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Objective-To test reliability ofjoint space width (JSW) measurements as a predictor of cartilage thickness in knees of patients with osteoarthritis (OA), using high definition microfocal radiography. Method-JSW was measured from weight bearing plain film macroradiographs taken in the tunnel view and compared with the sum of femoral and tibial cartilage thicknesses measured from double contrast macroarthrograms of the same regions of the same knees obtained in the non-weight bearing lateral position.

Objective-To determine whether fractal signature analysis (FSA) of digitised macroradiographs of knees quantifies alterations in trabecular structure in the tibial cancelious bone of osteoarthritic patients with either early or definite joint space narrowing compared with non-arthritic subjects. (Ann Rheum Dis 1996;55:749-755) In evaluating the pathogenesis of osteoarthritis, studies have concentrated on the assessment of articular cartilage degeneration and loss, since this is considered to be the pathological hallmark of osteoarthritis.' However, articular cartilage is intimately associated with subchondral bone. Together they act as a system that mediates and adapts to mechanical stress, to the extent that it is difficult to isolate events in one tissue compartment that do not affect the other.2 3 Subchondral sclerosis, seen as an increase in the thickness of the subarticular cortex and cancellous bone, is attributed to the degeneration and loss of cartilage and the consequent increase in mechanical load upon the subjacent bone.4 5 To understand the processes involved in the dialogue between bone and cartilage, methods are required that will provide quantitative data on changes in subchondral cancellous bone from images of the bones of patients. Although

SUMMARY The serum concentrations of serum amyloid-A protein (SAA), C-reactive protein (CRP), and alpha,-acid glycoprotein (alpha,-AGP) have been measured in 185 patients with rheumatoid arthritis. SAA and CRP concentrations correlated well (r=086) both within and above the normal ranges, though SAA showed a greater incremental increase than CRP. All patients with normal SAA levels also had normal CRP and alpha1-AGP concentrations. In contrast, in 40 % of patients with normal CRP and alpha1-AGP concentrations the SAA was raised, sometimes markedly so. The clinical and serological assessments of disease activity in these patients were not significantly different from those with concomitantly raised levels of CRP. These findings suggest that SAA is a more sensitive marker of inflammation than is CRP. The role of the measurement of SAA as a monitor for inflammatory disease activity is discussed.

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