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Clinical and epidemiological research
Extended report
Risk factors for medial meniscal pathology on knee MRI in older US adults: a multicentre prospective cohort study
  1. Martin Englund1,2,
  2. David T Felson2,
  3. Ali Guermazi2,
  4. Frank W Roemer2,3,
  5. Ke Wang2,
  6. Michel D Crema2,
  7. John A Lynch4,
  8. Leena Sharma5,
  9. Neil A Segal6,
  10. Cora E Lewis7,
  11. Michael C Nevitt4
  1. 1Lund University, Lund, Sweden
  2. 2Boston University School of Medicine, Boston, Massachusetts, USA
  3. 3Klinikum Augsburg, Augsburg, Germany
  4. 4University of California San Francisco, San Francisco, California, USA
  5. 5Northwestern University, Chicago, Illinois, USA
  6. 6University of Iowa, Iowa City, Iowa, USA
  7. 7University of Alabama, Birmingham, Alabama, USA
  1. Correspondence toDr Martin Englund, Musculoskeletal Sciences, Department of Orthopedics, Skåne University Hospital, Klinikgatan 22, SE-221 85 Lund, Sweden; martin.englund{at}med.lu.se

Abstract

Objectives Meniscal pathology in which the aetiology is often unclear is a frequent finding on knee MRI. This study investigates potential risk factors for medial meniscal lesions or extrusion in middle-aged and elderly persons.

Methods Prospective cohort study using population-based subjects from Birmingham, Alabama and Iowa City, Iowa, USA (the Multicenter Osteoarthritis Study). 644 men and women aged 50–79 years with or at high risk of knee osteoarthritis (Kellgren and Lawrence grade 0–2) but with normal medial meniscal status at baseline were studied. Paired baseline and 30-month 1.0 T knee MRI were scored for meniscal lesions and extrusion (pathology) and the following systemic, knee-specific and compartment-specific potential risk factors were evaluated: age, sex, body mass index, bony enlargement of finger joints, knee trauma, leg-length inequality and knee alignment.

Results Of 791 knees, 77 (9.7%) had medial meniscal pathology at 30 months follow-up. 61 of the 77 (81%) had no report of trauma during follow-up. Including all potential risk factors in the multivariable model, the adjusted OR for medial meniscal pathology was 4.14 (95% CI 2.06 to 8.31) for knee trauma during follow-up, 1.64 (1.00 to 2.70) for five or more bony enlargements of finger joints (vs ≤4) and 2.00 (1.18 to 3.40) for varus alignment (vs not varus) at baseline examination. Obesity was a risk factor for the development of meniscal extrusion, OR 3.04 (1.04 to 8.93) but not for meniscal lesions, OR 1.15 (0.52 to 2.54).

Conclusions Apart from knee trauma, possible generalised osteoarthritis, expressed as multiple bony enlargements of finger joints, varus alignment and obesity are risk factors for medial meniscal pathology.

https://doi.org/10.1136/ard.2011.150052

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    In the tibiofemoral compartment of the knee there are two wedge-shaped discs of fibrocartilage, the medial and lateral meniscus. They provide important functions in absorbing shocks and distributing load over the surrounding joint cartilage.1,–,3 When a meniscus is damaged or removed by surgery, there is a greatly increased risk of developing knee osteoarthritis.4,–,7 The knee is one of the most common sites of osteoarthritis, causing pain, reduced knee function and disability to a large proportion of middle-aged and elderly persons.8 Osteoarthritis is an increasingly important health concern in most developed countries and is, according to the WHO, among the top 10 conditions in Europe with respect to a burden on society.8

