Osteochondritis dissecans of the knee

Abstract

Osteochondritis dissecans (OCD) characterises a disease process predominately affecting male teenagers and young adults which, as its end-product, yields the separation of osteochondral fragments from the joint surface. Although OCD may occur in many joints, the knee appears to be by far the most commonly involved. Hence painful locking in a teenage knee should always raise the suspicion of OCD. The cause of the disease remains unclear and many theories have been developed, none of which has received unequivocal agreement. A multifactorial aetiology including elements of repetitive trauma and vascular insufficiency is henceforth considered most likely.The fundamental principle in the treatment of OCD is the timely recognition of the condition as lesions in the early disease process are more likely to be treated successfully. Proper initial assessment and grading of the lesion will allow for the right treatment protocol to be chosen. MRI may help in the staging process and in determining the lesions healing potential. Most cases fair well with conservative measures. In more advanced stages of the disease, surgical intervention ranging from subchondral drilling to fragment refixation may be required. The primary aim of any intervention is to achieve healing of the subchondral bone, and preservation of the articular cartilage as fragment separation may pave the way for subsequent development of osteoarthritis. Osteochondritis dissecans (OCD) characterises a disease process predominately affecting male teenagers and young adults which, as its end-product, yields the separation of osteochondral fragments from the joint surface. Although OCD may occur in many joints, the knee appears to be by far the most commonly involved. Hence painful locking in a teenage knee should always raise the suspicion of OCD. The cause of the disease remains unclear and many theories have been developed, none of which has received unequivocal agreement. A multifactorial aetiology including elements of repetitive trauma and vascular insufficiency is henceforth considered most likely. The fundamental principle in the treatment of OCD is the timely recognition of the condition as lesions in the early disease process are more likely to be treated successfully. Proper initial assessment and grading of the lesion will allow for the right treatment protocol to be chosen. MRI may help in the staging process and in determining the lesions healing potential. Most cases fair well with conservative measures. In more advanced stages of the disease, surgical intervention ranging from subchondral drilling to fragment refixation may be required. The primary aim of any intervention is to achieve healing of the subchondral bone, and preservation of the articular cartilage as fragment separation may pave the way for subsequent development of osteoarthritis. IntroductionOsteochondritis dissecans or OCD, is a misnomer in terms of phrase, as it wrongly implies an inflammatory aetiology. It describes an intra-articular pathology affecting subchondral bone and surface cartilage in diarthrodial joints, which most commonly occurs in children and adolescents of male gender. It may result in the partial or total separation of the osteochondral fragment, thus creating a loose body. If untreated, this may ultimately jeopardise the integrity of the joint and lead to the development of osteoarthritis. The disease may in principle affect any joint and is known to occur in the knee, elbow, ankle and hip. The knee, however, appears to be the site of predilection, with reported figures of 65–75%.Historical reviewThe first description of loose bodies in the knee joint dates back to the 17th century and is credited to Ambroise Paré, who also appears to be the first surgeon who successfully attempted their surgical removal.1Paré A. Oeuveres Completes, vol. 3. Paris: JB Balliere; p. 1840–18; 32.Google Scholar, 2Paré A. The case reports and autopsy records of Ambroise Paré.in: Hamby W.B. Charles C. Thomas, Springfield, IL1960Google Scholar Monroe, in 1726, discovered a pea size loose body originating from the lateral femoral condyle during a cadaver examination, which he believed was caused by trauma.3Monroe A. Part of the cartilage of the joint separated and ossified.Med Essays Observations. 