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  2. Abstract


To evaluate the effect of meniscal damage on the development of frequent knee pain, aching, or stiffness in middle-aged and older adults.


The Multicenter Osteoarthritis Study is a prospective study of 3,026 individuals 50 years of age or older who have or are at high risk of developing knee osteoarthritis (OA). We investigated knees at baseline and at 15 months. Case knees (n = 110) were those with no pain, aching, or stiffness on most days at baseline, but that had developed frequent pain, aching, or stiffness at 15 months. Control knees (n = 220) were drawn randomly from knees with no frequent symptoms at baseline that did not become case knees. Using 1.0T magnetic resonance imaging performed at baseline and at followup, 2 musculoskeletal radiologists blinded to the case–control status assessed the meniscal damage using the following scale: 0 = intact, 1 = minor tear, 2 = nondisplaced tear or prior surgical repair, and 3 = displaced tear, resection, maceration, or destruction. The effect of meniscal damage was analyzed by contingency tables and logistic regression.


Meniscal damage was common at baseline both in case knees (38%) and in control knees (29%). Although there was a modest association between the meniscal damage score (range 0–3) and the development of frequent knee pain, aching, or stiffness (odds ratio [OR] 1.21, 95% confidence interval [95% CI] 0.96–1.51, adjusted for age, sex, and body mass index), meniscal damage was mostly present in knees with OA. When considering the co-occurrence of OA, we found no independent association between meniscal damage and the development of frequent knee symptoms (OR 1.05, 95% CI 0.80–1.37).


In middle-aged and older adults, any association between meniscal damage and the development of frequent knee pain seems to be present because both pain and meniscal damage are related to OA and not because of a direct link between the two.

The knee menisci are 2 semicircular fibrocartilaginous structures located between the articular cartilage surfaces of the femur and tibia in the medial and lateral joint compartments. The main functions of the menisci are shock absorption and load transmission in the knee, mainly through distribution of mechanical stress over a large area of the joint cartilage (1–4). Loss of meniscal function is recognized as a potent risk factor for both the development of knee osteoarthritis (OA) and cartilage loss in OA (5, 6). In the US, ∼6% of the population ≥30 years of age and 11–15% of those ≥65 years of age have symptomatic knee OA, and the prevalence is increasing (7).

The meniscus may tear as a result of knee trauma or it may tear spontaneously due to aging and degenerative processes (8–10). Magnetic resonance imaging (MRI) is frequently used in the diagnosis of meniscal damage and has high sensitivity and specificity (11, 12). Although population-based epidemiologic data are lacking, we know that meniscal damage is a common finding of MRI (13), especially in the OA knee (14, 15).

The outer one-third of the meniscus has neural innervation including nociceptors, and it is conceivable that meniscal lesions that extend into this location affect knee pain (16). It is also possible that the increased joint stress that occurs as a consequence of compromised meniscal function might elicit knee pain from other structures. While meniscal tears are weakly associated with knee pain cross-sectionally (14, 17), it is not known whether meniscal damage foreshadows the development of knee pain, and if it does, does it directly cause the symptoms? The only longitudinal study performed suggested an increased risk of developing knee symptoms if meniscal damage was present, but possible confounding of OA or effects relayed through other structural changes of OA as an intermediate variable was not evaluated (18).

The etiology of symptoms in OA is complex and poorly understood, with symptoms potentially emanating from a number of different concurrent processes in tissues within the synovial joint, and pain is influenced by psychosocial factors. We need to know more about the natural history of meniscal damage and whether a lesion that causes no or only minor symptoms may predict increased knee discomfort. Therefore, in a case–control study nested within a large prospective cohort, we investigated the effect of meniscal damage on the development of frequent knee pain, aching, or stiffness over 15 months.


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  2. Abstract

Study design.

The Multicenter Osteoarthritis (MOST) Study is a prospective epidemiologic cohort study with the goal of identifying risk factors for incident symptomatic knee OA and progressive knee OA. Individuals recruited for the MOST Study were ages 50–79 years and either had symptomatic knee OA at baseline or were at high risk of developing it. Those considered at high risk included persons who were overweight or obese; those with frequent knee pain, aching, or stiffness (but without OA shown on radiographs); those with a history of major knee injury; and those who had undergone previous knee surgery. All 3,026 subjects were recruited from 2 US communities, Birmingham, Alabama, and Iowa City, Iowa, through mass mailing of letters and study brochures, supplemented by media and community outreach campaigns. Each center also recruited ethnic minorities according to their representation in the community.

