TY - JOUR
T1 - Predictive and concurrent validity of cartilage thickness change as a marker of knee osteoarthritis progression
T2 - data from the Osteoarthritis Initiative
AU - Wirth, W.
AU - Hunter, D. J.
AU - Nevitt, M. C.
AU - Sharma, L.
AU - Kwoh, C. K.
AU - Ladel, C.
AU - Eckstein, F.
N1 - Funding Information:
This work is based on data from the OAI: The OAI is a public-private partnership comprised of five contracts ( N01-AR-2-2258 ; N01-AR-2-2259 ; N01-AR-2-2260 ; N01-AR-2-2261 ; N01-AR-2-2262 ) funded by the National Institutes of Health . Funding partners include Merck Research Laboratories ; Novartis Pharmaceuticals Corporation ; GlaxoSmithKline ; and Pfizer, Inc . Private sector funding for the Consortium and OAI is managed by the FNIH .
Funding Information:
C.K. Kwoh has received research support from Merck Serono and Abbvie.
Funding Information:
The image analysis in this study was partly funded by the FNIH OA Biomarkers Consortium, with grants, direct and in-kind contributions, provided by: AbbVie; Amgen Inc.; Arthritis Foundation; Bioiberica S.A.; DePuy Mitek, Inc.; Flexion Therapeutics, Inc.; GlaxoSmithKline; Merck KGaA; Rottapharm | Madaus; Sanofi; and Stryker. Other parts of funding were provided by a direct grant from Merck KGaA, by a contract with the University of Pittsburgh (Pivotal OAI MRI Analyses [POMA]: NIH/NHLBI Contract No. HHSN2682010000 21C), by a vendor contract from the OAI coordinating center at University of California, San Francisco (N01-AR-2-2258), and by an ancillary study to the OAI held by the Division of Rheumatology, Feinberg School of Medicine, Northwestern University (R01 AR52918).
Funding Information:
The image analysis in this study was partly funded by the FNIH OA Biomarkers Consortium, with grants, direct and in-kind contributions, provided by: AbbVie ; Amgen Inc. ; Arthritis Foundation ; Bioiberica S.A. ; DePuy Mitek, Inc. ; Flexion Therapeutics, Inc. ; GlaxoSmithKline ; Merck KGaA ; Rottapharm | Madaus ; Sanofi ; and Stryker . Other parts of funding were provided by a direct grant from Merck KGaA, by a contract with the University of Pittsburgh (Pivotal OAI MRI Analyses [POMA]: NIH/NHLBI Contract No. HHSN2682010000 21C), by a vendor contract from the OAI coordinating center at University of California, San Francisco (N01-AR-2-2258), and by an ancillary study to the OAI held by the Division of Rheumatology, Feinberg School of Medicine, Northwestern University (R01 AR52918).
Funding Information:
F. Eckstein is CEO/CMO and co-owner of Chondrometrics GmbH, which has received funding from the FNIH OA Biomarker Consortium for the quantitative analysis of cartilage data in this study. He has received consulting fees from Merck KGaA as well as honoraria from Medtronic (less than $10,000 each).
