REVIEW - Premorbid knee OA is not characterized by diffuse cartilage thinness

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Ann Rheum Dis. Published Online First: 24 January 2008.

doi:10.1136/ard.2007.076810

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Extended Report

Premorbid knee OA is not characterized by diffuse thinness: The

Framingham Study

D J Hunter 1*, JB Niu 1, Y Zhang 1, M LaValley 1, C E McClennan 1, M

Hudelmaier 2, F Eckstein 2 and D T Felson 1

1 Boston University, United States

2 Paracelsus Medical University, Austria

Abstract

It is hypothesized that, like low bone density and fracture, thin

cartilage predisposes to OA. Inferences about the effects of cartilage

thickness on the development of OA can be made by evaluating the

status of an unaffected non-diseased contralateral knee, in persons

with unilateral osteoarthritis, which we shall label the 'premorbid

knee'. The primary objective of this analysis was to compare cartilage

thickness in premorbid knees with non-OA knees drawn from persons

without any knee OA to determine if cartilage in the premorbid knee

was thinner than in the knee drawn from someone without OA in either

knee. From 2002-2005, The Framingham Osteoarthritis Study recruited

subjects without respect to OA from the community. We obtained PA,

semiflexed and lateral films of both knees and knee MRI for

quantitation of cartilage volume in one knee. The cartilage plates of

the patella, medial and lateral femur, medial and lateral tibia were

quantified, using a 3D FLASH-water excitation sequence (in plane

resolution 0.3x0.3 mm, 512 matrix, slice thickness 1.5mm) and digital

post-processing, involving three-dimensional reconstruction.

Radiographs were used to define the OA status of knees with disease

defined as K & L grade 2 and or PF OA on the lateral film. Of 1020

participants included in this analysis, 720 had no OA in either knee

(no knee OA sample), and 55 subjects had no OA in MRI knee and OA in

the contralateral knee (premorbid knee OA sample). We compared

cartilage thickness and percent of cartilage coverage (total bone

interface covered with cartilage) between these groups. After initial

plate-specific univariate comparisons we performed a multiple

regression to assess the association between OA status (premorbid vs.

no OA knee) and cartilage thickness adjusting for age, sex and BMI. We

used GEE to account for correlation between plates. To further

determine if the cartilage was diffusely thinned or had only increased

areas of denuded cartilage, we removed plates with denuded areas (less

than 95% cartilage coverage) from the analysis. 55% of subjects were

women. There was no difference in cartilage thickness between the

premorbid knees and the no knee OA sample. After adjusting for age,

sex and BMI and removing plates with less than 95% coverage from the

analysis, we found the same or even thicker cartilage in premorbid

knees compared with the knee OA sample. Premorbid knees do not have

diffuse cartilage thinness. Rather the cartilage is normal or thicker

with denuded areas suggesting that this may be the initial pathology

rather than diffuse thinning.

http://ard.bmj.com/cgi/content/abstract/ard.2007.076810v1?papetoc

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