Knee Cartilage Loss Research Articles

Association of Baseline Knee Bone Size, Cartilage Volume, and Body Mass Index with Knee Cartilage Loss Over Time: A Longitudinal Study in Younger or Middle-aged Adults

To determine the association of knee bone size, cartilage volume, and body mass index (BMI) at baseline with knee cartilage loss over 2 years in younger or middle-aged adults. A total of 324 subjects (mean age 45 yrs, range 26-61) were measured at baseline and about 2 years later. Knee cartilage volume and bone size were determined using T1-weighted fat-saturated magnetic resonance imaging. In multivariable analysis, baseline knee bone size was negatively associated with annual change in knee cartilage volume at medial and lateral tibial sites (ß = -0.62% to -0.47%/cm(2), all p < 0.001). The associations disappeared at medial tibial site after adjustment for baseline cartilage volume and became of borderline statistical significance at lateral tibial site after adjustment for both baseline cartilage volume and osteophytes (ß = -0.29, p = 0.059). Baseline knee cartilage volume was consistently and negatively associated with annual change in knee cartilage volume at all 3 medial tibial, lateral tibial, and patellar sites (ß = -4.41% to -1.37%/ml, all p < 0.001). Baseline BMI was negatively associated with an annual change in knee cartilage volume, but only in subjects within the upper tertile of baseline cartilage volume, even after adjusting for cartilage defects (ß = -0.16% to -0.34%/kg/m(2), all p < 0.05). Our study suggests that both higher baseline tibial bone area and knee cartilage volume (most likely due to cartilage swelling) are associated with greater knee cartilage loss over 2 years. A higher BMI was associated with greater knee cartilage loss only in subjects with higher baseline cartilage volume.

MRI-based extended ordered values more efficiently differentiate cartilage loss in knees with and without joint space narrowing than region-specific approaches using MRI or radiography – data from the OA initiative

The sensitivity to change of quantitative analysis of cartilage in knee osteoarthritis using magnetic resonance imaging (MRI) is compromised by the spatial heterogeneity of cartilage loss. We explore whether extended (medial-lateral) "ordered values" (OVs) are superior to conventional approaches of analyzing subregional cartilage thickness loss and to radiography, in differentiating rates of progression in knees with and without joint space narrowing (JSN). 607 Osteoarthritis Initiative (OAI) participants (308 without and 299 with baseline JSN at baseline) were studied over 12 months. Subregional femorotibial cartilage loss was determined in all knees, and changes in minimum joint space width (mJSW) in a subset of 290 knees. Subregional thickness changes in medial and lateral tibial and femoral cartilages were sorted in ascending order (OV1-16). A Wilcoxon rank-sum test was used to compare rates of change in knees with and without JSN. JSN-knees displayed greater cartilage loss than those without JSN, with minimal P-values of 0.008 for femorotibial subregions, 3.3×10(-4) for medial OV1, and 5.4×10(-7) for extended (medial and lateral) OV1. mJSW measurements (n=290) did not discriminate between longitudinal rates of change in JSN vs no-JSN knees (P=0.386), whereas medial OV1 (P=5.1×10(-4)) and extended OV1 did (P=2.1×10(-5)). Extended OVs showed higher sensitivity to detecting differences in longitudinal rates of cartilage loss in knees with and without baseline JSN than anatomical (sub)regions and radiography. The OV technique also circumvents challenges of selecting particular regions "a priori" in clinical trials and may thus provide a powerful tool in studying risk factors or treatment efficacy in osteoarthritis.

