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.

(1) Gabrion A, Aimedieu P, Laya Z, Havet E, Mertl P, Grebe R, et al. Relationship between ultrastructure and biomechanical properties of the knee meniscus. Surgical & Radiologic Anatomy 2005 Dec;27(6):507-510.

(2) McDermott I. (ii) Meniscal Tears. Current Orthopaedics 2007;20:85–94.

(3) Englund M, Roos EM, Roos HP, Lohmander LS. Patient-relevant outcomes fourteen years after meniscectomy: influence of type of meniscal tear and size of resection. Rheumatology 2001 Jun;40(6):631-639.

(4) Salata MJ, Gibbs AE, Sekiya JK. A systematic review of clinical outcomes in patients undergoing meniscectomy. Am J Sports Med 2010 Sep;38(9):1907-1916.

(5) Rangger C, Kathrein A, Klestil T, Glotzer W. Partial meniscectomy and osteoarthritis. Implications for treatment of athletes. Sports Medicine 1997 Jan;23(1):61-68.

(6) McMurray T. The semilunar cartilages. British Journal of Surgery 1942;29:407–414.

(7) Hwa-Jae Jeong, MD, Seung-Hee Lee, MD, Chun-Suk Ko, MD. Meniscectomy. Knee Surgery and Related Research 2012;24(3):129–136.

(8) McDermott I. Meniscal tears, repairs and replacement: their relevance to osteoarthritis of the knee. Br J Sports Med 2011 Apr;45(4):292-297.

(9) Herrlin SV, Wange PO, Lapidus G, Hallander M, Werner S, Weidenhielm L. Is arthroscopic surgery beneficial in treating non-traumatic, degenerative medial meniscal tears? A five year follow-up. Knee Surgery, Sports Traumatology, Arthroscopy 2013 Feb;21(2):358-364.

(10) Surgery or physiotherapy for meniscal tears?. BMJ 2013 346(Clinical research ed):Arte Number: f1921. ate of Pubaton: 2013.

(11) Rimington T, Mallik K, Evans D, Mroczek K, Reider B. A prospective study of the nonoperative treatment of degenerative meniscus tears. Orthopedics 2009 Aug;32(8).

(12) Hare KB, Lohmander LS, Christensen R, Roos EM. Arthroscopic partial meniscectomy in middle-aged patients with mild or no knee osteoarthritis: a protocol for a double-blind, randomized sham-controlled multi-centre trial. BMC Musculoskeletal Disorders 2013;14:71.

(13) Beaufils P, Hulet C, Dhenain M, Nizard R, Nourissat G, Pujol N. Clinical practice guidelines for the management of meniscal lesions and isolated lesions of the anterior cruciate ligament of the knee in adults. Orthopaedics & traumatology, surgery & research 2009 Oct;95(6):437-442.

(14) Cyteval C. [MR imaging of the knees in patients over 50 years of age: incidental meniscal lesions]. J Radiol 2008 Dec;89(12):1897-1899.

(15) Englund M, Lohmander LS. Patellofemoral osteoarthritis coexistent with tibiofemoral osteoarthritis in a meniscectomy population. Ann Rheum Dis 2005 Dec;64(12):1721-1726.

(16) Noble J HD. The Pathology of the Degenerate Meniscal Lesion. The Journal of Bone and Joint Surgery 1975;57-B(2):180–186.

(17) Abraham AC, Donahue TL. From meniscus to bone: a quantitative evaluation of structure and function of the human meniscal attachments. Acta Biomaterialia 2013 May;9(5):6322-6329.

(18) Seedhom BB, Dowson D, Wright V. Proceedings: Functions of the menisci. A preliminary study. Ann Rheum Dis 1974 Jan;33(1):111.

(19) Markolf KL, Mensch JS, Amstutz HC. Stiffness and laxity of the knee–the contributions of the supporting structures. A quantitative in vitro study. Journal of Bone & Joint Surgery – American Volume 1976 Jul;58(5):583-594.

(20) Zimny ML, Albright DJ, Dabezies E. Mechanoreceptors in the human medial meniscus. Acta Anat 1988;133(1):35-40.

(21) Schillhammer CK, Werner FW, Scuderi MG, Cannizzaro JP. Repair of lateral meniscus posterior horn detachment lesions: a biomechanical evaluation. Am J Sports Med 2012 Nov;40(11):2604-2609.

