Calcification of articular cartilage in human osteoarthritis.

Standard

Calcification of articular cartilage in human osteoarthritis. / Fuerst, Martin; Bertrand, J; Lammers, L; Dreier, R; Echtermeyer, F; Nitschke, Y; Rutsch, F; Schäfer, F K W; Niggemeyer, O; Steinhagen, J; Lohmann, C H; Pap, T; Rüther, Wolfgang.

In: ARTHRITIS RHEUM-US, Vol. 60, No. 9, 9, 2009, p. 2694-2703.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Fuerst, M, Bertrand, J, Lammers, L, Dreier, R, Echtermeyer, F, Nitschke, Y, Rutsch, F, Schäfer, FKW, Niggemeyer, O, Steinhagen, J, Lohmann, CH, Pap, T & Rüther, W 2009, 'Calcification of articular cartilage in human osteoarthritis.', ARTHRITIS RHEUM-US, vol. 60, no. 9, 9, pp. 2694-2703. <http://www.ncbi.nlm.nih.gov/pubmed/19714647?dopt=Citation>

APA

Fuerst, M., Bertrand, J., Lammers, L., Dreier, R., Echtermeyer, F., Nitschke, Y., Rutsch, F., Schäfer, F. K. W., Niggemeyer, O., Steinhagen, J., Lohmann, C. H., Pap, T., & Rüther, W. (2009). Calcification of articular cartilage in human osteoarthritis. ARTHRITIS RHEUM-US, 60(9), 2694-2703. [9]. http://www.ncbi.nlm.nih.gov/pubmed/19714647?dopt=Citation

Vancouver

Fuerst M, Bertrand J, Lammers L, Dreier R, Echtermeyer F, Nitschke Y et al. Calcification of articular cartilage in human osteoarthritis. ARTHRITIS RHEUM-US. 2009;60(9):2694-2703. 9.

Bibtex

@article{88f7a167f5994c15af786db7f35631c3,
title = "Calcification of articular cartilage in human osteoarthritis.",
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.",
author = "Martin Fuerst and J Bertrand and L Lammers and R Dreier and F Echtermeyer and Y Nitschke and F Rutsch and Sch{\"a}fer, {F K W} and O Niggemeyer and J Steinhagen and Lohmann, {C H} and T Pap and Wolfgang R{\"u}ther",
year = "2009",
language = "Deutsch",
volume = "60",
pages = "2694--2703",
journal = "ARTHRITIS RHEUMATOL",
issn = "2326-5191",
publisher = "John Wiley and Sons Ltd",
number = "9",

}

RIS

TY - JOUR

T1 - Calcification of articular cartilage in human osteoarthritis.

AU - Fuerst, Martin

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, Wolfgang

PY - 2009

Y1 - 2009

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.

AB - 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.

M3 - SCORING: Zeitschriftenaufsatz

VL - 60

SP - 2694

EP - 2703

JO - ARTHRITIS RHEUMATOL

JF - ARTHRITIS RHEUMATOL

SN - 2326-5191

IS - 9

M1 - 9

ER -