Circulating levels of IL-6 and TNF-α are associated with knee radiographic osteoarthritis and knee cartilage loss in older adults

The role of inflammation in osteoarthritis (OA) pathogenesis is unclear, and the associations between inflammatory cytokines and cartilage loss have not been reported. We determined the associations between serum levels of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), knee radiographic OA (ROA) and cartilage loss over 2.9 years in older adults. A total of 172 randomly selected subjects (mean 63 years, range 52-78, 47% female) were studied at baseline and approximately 3 (range 2.6-3.3) years later. IL-6 and TNF-α were assessed by radioimmunoassay. T1-weighted fat-suppressed magnetic resonance imaging of the right knee was performed at baseline and follow-up to determine knee cartilage volume. Knee ROA of both knees was assessed at baseline. At baseline, quartiles of IL-6 and TNF-α were associated with increased prevalence of medial tibiofemoral joint space narrowing (OARSI grade ≥ 1) in multivariate analyses [odds ratio (OR): 1.42 and 1.47 per quartile, respectively, both P<0.05]. Longitudinally, baseline IL-6 predicted loss of both medial and lateral tibial cartilage volume (β: -1.19% and -1.35% per annum per quartile, P<0.05 and P<0.01, respectively), independently of TNF-α. Change in IL-6 was associated with increased loss of medial and lateral tibial cartilage volume (β: -1.18% and -1.06% per annum per quartile, both P<0.05) and change in TNF-α was also negatively associated with change in medial cartilage volume (β: -1.27% per annum per quartile, P<0.05). Serum levels of IL-6 and TNF-α are associated with knee cartilage loss in older people suggesting low level inflammation plays a role in the pathogenesis of knee OA.

An Open-Label Pilot Study Evaluating by Magnetic Resonance Imaging the Potential for a Disease-Modifying Effect of Celecoxib Compared to a Modelized Historical Control Cohort in the Treatment of Knee Osteoarthritis

The aim of the study was to evaluate by quantitative magnetic resonance imaging the effect of celecoxib 200 mg daily on cartilage volume loss over 12 months in knee osteoarthritis. The primary outcome of this study was to evaluate cartilage volume loss in the medial compartment of the knee (femoral condyle and tibial plateau) assessed by quantitative magnetic resonance imaging on subjects receiving continuous treatment with celecoxib 200 mg daily for 12 months compared with a modelized historical control cohort, as expressed by the percentage loss from baseline. Safety of the medication was also assessed. Comparison of the observed volume loss to the expected loss was evaluated by a multivariate linear regression model based on a historical cohort. For the primary outcome, the 95% confidence intervals for the mean observed celecoxib cohort joint medial compartment cartilage volume loss (6.81% [6.01; 7.60]) and mean predicted loss (modelized historical cohort) (5.65% [5.10; 6.19]) overlap, indicating no significant difference and hence no effect of celecoxib on the medial compartment cartilage volume loss. Similar findings were demonstrated for the lateral compartment cartilage loss. The safety data reported several minor adverse events similar to those typically seen in a 1-year clinical trial. Although celecoxib was demonstrated to be safe for knee osteoarthritis at a 200 mg daily dose, it did not provide a protective effect on knee cartilage loss. Cohort modelization is an efficient and unbiased way to provide a comparator group for the assessment of novel treatments when classic head-to-head randomized controlled trials are not feasible.

The association between subchondral bone cysts and tibial cartilage volume and risk of joint replacement in people with knee osteoarthritis: a longitudinal study

IntroductionTo examine the natural history of subchondral bone cysts and to determine whether knee cartilage loss and risk of joint replacement is higher in knees with cysts, compared with those with bone marrow lesions (BMLs) only or those with neither BMLs nor cysts.MethodsThe symptomatic knee in 132 subjects with knee osteoarthritis (OA) was imaged by using magnetic resonance imaging at baseline and 2 years later. Tibial cartilage volume, subchondral bone cysts, and BMLs were measured by using validated methods. Knee arthroplasty over a 4-year period was ascertained.ResultsBone cysts were present in 47.7% of subjects, 98.1% of whom also had BMLs. Over a 2-year period, 23.9% of subjects had cysts progress, 13.0% developed new cysts, and 11.4% had cysts regress. Bone cysts at baseline were associated with lower medial and lateral tibial cartilage volume compared with those with BMLs only or those with neither (P for trend 0.004 and <0.001, respectively). Annual medial cartilage volume loss was greatest in those with bone cysts compared with those with BMLs only or those with neither (9.3%, 6.3%, and 2.6%, respectively; P for trend, <0.001). As the severity of bone abnormality in the medial compartment increased from no BMLs or cysts present, to BMLs only, to subchondral bone cysts present, the risk of knee replacement was increased (odds ratio, 1.99; 95% confidence interval (CI), 1.01 to 3.90; P = 0.05).ConclusionsWhen cysts are present, cartilage loss and risk of knee replacement are higher than if only BMLs are present, suggesting that cysts identify those most likely to benefit from prevention of disease progression. As cysts can regress, they may also provide therapeutic targets in knee OA.

