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Experimental colitis impairs linear bone growth independent of nutritional factors
S G Koniaris1, S E Fisher, C T Rubin
1Department of Pediatrics, North Shore University Hospital-New York University School of Medicine, Manhasset, USA.
Insights
Experimental colitis in rats led to impaired bone growth, independent of nutrition. Elevated inflammatory markers suggest a link between gut inflammation and growth delay in children with inflammatory bowel disease.
Area of Science:
- Pediatric Gastroenterology
- Pediatric Endocrinology
- Inflammatory Bowel Disease Research
Background:
- Children with chronic inflammatory bowel disease (IBD) often experience poor linear growth.
- Inflammatory mediators are suspected contributors to growth delay in pediatric IBD.
- This study investigates the impact of experimental colitis on bone growth in a controlled rat model.
Purpose of the Study:
- To evaluate the effect of experimental colitis on linear bone growth in rats.
- To determine if nutritional intake influences the observed growth effects.
- To explore the role of inflammatory mediators in colitis-induced growth impairment.
Main Methods:
- Male Sprague-Dawley rats underwent experimental colitis induction via trinitrobenzene sulfonic acid enema.
- Control and colitis groups were pair-fed a liquid diet for 14 days.
- Bone growth was assessed using tibial growth-plate histomorphometry, and serum/urine mineral levels and interleukin-6 were analyzed.
Main Results:
- Histology confirmed active colitis in treated rats.
- No significant differences in weight gain or serum/urine calcium, zinc, and magnesium were observed between groups.
- Experimental colitis resulted in decreased linear bone growth, characterized by a larger resting zone, smaller proliferative zone, and reduced terminal hypertrophic chondrocytes.
Conclusions:
- Experimental colitis significantly impairs linear bone growth in rats, irrespective of nutritional status.
- Elevated interleukin-6 levels suggest that circulating cytokines from intestinal inflammation may suppress bone growth.
- Findings imply a potential mechanism for growth delay in children with inflammatory bowel disease.
Background:
Poor linear growth frequently complicates chronic inflammatory bowel disease in children. Circulating inflammatory mediators may play a role in this growth delay. We evaluated the effect of experimental colitis on bone growth in a nutritionally controlled rat model.
Methods:
Experimental colitis was induced in male Sprague-Dawley rats (125-150 g) by enema with trinitrobenzene sulfonic acid in 50% ethanol on day 1 and 11 of a 14-day protocol. Control animals were pair-fed and all animals received a liquid rat diet (1 kcal/ml). Twenty-four-hour urine, collected on days 2 and 12 and serum samples, collected at death, were analyzed for calcium, zinc, and magnesium. Serum samples from a separate set of animals were studied for serial interleukin-6 levels. Right proximal tibias were processed for growth-plate histomorphometry, in which linear growth is proportional to the heights of the proliferative zone, and terminal hypertrophic chondrocyte, but inversely proportional to the height of the resting zone.
Results:
Histology confirmed active inflammation in the animals given trinitrobenzene sulfonic acid. Weight gain and both urinary excretion and serum levels of zinc, calcium, and magnesium did not differ between treatment and nontreatment groups. Histologically, there was impaired linear bone growth. The resting zone was greater in the colitis group (94.5 +/- 32.6 microns versus 3.9 +/- 5.4 microns; p < 0.05); the proliferative zone was smaller in the colitis group (123.7 +/- 18.2 microns versus 78.9 +/- 11.2; p < 0.05 micron); the terminal hypertrophic chondrocyte was reduced in the colitis group (19.5 +/- 1.4 microns versus 28.8 +/- 3.6 microns; p < 0.05). At 6 and 24 hours after induction, the level of interleukin-6 was elevated in the colitis group.
Conclusions:
Experimental colitis results in a decreased linear bone growth, independent of nutritional intake. Circulating cytokines derived from intestinal inflammation may contribute to the suppression of bone growth.