1738; 4: 305Google Scholar Another important historical description dates back to 1817, when the French surgeon Laennec described intra-articular loose bodies as joint mice or arthrophytes.4Nagura S. The so-called osteochondritis dissecans of König.Clin Orthop. 1960; 18: 100-122Google Scholar By expressing his belief that loose bodies arise from the proliferation of cartilage of the periarticular synovial tissue he may have inadvertently described a condition later known as synovial chondromatosis, rather than OCD. Broca, in 1854, opposed both Monroe's and Laennec's opinion by promoting the theory that loose bodies are caused by ‘spontaneous necrosis’ of part of the articulating cartilage.4Nagura S. The so-called osteochondritis dissecans of König.Clin Orthop. 1960; 18: 100-122Google ScholarSir James Paget is credited with the classic account of OCD, which he described as ‘quiet necrosis’.5Paget J. On the production of some of the loose bodies in joints.St Barth Hosp Rep. 1870; 6: 1-4Google Scholar In 1870 he reported on two children, both of whom suffered loose bodies in their knee. One, a little girl, was known to break thick pieces of wood over her knee whilst the other was an athletic school boy ‘with many blows and strains to his knee from sports’. Paget wrote: ‘How can such pieces of articular cartilage be detached from living bone? They cannot be chipped off—no force can do this. These bodies are sequestra exfoliated after necrosis of injured portions of cartilage without inflammation’. He differentiated OCD from an acute osteochondral fracture and noted that the process involved an avascular sequestrum without evidence of inflammatory change.The phrase ‘Osteochondritis dissecans’ however, was not coined until 1887. Franz König, Professor of Surgery in Göttingen, described a series of young and otherwise healthy adults suffering loose cartilaginous fragments in their knee, ankle or elbow.6König F. Über freie Körper in den Gelenken.Dtsch Z Chir. 1887; 27: 90-109Crossref Scopus (274) Google Scholar Through the lack of trauma in all but one case and the absence of any disease he became intrigued about the aetiology of this condition, which he thought might be caused by a spontaneous process. In König's opinion, even severe trauma was unlikely to create osteochondral fragments in the common locations observed without creating significant damage to other structures. However, he did not rule out that in a minority of patients a localised joint surface contusion might induce a process of subchondral necrosis, followed by an inflammatory response and subsequent fragment dissecation. König deliberately used the suffix ‘–itis’, as he was under the impression that these ‘corpora mobile’ were caused primarily by an inflammatory response to subchondral necrosis, which he based on the finding of giant cells in one of the retrieved specimens. König was, however, unable to explain what initiated the process of osteochondritis, and hence concluded his article by saying that the true aetiology of OCD remained unknown.Although it is widely thought that the lesion should be more accurately termed ‘osteochondrosis’ or ‘osteochondrolysis’, the term OCD has prevailed.7Aichroth P. Osteochondritis dissecans of the knee. A clinical survey.JBJS. 1971; 53-B: 440-447Google Scholar, 8Jonasch E. Das Kniegelenk. Berlin: deGruyter; 1964. p. 231–8.Google ScholarIt is of interest to note that some confusion arose after König had published his original account on OCD in the late 1880s, through substitution of the word dissecans with desiccans. ‘One author has brought his facts into line with the error in nomenclature by finding that the loose bodies he described were desiccated’, as quoted by Timbrell Fisher in his excellent article on the pathology and aetiology of loose bodies.9Fisher A.G.T. A study of loose bodies composed of cartilage or of cartilage and bone occurring in joints. With special reference to their pathology and aetiology.Br J Surg. 1920; 8: 493-526Crossref Scopus (25) Google ScholarAetiologyA review of the literature reveals the lack of agreement among investigators concerning the aetiology of OCD. The most commonly quoted theories include