Extended reports
Synovial fluid chondroitin and keratan sulphate epitopes,
glycosaminoglycans, and hyaluronan in arthritic and normal knees
a Rheumatology Unit,
City Hospital, Nottingham , b Biochemistry
Division, Kennedy Institute of Rheumatology, Hammersmith, London
Correspondence to: Professor M Doherty, Rheumatology Unit, City Hospital, Hucknall Road, Nottingham NG5 1PB.
Accepted for publication 26 February 1997
OBJECTIVES
To determine concentrations of
chondroitin sulphate (CS) and keratan sulphate (KS) epitopes,
glycosaminoglycans (GAGs) and hyaluronan (HA) in knee synovial fluid
(SF) from normal subjects and patients with osteoarthritis (OA) or
rheumatoid arthritis (RA), to test whether these variables may be used
as markers of the OA process.
METHODSOA was subdivided into large joint OA
(LJOA), nodal generalised OA (NGOA), and OA with calcium pyrophosphate
crystal deposition (CPA). Clinical assessment of inflammation (0-6) was
undertaken on OA and RA knees. Knee SF was examined by enzyme linked
immunosorbent assay for: CS epitopes, using monoclonal antibodies 3-B-3
and 7-D-4; KS epitope using monoclonal antibody 5-D-4; and HA, using biotinylated HA binding region of cartilage proteoglycan. Total sulphated GAGs were measured by dye binding with 1:9 dimethylmethylene blue.
RESULTSIncreased SF 3-B-3 concentrations and
3-B-3/GAG ratio were found in OA, compared with RA or normal knees,
with higher 3-B-3 and 3-B-3/GAG in LJOA and NGOA than in CPA. SF 7-D-4
and 7-D-4/GAG were reduced in RA, compared with normal and OA; SF 5-D-4
was reduced in OA compared with normal. GAG and HA concentrations were
decreased in both OA and RA. No correlations with radiographic scores
were observed, but SF 7-D-4 was lower in `inflamed' compared with
`non-inflamed' RA and OA knees. In patients with bilateral samples
there were strong correlations between right and left knees for all SF variables.
CONCLUSIONSChanged concentrations of SF CS and
KS can be detected in OA with a profile that differs from that seen in
RA. Clinical subgrouping and local joint inflammation may influence
these measures, supporting different pathogenesis within OA subgroups
and requirement for careful patient characterisation in SF studies.
© 1997 by Annals of the Rheumatic Diseases
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