Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose:
Diabetes is a causative factor in joint diseases and amplifies the damage induced by other agents as well. According to an accepted hypothesis, damaged joint tissue in diabetes is caused by an excess of advanced glycation end products, which forms covalent cross-links within collagen (COL) fibers and alters their structure and function. In this context the remodeling process of the collagen fibers in different structures in the joint probably is the trigger of the joints disorders observed in these patients.The main of this study was to analyze the synovial collagen fibers in the rat diabetic joints induced by streptozotocin and their correlation with the temporal evolution of the diabetes.
Methods:
Twenty diabetic Wistar rats (2.5 months of age and 200-250g) induced by infusion of streptozotocin (35mg/kg) were divided in two groups. The first group (G1=10) was euthanized after 2 weeks of induction and the second group (G2=10) after 2 months of diabetic induction. The control (C1=10 and C2=10) groups received only saline infusion. The experimental protocol complies the rules adopted by the Brazilian College of Animal Experimentation (COBEA) and was approved by the internal Ethics Committee of the University of São Paulo Medical School, protocol # 10501/13. After the euthanasia, weight, blood glucose and plasmatic anti-carboximetilisin (ACML) analysis were performed. The synovial tissues of the knee were included in paraffin and histological sections were stained with Hematoxylin and Eosine. 4-hydroxyproline analysis, picrosirius red stained, immunofluorescence and image analysis were used to evaluated the amount of total collagen and the COL I, COL III and V in the synovial tissues.
Results: Blood glucose was statistical significant increases in the diabetic groups when compared with control groups (,p<0,005). In contrast, the weight of the diabetic animals decreased when compared with the control groups ( p <0.001). Increased quantities of collagen was observed by 4-hydroxyproline analysis in G2 group when compared to C2 (p <0.005) group. Similar situation was observed between G1 and C1 but without statistical significance. The morphology analysis showed a substitution of the sub-synovial layer fat by fibrotic tissue in the diabetic groups with important deposition of collagen fibers around small vessels. Indeed, the histomorphometry analysis showed an increased amount of coarse collagen fibers (22.70 ± 8.20) with a reduction of fine collagen fibers in G2 (16:29 ± 6:10%) when compared with C2 (14:45 ± 5:39%, 21:39 ± 6.14, respectively, p <0.05) group. Similar situation was observed between G1 and C1 but without statistical significance. The COL I, III and V analysis showed a statistical increased of these fibers in G2 when compared with C2. Between G1 and C1 this increase was observed but without significance.
Conclusion: The morphologic changes observed in the synovial tissues from diabetic rats and the increased amount of the collagen fibers deposition in this structure reinforce the idea that the collagen fibers deposition and remodeling are part of the pathogenic pathway progression in the joint from diabetic patients.
Disclosure:
P. C. Andrade,
None;
A. P. P. Velosa,
None;
J. Morais,
None;
E. R. Parra,
None;
C. Goldeinstein-Schainberg,
None;
V. L. Capelozzi,
None;
W. R. Teodoro,
None.
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/abnormal-collagen-fibers-deposition-in-the-synovial-joints-is-a-characteristic-of-the-temporal-evolution-of-the-diabetic-rats-model-induced-by-streptozotocin/