trauma, followed by ischaemia and abnormal ossification through accessory centres of ossification within the epiphysis. There also appears to be some support for a genetic predisposition. Riedel, in 1896, at the 25th Congress of the German surgical Society, spoke on the subject ‘Contribution to the theory of arthrophytes’ by saying ‘Foreign bodies arise in the joints not only through trauma or as a consequence of arthritis deformans, but also through König's OCD. Until now, only the end-products of this disease in the form of completely detached bone-cartilage pieces are known’.10Riedel. Verhandlungen des 25 Kongress der Deutschen Gesellschaft für Chirurgie 1896.Google Scholar In many respects little has changed since Riedel's account some 110 years ago. Although the frequent occurrence of OCD in patients involved in sporting activities would support a repetitive trauma aetiology, on the basis of the currently available knowledge a multifactorial aetiology of OCD appears more likely.TraumaMost theories on OCD aetiology centre on trauma, described either as an initial macro-trauma followed by repetitive micro-trauma or persistent repetitive micro-trauma alone. Both Paget and König are often falsely associated as being proponents of the trauma theory, which could not be further from the truth. On reading their original accounts it would appear that both men believed that trauma, when it occurs, should be considered incidental rather than causative in the aetiology of OCD.5Paget J. On the production of some of the loose bodies in joints.St Barth Hosp Rep. 1870; 6: 1-4Google Scholar, 6König F. Über freie Körper in den Gelenken.Dtsch Z Chir. 1887; 27: 90-109Crossref Scopus (274) Google ScholarMany authors, however, have considered trauma as the predisposing factor in the aetiology of OCD. Their theories are based on anatomical and biomechanical peculiarities of the knee joint. Fick, in 1904, demonstrated the importance of the tibial spines and the inner aspects of the femoral condyles for absorbing compressive forces and for providing guidance under varus, valgus and rotational stress,11Fick A. Handbuch der Anatomie und Mechanik der Gelenke, vol. 1. Anatomie der Gelenke. Gustav Fischer, Jena1904Google Scholar an observation later confirmed by Goodfellow and O’Connor.12Goodfellow J. O’Connor J. The mechanics of the knee and prosthesis design.JBJS. 1978; 60-B: 358-369PubMed Google Scholar Owing to the central position of the eminence and its antero-posterior course, guidance is most effective in mid flexion and thus at a point where a high degree of rotational freedom is combined with a high axial load.Ludloff, in 1908, was the first to express the view that low-grade trauma slightly above physiological levels may be causative for OCD.13Ludloff R. Zur Frage der Osteochondritis dissecans am Knie.Arch Klin Chir. 1908; 87: 552-570Google Scholar In 1922, Roesner published a landmark article with the title ‘The development mechanics of OCD of the knee’.14Roesner E. Die Entstehungsmechanik der sogenannten Osteochondritis dissecans am Kniegelenk.Brun's Beitr Klin Chir. 1922; 127: 537-561Google Scholar Based on Adolf Fick's biomechanical principles of knee motion, Roesner believed that the mechanism of trauma was due to the repetitive impingement of the intercondylar eminence against the lateral aspect of the medial femoral condyle (MFC) during external tibial rotation—a movement pattern known as the ‘screw-home-mechanism’. In his cadaver experiments he observed surface cartilage damage in common OCD locations after repeated leg extensions with the tibia held in fixed external rotation. He believed that through this mechanism a ‘dry fracture’ of the subchondral bone is created. He used the term ‘dry fracture’, as he thought that continuing external pressure through ongoing impingement prevented a subchondral haematoma, leading to a non-union and subsequent fragment dissecation.Fairbanks, in 1933, published his version of an impingement theory which, contrary to Roesner's ‘screw home mechanism’, was based on a ‘violent rotation inwards of the tibia, driving the anterior tibial spine against the inner condyle’,15Fairbanks H.A.T. Osteochondritis dissecans.Br J Surg. 1933; 21: 67-82Crossref Scopus (101) Google Scholar a notion