Magnetic resonance imaging‐based cartilage loss in painful contralateral knees with and without radiographic joint space narrowing: Data from the osteoarthritis initiative

To determine by magnetic resonance imaging (MRI), whether knees with advanced radiographic disease (medial joint space narrowing [mJSN]) encounter greater longitudinal cartilage loss than contralateral knees with earlier disease (no or less mJSN). Participants were selected from 2,678 cases in the Osteoarthritis Initiative, based on exhibition of bilateral pain, body mass index >25 (kg/m(2)), mJSN in 1 knee, no or less mJSN in the contralateral knee, and no lateral JSN in both knees. Eighty participants (mean +/- SD age 60.6 +/- 9.1 years) fulfilled these criteria. Medial tibial and femoral cartilage morphology was analyzed from the baseline and the 1-year followup MRI (sagittal double echo at steady state by 3.0T) of both knees by experienced readers blinded to the time point and mJSN status. Knees with more radiographic mJSN displayed greater medial cartilage loss (-80 mum) assessed by MRI than contralateral knees with less mJSN (-57 mum). The difference reached statistical significance in participants with an mJSN grade of 2 or 3 (P = 0.005-0.08), but not in participants with an mJSN grade of 1 (P = 0.28-0.98). In knees with more mJSN, cartilage loss increased with higher grades of mJSN (P = 0.003 in the medial femur). Knees with an mJSN grade of 2 or 3 displayed greater cartilage loss in the weight-bearing medial femur than in the posterior femur or in the medial tibia (P = 0.048). Knees with advanced mJSN displayed greater cartilage loss than contralateral knees with less mJSN. These data suggest that radiography can be used to stratify fast structural progressors, and that MRI cartilage thickness loss is more pronounced at advanced radiographic disease stage.

Serum levels of vitamin D, sunlight exposure, and knee cartilage loss in older adults: The Tasmanian older adult cohort study

To determine the associations between serum levels of vitamin D, sunlight exposure, and knee cartilage loss cross-sectionally and longitudinally in older adults. A total of 880 randomly selected subjects (mean age 61 years [range 51-79 years], 50% women) were studied at baseline, and 353 of these subjects were studied 2.9 years later. Serum levels of 25-hydroxyvitamin D (25[OH]D) were assessed by radioimmunoassay, and sunlight exposure was assessed by questionnaire. T1-weighted fat-suppressed magnetic resonance imaging (MRI) of the right knee was performed to determine knee cartilage volume and defects. Knee radiographic osteoarthritis (OA) and knee pain were also assessed. The mean 25(OH)D serum level was 52.8 nmoles/liter at baseline (range 13-119 nmoles/liter). Winter sunlight exposure and serum 25(OH)D level were both positively associated with medial and lateral tibial cartilage volume, and a serum 25(OH)D level<50 nmoles/liter was associated with increased medial tibiofemoral joint space narrowing (all P<0.05). Longitudinally, baseline serum 25(OH)D level predicted change in both medial and lateral tibial cartilage volume (beta=+0.04% per annum per nmole/liter for both; P<0.05), and change in serum 25(OH)D level was positively associated with change in medial tibial cartilage volume. These associations were consistent in subjects with radiographic OA and knee pain and/or in women, but not in men or in subjects without radiographic OA or knee pain. Sunlight exposure and serum 25(OH)D levels are both associated with decreased knee cartilage loss (assessed by radiograph or MRI). This is best observed using the whole range of 25(OH)D levels rather than predefined cut points and implies that achieving vitamin D sufficiency may prevent and/or retard cartilage loss in knee OA.

