Editorials and publications

Meniscopathy – Paul Welford, Nov 2013


Once dismissed as simply vestigial remnants from an obsolete muscle(1), the semi-lunar cartilages, or menisci as they are now known, are now understood to play key roles in knee joint health and function(2). Having historically been left in-situ, surgical removal of pathological menisci became popular in the latter half of the 19th century(3).

The menisci are the most frequently injured structures in the knee joint, with well-described sequelae of instability and tibiofemoral degenerative changes associated with the loss of functional meniscal tissue(4). In fact, up to 89% of patients experience osteoarthritis following meniscectomy(5).

Alongside our improved scientific understanding, clinical practice has seen a paradigm shift. To this day a name almost synonymous with meniscal lesions, McMurray once advocated removal of a meniscus found to be healthy at operation, provided that pathology had been previously suspected(6). Current treatments aim to preserve as much viable meniscus as possible(7) and include arthroscopic repair, partial meniscectomy and meniscal replacement surgery(8).

In keeping with this drive for meniscal preservation, conservative treatments such as exercise therapy have recently been advocated for the management of atraumatic, degenerative meniscal tears, which are frequently not amenable to repair(9-12). Recent guidelines question the outcomes of arthroscopic meniscectomy in this group, and actively recommend against its use where joint-space narrowing co-exists(13).

Asymptomatic, degenerative meniscal tears are a well documented incidental finding during MRI(14), being confirmed on the scans of 1 in 3 middle-aged or elderly knees(15) . In addition, degenerative horizontal cleavage tears have been reported in at least one knee of up to 60% of cadavers(16).

The positive outcomes to non-operatively treated degenerative tears and the high rate of asymptomatic tears raises several important questions: Is the pain associated with this pathology actually related to the tear at all? Do intra-substance degenerative meniscal changes mediate pain via a mechanical pathway, a biochemical mechanism, or by some other means? Are we able to selectively diagnose degenerative tears and prevent unnecessary (and potentially unhelpful) surgery? Is there a more appropriate classification system for this common condition? Are there any alternative methods of treatment for this patient sub-group?

Much of the literature examining degenerative pathology of the meniscus focuses on the tearing of meniscal tissue (9,12) .  This body of evidence will be explored, drawing parallels to similar conditions where appropriate. The potential merits of a new diagnostic category based on intra-substance changes and clinical signs rather than meniscal tears will then be discussed.

Structure and Function of the Menisci

The menisci are semi-lunar fibrocartilaginous complexes, triangular in cross-section(17), that help share load across the tibiofemoral joint by increasing joint congruence; The medial meniscus transfers 50% of medial compartmental load, while the lateral meniscus conveys 70% of lateral stress(18). In support of the ligaments, the menisci also confer stability to the knee joint(19). Further roles of the menisci include shock absorption, nutrition of articular cartilage and, via mechanoreceptors in the peripheral zone, proprioception(20).

The bodies of the menisci facilitate shock-absorption by transducing compressive load into ‘hoop stresses’, which are transferred to the tibial plateau where they are attenuated via the fibrocartilaginous entheses(17). Injury to these entheses, particularly common at the posterior horn of the lateral meniscus, causes a significant increase in tibiofemoral contact pressure(21). In addition to their bony attachments, the menisci have attachments to the patella via the patellomeniscal ligaments. The medial meniscus is anchored to the medial collateral ligament, which restricts its mobility and is thought to contribute to the increased rate of medial versus lateral meniscal tears(22).

The extracellular matrix of the menisci consists of type I collagen, with the addition of type II collagen in the white (avascular) zone(23). The ability of the meniscus to withstand high levels of compressive load is a result of high levels of glycosaminoglycans (GAGs) in the extracellular matrix(24).

The inner region of the meniscus consists of large collagen bundles with a regular arrangement, whereas the outer zone contains smaller bundles with a more irregular orientation(25). Broadly described in terms of circumferential and radially orientated collagen fibrils, it has recently been demonstrated that these fibres are uniquely bundled. Differences in micro-architecture between individuals may explain variation in the response to injury(26).

Functionally, the meniscus is divided into an outer, vascular portion and avascular middle and inner portions where, due to an inability to heal, an injury can be devastating. There is evidence of lower levels of GAGs in the middle and inner thirds(24).