(22) Lento PH AV. Meniscal Injuries: A Critical Review. Journal of Back and Musculoskeletal Rehabilitation 2000;15:55–62.

(23) Athanasiou Kyriacos A., Sanchez-Adams Johannah. Engineering the knee meniscus. : Morgan and Claypool; 2009.

(24) Sanchez-Adams J, Willard VP, Athanasiou KA. Regional variation in the mechanical role of knee meniscus glycosaminoglycans. J Appl Physiol 2011 Dec;111(6):1590-1596.

(25) Ashraf S, Wibberley H, Mapp PI, Hill R, Wilson D, Walsh DA. Increased vascular penetration and nerve growth in the meniscus: a potential source of pain in osteoarthritis. Ann Rheum Dis 2011 Mar;70(3):523-529.

(26) Rattner JB, Matyas JR, Barclay L, Holowaychuk S, Sciore P, Lo IK, et al. New understanding of the complex structure of knee menisci: implications for injury risk and repair potential for athletes. Scand J Med Sci Sports 2011 Aug;21(4):543-553.

(27) Limbird TJ. Application of laser Doppler technology to meniscal injuries. Clinical Orthopaedics & Related Research 1990 Mar(252):88-91.

(28) Day B, Mackenzie WG, Shim SS, Leung G. The vascular and nerve supply of the human meniscus. Arthroscopy 1985;1(1):58-62.

(29) Noble J EK. In Defence of Meniscus. The Journal of Bone and Joint Surgery 1980;62-B(1):7–11.

(30) Joseph GB, Baum T, Alizai H, Carballido-Gamio J, Nardo L, Virayavanich W, et al. Baseline mean and heterogeneity of MR cartilage T2 are associated with morphologic degeneration of cartilage, meniscus, and bone marrow over 3 years–data from the Osteoarthritis Initiative. Osteoarthritis & Cartilage 2012 Jul;20(7):727-735.

(31) Hede A, Jensen DB, Blyme P, Sonne-Holm S. Epidemiology of meniscal lesions in the knee. 1,215 open operations in Copenhagen 1982-84. Acta Orthop Scand 1990 Oct;61(5):435-437.

(32) Louboutin H, Debarge R, Richou J, Selmi TA, Donell ST, Neyret P, et al. Osteoarthritis in patients with anterior cruciate ligament rupture: a review of risk factors. Knee 2009 Aug;16(4):239-244.

(33) McMillan G, Nichols L. Osteoarthritis and meniscus disorders of the knee as occupational diseases of miners. Occupational & Environmental Medicine 2005 Aug;62(8):567-575.

(34) Kai B, Mann SA, King C, Forster BB. Integrity of articular cartilage on T2 mapping associated with meniscal signal change. Eur J Radiol 2011 Sep;79(3):421-427.

(35) Roemer FW, Guermazi A, Hunter DJ, Niu J, Zhang Y, Englund M, et al. The association of meniscal damage with joint effusion in persons without radiographic osteoarthritis: the Framingham and MOST osteoarthritis studies. Osteoarthritis & Cartilage 2009 Jun;17(6):748-753.

(36) Fauno P, Nielsen AB. Arthroscopic partial meniscectomy: a long-term follow-up. Arthroscopy 1992;8(3):345-349.

(37) Smillie IS. The current pattern of the pathology of meniscus tears. Proc R Soc Med 1968 Jan;61(1):44-45.

(38) Campbell SE, Sanders TG, Morrison WB. MR imaging of meniscal cysts: incidence, location, and clinical significance. AJR.American Journal of Roentgenology 2001;177(2):409-413.

(39) Fernandes JC, Martel-Pelletier J, Pelletier JP. The role of cytokines in osteoarthritis pathophysiology. Biorheology 2002;39(1-2):237-246.

(40) Maffulli N, Petricciuolo F, Pintore E. Lateral meniscal cyst: arthroscopic management. Medicine & Science in Sports & Exercise 1991 Jul;23(7):779-782.

(41) Franceschi F, Longo UG, Ruzzini L, Simoni P, Zobel BB, Denaro V. Bilateral complete discoid medial meniscus combined with posterior cyst formation. Knee Surgery, Sports Traumatology, Arthroscopy 2007 Mar;15(3):266-268.

(42) Spina M, Sabbioni G, Tigani D. Medial meniscal cyst: a case report. Chirurgia Degli Organi di Movimento 2008 Dec;92(3):175-178.

