Cartilage Thickness Loss Research Articles

Five-year followup of knee joint cartilage thickness changes after acute rupture of the anterior cruciate ligament.

Anterior cruciate ligament (ACL) rupture involves an increased risk of osteoarthritis. The purpose of this study was to explore changes in cartilage thickness over 5 years after ACL rupture. A total of 121 young active adults (ages 18-35 years; 26% women) from the Knee ACL, Nonsurgical versus Surgical Treatment (KANON) study, who had acute traumatic rupture of the ACL were studied. Sagittal magnetic resonance images were acquired within 4 weeks of ACL rupture (baseline) and at the 2-year and 5-year followup assessments. Medial and lateral femorotibial cartilage was segmented (with blinding to acquisition order), and the mean cartilage thickness was computed across 16 femorotibial subregions. Total femorotibial cartilage thickness change was the primary analytic focus. Maximal subregional mean cartilage thickness loss (ordered value 1 [OV1]) and gain (ordered value 16 [OV16]), independent of its specific location in individual knees, were the secondary analytic focus. Overall femorotibial cartilage thickness increased by 31 μm/year over 5 years (95% confidence interval 18, 44). The increase was similar in men and women and was significantly greater in those younger, as compared with those older, than the median age (25.3 years). The rate of total cartilage thickness change did not differ significantly between the first 2 years and the later 3 years. However, the maximal annualized subregional cartilage loss (OV1) and gain (OV16) were both significantly greater (P < 0.001 and P < 0.05, respectively) during the earlier interval than during the later interval (-115 versus -54 μm [OV1] and 116 versus 69 μm [OV16]). Cartilage thickening was observed over 5 years following ACL injury, particularly in the medial femorotibial compartment and in younger subjects. Major perturbations in cartilage homeostasis were seen over the first 2 years after ACL rupture, with simultaneous subregional thinning and thickening occurring within the same cartilage plate or compartment.

Mitochondrial DNA (mtDNA) haplogroups influence the progression of knee osteoarthritis. Data from the Osteoarthritis Initiative (OAI).

ObjectiveTo evaluate the influence of the mtDNA haplogroups on knee osteoarthritis progression in Osteoarthritis Initiative (OAI) participants through longitudinal data from radiographs and magnetic resonance imaging (MRI).MethodsFour-year knee osteoarthritis progression was analyzed as increase in Kellgren and Lawrence (KL) grade, in addition to increase in OARSI atlas grade for joint space narrowing (JSN), osteophytes and subchondral sclerosis in the tibia medial compartment of 891 Caucasian individuals from the progression subcohort. The influence of the haplogroups on the rate of structural progression was also assessed as the four-year change in minimum joint space width (mJSW in millimetres) in both knees of (n = 216) patients with baseline unilateral medial-tibiofemoral JSN. Quantitative cartilage measures from longitudinal MRI data were those related to cartilage thickness and volume with a 24 month follow-up period (n = 381).ResultsDuring the four-year follow-up period, knee OA patients with the haplogroup T showed the lowest increase in KL grade (Hazard Risk [HR] = 0.499; 95% Confidence Interval [CI]: 0.261–0.819; p<0.05) as well as the lowest cumulative probability of progression for JSN (HR = 0.547; 95% CI: 0.280–0.900; p<0.05), osteophytes (HR = 0.573; 95% CI: 0.304–0.893; p<0.05) and subchondral sclerosis (HR = 0.549; 95% CI: 0.295–0.884; p<0.05). They also showed the lowest decline in mJSW (standardized response means (SRM) = −0.39; p = 0.037) in those knees without baseline medial JSN (no-JSN knees). Normalized cartilage volume loss was significantly lower in patients carrying the haplogroup T at medial tibia femoral (SRM = −0.33; p = 0.023) and central medial femoral (SRM = −0.27; p = 0.031) compartments. Cartilage thickness loss was significantly lower in carriers of haplogroup T at central medial tibia-femoral (SRM = −0.42; p = 0.011), medial tibia femoral (SRM = −0.32; p = 0.018), medial tibia anterior (SRM = +0.31; p = 0.013) and central medial femoral (SRM = −0.19; p = 0.013) compartments.ConclusionsMitochondrial genome seems to play a role in the progression of knee osteoarthritis. mtDNA variation could improve identification of patients predisposed to faster or severe progression of the disease.