Previously considered inert structures, the menisci are now known to have a characteristic blood and nerve supply(27). To appreciate the status of the menisci as living tissue is of great importance when considering the process of meniscal degeneration. The vascular supply to the medial and lateral meniscus comprises a perimeniscal ring of vascular synovial tissue, arising from the medial, lateral inferior and middle geniculate arteries(28). Larger nerves follow these vessels, coursing circumferentially, with smaller fibres projecting radially into the outer third of the meniscal substance(28).

Degenerative Meniscal Pathology – Definition

The literature offers little agreement as to what constitutes a definition of meniscal degeneration. Previous studies have tended to focus on meniscal tears, despite limited evidence that the tear is itself the cause of symptoms(14,15).

Definitions of degenerative meniscal tear include, “the clinical signs of meniscal tear in the absence of any history of trauma.” This definition, combined with signs of meniscal tear on MRI, has been successfully used to compare the effects of arthroscopic versus non-operative therapy for degenerative meniscal tears in Sweden(9). Broadly speaking, any tear occurring in abnormal fibrocartilage is generally labeled degenerative(2) .

Defining the concept of meniscal degeneration is also confounded by a lack of universally accepted descriptive terminology. Terms such as mucoid degeneration(29), myxoid degeneration, intra-substance degeneration(30) and cystic degeneration(16) appear to be used interchangeably. To avoid confusion, the simple term ‘meniscal degeneration’ will be used here unless otherwise specified.

Risk Factors

Risk factors for developing meniscal degeneration have not been thoroughly investigated but appear to be to be similar to those for osteoarthritis of the knee(30).

Examples include advancing age, male gender(31), obesity, history of anterior cruciate ligament rupture, prior knee surgery and family history of total knee replacement(30,32). Occupations such as mining, which involve significant amounts of time spent kneeling, also appear to increase the risk of experiencing meniscal disorders and osteoarthritis of the knee(33).

Progressive development of intra-substance meniscal degeneration over time is associated with co-morbid articular cartilage degeneration, though it is unknown whether this is a causative relationship(30,34). In addition, persistent effusion is common in knees with meniscal pathology; synovial activation has implicated in pathophysiology of degenerative joint disease(35).

Both partial and total meniscectomy are known to significantly increase the risk of subsequently developing degenerative joint disease(8), particularly where there is postoperative malalignment(36).



The mean annual incidence of new meniscal lesions was reported as 9.0 per 10,000 in men and 4.2 in women by a large Danish study(31). 23% of the males and 36% of the women with meniscal pathology reported no history of trauma. There is a probably that these figures are lower that actual values, due to under-reporting of sub-clinical meniscal lesions and spontaneous resolution of symptoms preventing medical attention being sought(31).


The mean age for developing degenerative meniscal tears in a 1968 report by Smillie was 43 years(37). The lesions tended to be horizontal cleavage tears, occurring in abnormal fibrocartilage, most frequently that of the posterior horn of the medial meniscus(37). A review of 3,000 meniscectomies confirmed that 50% of tears resected were degenerative(37). 38% of patients with horizontal meniscal tears do not give a history of trauma, compared to only 19% of patients with vertical tears. Symptoms of locking were most common with vertical or oblique tears(29).

Both meniscal tears and meniscal cysts present twice as frequently in the medial compartment when compared to the lateral compartment(38). Microscopic degeneration however, is seen with equal frequency in both menisci(16).

Evidence of meniscal degeneration at microscopy has been reported to be an almost universal finding in subjects over the ages of 40, on the basis of examination at necroscopy(16). There are no further epidemiological data available for meniscal degeneration in the absence of either a tear or osteoarthritis(39).


Meniscal degeneration involves combination of macroscopic and microscopic changes occurring within the substance of the meniscus(16).

Macroscopic changes include ‘fern leaf’ calcification, and horizontal-cleavage tears which are commonly, but not exclusively, found in degenerative knee joint compartments(16). Horizontal cleavage tears may occasionally present with an associated meniscal cyst. The lateral meniscus is affected 3 to 10 times more frequently affected than medial(40). Occasionally the finding of a meniscal cyst may represent an underlying discoid meniscus(41), but in 90% of cases it the confirms the presence of a horizontal meniscal tear(38,42). Degenerative tears are frequently complex in morphology(2). Fraying, softening, discolouration and fibrillation have also been identified as markers of degeneration(29).