later supported by Wilson16Wilson J.N. A diagnostic sign in osteochondritis dissecans of the knee.JBJS. 1967; 49-A: 477-480Google Scholar and Smillie.17Smillie I.S. Osteochindritis dissecans. Livingstone, London1960Google Scholar Fairbanks’ theory of anterior tibial spine impingement through internal tibial rotation, however, failed to explain lesions in the most common locations of the postero-lateral aspect of the medial femoral condyle.Whilst the impingement theses may explain the development of OCD around the lateral aspect of the medial femoral condyle, they do not account for lesions occurring at other sites such as the lateral femoral condyle and patella. Furthermore, tibial eminence impingement is not seen during normal walking or running and evidence of abnormal tibial eminence morphology or abnormalities in the relationship between tibial eminence to the MFC in OCD cases is missing. Green reported on a number of cases with incomplete separation of the osteo-articular fragment, all of which presented intact surface cartilage in the area closest to the tibial eminence, henceforth questioning the validity of Fairbanks's and Roesner's theory of impingement.18Green J.P. Osteochondritis dissecans of the knee.JBJS [Br]. 1966; 48-B: 82-91Google ScholarOther theories consider pressure exerted from the patella onto the lateral aspect of the MFC between 90° and 130° of knee flexion as a potential pathomechanism.19Baumgartl F. Das Kniegelenk. Springer, Berlin1964Google Scholar Bandi based his theory on the observation that during mid-flexion the area of OCD predilection on the MFC becomes trapped between patella and tibia.20Bandi W. Die retropatellaren Kniegelenkschäden. Huber, Bern1981Google Scholar He believed that both tibia and patella work like a pair of pliers, exerting pressure onto the femoral condyle. Through the creation of a perpendicular pressure gradient, which he described as ‘strain waves’, subchondral bone bulges forward and eventually demarcates, thus explaining the often observed chondral prominence of OCD lesions (Fig. 1).A number of experimental studies have given support to the trauma hypothesis. Rehbein performed an experimental study on dogs in which he reproduced OCD like lesions by exposing the anterior aspect of their knees to repetitive micro-trauma. He observed a fibrous demarcation surrounding the surface cartilage and subchondral bone, which was histologically indistinguishable from OCD lesions seen in humans.21Rehbein F. Die Entstehung der Osteochondritis Dissecans.Arch Klin Chir. 1950; 265: 69-114PubMed Google Scholar Langenskiold produced lesions, which histologically and radiologically resembled OCD, by cutting a segment of articular cartilage in young rabbits, leaving the cartilage attached to the synovium and replacing the fragment in its bed. He concluded that OCD might be caused by a cartilage fracture in childhood.22Langenskiold A. Can osteochondritis dissecans arise as a sequel of cartilage fracture in early childhood?.Acta Chir Scand. 1955; 109: 206-209PubMed Google Scholar Aichroth conducted a similar study using adult New Zealand White rabbits.7Aichroth P. Osteochondritis dissecans of the knee. A clinical survey.JBJS. 1971; 53-B: 440-447Google Scholar He was able to show that undisplaced but stable osteochondral fractures resembled OCD in humans both radiologically and histologically. Lesions that were stabilised healed but those with tenuous stability developed into avascular unstable lesions.Clinical and observational studies have also confirmed the association between OCD and trauma. Rosenberg examined osteochondral fractures involving the lateral femoral condyle, which had been caused by endogenous trauma.23Rosenberg N.J. Osteochondral fractures of the lateral femoral condyle.JBJS. 1964; 46-A: 1013-1026Google Scholar He demonstrated that un-united osteochondral fractures become indistinguishable from OCD both radiologically and microscopically. Kennedy et al.24Kennedy J.C. Grainger R.W. McGraw R.W. Osteochondral fractures of the femoral condyles.JBJS. 1966; 48-B: 436-440Google Scholar found two clinical groups in their study of osteochondral fractures of the femoral condyles. They distinguished between those patients who sustained ‘exogenous’ fractures caused by direct trauma (e.g. direct blow), to patients with ‘endogenous’ fractures caused by rotatory and compressive forces. They were able to reproduce some of these lesions in cadaver knees, although the variety of locations observed in OCD has not been reproduced experimentally. A history of previous knee trauma, usually of moderate degree, is reported in approximately 50% of all patients suffering OCD.7Aichroth P. Osteochondritis dissecans of the knee. A clinical survey.JBJS. 1971; 53-B: 440-447Google Scholar, 18Green J.P. Osteochondritis dissecans of the knee.JBJS [Br]. 