Subjects were excluded if they screened positive for rheumatoid arthritis (19), had ankylosing spondylitis, psoriatic arthritis, reactive arthritis, or a severe medical condition that made continued participation in the study unlikely, had undergone previous bilateral knee replacement surgery, were unable to walk without the help of another person or a walker, or were planning to move out of the area in the next 3 years.

Both the baseline assessment and the 15-month assessment followed a similar protocol. Each included a telephone interview and a clinic visit. Subjects answered validated questions about knee symptoms, such as the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) instrument (20); completed surveys on medication use and history of knee injury or knee surgery; and were weighed (without shoes, on a balance-beam scale) and had their height measured. The interviews and medication surveys administered at the baseline and 15-month assessments were identical.

Definitions of case and control knees.

For the present study, knees eligible for the development and/or occurrence of frequent knee pain, aching, or stiffness at 15 months consisted of those for which the subject said there was no frequent pain, aching, or stiffness at both the baseline telephone interview and the baseline clinic visit. The exact phrasing of the question was, “During the past 30 days, have you had pain, aching, or stiffness in your knee on most days?” (The question was asked about the left and right knee separately.) Among the eligible knees, we defined a knee as a case knee at 15 months if the participant answered “yes” to the question for that knee during both the telephone interview and the clinic visit. All case knees with readable MR images identified by March 2006 at both baseline and 15 months were included (n = 110).

From the remaining eligible knees with readable MR images that did not fulfill the criteria for being a case knee, we randomly selected 2 controls per case, frequency matched by study center and by number of eligible knees from each subject (Figure 1 and Table 1). The phone interview and clinic visit at 15 months for controls followed an identical protocol as that for cases, including repeat knee MRIs at the clinic visit. The median number of days between the telephone interview and the clinic visit was 34 days at baseline and 29 days at the 15-month followup.

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Figure 1. Selection process for knees analyzed in the study. MRI = magnetic resonance imaging.

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Table 1. Characteristics of the study subjects at baseline*
 Cases (n = 102 subjects, 110 knees)Controls (n = 208 subjects, 220 knees)
  • *

    BMI = body mass index; OA = osteoarthritis; K/L = Kellgren/Lawrence; WOMAC = Western Ontario and McMaster Universities Osteoarthritis Index.

  • Cases were subjects who developed frequent knee pain, aching, or stiffness at 15 months. Controls were randomly selected at baseline from the same source population as the cases and did not meet criteria to be cases.

  • Highest score obtained from the medial or lateral meniscus.

  • §

    P = 0.003 versus controls, by generalized estimating equation.

Age, mean ± SD years62.9 ± 8.361.2 ± 8.3
Female, no. (%)79 (72)132 (60)
BMI, mean ± SD kg/m229.5 ± 4.629.7 ± 4.3
Knee OA (K/L grade ≥2), no. (%)33 (30)47 (21)
Mechanical axis valgus (>181 degrees), no. (%)26 (24)36 (16)
Mechanical axis varus (<179 degrees), no. (%)52 (47)89 (40)
Meniscal score ≥1 (damage), no. (%)42 (38)63 (29)
Meniscal score, median (range)0 (0–3)0 (0–3)
Self-report of knee injury, no. (%)20 (18)45 (20)
Self-report of knee surgery, no. (%)5 (5)18 (8)
Pain, mean ± SD WOMAC index score1.8 ± 2.2§1.1 ± 1.8

Knee MRI.

Baseline and 15-month MRI scans were obtained with a 1.0T MR system (OrthOne; ONI Medical Systems, Wilmington, MA) equipped with a circumferential transmit–receive extremity coil and included sagittal and axial fat-suppressed fast spin-echo proton density–weighted sequences (time to recovery [TR] 5,800/2,500 msec, time to echo [TE] 35 msec, slice thickness 3 mm, interslice gap 0 mm, field of view [FOV] 14 cm, and 288 × 192–pixel matrix) as well as coronal STIR sequences (TR 7,820 msec, TE 15 msec, slice thickness 3 mm, interslice gap 0 mm, FOV 14 cm, and 256 × 256–pixel matrix) (21).