Publisher Copyright:
© 2017 Osteoarthritis Research Society International
PY - 2017/12
Y1 - 2017/12
N2 - Objective To investigate the predictive and concurrent validity of magnetic resonance imaging (MRI)-based cartilage thickness change between baseline (BL) and year-two (Y2) follow-up (predictive validity) and between Y2 and Y4 follow-up (concurrent validity) for symptomatic and radiographic knee osteoarthritis (OA) progression during Y2→Y4. Methods 777 knees from 777 Osteoarthritis Initiative (OAI) participants (age: 61.3 ± 9.0 years, BMI: 30.1 ± 4.8 kg/m2) with Kellgren Lawrence (KL) grade 1–3 at Y2 (visit before progression interval) had cartilage thickness measurements from 3T MRI at BL, Y2 (n = 777), and Y4 (n = 708). Analysis of covariance and logistic regression were used to assess the association of pain progression (≥9 WOMAC units [scale 0–100], n = 205/572 with/without progression) and radiographic progression (≥0.7 mm minimum joint space width (mJSW) loss, n = 166/611 with/without progression) between Y2 and Y4 with preceding (BL→Y2) and concurrent (Y2→Y4) change in central medial femorotibial (cMFTC) compartment cartilage thickness. Results Symptomatic progression was associated with concurrent (Y2→Y4: −305 ± 470 μm vs −155 ± 346 μm, Odds ratios (OR) = 1.5 [1.2, 1.7]) but not with preceding cartilage thickness loss in cMFTC (−150 ± 276 μm vs −151 ± 299 μm, OR = 0.9 95% CI: [0.8, 1.1]). Radiographic progression, in contrast, was significantly associated with both concurrent (−542 ± 550 μm vs −98 ± 255 μm, OR = 3.4 [2.6, 4.3]) and preceding cMFTC thickness loss (−229 ± 355 μm vs −130 ± 270 μm, OR = 1.3 [1.1, 1.5]). Conclusions These results extend previous reports that did not discern predictive vs concurrent associations of cartilage thickness loss with OA progression. The observed predictive and concurrent validity of cartilage thickness loss for radiographic progression and observed concurrent validity for symptomatic progression provide an important step in qualifying cartilage thickness loss as a biomarker of knee OA progression. Clinicaltrials.gov identification NCT00080171.
AB - Objective To investigate the predictive and concurrent validity of magnetic resonance imaging (MRI)-based cartilage thickness change between baseline (BL) and year-two (Y2) follow-up (predictive validity) and between Y2 and Y4 follow-up (concurrent validity) for symptomatic and radiographic knee osteoarthritis (OA) progression during Y2→Y4. Methods 777 knees from 777 Osteoarthritis Initiative (OAI) participants (age: 61.3 ± 9.0 years, BMI: 30.1 ± 4.8 kg/m2) with Kellgren Lawrence (KL) grade 1–3 at Y2 (visit before progression interval) had cartilage thickness measurements from 3T MRI at BL, Y2 (n = 777), and Y4 (n = 708). Analysis of covariance and logistic regression were used to assess the association of pain progression (≥9 WOMAC units [scale 0–100], n = 205/572 with/without progression) and radiographic progression (≥0.7 mm minimum joint space width (mJSW) loss, n = 166/611 with/without progression) between Y2 and Y4 with preceding (BL→Y2) and concurrent (Y2→Y4) change in central medial femorotibial (cMFTC) compartment cartilage thickness. Results Symptomatic progression was associated with concurrent (Y2→Y4: −305 ± 470 μm vs −155 ± 346 μm, Odds ratios (OR) = 1.5 [1.2, 1.7]) but not with preceding cartilage thickness loss in cMFTC (−150 ± 276 μm vs −151 ± 299 μm, OR = 0.9 95% CI: [0.8, 1.1]). Radiographic progression, in contrast, was significantly associated with both concurrent (−542 ± 550 μm vs −98 ± 255 μm, OR = 3.4 [2.6, 4.3]) and preceding cMFTC thickness loss (−229 ± 355 μm vs −130 ± 270 μm, OR = 1.3 [1.1, 1.5]). Conclusions These results extend previous reports that did not discern predictive vs concurrent associations of cartilage thickness loss with OA progression. The observed predictive and concurrent validity of cartilage thickness loss for radiographic progression and observed concurrent validity for symptomatic progression provide an important step in qualifying cartilage thickness loss as a biomarker of knee OA progression. Clinicaltrials.gov identification NCT00080171.
KW - Cartilage thickness
KW - MRI
KW - Osteoarthritis
KW - Progression
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U2 - 10.1016/j.joca.2017.08.005
DO - 10.1016/j.joca.2017.08.005
M3 - Article
C2 - 28838858
AN - SCOPUS:85028705237
VL - 25
SP - 2063
EP - 2071
JO - Osteoarthritis and Cartilage
JF - Osteoarthritis and Cartilage
SN - 1063-4584
IS - 12
ER -