Rates and sensitivity of knee cartilage thickness loss in specific central reading radiographic strata from the osteoarthritis initiative

To compare the rate and sensitivity to change of quantitative cartilage thickness change with magnetic resonance imaging (MRI) across specific radiographic strata of knee osteoarthritis (KOA) from central expert readings of the Osteoarthritis Initiative (OAI). Specifically, we explored whether Kellgren Lawrence grade (KLG) 2 knees with radiographic joint space narrowing (JSN) displayed greater cartilage loss than those without JSN, and whether knees with medial JSN grade2 had greater loss than those with grade1. One-year femorotibial cartilage thickness change was obtained for 836 knees, 112 without, and 724 with definite radiographic KOA based on baseline site readings. The maximum subregional cartilage loss, and cartilage thickness change in the total femorotibial joint (FTJ) and medial femorotibial compartment (MFTC) were analyzed across different radiographic strata (central vs site readings). The maximum subregional rate of change was significantly greater in central_KLG2 knees with than in those without JSN (172 ± 152 vs 134 ± 100 μm; P = 0.03). In contrast, the rate did not differ significantly between central_KLG1 knees with and without JSN. MFTC cartilage loss in central_medial_grade2 JSN knees was substantially and significantly greater than in grade1 knees (-70 ± 159 vs -31 ± 126 μm; P = 0.02). For comparison, the loss in grade3 knees was -72 ± 122 μm. In KLG2 knees, presence of radiographic JSN was associated with significantly and substantially greater rates of subregional cartilage loss. Differentiating knees with mild vs moderate medial JSN, and definite radiographic OA knees with vs without JSN is important in predicting structural progression of KOA, and for planning clinical trials testing the efficacy of disease modifying drugs (DMOADs).

Intraarticular sprifermin (recombinant human fibroblast growth factor 18) in knee osteoarthritis: a randomized, double-blind, placebo-controlled trial.

To evaluate the efficacy and safety of intraarticular sprifermin (recombinant human fibroblast growth factor 18) in the treatment of symptomatic knee osteoarthritis (OA). The study was a randomized, double-blind, placebo-controlled, proof-of-concept trial. Intraarticular sprifermin was evaluated at doses of 10 μg, 30 μg, and 100 μg. The primary efficacy end point was change in central medial femorotibial compartment cartilage thickness at 6 months and 12 months as determined using quantitative magnetic resonance imaging (qMRI). The primary safety end points were nature, incidence, and severity of local and systemic treatment-emergent adverse events (AEs) and acute inflammatory reactions, as well as results of laboratory assessments. Secondary end points included changes in total and compartment femorotibial cartilage thickness and volume as assessed by qMRI, changes in joint space width (JSW) seen on radiographs, and pain scores on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). One hundred ninety-two patients were randomized and evaluated for safety, 180 completed the trial, and 168 were evaluated for the primary efficacy end point. We found no statistically significant dose response in change in central medial femorotibial compartment cartilage thickness. Sprifermin was associated with statistically significant, dose-dependent reductions in loss of total and lateral femorotibial cartilage thickness and volume and in JSW narrowing in the lateral femorotibial compartment. All groups had improved WOMAC pain scores, with statistically significantly less improvement at 12 months in patients receiving the 100-μg dose of sprifermin as compared with those receiving placebo. There was no significant difference in serious AEs, treatment-emergent AEs, or acute inflammatory reactions between sprifermin and placebo groups. No statistically significant relationship between treatment group and reduction in central medial femorotibial compartment cartilage thickness was observed; however, prespecified structural secondary end points showed statistically significant dose-dependent reductions after sprifermin treatment. Sprifermin was not associated with any local or systemic safety concerns.

THU0195 Semiquantitatively Assessed Bone Marrow Lesions, Cartilage Damage, Meniscal Damage and Extrusion PREDICT Quantitatively Measured Cartilage Thickness Loss in the Same Femorotibial Compartment: the Most Study

BackgroundStudies have shown associations of structural progression of knee OA with several MRI-assessed pathologic features such as bone marrow lesions (BMLs) cartilage damage and meniscal lesions1,2. However previous studies commonly...