Patterns of femorotibial cartilage loss in knees with neutral, varus, and valgus alignment

Malalignment is known to alter medial-to-lateral femorotibial load distribution and to affect osteoarthritis (OA) progression in the mechanically stressed compartment. We investigated the pattern of cartilage loss in neutral, varus, and valgus knees. Alignment was measured from full-limb radiographs in 174 participants with symptomatic knee OA. Coronal magnetic resonance images were acquired at baseline and a mean +/- SD of 26.6 +/- 5.4 months later. The weight-bearing femorotibial cartilages were segmented from paired images. Cartilage volume, surface area, and thickness were determined in total cartilage plates and defined subregions using proprietary software. The medial-to-lateral ratio of femorotibial cartilage loss was 1.4:1 in neutral knees (n = 74), 3.7:1 in varus knees (n = 57), and 1:6.0 in valgus knees (n = 43). The relative contribution of cartilage thickness change tended to be greater in knees with mild cartilage loss, whereas the increase of denuded area was greater in knees with accelerated cartilage loss. In both varus and neutral knees, the greatest changes were observed in the same subregions of the medial femorotibial compartment (central and external medial tibia, and central medial femur). In valgus and neutral knees, the subregions with the greatest changes in the lateral femorotibial compartment were also similar (internal and central lateral tibia, external lateral femur). The medial-to-lateral rate of femorotibial cartilage loss strongly depended on alignment. Subregions of greater-than-average cartilage loss within the stressed compartment were, however, similar in neutral, varus, and valgus knees. This indicates that the medial-to-lateral loading pattern is different, but that the (sub)regional loading pattern may not differ substantially between neutral and malaligned knees.

Bone marrow lesions predict increase in knee cartilage defects and loss of cartilage volume in middle-aged women without knee pain over 2 years

Objective:Bone marrow lesions (BML) are important in established knee osteoarthritis, predicting pain and progression of disease. Whether BML are also associated with longitudinal changes in knee structure in an asymptomatic...

Relationship of meniscal damage, meniscal extrusion, malalignment, and joint laxity to subsequent cartilage loss in osteoarthritic knees

Progressive knee osteoarthritis (OA) is believed to result from local factors acting in a systemic environment. Previous studies have not examined these factors concomitantly or compared quantitative and qualitative cartilage loss outcomes. The aim of this study was to test whether meniscal damage, meniscal extrusion, malalignment, and laxity each predicted tibiofemoral cartilage loss after controlling for the other factors. Laxity and alignment were measured at baseline in individuals with knee OA. Magnetic resonance imaging included spin-echo coronal and sagittal imaging for meniscal scoring and axial and coronal spoiled gradient echo sequences with water excitation for cartilage quantification. Tibial and weight-bearing femoral condylar subchondral bone area and cartilage surface were segmented. Cartilage volume, denuded bone area, and cartilage thickness were quantified in each plate, with progression defined as cartilage loss >2 times the coefficient of variation for each plate. Qualitative outcome was assessed as worsening of the cartilage score. Logistic regression analysis with generalized estimating equations yielded odds ratios for each factor, adjusting for age, sex, body mass index, and the other factors. We studied 251 knees in 153 persons. After full adjustment, medial meniscal damage predicted medial tibial cartilage volume loss and tibial and femoral denuded bone increase, while varus malalignment predicted medial tibial cartilage volume and thickness loss and tibial and femoral denuded bone increase. Lateral meniscal damage predicted every lateral outcome. Laxity and meniscal extrusion had inconsistent effects. After full adjustment, no factor except medial laxity predicted qualitative outcome. Using quantitative cartilage loss assessment, local factors that independently predicted tibial and femoral loss included medial meniscal damage and varus malalignment (medially) and lateral meniscal damage (laterally). A measurement of quantitative outcome was more sensitive at revealing these relationships than a qualitative approach.

