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Published on: March 18, 2022
Inflammatory bowel disease causes reversible suppression of osteoblast and chondrocyte function in mice
Laura Harris1, Patricia Senagore, Vincent B Young
1Department of Physiology, Michigan State University, East Lansing, Michigan, USA.
Insights
Inflammatory bowel disease (IBD) in young mice reduced bone density and growth. Bone parameters recovered during IBD remission, indicating potential for skeletal recovery in pediatric IBD patients.
Area of Science:
- Pediatric skeletal biology
- Inflammatory bowel disease research
- Bone metabolism and growth
Background:
- Pediatric inflammatory bowel disease (IBD) is linked to reduced bone density and stature.
- The broad skeletal impact of IBD during growth remains poorly understood.
Purpose of the Study:
- To investigate the effects of an acute inflammatory bowel disease (IBD) episode on growing bone in a pediatric mouse model.
- To assess skeletal recovery following the resolution of active disease.
Main Methods:
- Induction of colitis in 4-week-old mice using dextran sodium sulfate (DSS).
- Monitoring of bone parameters (density, volume, thickness, strength) via histology, serum analysis, and gene expression.
- Assessment of growth plate dynamics and serum cytokine levels (TNF-alpha, IGF-I).
Main Results:
- Active IBD and early recovery decreased trabecular and cortical bone density, volume, and thickness.
- Bone strength was maintained despite density changes; marrow adiposity did not increase.
- Bone length decreased, correlating with reduced growth plate thickness and chondrocyte markers; serum TNF-alpha increased and IGF-I decreased.
- A growth spurt during recovery normalized bone parameters and gene expression, with serum markers returning to baseline.
Conclusions:
- Acute IBD significantly impacts growing bone, affecting both density and length through mechanisms involving osteoblast function and growth plate activity.
- Skeletal parameters and growth can recover following IBD remission, suggesting potential for catch-up growth.
- Serum TNF-alpha and IGF-I levels may play a role in the skeletal response to IBD and its recovery.
Abstract:
Decreased bone density and stature can occur in pediatric patients with inflammatory bowel disease (IBD). Little is known about how IBD broadly impacts the skeleton. To evaluate the influence of an acute episode of IBD on growing bone, 4-wk-old mice were administered 5% dextran sodium sulfate (DSS) for 5 days to induce colitis and their recovery was monitored. During active disease and early recovery, trabecular bone mineral density, bone volume, and thickness were decreased. Cortical bone thickness, outer perimeter, and density were also decreased, whereas inner perimeter and marrow area were increased. These changes appear to maintain bone strength since measures of moments of inertia were similar between DSS-treated and control mice. Histological (static and dynamic), serum, and RNA analyses indicate that a decrease in osteoblast maturation and function account for changes in bone density. Unlike some conditions of bone loss, marrow adiposity did not increase. Similar to reports in humans, bone length decreased and correlated with decreases in growth plate thickness and chondrocyte marker expression. During disease recovery, mice experienced a growth spurt that led to their achieving final body weights and bone length, density, and gene expression similar to healthy controls. Increased TNF-alpha and decreased IGF-I serum levels were observed with active disease and returned to normal with recovery. Changes in serum TNF-alpha (increased) and IGF-I (decreased) paralleled changes in bone parameters and returned to normal values with recovery, suggesting a potential role in the skeletal response.
