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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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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- SUBJECTS AND METHODS
- AUTHOR CONTRIBUTIONS
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.