Two musculoskeletal radiologists (AG and FWR) who were blinded to the case/control status and clinical data read paired images (with knowledge of the time sequence). Meniscal tears, maceration, and/or resection (referred to in this study as meniscal damage) were graded using the Whole-Organ MRI Score (WORMS) (22). The anterior horn, body segment, and posterior horn of the medial and lateral menisci were graded separately on a scale from 0 to 4, as follows: 0 = intact, 1 = minor radial tear or parrot-beak tear, 2 = nondisplaced tear or prior surgical repair, 3 = displaced tear or partial resection, and 4 = complete maceration/destruction or complete resection (interrater κweighted = 0.80). The readers regarded an intrameniscal signal as a meniscal tear when it communicated with the meniscal inferior or superior margin on at least 2 slices. A meniscal score (range 0–3) was determined for each of the medial and lateral menisci (Table 2). We used a collapsed version of the original 7-item WORMS total meniscal score (22) because of low numbers of subjects with higher grades. The highest score from the medial or lateral side was used for analysis. For a dichotomized predictor variable, we defined meniscal damage as a meniscal score ≥1.

Table 2. Determination of meniscal score*
Meniscal scoreCollapsed WORMS scoreDefinition
  • *

    The anterior horn, body segment, and posterior horn of the medial and lateral menisci were graded using a collapsed version of the Whole-Organ Magnetic Resonance Imaging (WORMS) total meniscal score.

0All regions scored as 0Intact meniscal morphology
1Score of 1 in at least 1 region, but no score >1Minor radial tear or parrot-beak tear
2Score of 2 in at least 1 region, but no score >2Nondisplaced tear or prior surgical repair
3Score of 3 or 4 in at least 1 regionDisplaced tear, resection, or complete maceration or destruction


All subjects underwent baseline weight-bearing posteroanterior fixed flexion view knee radiographs using the SynaFlexer positioning frame (Synarc, San Francisco, CA) (23, 24). Body weight was equally distributed between the 2 legs, and the great toes of the feet and the front of the thighs were placed in contact with the front plate of the Plexiglas frame. The external rotation of the feet was fixed at 10 degrees, using a V-shaped foot angulation support on the frame. The central x-ray beam was directed downward at an ∼10-degree angle at a site midway between the knees at the level of the popliteal crease (film-focus distance 183 cm).

One rheumatologist (DTF) and one musculoskeletal radiologist who were both experienced in reading study films graded all baseline posteroanterior view radiographs according to the Kellgren/Lawrence (K/L) scale (25), under blinded conditions with regard to case/control status and clinical data. Radiographic OA was considered to be present if the K/L grade was ≥2.

Full-limb radiographs of both legs were obtained at baseline. The mechanical axis was defined as the angle formed by the intersection of a line from the center of the head of the femur to the center of the tibial spines and a line from the center of the talus to the center of the tibial spines. The interobserver intraclass correlation coefficient for the mechanical axis was 0.99 (P < 0.0001).

Statistical analysis.

All statistical analyses were computed using SAS statistical software for Windows, version 9.1 (SAS Institute, Cary, NC). We calculated means for continuous variables and proportions for categorical variables, then compared the difference in means and proportions between cases and controls using the generalized estimating equation (GEE) to account for correlated knees. For analysis of associations, contingency tables were used to examine the effect of meniscal damage according to radiographic OA severity (K/L score). Logistic regression with GEEs was used to evaluate the effect of meniscal damage, adjusted for age, sex, body mass index (BMI), and radiographic K/L score. Additional analyses were also performed with adjustment for malalignment and change in pain medication. Assuming the prevalence of meniscal damage was ∼20% among knees without frequent pain, aching, or stiffness in subjects ages 50–79 years, with 220 control knees and 110 case knees, our study had 80% power to detect an odds ratio (OR) of 2.0 (using binary predictor variables) with α = 0.05. All P values were 2-tailed, and P values less than or equal to 0.05 were considered significant.


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  2. Abstract

Baseline characteristics and WOMAC pain scores.

The group of case knees (n = 110), i.e., knees that had developed frequent pain, aching, or stiffness at 15 months, showed a tendency toward a higher frequency of female subjects (72% versus 60%; P = 0.06) and toward a higher frequency of baseline radiographic OA (30% versus 21%; P = 0.10) than control knees (n = 220) (Table 1). The group of case knees also showed a tendency toward a higher frequency of severe radiographic OA (K/L grade ≥3) than in control knees (20% versus 8%; P = 0.002).

The baseline mean WOMAC pain score (0–20 scale) was 1.8 for case knees and 1.1 for control knees. The mean change in WOMAC pain score from baseline to the 15-month followup was +4.5 for cases and +0.5 for controls (P < 0.001).

