental injury. I disagreewith this position. In the cases they present, what wouldhave happened if the swelling and leg abnormalities werenot noted until after the newborn infants had been dis-charged from the hospital and were in the care of theparents? Child abuse would have been alleged against theparents. There is a differential diagnosis for metaphysealfractures that includes copper deficiency, Menkes disease,scurvy, hyperparathyroidism, osteogenesis imperfecta, tem-porary brittle bone disease from fetal immobilization,physical therapy for clubfoot, breech presentation with/without external version, the bone disease of prematurity,fetal exposure to magnesium, and child abuse [1, 13, 14].

Pediatr Radiol (2008) 38:598–599DOI 10.1007/s00247-008-0758-4

DO00758; No of Pages

M. Miller (*)Department of Pediatrics,Wright State University Boonshoft School of Medicine,Children’s Medical Center, 1 Children’s Plaza,Dayton, OH 45404, USAe-mail: millerme@childrensdayton.org

Normal metaphyseal variants and the metaphyseal abnor-malities of rickets can also be confused with child abuse[15]. Consideration of this differential diagnosis will result ina greater likelihood of establishing a correct diagnosis in theproblematic cases of infants with unexplained metaphysealfractures.

References

1. O’Connell A, Donoghue VB (2007) Can classic metaphyseallesions follow uncomplicated cesarean delivery? Pediatr Radiol37:488–491

2. Frost H (2001) From Wolf’s law to the Utah paradigm: insightsabout bone physiology and its critical application. Anat Rec262:398–419

3. Miller ME, Hangartner TN (1999) Temporary brittle bone disease:association with decreased fetal movement and osteopenia. CalcifTissue Int 64:137–143

4. Miller ME (2005) Hypothesis: fetal movement influences fetaland infant bone strength. Med Hypotheses 65:880–886

5. Mimouni F, Steichen JJ, Tsang RC et al (1988) Decreased bonemineral content in infants of diabetic mothers. Am J Perinatol5:339–343

6. Demarini S, Specker B, Sierra RI et al (1995) Evidence ofincreased intrauterine bone resorption in term infants of motherswith insulin-dependent diabetes. J Pediatr 126:796–798

7. Robertson SS, Dierker LJ (2003) Fetal cyclic motor activity indiabetic pregnancies: sensitivity to maternal blood glucose. DevPsychobiol 42:9–16

8. Miller ME (2003) The lesson of temporary brittle bone disease: allbones are not created equal. Bone 33:466–474

9. Grayev AA, Boal DK, Wallach DW et al (2001) Metaphysealfractures mimicking abuse during treatment for clubfoot. PediatrRadiol 31:559–563

10. Miller ME (2002) Letter to the Editor. Fractures during physicaltherapy. Pediatr Radiol 32:536–537

11. Rodriguez JI, Palacios J, Garcia-Alix A et al (1988) Effects ofimmobilization on fetal bone development. A morphometric studyin newborns with congenital neuromuscular diseases with intra-uterine onset. Calcif Tissue Int 43:335–339

12. Rodriguez JI, Garcia-Alix A, Palacios J et al (1988) Changes inthe long bones due to fetal immobility caused by neuromusculardisease. J Bone Joint Surg Am 70:1052–1060

13. Paterson CR (2003) Radiological features of the brittle bonestates. J Diagn Radiogr Imaging 5:39–45

14. Wedig KE, Kogan J, Schorry E et al (2006) Skeletal demineralizationand fractures caused by fetal magnesium toxicity. J Perinatol 26:371–374

15. Kleinman P, Belanger PL, Karellas A et al (1991) Normalmetaphyseal radiologic variants not to be confused with findingsof infant abuse. AJR 156:781–783

Pediatr Radiol (2008) 38:598–599 599