The microscopic features of degenerative meniscus were originally described in 1975 by Noble(16). Features reported include degeneration of the cartilaginous matrix, with some areas of the meniscus showing chondrocyte proliferation, whereas apoptosis was predominant in others. Infiltration of eosinophils into the chondrous matrix was associated with microcyst formation. Fragmentation of collagen bundles and gross degeneration of the matrix resulted in the development of planes of cleavage within the meniscus. These planes of cleavage were associated with in-growth of blood vessels and round cell proliferation(16 .

Meniscal degeneration has been linked to repression of genes associated with cartilage development and extracellular matrix stimulation. Genes implicated in immune response, inflammation, and apoptosis were stimulated(43).

In 1975, Noble identified parallels between the pathophysiology of meniscal degeneration and that of both osteoarthritis and intervertebral disc degeneration(16). More recent research in the fields of osteoarthritis and tendinopathy demonstrates further similarities. Neovascularisation (angiogenesis) has been reported in both these conditions by several authors (25,44-47). Abnormal control of cellular apoptosis has been confirmed in tendinopathy(48), associated with matrix disorganisation and increased incidence of tears or rupture. In fact, 98% of Achilles ruptures occur in pathological tendon(49).

Growth of new sensory nerves accompanies angiogenesis in the peripheral zone of the degenerative meniscus and has been hypothesised to be a potential pain source(25). This may explain the poor correlation between clinical symptoms and the presence of a meniscal tear(14).

Originally thought to be a primary inflammatory pathology, tendinopathy was later described as degenerative. Now, tendinopathy is understood to be a heterogenous condition, presenting along a continuum, with optimised treatment reflecting the stage of the pathology(49). Staging of pathology into the clinical sub-categories of reactive tendinopathy, dysrepair and degenerative tendinopathy is achieved via clinical examination and diagnostic ultrasound(49).

The scientific literature is rich with studies investigating the aetiology and pathophysiology of osteoarthritis(50,51). This process of articular cartilage breakdown, recently thought to be degenerative, has once-again been proposed to have an autoimmune, inflammatory component(51). Cytokine profiles(39) activated T-cells, and abnormally high expression of complement in osteoarthritic joints support this theory(52). Specifically, both articular cartilage and meniscus show catabolic responses to interleukin 1a (53). Osteoarthritis is, however, a pathology affecting the entire joint(54) and meniscal degeneration has been proposed as a stage in this disease process(55). It has been demonstrated that significant degenerative changes of both articular cartilage and meniscus may be present in knees that appear normal on plain radiographs(55).

While meniscal damage has been identified as a feature of knee osteoarthritis(25) and there do appear to be risk factors common to both conditions(31), it is known that horizontal meniscal tears can exist in the presence of normal articular cartilage; 19% of otherwise normal joint compartments examined in cadavers contained a horizontal tear(16).

The presence of a degenerative meniscal tear is associated with reduced balance and walking ability when compared to knees with similar levels of articular cartilage degeneration, but no meniscal tear(56).

Although significant progress appears to have been made in the understanding of osteoarthritis, the contribution of meniscal degeneration to knee pain and overall morbidity remains unclear(25).


Clinical examination and diagnosis


Clinical examination of the knee is central to the diagnosis of meniscal tear and has been reported to be up to 90% accurate (sensitive and specific)(8,57). Combined clinical examination has been demonstrated to be more sensitive, but less specific, than MRI for diagnosis of medial meniscal tears(58). While no single clinical feature is pathognomonic, acute meniscal tears typically present with a history of trauma and sudden pain followed by an insidious onset of effusion and locking or ‘catching’ of the knee(59).

Degenerative pathology of the meniscus, including horizontal cleavage or incomplete meniscal tear, does not always interfere with normal joint mechanics and may elude diagnosis(60). Presence of pathological meniscus is, however, associated with persistent knee joint effusion(35).