    The mechanism by which meniscal tear occurs is traditionally considered to be caused by acute knee trauma.9 However, meniscal lesions are frequent incidental findings in middle-aged and elderly persons on knee MRI, with an overall prevalence ranging from approximately 19% in the knees of women 50–59 years of age to 56% in the knees of men 70–90 years of age.10 These meniscal lesions are typically horizontal cleavage lesions or flap tears of the body or posterior horn of the medial meniscus with or without fibrillation, and are often accompanied by meniscal extrusion (radial displacement of the meniscus outside the joint margin).10,–,12 In the general population most of these meniscal pathologies do not per se cause symptoms,10 but as diminishing meniscal function is a strong risk factor for knee osteoarthritis and osteoarthritis progression,4 13 14 any such pathology may still be a key factor in several aspects, in particular in early-stage knee osteoarthritis. These findings are sometimes referred to as being of degenerative character, even if there is little evidence of their aetiology.15 To date, there have been no longitudinal studies of risk factors for such meniscal pathology. One reason for the lack of studies is the difficulty of ascertaining meniscal status at both baseline and follow-up. This requires repeated, expensive, and time-consuming imaging methods such as knee MRI. Therefore, there is a strong rationale for the present study, in which we use data from a large on-going cohort study. For risk factors, we focused on the effects of common systemic and biomechanical factors that are likely to precede and possibly cause meniscal pathology. Cartilage damage or bone marrow lesions were not evaluated as risk factors because they may often be a consequence of meniscal pathology.13 14 16 Therefore, using a prospective cohort study design with repeat knee MRI examinations over 30 months our aim was to evaluate common demographic, systemic, but also certain biomechanical knee-specific potential risk factors that may be casually associated with meniscal pathology.

    Methods

    Design overview

    The Multicenter Osteoarthritis Study (MOST) is a large, prospective cohort study of individuals aged 50–79 years in which the primary goal was to identify risk factors for incident and progressive knee osteoarthritis.17 Study subjects either had knee osteoarthritis at baseline or were at high risk of developing the disease. Factors considered to contribute to a high risk of knee osteoarthritis included being overweight or obese, having either knee pain, aching, or stiffness on most of the preceding 30 days, a previous knee injury that made it difficult to walk for at least 1 week, or previous knee surgery. Written informed consent was obtained before participation at each visit, as approved by the institutional review boards of the participating institutions.

    Setting and participants: MOST parent study

    All 3026 subjects in MOST were recruited from two communities in the USA (Birmingham, Alabama and Iowa City, Iowa) through mass mailing of letters and study brochures, supplemented by media and community outreach campaigns. Recruitment was based on the presence of one or several risk factors for osteoarthritis as detailed above. Subjects were excluded if they screened positive for rheumatoid arthritis,18 had ankylosing spondylitis, psoriatic arthritis, chronic reactive arthritis, a severe medical condition that made continued participation in the study unlikely, bilateral knee replacement surgery, inability to walk without the help of another person or walker, or were planning to move out of the area during the next 3 years.

    At the baseline clinic visits, subjects underwent weight-bearing posteroanterior knee radiography, using a fixed flexion protocol.19 20 One musculoskeletal radiologist and one of two rheumatologists graded all films according to the Kellgren and Lawrence (KL) scale;21 discrepancies were adjudicated by a panel of three readers. Readers were blinded to MRI findings and clinical data. The two-person interobserver reliability for determining the KL grade ranged from κ=0.77 to κ=0.80. Subjects were also weighed and had their height measured at baseline.

    Knee MRI scans and sampling

    At baseline and 30-month follow-up, knee MRI of all MOST participants who were willing and had no contraindications were obtained with a 1.0 T MR system (OrthOne; ONI, Wilmington, Massachusetts, USA) with a circumferential transmit–receive extremity coil. MRI were performed using sagittal and axial fat-suppressed fast spin-echo proton density-weighted sequences (repetition time 5800/2500 ms, time to echo 35 ms, slice thickness 3 mm, field of view 14 cm, matrix 288×192 pixels), and coronal Short Tau Inversion Recovery (STIR) sequence (repetition time 7820 ms, time to echo 15 ms, slice thickness 3 mm, field of view 14 cm, matrix 256×256 pixels).22 23 Two musculoskeletal radiologists blinded to clinical and radiographic data read the paired images separately with knowledge of the time sequence.