High sensitivity C-reactive protein is associated with lower tibial cartilage volume but not lower patella cartilage volume in healthy women at mid-life

IntroductionElevated serum high sensitivity C-reactive protein (hsCRP) has been reported in established osteoarthritis (OA). The aim of this study was to determine whether serum levels of hsCRP are associated with the variation in tibial and patella cartilage volumes in women without evidence of OA.MethodsParticipants were recruited from a database established from the Australian electoral roll, and were aged 40 to 67 years, were not hysterectomized and had no significant knee pain or knee injury in the last 5 years. Tibial and patella cartilage volumes were measured from magnetic resonance imaging (MRI) of each woman's dominant knee and hsCRP measured in serum. Linear regression models were used to explore the major determinants of variation in both tibial and patella cartilage volume and to assess whether serum hsCRP made an independent contribution to variation in the volumes of cartilage in the two knee compartments.ResultsThe mean age of the 176 participants was 52.3 ± 6.6 years. Compared with a standard model for tibial cartilage volume that included bone area, age, smoking and alcohol status, the addition of an hsCRP term made an independent negative contribution to variation in tibial cartilage volume, irrespective of whether body mass index (BMI) was included in the model or not. By contrast, using a similar approach, hsCRP did not contribute independently to variation in patella cartilage volume.ConclusionIn asymptomatic women aged 40 to 67 years, serum hsCRP is independently negatively associated with the volume of tibial but not patella cartilage suggesting that subclinical inflammation may predispose to knee cartilage loss in the tibial compartment. This should be further assessed by a longitudinal study.

Two-year prospective longitudinal study exploring the factors associated with change in femoral cartilage volume in a cohort largely without knee radiographic osteoarthritis

To identify factors associated with change in femoral cartilage volume over 2 years in a cohort largely without knee radiographic osteoarthritis. A total of 252 subjects (mean 45 years, range 28-60) were used for this study. T1-weighted fat saturation magnetic resonance imaging was performed at baseline and approximately 2 years later. Knee femoral condyle cartilage volume, femoral cartilage defect (0-4 scale) and tibial bone size were determined. The total femoral cartilage volume loss was 6.3% for the 2.3-year period. Factors associated with this annual change were female gender (females vs males: -1.69%, P<0.01), age (over vs under 40 years: -0.96%, P=0.01), smoking (beta: -0.04% per pack-years, P<0.01), as well as lower limb muscle strength (r: +0.32, P<0.01) and its change (beta: +0.34% per quartile, P<0.05). Structural factors associated with change included baseline femoral cartilage volume (beta: -0.36% per ml, P<0.01), femoral cartilage defects (beta: +1.07% per grade, P<0.01), tibial bone area (beta: +0.13% per cm(2), P<0.05), lateral osteophytes (beta: -1.91% per grade, P<0.01) and change in femoral cartilage defects (beta: -0.8% per grade, P<0.001). This study provides evidence confirming that significant risk factors are associated with femoral cartilage loss and these include gender (female), age, smoking, and severity of lower limb muscle weakness. It also supports the hypothesis that femoral cartilage swelling reflected by an increased baseline cartilage volume could be a predictor of disease progression. Our findings also provide interesting clues to implement preventive measures that can possibly prevent or reduce knee cartilage loss.

Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development

To describe the effects of smoking on change in knee cartilage volume and increases in knee cartilage defects, and to test for interaction between smoking and family history of osteoarthritis (OA). Subjects with at least 1 parent having severe primary knee OA (offspring) and randomly selected controls without this history (a total of 325 subjects with a mean age of 45 years) were measured at baseline and 2.3 years later. Knee cartilage volume and defect score (on a 0-4 scale) were determined using T1-weighted fat-saturated magnetic resonance imaging. Smoking status and duration and number of cigarettes were recorded by questionnaire. In offspring, smoking was associated with annual change in medial and lateral tibial cartilage volume (beta = -2.20% and beta = -1.45%, respectively, for current smokers versus former smokers and those who had never smoked; beta = -0.07%/pack-year at both tibial sites, for smoking severity) in multivariate analysis. Smoking was also associated with increases (change >or=1) in medial and lateral tibiofemoral cartilage defect scores (odds ratio [OR] 4.91 and OR 2.98, respectively, for current smokers versus those who had never smoked; OR 9.90 and OR 12.98, respectively, for heavy smoking [total of >20 pack-years] versus never smoking) (all P < 0.05). In contrast, smoking was not associated with any of the above in controls except for change in lateral tibial cartilage volume. There was significant interaction between smoking and offspring-control status for change in medial tibial cartilage volume (P = 0.047) and increases in medial (P = 0.03) and lateral (P = 0.049) tibiofemoral cartilage defects. Smoking leads to knee cartilage loss and defect development primarily in individuals with a family history of knee OA. This provides evidence for a gene-environment interaction in the etiology of knee OA.

A longitudinal study of the effect of sex and age on rate of change in knee cartilage volume in adults

To describe the association between sex, age and rate of change in knee cartilage volume in adults. A total of 325 subjects (mean age 45 yrs, range 26-61) was measured at baseline and approximately 2 yrs later. Knee cartilage volume and bone size were determined using T1-weighted fat saturation magnetic resonance imaging (MRI). Height, weight, body mass index and radiographic osteoarthritis (ROA) were measured by standard protocols. Knee cartilage volume decreased by 1.5-4.2% per annum. In multivariable analysis, females had higher rates of change per annum in knee cartilage volume than males (medial tibia: -3.5%, P < 0.001; lateral tibia: -2.6%, P < 0.001 and patella: -0.8%, P = 0.053). The sex difference first appeared at age 40 and became more marked with increasing age at the medial tibial site only (P = 0.039). Age was significantly associated with annual change in knee cartilage volume at all three sites (beta = -0.06 to -0.12%/yr, all P < 0.05), and these associations were stronger in females. With the exception of the medial site (beta = -0.05/yr, P = 0.117 for ROA exclusion, and beta = -0.06%/yr, P = 0.056 for ROA adjustment), the association with age did not change when subjects with ROA were excluded from analyses or after further adjustment for ROA. Within the age range we studied, knee cartilage volume declines at a faster rate with increasing age. This is partly mediated by ROA at the medial tibial site only. Furthermore, women have substantially higher knee cartilage loss than men, and these sex differences first appear at age 40 and become more marked with increasing age, which has implications for prevention of cartilage loss from middle age.

Urinary pentosidine does not predict cartilage loss among subjects with symptomatic knee OA: the BOKS Study

