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Annals of the Rheumatic Diseases logoLink to Annals of the Rheumatic Diseases
. 2005 Jun;64(6):886–890. doi: 10.1136/ard.2004.029140

Increased pentosidine, an advanced glycation end product, in serum and synovial fluid from patients with knee osteoarthritis and its relation with cartilage oligomeric matrix protein

L Senolt 1, M Braun 1, M Olejarova 1, S Forejtova 1, J Gatterova 1, K Pavelka 1
PMCID: PMC1755507  PMID: 15897309

Abstract

Background: Pentosidine, an advanced glycation end product, increasingly accumulates in articular cartilage with age, and contributes to the pathogenesis of osteoarthritis (OA). Increased pentosidine concentrations are associated with inflammatory disorders—for example, rheumatoid arthritis.

Objective: To compare pentosidine serum concentrations in patients with knee OA and in healthy volunteers and to determine a relationship between pentosidine and cartilage oligomeric matrix protein (COMP)—a marker of articular cartilage destruction.

Methods: Paired serum and synovial fluid samples were obtained by arthrocentesis from 38 patients with knee OA and from 38 healthy volunteers. Pentosidine concentration was measured by reverse phase high performance liquid chromatography with fluorescent detection and COMP was determined by sandwich ELISA.

Results: Significantly increased serum pentosidine (p<0.01) and COMP (p<0.05) levels were detected in the patients with OA compared with the control group. Serum pentosidine correlated significantly with synovial fluid pentosidine (p<0.001). Pentosidine in synovial fluid (p<0.05) and in serum (p<0.05) correlated significantly with synovial fluid COMP. Pentosidine and COMP concentrations did not correlate significantly with the radiological stage of the disease.

Conclusion: Increased pentosidine serum concentration in patients with OA and its correlation with the cartilage destruction marker COMP in synovial fluid suggests that pentosidine may be important in OA pathology and is a new potential OA marker.

Full Text

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Figure 1.

Figure 1

 Comparison of the serum levels of (A) pentosidine and (B) COMP in patients with OA and in controls.

Figure 2.

Figure 2

 Correlation between serum (S) and synovial fluid (SF) levels of (A) pentosidine and (B) COMP in patients with OA.

Figure 3.

Figure 3

 Correlation between (A) pentosidine and COMP in synovial fluid (SF) and (B) pentosidine in serum (S) and COMP in SF in patients with OA.

Figure 4.

Figure 4

 (A) Serum levels of pentosidine are significantly increased compared with levels in synovial fluid (SF) in patients with OA (p<0.001). (B) In contrast, serum levels of COMP are significantly decreased compared with levels in SF in patients with OA (p<0.001).

Selected References

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