(43) Rai MF, Patra D, Sandell LJ, Brophy RH. Transcriptome analysis of injured human meniscus reveals a distinct phenotype of meniscus degeneration with aging. Arthritis & Rheumatism 2013 Aug;65(8):2090-2101.

(44) Bonnet CS, Walsh DA. Osteoarthritis, angiogenesis and inflammation. Rheumatology 2005 Jan;44(1):7-16.

(45) Ashraf S, Walsh DA. Angiogenesis in osteoarthritis. Curr Opin Rheumatol 2008 Sep;20(5):573-580.

(46) Sahin H, Tholema N, Petersen W, Raschke MJ, Stange R. Impaired biomechanical properties correlate with neoangiogenesis as well as VEGF and MMP-3 expression during rat patellar tendon healing. Journal of Orthopaedic Research 2012 Dec;30(12):1952-1957.

(47) Willberg L, Sunding K, Ohberg L, Forssblad M, Alfredson H. Treatment of Jumper’s knee: promising short-term results in a pilot study using a new arthroscopic approach based on imaging findings. Knee Surgery, Sports Traumatology, Arthroscopy 2007 May;15(5):676-681.

(48) Nell EM, van der Merwe L, Cook J, Handley CJ, Collins M, September AV. The apoptosis pathway and the genetic predisposition to Achilles tendinopathy. Journal of Orthopaedic Research 2012 Nov;30(11):1719-1724.

(49) Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med 2009 Jun;43(6):409-416.

(50) Soder S, Aigner T. [Osteoarthritis. Etiology, typing, staging and histological grading]. Pathologe 2011 May;32(3):183-192.

(51) Kapoor M, Martel-Pelletier J, Lajeunesse D, Pelletier JP, Fahmi H. Role of proinflammatory cytokines in the pathophysiology of osteoarthritis. Nature Reviews Rheumatology 2011 Jan;7(1):33-42.

(52) Frisenda S, Perricone C, Valesini G. Cartilage as a target of autoimmunity: a thin layer. Autoimmunity Reviews 2013 Mar;12(5):591-598.

(53) McNulty AL, Rothfusz NE, Leddy HA, Guilak F. Synovial fluid concentrations and relative potency of interleukin-1 alpha and beta in cartilage and meniscus degradation. Journal of Orthopaedic Research 2013 Jul;31(7):1039-1045.

(54) Weinans H, Siebelt M, Agricola R, Botter SM, Piscaer TM, Waarsing JH. Pathophysiology of peri-articular bone changes in osteoarthritis. Bone 2012 Aug;51(2):190-196.

(55) Gudbergsen H, Lohmander LS, Jones G, Christensen R, Bartels EM, Danneskiold-Samsoe B, et al. Correlations between radiographic assessments and MRI features of knee osteoarthritis–a cross-sectional study. Osteoarthritis & Cartilage 2013 Apr;21(4):535-543.

(56) Lange AK, Fiatarone Singh MA, Smith RM, Foroughi N, Baker MK, Shnier R, et al. Degenerative meniscus tears and mobility impairment in women with knee osteoarthritis. Osteoarthritis & Cartilage 2007 Jun;15(6):701-708.

(57) Mohan BR, Gosal HS. Reliability of clinical diagnosis in meniscal tears. Int Orthop 2007 Feb;31(1):57-60.

(58) Sharma UK, Shrestha BK, Rijal S, Bijukachhe B, Barakoti R, Banskota B, et al. Clinical, MRI and arthroscopic correlation in internal derangement of knee. Kathmandu University Medical Journal 2011 Jul-Sep;9(35):174-178.

(59) Solomon DH, Simel DL, Bates DW, Katz JN, Schaffer JL. The rational clinical examination. Does this patient have a torn meniscus or ligament of the knee? Value of the physical examination. JAMA 2001 Oct 3;286(13):1610-1620.

(60) Harrison BK, Abell BE, Gibson TW. The Thessaly test for detection of meniscal tears: validation of a new physical examination technique for primary care medicine. Clinical Journal of Sport Medicine 2009 Jan;19(1):9-12.

(61) Galli M, Ciriello V, Menghi A, Aulisa AG, Rabini A, Marzetti E. Joint line tenderness and McMurray tests for the detection of meniscal lesions: what is their real diagnostic value?. Archives of Physical Medicine & Rehabilitation 2013 Jun;94(6):1126-1131.