1966; 48-B: 82-91Google Scholar, 25Linden B. The incidence of osteochondritis dissecans in the condyles of the femur.Acta Orthop Scand. 1976; 47: 664-667Crossref PubMed Scopus (180) Google Scholar, 26Green W.T. Banks H.H. Osteochondritis dissecans in children.JBJS. 1953; 35-A: 26-47PubMed Google Scholar, 27Scott Jr, D.J. Stevenson C.A. Osteochondritis dissecans of the knee in adults.Clin Orthop. 1971; 76: 82-86Crossref PubMed Scopus (26) Google Scholar, 28Chiroff R.T. Cooke III, C.P. Osteochondritis dissecans. A histologic and microradiographic analysis of surgically excised lesions.J Trauma. 1975; 15: 689-696Crossref PubMed Scopus (79) Google Scholar, 29Johnson L.L. Uitvlugt G. Austin M.D. Osteochondritis dissecans of the knee. Arthroscopic compression screw fixation.Arthroscopy. 1990; 6: 179-189Abstract Full Text PDF PubMed Scopus (103) Google ScholarIn light of the clinical and experimental evidence it would appear that direct and indirect trauma, usually related to sports injuries, are implicated in the pathogenesis of OCD, although it is widely agreed that acute macro-trauma when it occurs appears to be incidental rather than causative.IschaemiaIt has been suggested that the interruption of blood-flow to end arteries of the femoral condyle may precipitate ischaemic necrosis with subsequent sequestration of the subchondral bone and articular cartilage.30Enneking WF. Clinical musculoskeletal pathology. Gainsville: Shorter Printing Co.; 1977. p. 147.Google Scholar Koch, in 1879, performed a series of experiments on bone necrosis and noted that subchondral bone infarction with loose body formation was the result of obstruction of the entire capillary bed of the area concerned.31Koch W. Über embolische Knochennekrosen.Arch Klin Chir. 1879; 23: 315Google Scholar Rieger suggested that fat emboli were responsible for blocking the end arteries.32Rieger H. Zur Pathologie von Gelenkmäusen.Münch Med Wschr. 1920; 67: 719-725Google Scholar Watson-Jones, however, believed in a systemic abnormality causing thrombosis or embolism of end arteries, which also helped to explain the large number of cases with multiple site involvement in the absence of antecedent trauma.33Watson-Jones R. Fractures and joint injuries. 4th ed., vol. 1. London: Livingstone; 1952. p. 97.Google ScholarThe anatomical microvascularity of the distal femur was first investigated by Rogers and Gladstone in the late 1940s.34Rogers W.M. Gladstone H. Vascular foramina and arterial supply of the distal end of the femur.JBJS. 1950; 32-A: 867-874Google Scholar They performed injection studies confirming a rich blood supply with numerous anastomoses in the subchondral bone. The authors concluded that ischaemia would be an unlikely factor in the aetiology of OCD. Enneking, a firm proponent of the ischaemic theory, compared the blood supply of the subchondral bone to that of the bowel mesentery with its end arterial arcades.30Enneking WF. Clinical musculoskeletal pathology. Gainsville: Shorter Printing Co.; 1977. p. 147.Google Scholar He found that the terminal branches within the subchondral bone poorly anastomose with their neighbours, hence infarction would result in necrosis of wedge-shaped areas immediately beneath the articular cartilage. Further support to the ischaemia hypothesis was provided by Ficat et al.35Ficat P. Arlet J. Mazières B. Osteochondritis dissecans and osteonecrosis of the lower end of the femur. Value of functional investigation of the bone marrow.Sem Hosp Paris. 