Osteochondritis dissecans

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Osteochondritis dissecans
A lateral X-ray of a knee showing the typical features of osteochondritis dissecans
ICD-10 M93.2
ICD-9 732.7
OMIM 165800
DiseasesDB 9320
eMedicine radio/495  sports/57 orthoped/639
MeSH D010008

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Osteochondritis dissecans (Template:PronEng, typically abbreviated to OCD) is a form of osteochondritis.[1] It is commonly accepted that trauma, avascular necrosis and other causative factors affecting the subchondral (below cartilage) bone can lead to the loss of support for adjacent cartilaginous structures and precede the separation of an articular fragment from the underlying bone and formation loose bodies.[2][3][4][5] König[6] coined the term osteochondritis dissecans in 1887, describing it as an inflammation of the bone-cartilage interface.[7] Other terms have been associated with OCD in the literature, including osteochondral (pertaining to cartilage) fracture, osteonecrosis, accessory ossification center, osteochondrosis, and hereditary epiphyseal dysplasia.[8]

The symptoms of osteochondritis dissecans are pain and swelling of the affected joint, catching and locking on movement and a restriction in the range of movement. These symptoms characterize many knee conditions and may have a broad range of other causes, making OCD relatively hard to clinically diagnose .[9] To confirm the diagnosis, X-rays, CT scans and often magnetic resonance imaging (MRI) are usually required.[10] OCD is classified by the progression of the disease in stages (I, II, III or IV),[11] and may be treated accordingly with a form of articular cartilage repair.[12]

OCD is identified most commonly in skeletally immature adolescents (whose growth plates have not closed), occurring in 15 to 30 people per 100,000 every year.[13] Osteochondritis dissecans may affect several other species of animals, with dogs—specifically the German Shepherd—being the most commonly affected.[14]

Classification

OCD is classified by the progression of the disease in stages. While "arthroscopic classifications of osteochondral lesions [are] the criterion standard", the Anderson MRI staging is the main form of staging used in this article. There are four staging classifications presented; two are determined arthroscopically while two are determined by different forms of diagnostic imaging. Regardless of the representation used, this staging represents the "natural progression of osteochondritis dissecans" and the "various pathologic conditions that may be evident."[11][15]

The Anderson MRI staging of osteochondral lesions is as follows:

  • Stage I (earliest) - Subchondral bone flattening in the epiphysis (growth plate) before growth plate closure
  • Stage II can be divided into two substages—IIA and IIB
    • Stage IIA (stable) - Subchondral cyst
    • Stage IIB (unstable) - Incomplete separation of the osteochondral fragment due to repetitive trauma
  • Stage III (unstable) - Effusions (fluid around an undetached, undisplaced osteochondral fragment)
  • Stage IV (terminal)- Complete separation (detachment) of osteochondral fragment(s); mechanical irregularities and formation of loose bodies.

Stages I and II are stable lesions, while stages III and IV describe unstable lesions in which not only is the cartilage breached, but synovial fluid exists between the fragment and underlying bone.

The Pritsch arthroscopic staging of osteochondral lesions is as follows:[16]

  • Grade I - Intact, firm, shiny articular cartilage
  • Grade II - Intact but soft articular cartilage
  • Grade III - Frayed articular cartilage

The Cheng arthroscopic staging of osteochondral lesions is as follows:[17]

  • Grade A - Articular cartilage is smooth and intact but may be soft or ballottable
  • Grade B - Articular cartilage has a rough surface
  • Grade C - Articular cartilage has fibrillations or fissures
  • Grade D - Articular cartilage with a flap or exposed bone
  • Grade E - Loose, nondisplaced osteochondral fragment
  • Grade F - Displaced osteochondral fragment

The Berndt and Harty radiographic classification of osteochondral lesions of the talus is as follows:[18]

  • Stage I - Normal radiograph (subchondral compression fracture of the talus with no ligamentous sprain)
  • Stage II - Partially detached osteochondral fragment
  • Stage III - Complete, nondisplaced fracture remaining within the bony crater
  • Stage IV - Detached, loose osteochondral fragment

Pathophysiology

An algorithm for management of osteochondritis dissecans of the knee. Appropriate treatment of OCD is determined by the stage of its progression (I, II, III or IV)