Age-related changes in articular cartilage are likely to play a role in the etiology of osteoarthritis (OA). One of the major changes in the extracellular matrix of cartilage is the age-related accumulation of advanced glycation end products (AGEs). Pentosidine, an AGE crosslink, is one of the few characterized AGEs and is considered an adequate marker for the many AGEs that are formed in vivo. We used data from a longitudinal observation study to determine if urinary pentosidine could serve as a marker to predict cartilage loss. We conducted a prospective analysis of data from the Boston Osteoarthritis of the Knee Study (BOKS); a completed natural history study of knee OA. All subjects in the study met American College of Rheumatology (ACR) criteria for knee OA. Knee magnetic resonance (MR) images were scored for cartilage in 14 plates of the knee using the Whole Organ Magnetic Resonance Imaging Score (WORMS) semiquantitative grading scheme. Within the BOKS population, a nested sample of 127 subjects (39% of the whole sample) who had both baseline pentosidine and longitudinal magnetic resonance imaging (MRI) measurements (MRIs performed at baseline and 30 months later) was assessed. Urinary pentosidine was assayed and normalized to creatinine to account for differences in urine concentrations. We analyzed the data using three different methods to assess if baseline measures of pentosidine predicted subsequent cartilage loss on MRI. These were (1) analysis 1: logistic regression with the outcome cartilage loss in any plate; (2) analysis 2: proportional odds model where the outcome was defined as 0=no cartilage loss, 1=cartilage loss in one plate, 2=cartilage loss in two plates, and 3=cartilage loss in at least three plates; and (3) analysis 3: Poisson regression with the outcome the number of plates with cartilage loss. All analyses were adjusted for age, sex and Body Mass Index (BMI). At baseline the mean (standard deviation) age was 67 (9) years and 54% were male. The results for the three analytic steps are as follows: Analysis 1: the odds ratio for cartilage loss is 1.01 (95% confidence interval (CI) 0.93-1.09) with 1 unit increase in pentosidine. Analysis 2: the odds ratio for more cartilage loss is 0.99 (95% CI 0.92-1.06) with 1 unit increase in pentosidine. Analysis 3: the relative number of plates with cartilage loss decreased was 1.00 (95% CI 0.95-1.03) with a 1 unit increase in pentosidine. Urinary pentosidine does not predict knee cartilage loss. Previous studies have suggested that local content within cartilage of AGEs is elevated in persons at high risk for progression. Our data suggest that these changes are not measurable systemically. Alternatively, urinary pentosidine levels reflect cartilage degradation in all joints (thus whole body cartilage breakdown) and may therefore not relate to OA severity in a single knee joint.

Lack of association between chondrocalcinosis and increased risk of cartilage loss in knees with osteoarthritis: Results of two prospective longitudinal magnetic resonance imaging studies

To evaluate the relationship between chondrocalcinosis and the progression of knee osteoarthritis (OA) using longitudinal magnetic resonance imaging (MRI) assessments. Longitudinal knee MRIs were obtained in the Boston OA Knee Study (BOKS) and in the Health, Aging and Body Composition (Health ABC) Study. Chondrocalcinosis was determined as present or absent on baseline knee radiographs. Cartilage morphology was graded on paired longitudinal MRIs using the Whole-Organ Magnetic Resonance Imaging Score in 5 cartilage subregions of each of the medial and lateral tibiofemoral joints. Cartilage loss in a subregion was defined as an increase in the cartilage score of > or = 1 (0-4 scale). The risk for change in the number of subregions with cartilage loss was assessed using Poisson regression, with generalized estimating equations to account for correlations. Analyses were adjusted for age, sex, body mass index, baseline cartilage score, and presence of damaged menisci. In BOKS, 23 of the 265 included knees (9%) had chondrocalcinosis. In Health ABC, 373 knees were included, of which 69 knees (18.5%) had chondrocalcinosis. In BOKS, knees with chondrocalcinosis had a lower risk of cartilage loss compared with knees without chondrocalcinosis (adjusted risk ratio [RR] 0.4, 95% confidence interval [95% CI] 0.2-0.7) (P = 0.002), and there was no difference in risk in Health ABC (adjusted RR 0.9, 95% CI 0.6-1.5) (P = 0.7). Stratification by intact versus damaged menisci produced similar results within each cohort. In knees with OA, the presence of chondrocalcinosis was not associated with increased cartilage loss. These findings do not support the hypothesis that chondrocalcinosis worsens OA progression.

