RESEARCH - Premorbid knee OA is not characterised by diffuse thinness: the Framingham Osteoarthritis Study

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Published Online First: 24 January 2008. doi:10.1136/ard.2007.076810

ls of the Rheumatic Diseases 2008;67:1545-1549

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CLINICAL AND EPIDEMIOLOGICAL RESEARCH

Premorbid knee osteoarthritis is not characterised by diffuse

thinness: the Framingham Osteoarthritis Study

D J Hunter 1,2, J B Niu 1, Y Zhang 1, M LaValley 1, C E McLennan 1,2,

M Hudelmaier 3, F Eckstein 3, D T Felson 1

1 Boston University School of Medicine, Massachusetts, USA

2 Division of Research, New England Baptist Hospital, Boston,

Massachusetts, USA

3 Institute of Anatomy and Musculoskeletal Research, Paracelsus

Private Medical University, Salzburg, Austria

Objective: It is hypothesised that, like low bone density and

fracture, thin cartilage predisposes to osteoarthritis (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 OA, 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.

Methods: From 2002 to 2005, The Framingham Osteoarthritis Study

recruited subjects without respect to OA from the community. We

obtained posteroanterior, semiflexed and lateral films of both knees

and knee magnetic resonance imaging to quantify 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 1.5 mm) and digital post-processing, involving

three-dimensional reconstruction. Radiographs were used to define the

OA status of knees with disease defined as Kellgren and Lawrence grade

2 and or patellofemoral 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 the knee that was examined using

magnetic resonance imaging and OA in the contralateral knee (premorbid

knee OA sample). We compared cartilage thickness and percentage 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 versus no OA knee) and

cartilage thickness adjusting for age, sex and body mass index. We

used the Generalised Estimating Equation 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.

Results: 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 body mass index 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.

Conclusions: 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/67/11/1545?etoc

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