Baseline meniscal status.

Meniscal damage was found in 38% of case knees and 29% of control knees (P = 0.08) (Table 1). Meniscal damage was more frequent in knees in which previous surgery (P < 0.001) or an injury limiting the ability to walk for at least 2 days (P < 0.001) had been reported.

The crude estimate of effect suggested a trend toward an increased risk of developing frequent knee pain, aching, or stiffness with higher baseline meniscal score (Table 3). After controlling for age, sex, and BMI, there was ∼20% increased odds of developing frequent knee pain, aching, or stiffness per unit increase in the baseline meniscal score (OR 1.21, 95% CI 0.96–1.51).

Table 3. Distribution of meniscal scores
Meniscal scoreNo. (%) of cases (n = 110)No. (%) of controls (n = 220)Crude OR (95% CI)*
  • *

    Crude effect estimates from logistic regression (generalized estimating equation). OR = odds ratio; 95% CI = 95% confidence interval.

068 (62)157 (71)Referent
19 (8)16 (7)1.3 (0.55–3.1)
217 (15)26 (12)1.5 (0.77–3.0)
316 (15)21 (10)1.8 (0.86–3.6)

However, meniscal damage was mostly present in knees with radiographic OA at baseline (Table 4). OA may be a causal intermediate on the pathway to symptoms or a confounder to the observed association. Other processes or structural changes related to OA may directly cause the symptoms. Therefore, we performed an analysis stratified by the presence of radiographic OA (with dichotomized predictor variables), which suggested a limited, if any, effect of meniscal damage per se on the development of frequent pain, aching, or stiffness. The pooled Mantel-Haenszel odds ratio estimate was null (1.1, 95% CI 0.65–2.0) (Table 5). After adjusting for age, sex, and BMI, no association was found between the 2 radiographic OA strata (K/L grade ≤1 and K/L grade ≥2; P = 0.35 and 0.57, respectively).

Table 4. Association between baseline Kellgren/Lawrence grade and meniscal damage in case and control knees combined (n = 330)
Kellgren/Lawrence gradeNo. of kneesMeniscal damage present, no. (%)*Mean meniscal score of knees with meniscal damage
  • *

    Meniscal score ≥1 in lateral or medial meniscus at baseline. P for trend < 0.0001, by chi-square test.

012524 (19)1.9
112533 (26)1.9
24116 (39)2.1
≥33932 (82)2.5
Table 5. Association between baseline meniscal damage and development of frequent knee pain, aching, or stiffness at 15-month followup, by Kellgren/Lawrence (K/L) grade
 K/L gradeK/L grades 0–4 (collapsed)
DamageNo damageDamageNo damageDamageNo damageDamageNo damageDamageNo damage
  • *

    Mantel-Haenszel summary odds ratio estimate 1.1 (95% confidence interval 0.65–2.0).

Odds ratio*1.0Referent1.4Referent1.4Referent0.45Referent1.5Referent

When controlling for K/L grade using the meniscal score in the multivariable model, the effect estimate also diminished (OR 1.05, 95% CI 0.80–1.37). Additional adjustment for malalignment and change in pain medication did not substantially alter the results (data not shown).

Incident meniscal damage at 15-month followup or increase in regional WORMS meniscal grade.

While the focus of our investigation was the relationship of baseline meniscal damage to later symptoms, 7 case (6%) and 4 control (2%) knees developed meniscal damage during followup, after previously having none. Twelve case (11%) and 11 control (5%) knees had increased WORMS meniscal grades, i.e., they either developed a new lesion after previously having none or there was worsening of an existing lesion in any subregion.


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  2. Abstract

We prospectively examined the effect of meniscal damage on the development of frequent knee pain, aching, or stiffness in a large observational study of subjects with or at risk of knee OA. Although there was indication of a modest crude association between having meniscal damage and developing frequent knee pain, aching, or stiffness over 15 months, we need to separate the direct effects of an exposure (meniscal damage) from the effects relayed through an intermediate variable or confounder (OA). Meniscal damage was highly associated with the presence of OA at baseline. In our further analyses taking into account OA occurrence, we found limited evidence that meniscal damage directly caused later symptoms. The findings are consistent with previous knowledge of a weak association between meniscal tears per se and symptoms in the older adult knee (14, 17).