Osteochondritis dissecans differs from "wear and tear" degenerative arthritis, which is primarily an articular surface problem. Instead, OCD is a problem of the underlying subchondral bone, which may secondarily affect the articular cartilage. Left untreated, OCD can lead to the development of degenerative arthritis secondary to joint incongruity and abnormal wear patterns.[19]

OCD occurs when a loose piece of bone or cartilage partially (or fully) separates from the end of the bone, often because of a loss of blood supply (osteonecrosis) and insufficient amounts of calcium. The loose piece may stay in place or slide around making the joint stiff and unstable. OCD in humans most commonly affects the knees[20] or ankles, but can also affect other joints such as the elbow.

Functional anatomy

In skeletally immature individuals, the vascularity to the epiphyseal bone (growth plate) is very good, supporting both osteogenesis and chondrogenesis. With disruption of the epiphyseal plate vessels, varying degrees and depth of necrosis occur, resulting in a cessation of growth to both osteocytes and chondrocytes. In turn, this pattern leads to "nonspecific changes that produce disordered intracartilaginous ossification," resulting in subchondral avascular necrosis or OCD.[21]

Four minor stages of OCD have been identified after trauma, including revascularization and formation of granulation (scar) tissue, absorbation of necrotic fragments, intertrabecular osteoid deposition, and remodeling of new bone. With delay in the revascularization stage, an OCD lesion develops. OCD lesions may lead to articular-surface irregularities, which can cause degenerative arthritic changes.[21]

Presentation

In osteochondritis dissecans, fragments of cartilage or bone have become loose within a joint, leading to pain and inflammation. These fragments are sometimes referred to as "joint mice"[22] due to a squeaking sound produced by bending the joint. Specifically, OCD is a type of osteochondrosis in which a lesion has formed within the cartilage layer itself, giving rise to secondary inflammation.

Patients with OCD complain of activity-related pain that develops gradually. Subjective complaints usually consist of mechanical symptoms, including pain, swelling, catching, locking, and "giving way"; the primary presenting symptom may be a restriction in the range of movement.[15][23] Symptoms typically present themselves within the first stage of OCD (I), however the onset of stage II is usually within months and the disease progresses rapidly. This quick progression of OCD, combined with a set of symptoms similar of other causes (sprains, strains), leads to a late diagnosis and subsequently further damage.[9]

Physical examination typically reveals an effusion, tenderness, and crepitus. The tenderness may be diffuse initially but often changes to well-defined focal tenderness as the lesion progresses. Acute osteochondral fracture has a similar presentation, but is usually associated with a fatty hemarthrosis. Although there is no significant pathologic gait or characteristic alignment abnormality associated with OCD, the patient may walk with the involved leg externally rotated in an attempt to avoid tibial spine impingement on the lateral aspect of the medial condyle femur.[8]

Causes

Although the etiology is not certain, possible causative factors include repetitive trauma, ischemia, hereditary and endocrine factors, avascular necrosis, rapid growth, deficiencies and imbalances in the ratio of calcium to phosphorus, and anomalies of ossification.[2][8][24][25][26][27][28][29]

Dr. Smillie[30] believes that anomalies in ossification can be observed up to the age of ten, and that these may determine the clinical onset of osteochondritis dissecans in the second decade. It is suggested that this is the normal pattern of development in the juvenile cases, but there are two qualifications: The first is that anomalies of ossification do not necessarily lead to the development of osteochondritis dissecans. The second is that some cases observed in the second decade of life may fit into the adult pattern rather than the juvenile.

Trauma, rather than avascular necrosis, is thought to be the factor which localizes and determines the development of osteochondritis dissecans in juveniles.[31] In the adult group of cases trauma is thought to be the main or perhaps the sole factor in determining the onset of osteochondritis dissecans. The trauma may be endogenous and/or exogenous.[30] Interestingly, the incidence of overuse injuries in young athletes is on the rise and accounts for a significant number of visits to the primary care office;[32] this reinforces the theory that OCD may be associated with increased participation in sports and subsequent trauma.[33][34]

Diagnosis

Template:Seealso Template:Image stack To determine whether pains are osteochondritis dissecans, an MRI[10], CT scan or X-ray can be performed to show necrosis of subchondral bone and/or formation of loose fragments. In specific cases, if caught early enough, a harmless dye will be injected into the blood stream to show where calcium will accumulate.

