Osteoarthritis and its origins: Disease development at the cellular and molecular level - Veterinary Medicine
  • SEARCH:
Medicine Center
DVM Veterinary Medicine Featuring Information from:

ADVERTISEMENT

Osteoarthritis and its origins: Disease development at the cellular and molecular level


Clinical Edge


Eicosapentaenoic acid also may decrease the expression of proinflammatory cytokines and the enzymes and metabolites involved in their signaling pathways.18 This includes IL-1, TNF-α, COX-2, and PGE2. In vitro examination in our laboratory has confirmed the effect on IL-1 and PGE2 in canine cells (R.P. Middleton; S.S. Hannah: Unpublished data, 2004).

Conclusion

Osteoarthritis is a disease characterized by an imbalance in catabolic and anabolic factors affecting the degradation and synthesis of the extracellular matrix. New techniques are allowing researchers to characterize this disease and evaluate potential therapeutic agents at the cellular and molecular level. Proinflammatory mediators and inflammatory cytokines play a central role in the gene-expression changes and resulting biochemical changes seen in the arthritic articular chondrocyte. Oral eicosapentaenoic acid administration has effectively managed osteoarthritis in several species. The continued identification of the molecular mechanisms involved in osteoarthritis not only increases our understanding of the disease, but helps researchers identify and understand nutritional interventions.

References

1. Aigner, T.; McKenna, L.: Molecular pathology and pathobiology of osteoarthritic cartilage. Cell Mol. Life Sci. 59:5-18; 2002.

2. Kevorkian, L. et al.: Expression profiling of metalloproteinases and their inhibitors in cartilage. Arthritis Rheum. 50 (1):131-141; 2004.

3. Aigner, T. et al.: Anabolic and catabolic gene expression pattern analysis in normal versus osteoarthritic cartilage using complementary DNA-array technology. Arthritis Rheum. 44 (12):2777-2789; 2001.

4. Middleton, R. et al.: Gene expression profiling of osteoarthritis from canine chondrocytes. The development of a canine OA microarray chip. Trans. Orthopaedic Res. Soc. 28:0741; 2003.

5. Amin, A.R. et al.: Regulation of nitric oxide and inflammatory mediators in human osteoarthritis-affected cartilage: implication for pharmacological intervention. The Pathophysiology & Clinical Applications of Nitric Oxide. (Rubanyi, G.M., ed.) Harwood Academic Publishers, Richmond, Va., 1999; pp 397-412.

6. Attur, M.G. et al.: Reversal of autocrine and paracrine effects of interleukin 1 (IL-1) in human arthritis by type II IL-1 decoy receptor. Potential for pharmacological intervention. J. Biol. Chem. 275:40307-40315; 2000.

7. Goldring, M.B.: The role of cytokines as inflammatory mediators in osteoarthritis: lessons from animal models. Connective Tissue Research. 40:1-11; 1999.

8. Johnston, S.A.: Osteoarthritis. Joint anatomy, physiology, and pathobiology. Vet. Clin. North Am. 27:699-723; 1997.

9. Cawston, T. Matrix metalloproteinases and TIMPs: properties and implications for the rheumatic diseases. Mol. Med. Today 4:130-137; 1998.

10. Roush, J.K. et al.: Understanding the pathophysiology of osteoarthritis. Vet. Med. 97:108-112; 2002.

11. Marini, S. et al.: A correlation between knee cartilage degradation observed by arthroscopy and synovial proteinases activities. Clin. Biochem. 36:295-304; 2003.

12. Tetlow, L.C. et al.: Matrix metalloproteinase and proinflammatory cytokine production by chondrocytes of human osteoarthritic cartilage: associations with degenerative changes. Arthritis Rheum. 44:585-594; 2001.

13. Hegemann, N. et al.: Biomarkers of joint tissue metabolism in canine osteoarthritic and arthritic joint disorders. Osteoarthritis Cartilage 10:714-721; 2002.


ADVERTISEMENT

Source: Clinical Edge,
Click here