Article

Natural history of bone metabolism and bone mineral density in children with inflammatory bowel disease

Division of Gastroenterology and Nutrition, Connecticut Children's Medical Center, Hartford, Connecticut 06106, USA.
Inflammatory Bowel Diseases (Impact Factor: 5.48). 01/2007; 13(1):42-50. DOI: 10.1002/ibd.20006
Source: PubMed

ABSTRACT In children with inflammatory bowel disease (IBD) it is not known whether reductions in bone mineral density (BMD) are a consequence of bone turnover alterations and if BMD improves with treatment.
In a cohort of children with IBD, we prospectively measured indicators of bone remodeling, body mass index (BMI), disease activity, intact parathyroid hormone, serum IL-6, and insulin-like growth factor-I at diagnosis and then every 6 months for 2 years. BMD was determined annually using dual x-ray absorptiometry (DXA). BMD Z-scores were calculated using height/age. Baseline measurements and calcium intake were compared with a group of age- and sex-matched healthy children.
We observed that at diagnosis total body BMD Z-score (mean +/- SD) was -0.78 +/- 1.02 for Crohn's disease (CD, n = 58), -0.46 +/- 1.14 for ulcerative colitis (UC, n = 18), and -0.17 +/- 0.95 for control (CL, n = 49) (P < 0.01, CD versus CL). In CD, a BMD Z-score <-1.0 was associated with lower BMI and higher serum IL-6. Patients with CD and UC had low bone turnover. Activation of bone formation paralleled clinical improvement, but BMC gain was less than expected over the 2-year study period, especially in CD. Prednisone use did not correlate with low BMD.
Decreased bone turnover occurs in children newly diagnosed with IBD. Although indicators of osteoblast activity increase with clinical improvement, bone mineral accrual does not accelerate. Children with low BMI may be considered for BMD screening, since they are at risk for low bone mass.

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    • "The predominant bone remodelling abnormality in inflammatory bowel disease appears to be a reduction in bone formation with inappropriately maintained bone resorption (Sylvester et al. 2007). In other states characterised by poor nutritional availability such as anorexia nervosa a similar uncoupling of bone resorption from formation with suppressed formation is seen (Soyka et al. 1999). "
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    • "However, it is now known that not only malabsorption of vitamin D and calcium [3] [4] [5] [6] [7] [8] [9] [10], but also a host of cytokines [6, 9, 11–13] can contribute to bone loss. A number of other inflammatory diseases such as inflammatory bowel disease [14] [15] [16] [17] [18], rheumatoid arthritis [19], juvenile idiopathic arthritis [20], and systemic lupus erythematosus [21], have documented low bone mineral density and, in some studies, resultant osteopenia and osteoporosis. Since BA is an inflammatory disorder [1] [22], with ongoing issues of malabsorption present even when surgery is successful, it is postulated that bone health might be compromised even when jaundice is not present. "
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    ABSTRACT: In children, as in adults, bone is a metabolically active tissue in a constant state of turnover called remodelling. Remodelling is a tightly coupled process involving sequential resorption of bone by osteoclasts, followed by bone formation by osteoblasts. It fulfils a maintenance role, repairing micro- defects in bone and preserving bone strength. However, unlike adults, children are also growing. Skeletal growth involves not only longitudinal growth by chondrocytes at the epiphyseal growth plate, with subsequent mineralisation by osteoblasts, but also growth in bone width and reshaping of bone to optimise bone strength in response to the forces imposed by growing muscles. This latter process is called modelling. In the long bones, increase in bone width is achieved by teams of osteoblasts creating new bone on the outer bone surface of newly synthesised osteoid while simultaneously teams of osteoclasts resorb bone from the inner surface of the bone cortex, increasing the bone marrow cavity. These processes are not coupled but work independently. The net effect is an increase in the amount of bone tissue. Type I collagen is the predominant collagen in bone and soft tissue. It is formed from a precursor procollagen molecule which undergoes extracellular processing to remove the bulky C- terminal and smaller N- terminal propeptides, allowing assembly of the collagen triple helices into fibrils that provide much of the tensile strength of bone. Mature type I collagen in bone subsequently forms intermolecular cross- links at the N- terminal and C- terminal telopeptide regions, helping to stabilise the fibrillar structure. However, the main structural strength of bone derives from its mineral component: hydroxyapatite, a crystalline form of calcium phosphate, that slots into specific grooves formed by the neatly staggered array of collagen molecules within fibrils. There are a number of biochemical markers of bone formation and bone resorption that reflect these dynamic processes (table 1). Bone formation markers are all measured in serum or plasma. Bone resorption markers may be measured in serum, plasma or urine, depending on the marker and the assay. Figure 1 shows a schematic representation of the synthesis and clearance of most of the commonly measured bone markers.
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