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Published on: April 11, 2012
Joint laxity in the parents of children with temporary brittle bone disease
Colin R Paterson1, Patricia A Mole
1Formerly Department of Medicine, University of Dundee, Dundee, Scotland, UK. c.s.paterson@btinternet.com
Insights
Parental joint laxity may indicate a risk for temporary brittle bone disease in children. This study found significant hypermobility in parents of children with unexplained fractures, suggesting a heritable factor.
Area of Science:
- Pediatrics
- Genetics
- Orthopedics
Background:
- Temporary brittle bone disease is a controversial cause of pediatric fractures.
- Premature birth, twin pregnancy, and fetal movement issues are contributing factors.
- Heritable factors are also considered important in its etiology.
Purpose of the Study:
- To investigate the role of parental joint laxity in children with unexplained fractures.
- To determine if hypermobility syndrome is more prevalent in parents of affected children.
- To explore the potential inheritance patterns of this risk factor.
Main Methods:
- Infants with temporary brittle bone disease findings were identified.
- Parental joint laxity was assessed using the nine-point Beighton scale.
- Parental scores were compared to control groups.
Main Results:
- 40 out of 81 children had at least one parent with a Beighton score ≥ 4.
- Fathers showed a significant difference in laxity compared to controls (P=0.013).
- The most flexible parent (mother or father) showed significant differences from controls (P=0.042 and P=0.0065).
Conclusions:
- Parental joint laxity is a significant risk factor for temporary brittle bone disease.
- Autosomal dominant inheritance is likely for this risk factor.
- Assessing parental joint laxity can aid in evaluating children with fractures.
Abstract:
One controversial cause of unexplained fractures in young children is temporary brittle bone disease. Contributory factors for this disorder include the following: premature birth, twin pregnancy and diminished foetal movement. Heritable factors may also be important. Infants with findings consistent with temporary brittle bone disease were identified from clinical and medico-legal referrals. The routine evaluation of each family included examination of both parents where available for joint laxity using the nine-point Beighton scale. Of 81 children in whom both parents had been examined personally, 40 had at least one parent with a Beighton score of four or more, conventionally regarded as indicative of the hypermobility syndrome. We found no significant difference in laxity when we compared the whole group of mothers with the controls (P = 0.081). The fathers were significantly different from their control group (P = 0.013). When we compared the figures for the most flexible parent of each child, there were significant differences from control subjects both in the mothers and in the fathers (P = 0.042 and P = 0.0065, respectively). We draw attention to the likely autosomal dominant inheritance of this risk factor for temporary brittle bone disease as well as the potential value of assessing parental joint laxity in evaluating children with fractures.
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