Joint-line tenderness is a commonly performed examination procedure in the suspicion of meniscal pathology. In isolation, it has been deemed to be of little diagnostic value, with sensitivity 63% and specificity 50%(61). Combined with a history of trauma these values may rise to 95% and 93%(62) respectively, with better diagnostic accuracy for tears of the lateral than the medial meniscus(63). For atraumatic, degenerative meniscal pathology, the value of joint-line palpation lies in its integration with the rest of the clinical examination(57).

Several orthopaedic tests, including McMurray’s, aim to confirm diagnosis by aim the reproduction of a painful clunk as the unstable portion of the torn meniscus is trapped in the joint line(57). However, in degenerative pathology, where there may be no mechanical features, these tests prove insensitive. This phenomenon has been borne out by the research, with reported sensitivity and specificity values for McMurrays test of 16%-58% and 77%-98% respectively(64).

Weight-bearing tests have since been proposed that report higher diagnostic accuracy values. These tests have been advocated for patients with pain upon tibial rotation but no mechanical symptoms(60), which might make them well-suited to the assessment of degenerative meniscal pathology. They aim to place the outer, circumferentially innervated portion of the meniscus under tensile stress to reproduce pain.  One of these, the Thessaly test, has reported sensitivity of 90% and specificity of 98%(60) though these results come from a single study with only one examiner.   It also is worth noting that these diagnostic accuracy values have been shown to significantly lower diagnostic accuracy values (sensitivity 79%, specificity 40%) in patients with anterior cruciate ligament deficient knee(65).

Investigations and Classification


Although rarely performed exclusively for diagnostic purposes, arthroscopy is widely considered to be the gold standard for the diagnosis of meniscal pathology(8,57,59).


Classification of meniscal injury typically occurs at arthroscopy, describing anatomical factors such as location, rim width, tear depth, tissue quality and pattern(66). Assessment of these classification criteria may require invasive examination, including probing of meniscal tissue(66) and histopathological examination of excised meniscus(16). Clearly, this method of describing and classifying meniscal pathology is impossible where conservative management is planned.

MRI, including modern techniques such a 3 Tesla (3T), may have value in the evaluation meniscal pathology(67). MRI traditionally examines tissue morphology(68), visualising tears of the menisci with reported diagnostic accuracy (sensitivity and specificity) around 70-80%(8).

3T MRI has recently been used to evaluate slow-motion interaction between macromolecular protons and bulk water. This technique facilitates assessment of proteoglycan loss in both meniscus and articular cartilage(68). A meniscal scoring system known as WORMs grading has hence been defined: grade 0, normal meniscus; grade 1, increased signal, no tear; grade 2, small radial tear; grade 3, single tear; grade 4: complex tear; grade 5, displaced tear; grade 6, macerated meniscus(69). Diagnostic accuracy has been shown to been more accurate for degenerative lesions of the medial meniscus than the lateral meniscus, particularly in the presence of complex tears. However, with combined medial and lateral sensitivity and specificity of 79% and 95% respectively, the diagnostic value of 3-T MRI should not be overestimated(67).

Indeed, with higher diagnostic accuracy values reported for clinical examination alone, the value of MRI appears to lie more in its ability to exclude associated knee joint pathology(8).

Within the broader context of the assessing the knee with early osteoarthritis, MRI demonstrates earlier detection of changes in the both the menisci and articular cartilage when compared to conventional radiology(55).

Management and prognosis


The initial management of degenerative meniscal pathology is conservative(7).  A recent double-blinded, placebo controlled randomised-controlled trial comparing arthroscopic meniscectomy for degenerative meniscal tears found no additional benefit when compared with sham arthroscopy(12). Another study involving 96 patients with MRI confirmed degenerative meniscal tears, but minimal radiographic osteoarthritis, compared arthroscopic partial meniscectomy plus exercise therapy with exercise therapy alone. Both groups showed equal improvement. Approximately one third of the patients were no better after exercise therapy, but subsequently improved following arthroscopy(9). The authors recommend exercise therapy as the initial treatment of choice for degenerative meniscal tear, a finding supported elsewhere in the literature(11,70).