    Of participants studied at baseline, 90% had 30-month follow-up clinical visits (figure 1). The study sample selected for MRI readings has previously been described.24 In this study we included all knees with KL grade 0–2 at baseline, ie, we elected not to include subjects with severe preexisting radiographic osteoarthritis (KL grade 3 or 4) as preexisting meniscal pathology is very frequent in these subjects. Furthermore, we restricted our analyses to include only knees with normal medial meniscal integrity and no extrusion of the medial meniscus on MRI at baseline (n=791). We focused on medial meniscal pathology only because lateral meniscal pathology is rarer,10 and our multivariable analysis included mechanical knee alignment, which is a compartment-specific risk factor.

    Figure 1
    Figure 1

    Study flow chart (please note that a person may contribute with one knee to the analysis while the other knee was excluded). MOST, Multicenter Osteoarthritis Study; OA, osteoarthritis.

    Meniscal outcome variable

    Meniscal integrity on paired baseline and 30-month MRI was assessed using the whole-organ MRI score method.25 Meniscal tear, maceration, and (or) destruction of the anterior horn, body segment and the posterior horn, collectively here referred to as meniscal lesions, were assessed using a five-item ordered scale, in which 0 is intact and 1 is minor radial or parrot-beak tear, 2 is non-displaced tear, 3 is displaced tear or partial maceration or destruction, or 4 is complete maceration, or destruction (interobserver weighted κ=0.80). The readers regarded an increased intrameniscal signal (often a linear signal within the meniscus) as a meniscal tear when it communicated with the inferior or superior margin and (or) free edge of the meniscus on at least two slices.

    Meniscal positioning was graded as 0 is no extrusion, or grade 1 or 2 (extrusion ≤50%, and extrusion ≥50%, respectively) from the midposterior coronal slice where the medial tibial spine was depicted to its maximum extent (interobserver weighted κ=0.60). The point of reference for meniscal extrusion was the tibial plateau osteochondral junction at the joint margin (excluding osteophytes).

    For this study, because meniscal lesions and extrusion are often related and have similar effects of increased risk for cartilage loss and bone marrow lesions,14 16 and to ensure sufficient numbers with the outcome, we primarily combined the two constructs meniscal integrity and meniscal positioning to create a dichotomous outcome variable for the medial compartment: no meniscal pathology is intact meniscus and no meniscal extrusion at both baseline and the 30-month examination versus new development of meniscal pathology is meniscal lesion or extrusion at 30 months but having had normal medial meniscal status at the baseline examination. However, we also evaluated meniscal lesions and meniscal extrusion as two separate outcomes.

    Exposure variables

    At both 15 and 30-month follow-up, subjects were asked if they had injured their left or right knee (and which side it was) badly enough to limit their ability to walk for at least 2 days since the last study visit.

    At the baseline clinic visit, examiners evaluated the finger joints for bony enlargement of study subjects' hands. These bony enlargements may indicate a predisposition towards generalised osteoarthritis, and hypothetically also to a greater risk of degenerative meniscal pathology.26,–,29 The examined joints were the first interphalangeal, distal interphalangeal (Heberden's nodes), proximal interphalangeal (Bouchard's nodes) and the first carpometacarpal joint (base of thumb). Using the median value of finger joints with bony enlargement (four joints), we created a dichotomised exposure variable, none to four versus five or more.