Meniscal tissue is partly innervated and is thus a structure to consider as a cause of knee pain not only in young athletes, but also in older adults (16). Little is known of the clinical course of existing meniscal lesions that cause no or few symptoms. The only previous longitudinal study comparing the clinical course of knees with and without such lesions concluded that knees with asymptomatic lesions risk becoming more symptomatic over a 30-month period compared with knees without such lesions, although the severity and impairment remained low (18). However, the study did not take into consideration any effect of OA or other pathologic processes in the joint. OA is a whole-joint disorder that is not only associated with knee pain, but is also highly associated with frequency of meniscal lesions, and thus, for possible clinical implications, OA must somehow be addressed in analysis (14, 15). If not, meniscal damage may incorrectly be interpreted as a direct cause of knee pain, and symptomatic treatment may be directed at an important but often “silent” feature of OA, while OA itself proceeds (26, 27). It is noteworthy that the current widespread surgical treatment of the degenerate and complex type of lesion is resection, because arthroscopic repair of these tears is not readily achievable (28). Thus, treatment is not expected to improve meniscal function.

The meniscus is a critical structure in the knee, and loss of its function is strongly associated with an increased risk for OA (5, 6). OA may lie as an intermediate variable in the causal chain between meniscal damage and developing knee pain. A variety of other structures or processes related to knee OA may very well be responsible for symptoms, e.g., bone marrow lesions, which may be initiated by altered loading patterns and chronic overloading due to the loss of meniscal function (29, 30). Also, it is plausible that the OA disease process may cause meniscal matrix degradation, leading to meniscal damage from normal joint loading or minor trauma. Once again, other structural changes or processes related to OA can be the direct cause of knee symptoms, while meniscal damage often is a clinically “silent” feature. In middle-aged or older adults in particular, OA may act as a confounder for the association observed between meniscal damage and knee symptoms.

It is conceivable that certain types of meniscal lesion may be directly responsible for knee pain, particularly in the early stages during its development, e.g., if the tear involves the peripheral one-third that is vascularized and innervated. Still, the high prevalence of meniscal damage in the older adult knee and the weak association with knee symptoms suggest that any such discomfort may often be a self-limited process that often can be treated conservatively (26).

While MRI generally has high sensitivity and specificity (80–95%) for the diagnosis of meniscal damage compared with the current gold standard, arthroscopic inspection and probing (11, 12), there are important limitations to this work. Even though this is the largest study of its kind, subject numbers were limited, and estimates of effect must be interpreted cautiously. The limited sample size made it necessary to collapse various types of meniscal damage into a single or a few categories for the statistical analyses. The relationship between site of damage or type of lesion and knee symptoms requires further study. Also, we could not classify tears that may have been unstable and at higher risk of becoming symptomatic.

Another limitation is that we did not have data on catching, which is a symptom that also may occur due to meniscal damage. However, we would advocate that most patient-relevant knee discomfort would be captured by our question asking about any knee pain, aching, or stiffness. Also, we note that developing frequent knee pain, aching, or stiffness required consistency of these symptoms at followup and no frequent knee symptoms at baseline, but our subjects who noted no frequent knee symptoms at baseline often reported some knee pain at baseline on the WOMAC questionnaire. Thus, for them, developing frequent knee pain, aching, or stiffness represents an increase in the frequency and severity of symptoms and not necessarily completely new symptoms.

Basic prevalence data of meniscal lesions and their association with knee symptoms in the general population of older adults remain to be elucidated. Meniscal lesions in this age category may often represent an integral part of aging and/or degenerative joint disease. It is a challenge for the healthcare professional to discriminate between knee pain cased by OA and pain that may arise from meniscal damage.

In conclusion, meniscal damage in older adults is highly associated with OA of the knee. However, meniscal damage often seems to not be directly responsible for later symptoms, while other features of OA may be so.


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  2. Abstract

Dr. Englund had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Study design. Englund, Lewis, Torner, Nevitt, Zhang, Felson.

Acquisition of data. Guermazi, Roemer, Lynch, Lewis, Torner, Nevitt, Felson.

Analysis and interpretation of data. Englund, Niu, Guermazi, Roemer, Hunter, Lynch, Lewis, Torner, Nevitt, Zhang, Felson.

Manuscript preparation. Englund, Guermazi, Roemer, Hunter, Lynch, Nevitt, Zhang, Felson.

Statistical analysis. Englund, Niu, Zhang.


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  2. Abstract
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