Changes in articular cartilage and posterior meniscus geometries after anterior cruciate ligament injury

s / Osteoarthritis and Cartilage 22 (2014) S57–S489 S356 an increased posterior-inferior directedmiddle cartilage (1.4 increase, p 1⁄4 0.0007) and posterior cartilage slope (3 increase, p < 0.0001), a decreasedmeniscus-bonewedge angle (1.8 decrease, p1⁄4 0.0004) and a decreased meniscus-cartilage height (0.2 mm decrease, p 1⁄4 0.0089) compared with the uninjured contralateral leg. In the medial compartment, the injured leg had an increased posterior-inferior directed posterior cartilage slope (1.5 increase, p 1⁄4 0.0002), a larger meniscuscartilage angle (1.4 increase, p 1⁄4 0.0009) and a smaller cartilage-bone height (0.2 mm decrease, p 1⁄4 0.0026) compared with the uninjured contralateral leg. In contrast, there were no side-to-side differences for all measurements of tibial plateau geometry for the control subjects. Conclusions: Our hypothesis was supported, ACL-injured subjects displayed side-to-side differences in tibial plateau geometry while uninjured control subjects did not. Consequently, the injured knee should not be used in prognostic studies designed to identify risk factors risk factors for ACL trauma, as the tibial plateau geometry is altered by the injury. ACL-injured subjects displayed differences in medial and lateral compartment articular cartilage and meniscus geometries but not in the geometry of the subchondral bone. These differences represent substantial alterations to tibiofemoral articular surfaces found soon after injury, such as increased posterior directed articular cartilage slope and decreased meniscus height. It is unclear whether these changes are produced by the initial trauma, a healing response over time or altered contact mechanics due to the ACL insufficiency at the time of MRI acquisition. The observed changes may be indicative of some of the earliest changes that influence the initial onset or progression of PTOA. 622 CARTILAGE DAMAGE, BONE MARROW LESIONS AND MENISCAL LESIONS PREDICT QUANTITATIVELY MEASURED LOSS OF CARTILAGE OVER 30-MONTHS: THE MOST STUDY A. Guermazi y, F. Eckstein z, D. Hayashi y, F.W. Roemer y, W. Wirth z, T. Yang y, J. Niu y, L. Sharma x, M.C. Nevitt k, C.E. Lewis{, J. Torner #, D.T. Felson y. yBoston Univ., Boston, MA, USA; z Paracelsus Med. Univ., Salzburg, Austria; xNorthwestern Univ., Chicago, IL, USA; kUniv. of California San Francisco, San Francisco, CA, USA; {Univ. of Alabama at Birmingham, Birmingham, AL, USA; Univ. of Iowa, Iowa City, IA, USA Purpose: Recent epidemiological studies have shown associations of structural progression of knee OA with several MRI-based pathological ORs for different MRI features predicting cartilage loss in the same femorotibial compartment Risk factor at baseline No. of compartments without cartilage loss (medialþlateral) (N 1⁄4 321) n (%) No. of compartments with cartilage loss (medial þlateral): (N 1⁄4 64) n (%) aOR (95% CI) Cartilage WORMS score 2 (per unit increase) 183 (57.01) 48 (76.19) 2.59 (1.36, 4.95) BML WORMS score 1 (per unit increase in max BML) 85 (26.48) 26 (41.27) 1.90 (1.10, 3.29) Meniscal damage WORMS score 1 (per unit increase) 49 (15.26) 25 (39.68) 4.47 (2.38, 8.40) Meniscal extrusion (present) (per unit increase) 59 (18.50) 28 (44.44) 3.32 (1.90, 5.80) Effusion synovitis WORMS score 1 (per unit increase) 224 (69.78) 46 (73.02) 1.82 (0.89, 3.75) Hoffa synovitis WORMS score 1 (per unit increase) 187 (58.26) 35 (55.56) 0.93 (0.52, 1.66) features of OA, including cartilage damage, bone marrow lesions and meniscal lesions. However, studies that examined these risk factors commonly evaluated one of them at a time and not their combination simultaneously, although these features are known to partly coexist. The aim of the current study was