    Full-limb radiographs of both legs for determination of mechanical axis and leg length were obtained at baseline. The mechanical axis was defined as the angle formed by the intersection of a line from the centre of the head of the femur to the centre of the femoral notch in the knee, and a second line from the centre of the talus to the centre of the tibial spines in the knee (for interobserver agreement intraclass correlation coefficient was 0.99, p<0.001). Based on earlier work, we defined varus as less than 179°.30

    Leg-length inequality has recently been reported to be a risk factor for the development and progression of knee osteoarthritis and could hypothetically be related to increased ground-reaction forces.31 32 We defined leg length as the distance from the centre of the femoral head to the tibial mid-plafond point. The mid-plafond point is the most distal portion of the tibia directly over the talar dome and does not include the ankle joint. For leg-length inequality, intra and interobserver intraclass correlation coefficients were 0.96 and 0.97, respectively (both p<0.001). We defined clinically significant leg-length inequality as a difference by 1 cm or more, and created a two-item categorical variable: leg-length inequality less than 1 cm and leg-length inequality by 1 cm or more.

    Statistical analysis

    To evaluate the effect of potential risk factors for medial meniscal pathology, we calculated adjusted OR using logistic regression. We used generalised estimating equations to account for the correlation between two knees from the same subject. In the model we evaluated age, gender, body mass index, finger joints with bony enlargements, knee injury limiting the ability to walk for at least 2 days during follow-up, knee alignment and leg-length inequality; all entered simultaneously. Furthermore, race and clinical site (Alabama or Iowa) were adjusted for because MRI readings were matched by clinical site. We also performed a couple of sensitivity analysis evaluating the effect of additional adjustment for KL grade and (or) with adjustment for MOST recruitment variables. As MOST is enriched with subjects with one or more risk factors for knee osteoarthritis, which may potentially bias the relative estimates of effect, we conditioned on study recruitment variables that were not already included in the model. These risk factors (the information obtained at the telephone screening interview) were a self-report of previous knee injury (so badly that it was difficult to walk for at least 1 week), previous knee surgery and the presence of knee pain, aching or stiffness on most days for the last 30 days. All tests were performed using SAS for Windows, version 9.1. p Values less than or equal to 0.05 were considered statistically significant.

    Results

    The study sample with normal medial meniscal status at baseline knee MRI consisted of 791 knees from 644 persons (64.6% women). The mean (SD) age of subjects was 60.0 (7.3) years with a mean (SD) body mass index of 29.5 (4.7) (table 1). At baseline, the distribution of severity of tibiofemoral radiographic osteoarthritis, KL grade, was 563 knees with grade 0, 143 knees with grade 1 and 112 knees with grade 2.

    View this table:
    Table 1

    Study sample characteristics at baseline and information on knee injury during follow-up shown by the outcome

    The analyses focused on medial meniscal pathology only. Of the 791 knees, 77 (9.7%) had such findings on MRI at the 30-month follow-up (figures 2–4). Of those, 31 had both meniscal lesion (tear, destruction or maceration) and meniscal extrusion, 28 cases had meniscal lesions but no extrusion, and 18 cases had meniscal extrusion but no definite meniscal lesion. The lesions predominantly involved the posterior horn (88%), followed by the meniscus body (53%). None (0%) involved the anterior horn.

    Figure 2
    Figure 2

    Meniscal tear. (A) Baseline sagittal fat-suppressed proton density-weighted 1.0 T MRI shows normal triangular appearance of the posterior horn of the medial meniscus without tear or intramensical signal alterations. (B) Follow-up image shows a meniscal tear reaching the superior and inferior surface of the posterior horn (arrow).

    Figure 3
    Figure 3

    Partial meniscal maceration. (A) Baseline coronal 1.0 T STIR MRI shows a normal body of the medial meniscus. (B) 30-Month follow-up image shows partial maceration of the meniscal body with an amputated triangular appearance (arrow).

    Figure 4
    Figure 4

    Meniscal extrusion. (A) Baseline coronal 1.0 T STIR MRI depicts a normal position of the body of the medial meniscus in alignment with the tibial plateau. (B) The 30-month follow-up image shows medial meniscal extrusion of 3 mm in regard to the tibial plateau (arrow).

