, 2009, 2010, 2011; D’Hooge et al., in press). There are some limitations to this study. The absence of differences in CSA between groups or sides may be related to small participant numbers. Further studies with larger sample size are required to confirm our findings. The MFI has not previously been applied in the lumbar region. The index has been used extensively in the cervical spine (Elliott et al., 2005, 2006). Unlike the cervical region, the fat ROI could not be drawn in a clear intermuscular fat area, but instead, peripherally from the lumbar muscles. This yielded comparable MK-1775 solubility dmso but slightly lower indices (range: 0.15–0.30), which might be due to calculating the MFI after

segmentation of visible fat. In conclusion, the current study shows a generalized increase in fatty infiltration in lean lumbar muscle GSK J4 ic50 tissue, in the absence of alterations in muscle size or macroscopic

fat deposition after resolution of LBP. It is hypothesized that decreased muscle quality may contribute to recurrence of LBP. The authors acknowledge Dr. Nele Dickx, Joke Vanhecke and Nele Vlieghe for assisting in data collection and Eng. Pieter Vandemaele for technical MRI support. This research was supported by Special Research Fund (BOF), Ghent University. “
“Benign joint hypermobility syndrome (BJHS) is a hereditable collagen disorder that features excessive flexibility of joints and chronic pain. It is closely associated with a genetic disorder, the hypermobile type of Ehlers Danlos Syndrome (EDS type III) (Grahame, 2008). Previously this condition was considered an insignificant finding due in part to the absence of any non-musculoskeletal symptoms. However over the past few decades, research into the area revealed important findings that link this symptom to more serious conditions

such as osteoarthritis (OA) (Bridges et al., 1992) or low back pain (LBP) (Murray, 2006). An abnormality of structure and distribution of type I collagen together with an increased ratio of collagen type III to type I is thought to be the underlying cause of BJHS (Russek, 1999), resulting in decreased stiffness and generalised ligament laxity, which constitutes until the clinical picture observed in patients. The effect of joint laxity ranges from joint pain to increased soft tissue injuries and joint subluxation or dislocation. Extra-articular manifestations may include mitral valve prolapse, which is three times more prevalent in BJHS populations than healthy populations, uterine and rectal prolapse and abdominal herniation. Other associations include increased incidence of anxiety disorders and delayed motor development in infants (Grahame, 1990). A diagnosis of BJHS may bring with it an increased risk of developing degenerative diseases such as OA (Grahame, 1989, Bridges et al., 1992 and Jonsson et al., 1996); one study reported that up to 60% of BJHS patients developed OA (Bridges et al., 1992).