AB0792 Regenerative Power of Autologous Peripheral Blood Stem Cell Injection in Knee Osteoarthritis by A NON Invasive Approach - MRI Study-

BackgroundOsteoarthritis (OA) describes age-related, heterogeneous group of disorders characterized pathologically by focal areas of loss of articular cartilage in synovial joints, associated with varying degrees of osteophyte formation, subchondral bone...

Trajectory of cartilage loss within 4 years of knee replacement – a nested case–control study from the Osteoarthritis Initiative

Knee replacement (KR) represents a clinically important endpoint of knee osteoarthritis (KOA). Here we examine the 4-year trajectory of femoro-tibial cartilage thickness loss prior to KR vs non-replaced controls. A nested case-control study was performed in Osteoarthritis Initiative (OAI) participants: Cases with KR between 12 and 60 month (M) follow-up were each matched with one control (without KR through 60M) by age, sex, and baseline radiographic stage. Femoro-tibial cartilage thickness was measured quantitatively using magnetic resonance imaging (MRI) at the annual visit prior to KR occurrence (T0), and at 1-4 years prior to T0 (T-1 to T-4). Cartilage loss between cases and controls was compared using paired t-tests and conditional logistic regression. One hundred and eighty-nine knees of 164 OAI participants [55% women; age 64 ± 8.7; body mass index (BMI) 29 ± 4.5] had KR and longitudinal cartilage data. Comparison of annualized slopes of change across all time points revealed greater loss in the central medial tibia (primary outcome) in KRs than in controls [94 ± 137 vs 55 ± 104 μm; P = 0.0017 (paired t); odds ratio (OR) 1.36 (95% confidence interval (CI): 1.08-1.70)]. The discrimination was stronger for T-2 → T0 [OR 1.61 (1.33-1.95), n = 127] than for T-1 → T0, and was not statistically significant for intervals prior to T-2 [i.e., T-4 → T-2, OR 0.97 (0.67-1.41), n = 60]. Results were similar for total medial femoro-tibial cartilage loss (secondary outcome), and when adjusting for pain and BMI. In knees with subsequent replacement, cartilage loss accelerates in the 2 years, and particularly in the year prior to surgery, compared with controls. Whether slowing this cartilage loss can delay KR remains to be determined.

Longitudinal (One‐Year) Change in Cartilage Thickness in Knees With Early Knee Osteoarthritis: A Within‐Person Between‐Knee Comparison

Objective: To test the hypothesis that cartilage displays significant longitudinal thickening in the external subregions of the central medial (ecMF) and lateral (ecLF) femur in knees with early radiographic osteoarthritis (ROA) compared with contralateral knees without ROA, and to explore differences in change in other subregions and in radiographic joint space width (JSW). Methods: 50 participants (50% women; age 61.1±9.7y; BMI 27.7±4.7kg/m2 ) were identified from the Osteoarthritis Initiative cohort with definite femorotibial osteophytes but no JSN in one knee (early ROA), and no osteophytes or JSN in the contralateral knee (non-ROA). A longitudinal within-person, between-knee comparison was performed using measures of subregional cartilage thickness based on analyses of sagittal DESSwe MR images obtained at baseline and 1-year. Medial JSW was evaluated from fixed flexion radiographs. Results: The change between baseline and 1-year was -6±94µm in ecMF and +18±91µm in ecLF in early ROA (p=0.78) vs. -1±68µm and +4±76µm in non-ROA knees (p=0.38). The variability of cartilage thickness change tended to be greater in early ROA than in non-ROA knees. Greater cartilage thickness loss in the lateral tibia and a greater reduction in minimum medial JSW was observed in early ROA vs. non-ROA knees. Conclusion: There was no direct evidence of longitudinal cartilage thickening in external subregions of the central femur in knees with early ROA compared with contralateral non-ROA knees. The observed greater variability in longitudinal thickness change in early ROA knees (but not in non-ROA knees) might be due to cartilage thickening and thinning occurring simultaneously in these knees.