    Of those knees reported to have sustained an injury leading to reduced ability to walk for at least 2 days during the follow-up, the adjusted OR for medial meniscal pathology was increased by over fourfold, OR 4.14 (95% CI 2.06 to 8.31) (table 2). Still, the majority, 62 of the 77 knees (81%) with meniscal pathology on the medial side did not have a report of knee injury during follow-up.

    View this table:
    Table 2

    Evaluation of potential risk factors for medial meniscal pathology on MRI over 30 months in knees (n=791) of middle-aged and elderly persons

    Keeping all potential risk factors in the model, including a report of knee injury or not, the estimate of risk was increased by approximately 60% if the subject had five or more bony enlargements of finger joints at baseline compared with four or less. Having a varus aligned knee was also associated with 100% increased estimate of risk compared with not being varus. Furthermore, obesity (body mass index of 30 or more) had an approximately 50% increased risk of medial meniscal pathology in the knee compared with having a body mass index of 25 or less, although this was not statistically significant. Age, gender and leg-length inequality were found not substantially to affect the risk of medial meniscal pathology over 30 months (table 2).

    Additional adjustment for KL grade at baseline and (or) the MOST recruitment variables did not essentially alter the estimates of risk (data not shown).

    The evaluation of risk factors for the development of meniscal lesions and extrusion as two separate outcomes yielded essentially the same overall picture as the model using the composite outcome, with the exception of the effect of body mass index. Obesity was a significant risk factor for the development of medial meniscal extrusion, OR 3.04 (95% CI 1.04 to 8.93), while it was not so for meniscal lesions, OR 1.15 (95% CI 0.52 to 2.54) (see supplementary appendix, available online only).

    Discussion

    This prospective cohort study provides novel evidence in support of the hypothesis that meniscus pathology is often a result of both systemic effects and local biomechanical factors, not only a result of acute knee trauma. Importantly, while knee trauma, which was associated with approximately a fourfold increased risk, was the most notable risk factor for medial meniscal pathology in this study, still 81% of persons who developed such pathology did not report knee trauma during follow-up.

    Of the systemic risk factors we evaluated, bony enlargements of finger joints can help identify subjects with generalised osteoarthritis and has strong genetic determinants.26 27 Furthermore, Heberden's nodes have been associated with the incidence and progression of knee osteoarthritis.33 We found that having multiple bony enlargements of finger joints was associated with an approximately 60% increased risk of developing meniscal pathology. In support of our findings, in subjects followed up after knee meniscectomy, those with radiographic hand osteoarthritis more often had a degenerative type of meniscal tear at the index surgery.28 Furthermore, systemic effects on, for example, collateral ligaments and degeneration of meniscal attachments may predispose to meniscal extrusion.34,–,36 The present longitudinal data support the hypothesis that the meniscal tissue is affected by degradation possibly related to an early-stage generalised osteoarthritis process.28 37

    Of the biomechanical risk factors that we evaluated, knee malalignment, which may be influenced by familiar factors,38 is an important compartment-specific risk factor for osteoarthritis progression,39 40 and has been associated with meniscal pathology in knee osteoarthritis.41 However, the role of malalignment in disease initiation remains controversial.42 43 We found that knees with varus malalignment at baseline, ie, increased loading of the medial compartment, versus not varus had an approximately 100% increased risk of meniscal pathology in the same compartment. The finding corroborates an arthroscopy series in which medial meniscal tear was associated with varus alignment.44 It is plausible that meniscal destruction and extrusion may also contribute directly to altered alignment of the knee. One challenge is the difficulty to tease out the effects of altered meniscus integrity and positioning from the effects of, for example, bone attrition and cartilage loss.41 45

    Our study failed to detect any significant effect of leg-length inequality with respect to the development of meniscal pathology. The number of subjects with leg-length inequality was however low. Negative findings must in general be interpreted with caution as a result of the outcome being uncommon and the low prevalence of certain risk factors. Importantly, the analyses evaluating meniscal lesions and meniscal extrusion as separate outcomes revealed that obesity seemed to be a stronger risk factor for extrusion than meniscal lesions. Results for the other risk factors were essentially the same for both meniscal lesions and extrusion (see supplementary appendix, available online only).