Arthroscopic partial meniscectomy may be indicated where symptoms impairing daily function persist, following appropriate conservative therapy. Other indications include mechanical symptoms such as locking, catching or giving way(7). Treatment via meniscectomy is specifically not recommended where there are radiological signs of osteoarthritis due to questionable benefit(13) and high rates of debilitating osteoarthritis post-operatively. Overall rates of patient satisfaction have been reported at 84% following partial medial meniscectomy and 73% following partial lateral meniscectomy, though these rates were not specific to degenerative meniscal pathology. Outcomes are generally less favourable where degenerative changes are present or malalignment persists postoperatively(4).


The rationale for partial meniscectomy lies in the preservation of the peripheral rim, which biomechanically crucial to the function of the menisci(7). Although associated to give better clinical outcomes and less osteoarthritis than total meniscectomy(4), increased incidence of radiographic degenerative changes has nonetheless been observed at 5 year follow-up to partial meniscectomy(71). Volume of meniscal tissue removed is negatively correlated with outcome(4). It has been demonstrated that the risk of developing radiographic osteoarthritis is significantly higher after lateral meniscectomy than after medial meniscectomy(72). The overall incidence of osteoarthritis following meniscectomy is up to 89%(5).

The value of supervised, exercise-based rehabilitation programmes following arthroscopic partial meniscectomy is not known. There are widespread issues surrounding the methodological quality of studies and conflicting results reported in the literature(73-75). A current line of research surrounds the effects of post-operative strengthening exercises on biomechanical knee loading and the subsequent incidence of osteoarthritis(76).

A novel approach to treating for degenerative meniscal tears was described in 2011. A series of 3 medial and 6 lateral menisci were repaired arthroscopically with exogenous fibrin clots, with all patients showing improvements in their functional scores and quality of life(77). Further research will shape the future of this technique as a potential treatment option.

Discussion and conclusion

Meniscal tears occur on a spectrum, from traumatic tears of normal fibrocartilage, to cleavages appearing spontaneously within grossly pathological meniscal tissue(2). Degenerative tears occur, without trauma, in abnormal menisci(9) and show poor correlation with knee pain(78). Partial meniscectomy is not recommended as a first treatment for degenerative tears(13). Therapeutic exercise reduces knee pain and improves function(9).

The mechanism of pain generation in meniscal degeneration may relate to angiogenesis and sensory nerve growth(25) or biochemical mediators, common to the development of osteoarthritis(39). Many degenerative meniscal tears do not cause symptoms(78). Where patients with degenerative tears do experience symptoms, the tear may not be their cause(14,51). Current diagnostic terminology, which aims to describe degenerative meniscal tears, may not be clinically useful.

It is possible that, as has been proposed for tendinopathy(49), meniscal pathology exists on a continuum. A broad diagnostic term, such as meniscopathy, may be useful in describing this continuum. As a diagnostic category, meniscopathy reduces the emphasis on the degenerative meniscal tear, which though reflecting the underlying matrix disintegration(16), may not be responsible for generating symptoms. Osteoarthritis is a broad diagnostic umbrella and the role of the meniscus in the experience of pain with this condition is poorly understood. Meniscal degeneration is just one of the pathological changes associated with osteoarthritis, but where symptoms relate to meniscal involvement, the diagnosis of meniscopathy may help inform treatment direction.

Diagnosis of meniscal pathology via clinical examination or imaging usually relies upon the detection of a tear. New MRI technologies, a revised attitude towards clinical examination and better understanding of pain mechanisms may assist in early diagnosis of meniscopathy, before macroscopic tears develop.

Management of meniscopathy on a continuum would aim to affect the pathology in a direction that favours resolution, rather than disease progression.

While exercise therapy has been shown to be beneficial, the exercise programmes themselves have been protocols rather than individualized treatments, based upon clinical findings. Future research should aim to expedite the diagnosis of early osteoarthritis and identify the role of meniscopathy in knee pain. In addition, staging the pathological changes involved in meniscopathy may allow identification of the exercises best suited to each of these stages.

Further understanding of risk factors for the development of meniscopathy would facilitate appropriate preventative action. Improved understanding of pain mechanisms in meniscopathy may allow the development of new pain relieving treatments aimed at, for example, destroying or arresting development of new blood vessels and sensory nerves in the meniscal periphery.

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