Cartilage damage, bone marrow lesions and meniscal lesions predict quantitatively measured loss of cartilage over 30-months: the most study

Cartilage damage, bone marrow lesions and meniscal lesions predict quantitatively measured loss of cartilage over 30-months: the most study

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

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

Lateral and medial joint space narrowing predict subsequent cartilage loss in the narrowed, but not in the non-narrowed femorotibial compartment – data from the Osteoarthritis Initiative

To determine the predictive value of unicompartimental joint space narrowing (JSN) for MRI-based cartilage thickness loss in the narrowed and the non-narrowed femorotibial compartment. 922 knees from 922 Osteoarthritis Initiative (OAI) participants (62.2 ± 9.0 years, 61% females) with radiographic OA (158 without JSN [noJSN], 175 with lateral JSN [latJSN], 589 with medial JSN [medJSN]) were analyzed using 3 T MRI. One-year cartilage thickness change was determined in the lateral (LFTC) and medial femorotibial compartment (MFTC), and in femorotibial subregions. The probability of subsequent cartilage loss was calculated using predefined thresholds. The predictive value of JSN for the probability and magnitude of cartilage loss was compared between latJSN, medJSN and noJSN knees using Fisher's exact and Mann-Whitney-U tests. The probability of cartilage loss was greater in the narrowed compartment of latJSN/medJSN knees (34.9%/32.4%) than in noJSN knees (13.3%/12.7%, P ≤ 6.4 × 10(-6)) and so was the magnitude of cartilage thickness change (P ≤ 8.2 × 10(-6)). No significant differences were observed between the narrowed compartments of latJSN vs. medJSN knees (probability: P = 0.58, magnitude: P = 0.19) or between the non-narrowed compartment of latJSN/medJSN vs. noJSN knees (probability: P ≥ 0.35, magnitude: P = ≥0.23). These results were confirmed by the location-independent ordered value (OV) analyses of femorotibial subregions. The predictive value of latJSN for lateral compartment cartilage loss was comparable to that of medJSN for medial compartment cartilage loss, whereas cartilage loss in the non-narrowed compartment was similar to that in noJSN knees. These findings provide important clues to predicting progression of knee OA, and in tailoring inclusion criteria for clinical trials.

The protective effect of osteoprotegerin on articular cartilage in a rabbit model of osteoarthritis: a histomorphometric study

Objective To observe the morphologic protection effect of intra-articular injection of osteoprotegerin (OPG)on articular cartilage in a rabbit model of osteoarthritis (OA).Methods Sixty male New Zealand rabbits were randomly divided into 3 groups:OPG group (n=20),sham-operated group (n=20) and PBS group (n=20).In OPG group and PBS group,each rabbit underwent anterior cruciate ligament transection (ACLT) in left knee joint,then 0.1 ml OPG solution or PBS were injected into the left knee for 8 weeks (5 times a week) in OPG group and PBS group,respectively.In sham-operated group,the anterior cruciate ligament was just exposed without transection,and then the incision was closed.All rabbits were sacrificed 12 weeks after operation,and the left knee joints were obtained.The Pelletier score and Mankin score were used to evaluate the macroscopic and microscopic cartilage morphology.Results The score of femoral condyle cartilage and tibial plateau cartilage was 1.80±0.89 and 1.80±0.77 in OPG group,respectively,and 3.10±0.97 and 3.20±0.77 in PBS group.However,there was no statistical difference in Pelletier score between the sham-operated group and the OPG group.Consistent with the macroscopic data,the OPG group has a significantly lower Mankin score involving cartilage structure (2.65±0.88),chondrocyte (1.35±0.71),Safranin O staining (1.83±0.83),tidemark integrity (0.30±0.47) and total score (6.13±1.97) compared with the PBS group (4.52±1.09,1.85±0.63,2.80±0.75,0.65±0.49,and 9.83±1.98,respectively).The OPG group has a significantly higher total Mankin score compared with the sham-operated group (4.80±1.25),however,there were no statistical differences in four subitem scores between the two groups.Moreover,the cartilage thickness in OPG group was 371.84±38.94 μm,255.09±74.82 μm in PBS group,and 404.68±15.97 μm in the sham-operated group,and the differences were statistically significant between three groups.Conclusion OPG has a protective effect on articular cartilage and can slow the progression of OA by reducing the grade of synovitis,decreasing the volume of osteophytes,and suppressing the loss of cartilage thickness. Key words: Osteoarthritis; Osteoprotegerin; Cartilage, articular

Contrast-Enhanced Nanofocus X-Ray Computed Tomography Allows Virtual Three-Dimensional Histopathology and Morphometric Analysis of Osteoarthritis in Small Animal Models.