    Knee osteoarthritis is often a result of increased biomechanical loading in susceptible individuals and the pathological response of joint tissues to such abnormal biomechanical stress.46 This study sheds further light on a plausible pathway by which knee malalignment and obesity could result in chronic overloading. Such overloading, coupled with degenerative meniscal matrix changes caused by ‘osteoarthritis in the meniscus’, could lead to meniscal fatigue and rupture/extrusion. Once the meniscus loses its critical function in the knee joint, increased biomechanical loading patterns on joint cartilage may result in cartilage loss,13 14 bone alterations including trabecular bone changes,47 increased bone mineral density,48 the development of subchondral bone marrow lesions16 and increasing malalignment. The vicious cycle of knee osteoarthritis is in motion.

    All of our exposure variables were observed independently of the MRI-based meniscal outcome variable, minimising the risk of dependent errors or other bias. However, measurements of the outcome and certain exposure variables are still subject to measurement error, which may result in misclassification. This misclassification is expected to be non-differential, biasing estimates of effect toward the null. We do not know the true nature or severity of the knee injuries reported. Therefore, we cannot exclude the possibility of recall bias, ie, more frequent recollection of knee injury if having a painful knee. Furthermore, there is one report of an increased prevalence of meniscal tears in professional floor layers exposed to frequent kneeling, suggesting that chronic overloading might be a risk factor.49 We cannot exclude the possibility of residual confounding as a result of physically demanding occupational or recreational activities increasing the risk for both bony enlargements of the hands and meniscal pathology. However, knee injury may to a certain extent serve as a proxy for such possible activities, and we controlled for that in our analyses. Our observation period of 30 months is a relatively short time perspective with respect to the development of degenerative changes of meniscal tissue. More time points and even longer follow-ups, including future studies of the association with patient-relevant outcomes such as knee pain, will provide further information on the natural course of meniscal pathology, its risk factors, and its impact in knee osteoarthritis. Further studies will also be required to study factors associated with meniscal pathology in younger individuals.

    In conclusion, this prospective study provides important evidence of a combined systemic and local biomechanical effect on the risk of developing meniscal pathology in middle-aged and elderly persons. For medial meniscal pathology, generalised osteoarthritis expressed as the presence of multiple bony enlargements of finger joints and varus alignment, and obesity were found to be risk factors in addition to knee injury.

    Acknowledgments

    The authors would like to thank all MOST staff and study participants at Birmingham, Alabama and Iowa City, Iowa, the UCSF MOST Coordinating Center, San Francisco, California (especially Charles McCulloch and Irina Tolstykh) and the staff at Boston University Clinical Epidemiology Research and Training Unit.

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    Supplementary materials

    Footnotes

    • Funding The Multicenter Osteoarthritis (MOST) Study is a cooperative epidemiological study of knee osteoarthritis funded by the National Institute on Aging (NIA): DTF, 1 U01 AG18820; Torner, 1 U01 AG18832; CEL, 1 U01 AG18947; MCN, 1 U01 AG19069. ME is supported by the Swedish Research Council and the Faculty of Medicine, Lund University, Sweden.

    • Competing interests AG is a shareholder of Boston Imaging Core Lab, LLC (BICL), Boston, Massachusetts, USA, a company providing radiological image assessment services, and Synarc Inc, and consultant to Merck Serono, Novartis, Genzyme, Facet Solutions and Stryker. FWR and MDC are shareholders of BICL. None of the other authors have declared any conflict of interest.

    • Patient consent Obtained.

    • Ethics approval This study was conducted with the approval of the institutional review boards from Boston University, University of Iowa and University of Alabama.

    • Provenance and peer review Not commissioned; externally peer reviewed.