1975; 51: 1907-1916PubMed Google Scholar who performed marrow pressure studies on patients suffering OCD and osteonecrosis. All of their patients had abnormal haemodynamics, with increased marrow pressure and circulatory obstruction owing to stasis.Löhr36Löhr W. Die Osteochondritis dissecans und das Gelenkmausleiden.Zbl Chir. 1929; 56: 2242Google Scholar and Lang37Lang F.J. Die Osteochondritis dissecans.Brun's Beitr Klin Chir. 1941; 171: 618Google Scholar both believed that irregularities in epiphyseal perfusion through changes from capsular to diaphyseal blood supply during epiphyseal closure are a key issue in the development of OCD. Their theory would appear plausible but fails to account for the occurrence of OCD in patients with a wide open physis.Accessory centres of ossificationThe development of separate ossific nuclei in the distal femoral epiphysis and their ossification process during maturation has led some researchers to conclude that OCD may simply be a variant of normal growth. Seidenstein38Seidenstein H. Osteochondritis dissecans of the knee with spontaneous healing in children.Bull Hosp Jt Dis. 1957; 28: 123-134Google Scholar, who considered this process to be a localised disturbance of condylar growth, observed spontaneous healing without active treatment. Ribbing39Ribbing S. The hereditary multiple epiphyseal disturbance and its consequences for the aetiogenesis of local malacias—particularly the osteochondrosis dissecans.Acta Orthop Scand. 1955; 24: 286-299Crossref PubMed Scopus (3) Google Scholar reviewed knee radiographs of 291 children for fragmentation of the ossific nucleus and compared those evidencing detached osseous islets within the articular cartilage outside the epiphysis to those with OCD. He found the locations similar in both groups and concluded that the ossification centre was a ‘locus minoris resistentiae’. He henceforth proposed the aetiology of OCD to be based on the separation of an accessory bone nucleus, which at least partially re-attaches during maturation, but which may completely separate if exposed to trauma.GeneticThis notion gained some popularity through a number of studies reporting a familial incidence of OCD.40Bernstein M.A. Osteochondritis dissecans.JBJS. 1925; 7: 319-329Google Scholar, 41Gardiner T.B. Osteochondritis dissecans in three members of one family.JBJS. 1955; 37-B: 139-141PubMed Google Scholar, 42Pick M.P. Familial osteochondritis dissecans.JBJS. 1955; 37-B: 142-145PubMed Google Scholar, 43Tobin W.J. Familial osteochondritis dissecans with associated tibia vara.JBJS. 1957; 39-A: 1091-1105PubMed Google Scholar, 44Stougaard J. The hereditary factor in osteochondritis dissecans.JBJS. 1961; 43-B: 256-258Google Scholar, 45Mubarak S.J. Carroll S.C. Familial osteochondritis dissecans of the knee.Clin Orthop. 1979; 140: 131-136PubMed Google Scholar Petrie, however, detected only one OCD case amongst first degree relatives of 34 patients suffering OCD, indicating the rarity of a potential hereditary influence.46Petrie P.W.R. Aetiology of osteochondritis dissecans.JBJS. 1977; 59-B: 366-367Google Scholar Multiple epiphyseal dysplasia, with its autosomal dominant and recessive hereditary patterns, should always be considered in patients with OCD. Hence, patients who are thought to have a familial form of OCD may, in fact, be suffering a variable expression of multiple epiphyseal dysplasia. Some authors have described an association of OCD with dwarfism, tibia vara and Perthes disease, indicating a possible genetic influence in isolated cases.43Tobin W.J. Familial osteochondritis dissecans with associated tibia vara.JBJS. 1957; 39-A: 1091-1105PubMed Google Scholar, 47White J. Osteochondritis dissecans in association with dwarfism.JBJS. 1957; 39-B: 261-267PubMed Google Scholar, 48Wiberg G. Spontaneous healing of osteochondritis dissecans in the knee joint.Acta Orthop Scand. 