title: Comparison of the ability of chondroitin sulfate derived from bovine, fish and pigs to suppress human osteoclast activity in vitro.
abstract: Chondroitin sulfate (CS) compounds are commonly used to manage OA symptoms. Recent literature has indicated that abnormal subchondral bone metabolism may have a role in the pathogenesis of OA. The aim of this study was to access the effects of chondroitin sulfate obtained from bovine, fish and porcine sources on human osteoclast formation and activity in vitro. Human osteoclasts were generated from blood mononuclear cells. Cells were cultured over 17 days with the addition of macrophage colony stimulating factor (M-CSF) and then stimulated with receptor activator of nuclear factor kappa B ligand from day 7. Cells were treated with the CS commencing from day 7 onwards. To assess effects on osteoclasts, tartrate resistant acid phosphatate (TRAP) expression and resorption of whale dentine assays were used. Bovine-derived CS consistently suppressed osteoclast activity at concentrations as low as 1 μg/ml. Fish and porcine CS was less consistent in their effects varying with different donor cells. All CS compounds had little effect on TRAP activity. mRNA analysis using real-time PCR of bovine CS treated cells indicated that the inhibition of activity was not due to inhibition of the late stage NFATc1 transcription factor (p > 0.05). These results are consistent with CS inhibition of mature osteoclast activity rather than the formation of mature osteoclasts. It would appear that there are differences in activity of the different CS compounds with bovine-derived CS being the most consistently effective inhibitor of osteoclast resorption, but the results need to be confirmed.
authors: Discipline of Anatomy and Pathology, School of Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
authors: M D
authors: MD
authors: Cantley
authors: K D
authors: KD
authors: Rainsford
authors: D R
authors: DR
authors: Haynes
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D050071:Bone Density Conservation Agents / Q000009:adverse effects / Q000378:metabolism*; D002417:Cattle; D002470:Cell Survival; D054338:Cell Transdifferentiation; D002478:Cells, Cultured; D002809:Chondroitin Sulfates / Q000009:adverse effects / Q000378:metabolism*; D003804:Dentin / Q000378:metabolism / Q000648:ultrastructure; D019587:Dietary Supplements / Q000009:adverse effects; D015536:Down-Regulation; D005399:Fishes; D006801:Humans; D066298:In Vitro Techniques; D007527:Isoenzymes / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000201:enzymology / Q000378:metabolism; D016173:Macrophage Colony-Stimulating Factor / Q000235:genetics / Q000378:metabolism; D010010:Osteoclasts / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D053245:RANK Ligand / Q000235:genetics / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism; D015203:Reproducibility of Results; D034421:Sus scrofa; D000071681:Tartrate-Resistant Acid Phosphatase; D014091:Tooth Resorption / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D014907:Whales
chemical_list: D050071:Bone Density Conservation Agents; D007527:Isoenzymes; D053245:RANK Ligand; D011994:Recombinant Proteins; C505688:TNFSF11 protein, human; D016173:Macrophage Colony-Stimulating Factor; D002809:Chondroitin Sulfates; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase
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