Objective:One of the early hallmarks of osteoarthritis (OA) is a progressive degeneration of the articular cartilage. Early diagnosis of OA-associated cartilage alterations would be beneficial for disease prevention and control, and for the development of disease-modifying treatments. However, early diagnosis is still hampered by a lack of quantifiable readouts in preclinical models.Design:In this study, we have shown the potency of contrast-enhanced nanofocus x-ray computed tomography (CE-nanoCT) to be used for virtual 3-dimensional (3D) histopathology in established mouse models for OA, and we compared with standard histopathology.Results:We showed the equivalence of CE-nanoCT images to histopathology for the modified Mankin scoring of the cartilage structure and quality. Additionally, a limited set of 3D cartilage characteristics measured by CE-nanoCT image analysis in a user-independent and semiautomatic manner, that is, average and maximum of the noncalcified cartilage thickness distribution and loss in glycosaminoglycans, was shown to be predictive for the cartilage quality and structure as can be evaluated by histopathological scoring through the use of an empirical model.Conclusions:We have shown that CE-nanoCT is a tool that allows virtual histopathology and 3D morphological quantification of multitissue systems, such as the chondro-osseous junction. It provides faster and more quantitative data on cartilage structure and quality compared with standard histopathology while eliminating user bias. CE-nanoCT thus should allow capturing subtle differences in cartilage characteristics, carefully mapping OA progression and, ultimately, asses the beneficial changes when testing a candidate disease-modifying treatment.

SAT0330 Large Areas of Cartilage Damage and Full Thickness Cartilage Loss Increase Risk for Incident Radiographic Osteoarthritis

BackgroundPrevalent cartilage damage is one of the strongest risk factors for progression of further cartilage loss in knees with and without OA. It is likely that prevalent cartilage damage also...

Relationship of Bone Mineral Density to Progression of Knee Osteoarthritis

To evaluate the longitudinal relationship between bone mineral density (BMD) and BMD changes and the progression of knee osteoarthritis (OA), as measured by cartilage outcomes. We used observational cohort data from the Vitamin D for Knee Osteoarthritis trial. Bilateral femoral neck BMD values as well as knee magnetic resonance imaging (MRI) scans in each subject were obtained at baseline and subsequently at 12 months and 24 months. The change in total cartilage volume and tibial and femoral cartilage thickness was measured by manual cartilage segmentation of 2 sequential knee MRI scans in each subject. Multivariable linear regression models were used to examine the associations of baseline BMD and BMD change with the cartilage outcomes, adjusting for baseline age, sex, body mass index, malalignment, and vitamin D treatment. Model fit and assumptions were validated. A total of 127 subjects were eligible for analysis. Longitudinal BMD loss was associated with loss of cartilage volume (β = 1.25 per 0.1 gm/cm(2) , P = 0.02) and loss of tibial cartilage thickness (β = 0.028, P = 0.03). BMD loss of a magnitude greater than the least significant change (<-4.7%) was associated with 1.02% cartilage volume loss per year (P = 0.005), 0.014 mm femoral cartilage thickness loss (P = 0.04), and 0.021 mm tibial cartilage thickness loss per year (P = 0.009). There were no significant associations between baseline BMD and any of the cartilage outcomes. Longitudinal BMD loss is associated with progressive cartilage loss in knees with OA. Further work to clarify the basis of this relationship could reveal novel therapeutic targets for knee OA.