Knee cartilage loss in symptomatic knee osteoarthritis over 4.5 years

The objective of this study was to describe the rate of change in knee cartilage volume over 4.5 years in subjects with symptomatic knee osteoarthritis (OA) and to determine factors associated with cartilage loss. One hundred and five subjects were eligible for this longitudinal study. Subjects' tibial cartilage volume was assessed by magnetic resonance imaging (MRI) at baseline, at 2 years and at 4.5 years. Of 105 subjects, 78 (74%) completed the study. The annual percentage losses of medial and lateral tibial cartilage over 4.5 years were 3.7 ± 4.7% (mean ± SD; 95% confidence interval 2.7 to 4.8%) and 4.4 ± 4.7% (mean ± SD; 95% confidence interval 3.4 to 5.5%), respectively. Cartilage volume in each individual seemed to track over the study period, relative to other study participants. After multivariate adjustment, annual medial tibial cartilage loss was predicted by lesser severity of baseline knee pain but was independent of age, body mass index and structural factors. No factors specified a priori were associated with lateral cartilage volume rates of change. Tibial cartilage declines at an average rate of 4% per year in subjects with symptomatic knee OA. There was evidence to support the concept that tracking occurs in OA. This may enable the prediction of cartilage change in an individual. The only significant factor affecting the loss of medial tibial cartilage was baseline knee pain, possibly through altered joint loading.

Association of prevalent and incident knee cartilage defects with loss of tibial and patellar cartilage: A longitudinal study

To describe the association between prevalent and incident knee cartilage defects and loss of knee cartilage in male and female adults. A convenience sample of 325 subjects (mean age 45 years; age range 26-61 years) was evaluated at baseline and approximately 2 years later. Knee cartilage volume, cartilage defect scores (0-4 scale), and joint surface area were determined using T1-weighted fat-suppression magnetic resonance imaging techniques. Height, weight, and radiographic evidence of osteoarthritis were measured by standard protocols. Multivariable analysis revealed that baseline cartilage defect scores at the medial tibia, lateral tibia, and patella had a dose-response association with the annual rate of change in knee cartilage volume at the corresponding site (beta = -1.3% to -1.2% per grade; P < 0.05 for all comparisons). In addition, an increase in knee cartilage defect score (change of > or =1) was associated with higher rates of knee cartilage volume loss at all sites (beta = -1.9% to -1.7% per year; P < 0.01 for all comparisons). Furthermore, a decrease in the knee cartilage defect score (change of less than or equal to -1) was associated with an increase in knee cartilage volume at all sites (beta = 1.0% to 2.7% per year; P < 0.05 for all comparisons). Prevalent knee cartilage defects are predictive of compartment-specific cartilage loss over 2 years. Both increases and decreases in knee cartilage defects are associated with changes in knee cartilage volume, which implies a potential for reversal of knee cartilage loss.

Genetic mechanisms of knee osteoarthritis: a population-based longitudinal study

To describe the differences in knee structure and non-knee structural factors between offspring having at least one parent with a total knee replacement for severe primary knee osteoarthritis and age- and sex-matched controls with no family history of knee osteoarthritis, a population-based longitudinal study of 163 matched pairs (mean age 45 years, range 26 to 61) was performed at baseline and about 2 years later. Knee cartilage defect score (0 to 4), cartilage volume and bone size were determined with T1-weighted fat saturation magnetic resonance imaging. Body mass index (BMI), lower-limb muscle strength, knee pain, physical work capacity at 170 beats/minute (PWC170) and radiographic osteoarthritis were measured by standard protocols. In comparison with controls, offspring had higher annual knee cartilage loss (-3.1% versus -2.0% at medial tibial site, -1.9% versus -1.1% at lateral tibial site and -4.7% versus -3.7% at patellar site, all P < 0.05), a greater increase in medial cartilage defect score (+0.15 versus -0.01, P < 0.05) and a greater decline in PWC170 (-0.7 watts/kg versus -0.4 watts/kg, P < 0.01). There were no significant differences in change in BMI, lower-limb muscle strength, knee pain or tibial bone area between these two groups; however, the differences in knee cartilage loss and cartilage defect change decreased in magnitude and became non-significant after adjustment for baseline cartilage volume, tibial bone area, BMI and knee pain. This longitudinal study suggests that knee cartilage loss, change in cartilage defects and decrease in physical fitness all have roles in the development of knee osteoarthritis, which is most probably polygenic but may reflect a shared environment. Importantly, the cartilage changes are largely dependent on baseline differences in cartilage volume, tibial bone area, BMI and knee pain, suggesting that these factors might have a role in their initiation.