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Calcification of articular cartilage in human osteoarthritis.
Arthritis Rheum. 2009 Sep; 60(9):2694-703.AR

Abstract

OBJECTIVE

Hypertrophic chondrocyte differentiation is a key step in endochondral ossification that produces basic calcium phosphates (BCPs). Although chondrocyte hypertrophy has been associated with osteoarthritis (OA), chondrocalcinosis has been considered an irregular event and linked mainly to calcium pyrophosphate dihydrate (CPPD) deposition. The aim of this study was to determine the prevalence and composition of calcium crystals in human OA and analyze their relationship to disease severity and markers of chondrocyte hypertrophy.

METHODS

One hundred twenty patients with end-stage OA undergoing total knee replacement were prospectively evaluated. Cartilage calcification was studied by conventional x-ray radiography, digital-contact radiography (DCR), field-emission scanning electron microscopy (FE-SEM), and synovial fluid analysis. Cartilage calcification findings were correlated with scores of knee function as well as histologic changes and chondrocyte hypertrophy as analyzed in vitro.

RESULTS

DCR revealed mineralization in all cartilage specimens. Its extent correlated significantly with the Hospital for Special Surgery knee score but not with age. FE-SEM analysis showed that BCPs, rather than CPPD, were the prominent minerals. On histologic analysis, it was observed that mineralization correlated with the expression of type X collagen, a marker of chondrocyte hypertrophy. Moreover, there was a strong correlation between the extent of mineralization in vivo and the ability of chondrocytes to produce BCPs in vitro. The induction of hypertrophy in healthy human chondrocytes resulted in a prominent mineralization of the extracellular matrix.

CONCLUSION

These results indicate that mineralization of articular cartilage by BCP is an indissociable process of OA and does not characterize a specific subset of the disease, which has important consequences in the development of therapeutic strategies for patients with OA.

Authors+Show Affiliations

Department of Orthopaedic Surgery, University Medical Center Hamburg-Eppendorf, Clinic Bad Bramstedt, Martinistrasse 52, Hamburg, Germany. mfuerst@uke.uni-hamburg.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19714647

Citation

Fuerst, M, et al. "Calcification of Articular Cartilage in Human Osteoarthritis." Arthritis and Rheumatism, vol. 60, no. 9, 2009, pp. 2694-703.
Fuerst M, Bertrand J, Lammers L, et al. Calcification of articular cartilage in human osteoarthritis. Arthritis Rheum. 2009;60(9):2694-703.
Fuerst, M., Bertrand, J., Lammers, L., Dreier, R., Echtermeyer, F., Nitschke, Y., Rutsch, F., Schäfer, F. K., Niggemeyer, O., Steinhagen, J., Lohmann, C. H., Pap, T., & Rüther, W. (2009). Calcification of articular cartilage in human osteoarthritis. Arthritis and Rheumatism, 60(9), 2694-703. https://doi.org/10.1002/art.24774
Fuerst M, et al. Calcification of Articular Cartilage in Human Osteoarthritis. Arthritis Rheum. 2009;60(9):2694-703. PubMed PMID: 19714647.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcification of articular cartilage in human osteoarthritis. AU - Fuerst,M, AU - Bertrand,J, AU - Lammers,L, AU - Dreier,R, AU - Echtermeyer,F, AU - Nitschke,Y, AU - Rutsch,F, AU - Schäfer,F K W, AU - Niggemeyer,O, AU - Steinhagen,J, AU - Lohmann,C H, AU - Pap,T, AU - Rüther,W, PY - 2009/8/29/entrez PY - 2009/8/29/pubmed PY - 2009/10/20/medline SP - 2694 EP - 703 JF - Arthritis and rheumatism JO - Arthritis Rheum VL - 60 IS - 9 N2 - OBJECTIVE: Hypertrophic chondrocyte differentiation is a key step in endochondral ossification that produces basic calcium phosphates (BCPs). Although chondrocyte hypertrophy has been associated with osteoarthritis (OA), chondrocalcinosis has been considered an irregular event and linked mainly to calcium pyrophosphate dihydrate (CPPD) deposition. The aim of this study was to determine the prevalence and composition of calcium crystals in human OA and analyze their relationship to disease severity and markers of chondrocyte hypertrophy. METHODS: One hundred twenty patients with end-stage OA undergoing total knee replacement were prospectively evaluated. Cartilage calcification was studied by conventional x-ray radiography, digital-contact radiography (DCR), field-emission scanning electron microscopy (FE-SEM), and synovial fluid analysis. Cartilage calcification findings were correlated with scores of knee function as well as histologic changes and chondrocyte hypertrophy as analyzed in vitro. RESULTS: DCR revealed mineralization in all cartilage specimens. Its extent correlated significantly with the Hospital for Special Surgery knee score but not with age. FE-SEM analysis showed that BCPs, rather than CPPD, were the prominent minerals. On histologic analysis, it was observed that mineralization correlated with the expression of type X collagen, a marker of chondrocyte hypertrophy. Moreover, there was a strong correlation between the extent of mineralization in vivo and the ability of chondrocytes to produce BCPs in vitro. The induction of hypertrophy in healthy human chondrocytes resulted in a prominent mineralization of the extracellular matrix. CONCLUSION: These results indicate that mineralization of articular cartilage by BCP is an indissociable process of OA and does not characterize a specific subset of the disease, which has important consequences in the development of therapeutic strategies for patients with OA. SN - 0004-3591 UR - https://www.unboundmedicine.com/medline/citation/19714647/Calcification_of_articular_cartilage_in_human_osteoarthritis_ L2 - https://doi.org/10.1002/art.24774 DB - PRIME DP - Unbound Medicine ER -