therefore to determine which semiquantitativeMRI-based OA features weremost predictive of subsequent cartilage loss in the same femorotibial compartment, with cartilage thickness change measured quantitatively using MRI. Methods: One knee of each participants of a subcohort of the Multicenter OA Study (MOST) was studied. The subcohort comprised participants who volunteered for a longitudinal study, in which quantitative MRI measurement of cartilage thickness and volume were performed. These participants also underwent conventional MRI allowing semiquantitative Whole Organ MRI Score (WORMS) based scoring of cartilage damage, bone marrow lesions (BML), meniscal damage and extrusion, effusion-synovitis, and Hoffa-synovitis at baseline and at 30-month follow-up. Progression in the medial or lateral femorotibial compartment (MFTC/LFTC) was defined as quantitative MRI-based cartilage thickness loss exceeding the change observed in OAI control cohort knees (mean 2xSD, MFTC/LFTC: -162mm/-145mm). All MRI predictors were dichotomized into being either “present” (score 2 for cartilage, 0 for others) or “absent”. Differences in baseline scores of predictor variables in the same femorotibial compartment were compared between progressor and non-progressor knees. This was done using multivariable logistic regression, adjusting for age, sex, body mass index, and anatomical alignment axis (degrees). We combined MFTC and LFTC to calculate adjusted odds ratio (aOR) and 95% CI of cartilage thickness loss across compartments (i.e. medial cartilage thinning with medial risk factors and lateral cartilage thinning with lateral risk factors), using Generalized Estimating Equations. Also, ORs and 95%CIs were calculated for MFTC and LFTC cartilage thickness loss, separately. Results: 196 participants with the mean age 59.8 6.3 years, mean BMI 29.5 4.6 kg/m2, and 62% women were studied. 46 knees had radiographic knee OA (Kellgren Lawrence grade 2) at baseline. In the MFTC/ LFTC, 35/29 progressors and 161/167 non-progressors were observed, respectively. Change in MFTC cartilage thickness was -63.0mm and that in LFTC cartilage thickness -25.10mm. For analysis combining MFTC and LFTC, predictors of cartilage thickness loss were baseline cartilage damage (aOR 2.6 [1.4-5.0]), BML (aOR 1.9 [1.1-3.3]), meniscal damage (aOR 4.5 [2.4-8.4]) and meniscal extrusion (aOR 3.3 [1.9-5.8]), all in the same femorotibial compartment. In contrast, effusion-synovitis or Hoffa-synovitis were not predictive of cartilage change. In MFTC-only analysis, MFTC progressors displayed higher aOR for having baseline medial meniscal damage (aOR 2.4, [95%CI 1.1-5.6]), medial meniscal extrusion (aOR 2.6 [1.1-5.8]), but not cartilage damage, BML, effusionsynovitis and Hoffa-synovitis. In the LFTC-only analysis, baseline lateral cartilage damage (aOR 3.4 [1.3-9.3]), lateral meniscal damage (aOR 13.9 [3.3-9.0]) and lateral meniscal extrusion (aOR5.0 [1.4-18.0]) predicted LFTC progression. Conclusion: Our study demonstrated that the presence of semiquantitatively assessed cartilage damage, BML, meniscal damage and extrusion in the same femorotibial compartment predict quantitatively measured cartilage thickness loss over 30-months. In contrast, baseline effusion-synovitis or Hoffa-synovitis were not significantly associated with subsequent cartilage loss. 623 REGIONAL CHANGES OF EARLY OSTEOARTHRITIS CARTILAGE AND SUBCHONDRAL BONE FRACTURE IN A RAT KNEE MODEL OF OA H. Iijima y, T. Aoyama z, A. Ito y, S. Yamaguchi y, M. Nagai y, J. Tajino y, X. Zhang y, H. Akiyama x, H. Kuroki y. yDept. of Motor Function Analysis, Graduate Sch. of Med., Kyoto Univ., kyoto, Japan; zDept. of Dev. and Rehabilitation of Motor Function, Graduate Sch. of Med., Kyoto Univ., kyoto, Japan; xDept. of Orthopaedic Surgery, Graduate Sch. of Med., Gifu