(62) Rose RE. The accuracy of joint line tenderness in the diagnosis of meniscal tears. West Indian Med J 2006 Oct;55(5):323-326.

(63) Eren OT. The accuracy of joint line tenderness by physical examination in the diagnosis of meniscal tears. Arthroscopy 2003 Oct;19(8):850-854.

(64) Malanga GA, Andrus S, Nadler SF, McLean J. Physical examination of the knee: a review of the original test description and scientific validity of common orthopedic tests. Archives of Physical Medicine & Rehabilitation 2003 Apr;84(4):592-603.

(65) Mirzatolooei F, Yekta Z, Bayazidchi M, Ershadi S, Afshar A. Validation of the Thessaly test for detecting meniscal tears in anterior cruciate deficient knees. Knee 2010 Jun;17(3):221-223.

(66) Anderson AF, Irrgang JJ, Dunn W, Beaufils P, Cohen M, Cole BJ, et al. Interobserver reliability of the International Society of Arthroscopy, Knee Surgery and Orthopaedic Sports Medicine (ISAKOS) classification of meniscal tears. Am J Sports Med 2011 May;39(5):926-932.

(67) von Engelhardt LV, Schmitz A, Pennekamp PH, Schild HH, Wirtz DC, von Falkenhausen F. Diagnostics of degenerative meniscal tears at 3-Tesla MRI compared to arthroscopy as reference standard. Archives of Orthopaedic & Trauma Surgery 2008 May;128(5):451-456.

(68) Wang L, Chang G, Xu J, Vieira RL, Krasnokutsky S, Abramson S, et al. T1rho MRI of menisci and cartilage in patients with osteoarthritis at 3T. Eur J Radiol 2012 Sep;81(9):2329-2336.

(69) Friedrich KM, Shepard T, de Oliveira VS, Wang L, Babb JS, Schweitzer M, et al. T2 measurements of cartilage in osteoarthritis patients with meniscal tears. AJR.American Journal of Roentgenology 2009;193(5):W411-5.

(70) Herrlin S, Ha ̊llander M, Wange P, Weidenhielm L, Werner S. Arthroscopic or conservative treatment of degenerative medial meniscal tears: a prospective randomized trial. Knee Surg Sports Traumatol Arthrosc 2007;15:393–401.

(71) Williams RJ, Warner KK, Petrigliano FA, Potter HG, Hatch J, Cordasco FA.        <br />MRI evaluation of isolated arthroscopic partial meniscectomy patients at a minimum five-year follow-up         HSS J 2007;3:35–43.

(72) Allen PR, Denham RA, Swan AV. Late degenerative changes after meniscectomy. Factors affecting the knee after operation. Journal of Bone & Joint Surgery – British Volume 1984 Nov;66(5):666-671.

(73) Morrissey MC, Milligan P, Goodwin PC. Evaluating treatment effectiveness: benchmarks for rehabilitation after partial meniscectomy knee arthroscopy. American Journal of Physical Medicine & Rehabilitation 2006 Jun;85(6):490-501.

(74) Goodwin PC, Morrissey MC, Omar RZ, Brown M, Southall K, McAuliffe TB. Effectiveness of supervised physical therapy in the early period after arthroscopic partial meniscectomy. Phys Ther 2003 Jun;83(6):520-535.

(75) Goodyear-Smith F, Arroll B. Rehabilitation after arthroscopic meniscectomy: a critical review of the clinical trials. Int Orthop 2001;24(6):350-353.

(76) Hall M, Hinman RS, Wrigley TV, Roos EM, Hodges PW, Staples M, et al. The effects of neuromuscular exercise on medial knee joint load post-arthroscopic partial medial meniscectomy: ‘SCOPEX’, a randomised control trial protocol. BMC Musculoskeletal Disorders 2012;13:233.

(77) Kamimura T, Kimura M. Repair of horizontal meniscal cleavage tears with exogenous fibrin clots. Knee Surgery, Sports Traumatology, Arthroscopy 2011 Jul;19(7):1154-1157.

(78) Englund M, Guermazi A, Gale D, Hunter DJ, Aliabadi P, Clancy M, et al. Incidental meniscal findings on knee MRI in middle-aged and elderly persons. N Engl J Med 2008 Sep 11;359(11):1108-1115.

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