Cartilage thickness loss and incidence of knee replacement in a subsample from the Osteoarthritis Initiative - a prospective cohort study

Cartilage thickness loss and incidence of knee replacement in a subsample from the Osteoarthritis Initiative - a prospective cohort study

Predictors of fatigue in patients with hip and knee osteoarthritis

s / Osteoarthritis and Cartilage 21 (2013) S63–S312 S250 Conclusions: Knees that were replaced (KRs) had lower baseline cartilage thickness and greater longitudinal (1 year) cartilage loss than nonKRs, the differences being strongest in both tibiae. Cartilage loss in the weight-bearing femur (a region commonly showing the greatest rate and sensitivity to change), in contrast showed less discrimination. The ability to discriminate between KRs and non-KRs was greater for “earlier” KRs (within 2 years after measurement of cartilage loss) than for those who received KR “later” (year 2-4 after measuring cartilage loss). 474 PREDICTORS OF FATIGUE IN PATIENTS WITH HIP AND KNEE OSTEOARTHRITIS K.D. Allen y,z, H.B. Bosworth y,z, C.J. Coffman y,z, A.S. Jeffreys y, E.Z. Oddone y,z, W.S. Yancy, Jr. y,z. yDurham VA Med. Ctr., Durham, NC, USA; zDuke Univ. Med. Ctr., Durham, NC, USA Purpose: Fatigue is emerging as an important outcome for patients with osteoarthritis (OA), but little is known about factors that predict fatigue severity. This study examined associations of demographic and clinical factors with fatigue in a cohort of patients with hip and / or knee OA. Methods: Participants were n1⁄4291 patients enrolled in a clinical trial of a combined patient and provider intervention for managing OA at the Durham Veterans Affairs Medical Center (mean age 1⁄4 61, SD1⁄49, 90% male, 53% non-white primarily African American). All measures were from baseline assessments. Fatigue was assessed with a 10cm visual analog scale (range 0-10) that asked participants to report how much fatigue has been a problem for them during the past week; anchors were “Fatigue is no problem” and “Fatigue is a major problem.” Potential predictors included participant age, race (white vs. nonwhite), gender, education (some vs. no college), self-rated health (excellent, very good, or good vs. fair or poor), pain severity (Western Ontario and McMasters University Osteoarthritis Index pain subscale), insomnia (Insomnia Severity Index), and depressive symptoms (Patient Health Questionnaire-8). Simple linear regression models examined associations of each individual predictor variable with fatigue, then a multivariable model was fit including all predictors that were significantly associated (p<0.01) with fatigue in simple regression models. Results: The mean fatigue score was 4.8 (SD1⁄43.1). In simple regression models, older age was associated with slightly lower fatigue (b1⁄4 0.07, 95%CI 1⁄4 -0.1, -0.04; p<0.001), and the following were associate with more fatigue: fair / poor self-rated health (b1⁄42.2, 95%CI 1⁄4 1.3, 3.1; p<0.001), greater insomnia severity (b 1⁄4 0.21, 95%CI 1⁄4 0.2, 0.3, p<0.001), greater pain severity (b1⁄4 0.4, 95%CI1⁄4 0.3, 0.5; p<0.001), and greater depressive symptoms (b 1⁄4 0.35, 95%CI 1⁄4 0.3, 0.4; p<0.001). In the multivariable model, variables that remained associated with fatigue were insomnia severity (b 1⁄4 0.06, 95%CI 1⁄4 0.01, 0.1; p1⁄40.0), pain severity (b 1⁄4 0.20, 95%CI 1⁄4 0.1, 0.3; p<0.001), depressive symptoms (b 1⁄4 0.21, 95%CI 1⁄4 0.1, 0.3; p<0.001). Conclusions: Fatigue severity was relatively high in this cohort of patients with OA; mean values on the fatigue visual analog scale were comparable to those seen in patients with rheumatoid arthritis. Demographic factors including age, as well as general health, were not associated with fatigue in the multivariable model. However, key clinical variables related to OA pain, depressive symptoms, and insomnia were associated with more fatigue. These results highlight that fatigue is part of a cluster of OA-related symptoms that generally worsen with greater disease severity. Because of its impact on daily activities and quality of life, fatigue is an important issue to address among patients