1943; 14: 270-277Crossref Scopus (6) Google Scholar, 49Woodward A.H. Decker J.S. Osteochondritis dissecans following Legg–Perthes disease.South Med J. 1976; 69: 943-944Crossref PubMed Scopus (7) Google Scholar It would, however, appear that heredity has little if any relationship with OCD other than a possible rare familial form that may exist.PathophysiologyPrecipitating insults at a vulnerable site causes a stress reaction, with locally impaired subchondral bone homoeostasis, which may progress into a stress fracture. If repetitive loading continues, the healing ability of bone may be impaired leading to avascularity and subsequent bone necrosis. Under ideal circumstances (early detection and treatment), resorption of the avascular bone is initiated by ingrowth of vascular buds and mesenchymal cells, creating a zone of granulation tissue between the viable and necrotic bone. This process of dead bone resorption and its replacement with new bone characterises the repair mechanism known as ‘creeping substitution’, which may, especially in juvenile patients, successfully re-establish the subchondral cancellous bone architecture.26Green W.T. Banks H.H. Osteochondritis dissecans in children.JBJS. 1953; 35-A: 26-47PubMed Google ScholarIn most cases, however, the repair is inadequate. The formed callus remains un-calcified, showing an exuberance of cartilaginous elements, which may shield-off the lesion preventing active repair. Expansion of this interstitial callus layer, which Roesner14Roesner E. Die Entstehungsmechanik der sogenannten Osteochondritis dissecans am Kniegelenk.Brun's Beitr Klin Chir. 1922; 127: 537-561Google Scholar described as ‘callus luxurians’, may elevate the osteo-articular fragment beyond the joint level increasing its mechanical vulnerability. This phenomenon is often observed during arthroscopy, when OCD lesions appear slightly protuberant despite intact surface cartilage. The lesion is biomechanically ill-equipped to withstand mechanical forces applied, especially if it is situated in a weight bearing area. Although the necrotic bone is held in place by the macroscopically intact overlying surface cartilage, it is assumed that this process also influences the basilar growth of the articular cartilage and its stress resilience. Once a subchondral non-union is established, the support for the articular cartilage is lost and degenerative changes are likely to occur. Under these circumstances the articular cartilage may fracture, leading to synovial fluid intrusion and inhibition of a potential healing response. Continuing hostile mechanical forces will further compromise fragment stability, eventually creating a loose osteochondral fragment.The fragment may remain in its crater, and through continuing joint movement be eroded. Once discarded into the joint cavity, a loose body is liable to impinge between tibia and femur, leading to third-body wear. The articular cartilage of the detached osteochondral fragment usually remains viable as it receives its nutrition from the synovial fluid. The subchondral bone, however, will undergo necrosis and complete resorption.50Fisher A.G.T. Internal derangements of the knee-joint. HK Lewis & Co, London1933Google ScholarEpidemiologyOCD has been classified according to the maturation status of the distal femoral physis into three groups: juvenile OCD in patients with wide open physis, adolescent OCD in patients with closing physis and adult OCD with fully closed physis. Juvenile OCD is by far the most common form observed. It has a peak prevalence between the age of 10 and 13 and is rarely seen in patients younger than 10 years of age.26Green W.T. Banks H.H. Osteochondritis dissecans in children.JBJS. 1953; 35-A: 26-47PubMed Google Scholar Boys are more commonly affected than girls, with a ratio of 5:3. Bilateral cases of OCD have been reported in up to 25% of affected individuals, with lesions usually being different in terms of size and symptoms.51Bednarz P.A. Paletta Jr, G.A. Stanitski C.L. Bilateral osteochondritis dissecans of the knee and elbow.Orthopedics. 1998; 21: 716-719PubMed Google Scholar, 52Schenk Jr, R.C. Goodnight J.M. Osteochondritis dissecans.JBJS. 1996; 78-A: 439-456Google ScholarAnatomic locationAichroth developed a classification system based on a survey of 200 patients, defining the various sites of OCD within the knee joint (Fig. 2).7Aichroth P. Osteochondritis dissecans of the knee. A clinical survey.JBJS. 1971; 53-B: 440-447Google Scholar The lesion most commonly involves the lateral posterior portion of the MFC, where it can be found in about 70% of cases. This is therefore described as the ‘classical’ OCD location.18Green J.P. Osteochondritis dissecans of the knee.JBJS [Br]. 1966; 48-B: 82-91Google Scholar A more wide-spread involvement of trochlea and central areas of the MFC is seen in about 15% of ca