Meniscus body position in the normal knee and its change over 4 years

used logistic regression models to evaluate if the presence of JSN or worsening of JSN (JSN progression), as dichotomous outcomes, were associated with BML volumewhile controlling for sex, body mass index, and age. We also used classification and regression trees (CART) to assess whether baseline BML volume or BML volume change was more influential in predicting JSN progression. To confirm the primary results we used data from the clinical trial (n 1⁄4 103) and performed logistic regression models to examine the association between manually measured BML size change (classified as BML regression, no change, or BML progression) and the outcome of cartilage thickness derived from manual cartilage segmentation (stratified into tertiles). Results: Among 362 knees with BML and JSN data, 240 (66%) had JSN at baseline including 25 knees with severe JSN (grade 3) that were excluded from analyses of JSN progression. Larger baseline BML volume was associated with the presence of baseline JSN (odds ratio [OR] 1⁄4 1.5; 95% confidence interval [CI]1⁄4 1.2 1.8) and JSN progression in the same TF compartment (OR 1⁄4 1.3; 95% CI 1⁄4 1.1 1.5). There was a trend that BML regression and BML progression may be associated with greater odds of JSN progression relative to knees with no or minimal changes in BML volume (Table). Sensitivity analyses, excluding knees with more severe lateral JSN, revealed that BML regression in the medial TF compartment was associated with greater odds of medial JSN progression (Table). In CART analyses baseline BML volume was the variable best able to discriminate between those who did and did not have JSN progression. Finally, confirmatory analyses demonstrated that knees with BML regression (OR 1⁄4 2.7; 95% CI 1⁄4 1.0 7.1) or BML progression (OR 1⁄4 2.0; 95% CI 1⁄4 0.9 4.6) had greater odds of cartilage thickness loss. Conclusions: Baseline BML size is an important assessment in knee OA but a reduction of BML size, as measured on traditional MRI, may not be associated with reduced odds of structural changes.

The pattern of cartilage damage in antero‐medial osteoarthritis of the knee and its relationship to the anterior cruciate ligament

Within antero-medial gonarthrosis (AMG) of the knee, there is a spectrum of damage seen in the functionally intact anterior cruciate ligament (ACL). Our aim was to correlate the degree of ACL damage to the geographical extent and degree of cartilage loss on the tibial plateau. Ninety tibial plateaus resected during unicompartmental arthroplasty were photographed and digitally mapped. The ACL damage was graded (0: normal, 1: synovium loss, 2: longitudinal splits), and dimensions of full thickness cartilage loss and damage recorded. The percentage of full thickness loss in patients with a normal ACL was compared to those with a damaged, but functionally intact ligament. All specimens showed similar elliptical loss of cartilage in the antero-medial part of the tibial plateau. A total of 45(50%) patients had a macroscopically normal ACL, 21(23%) had synovial loss, and 24(27%) had longitudinal splits. An increase in the area of cartilage damage was seen with progressive ACL damage (p < 0.001). The area of macroscopically normal cartilage found posteriorly did not change. This study demonstrates that phenotypic distribution of cartilage damage in AMG is highly reproducible with a pattern of increasing cartilage erosion associated with increasing ACL damage.

Using magnetic resonance imaging to determine the compartmental prevalence of knee joint structural damage

To describe the prevalence of magnetic resonance imaging (MRI) detected structural damage in the patellofemoral joint (PFJ) and tibiofemoral joint (TFJ) in a population-based cohort. A secondary aim was to evaluate the patterns of compartmental involvement in knees with pain, between men and women, and in different age and body mass index (BMI) categories. We studied 970 knees, one knee per subject, from the Framingham Osteoarthritis Study, a population-based cohort study of persons 51-92 years old. Cartilage damage and bone marrow lesions (BMLs) were assessed using the Whole Organ Magnetic Resonance Imaging Score (WORMS). The prevalence of isolated PFJ, isolated TFJ, and mixed structural damage was determined using the following definitions: any cartilage damage, full thickness cartilage loss, any BML, and the combination of full thickness cartilage loss with any BML. The mean age and BMI was 63.4 years and 28.6m/kg(2), respectively; 57% were female. Isolated PFJ damage occurred in 15-20% of knees and isolated TFJ damage occurred in 8-17% of knees depending on the definition used. The prevalence of isolated PFJ damage was greater than isolated TFJ damage using all definitions except the any BML definition. This pattern was similar between genders and among age and BMI categories. In those with knee pain, isolated PFJ was at least as common as TFJ damage depending on the definition used. Using MRI to assess knee joint structural damage, isolated PFJ damage was at least as common as, if not more common than, isolated TFJ damage.