Physical examination

A special test known as the "Wilson sign" has been described to locate OCD lesions of the femoral condyle.[35] The test is performed by slowly extending the knee from 90 degrees while maintaining internal rotation. Pain reported at 30 degrees of flexion and relief with tibial external rotation is a positive result.

The possibility of microtrauma contributing to OCD underscores the importance of evaluating biomechanical forces at the knee during the physical examination. An evaluation of the alignment and rotation of all major joints in the involved extremity; as well as extrinsic and intrinsic abnormalities of the joint, including joint laxity, should be considered.

Diagnostic imaging

Plain radiographs show lucency of the ossification front, representing growth inhibition, in young patients. In older adolescents, the OCD lesion frequently appears as a well-circumscribed area of sclerotic subchondral bone with a radiolucent line between the defect and the epiphysis. The apparent size of the lesion depends on its location on the condyle and on the amount of knee flexion used. By viewing the lateral (side) radiograph, Harding described a method to identify the most common site of an OCD lesion.[36] Cahill and Berg described a method to record the location of OCD based on radiographs by plotting the lesion with coordinates; the letters A--C are used for the lateral view, and the numbers 1--5 are used for the anteroposterior view (dividing both condyles into two equal halves and a separate area over the intercondylar notch).[37][38]

Magnetic resonance imaging is useful for staging OCD lesions, evaluating the integrity of the joint surface, and distinguishing normal variants from OCD by showing bone and cartilage edema in the area of the irregularity. MRI provides information regarding features of the articular cartilage and underlying subchondral (below cartilage) bone, including edema, fractures, fluid interfaces, articular surface integrity, and fragment displacement.[39][40] High signal at the fragment interface is seen in active lesions, which is considered to be potentially unstable or to have current or recent microfractures. MRI and arthroscopy have been reported to have a close correlation, while MRI and plain radiographs have been shown to have a poorer correlation.[40]

CT (computed tomography) scans and technetium bone scintigraphy are also sometimes used to monitor the progress of treatment. Unlike plain radiographs (X-rays), CT scans, along with MRI's, can show the exact location and extent of the lesion.[41] Technetium bone scintigraphy can detect osteoblastic activity, regional blood flow, and the amount of osseous uptake, which seem to be correlated to the potential amount of healing possible in the osteochondral fragment.[42][43]

Prognosis

"The natural history and prognosis from different treatments vary depending on the age of the patient, the joint affected, [the] stage of the lesion," and most importantly the status of the growth plate.[44] The juvenile form of the disease occurs in children with open growth plates, usually between the ages 5 and 15 years. The adult form, which occurs in those who have reached skeletal maturity, is most commonly found in patients of ages 16 to 50 years.[45]

Still, prognosis is favorable in stable lesions (stage I and II) in juveniles with open growth plates; indicating the use of non-operative treatment. However, unstable, large, full thickness lesions (stage III and IV) or lesions of any stage found in skeletally mature patients (closed growth plates) are more likely to fail non-operative treatment and offer a worse prognosis.[45][46]

Treatment

Treatment options include modified activity with or without weight-bearing; immobilization; cryotherapy; anti-inflammatories; drilling of subchondral bone to improve vascularity; microfracture; reattachment and removal of loose bodies and autologous osteochondral plugs (OATS).[33] The principles of treatment are to enhance the healing potential of subchondral bone, fix unstable fragments while maintaining joint congruity, and to replace the damaged bone and cartilage with implant tissues or cells that can replace bone and grow cartilage.[47] However, the capacity of articular cartilage for repair is limited. Partial-thickness defects in the articular cartilage do not heal spontaneously. "Injuries of the articular cartilage that do not penetrate the subchondral bone" do not heal and usually progress to the "degeneration of the articular surface."[48] As a result, surgery is often required in even moderate cases (stage II, III) of OCD.

Non-surgical treatment

Candidates for non-operative treatment include those who are skeletally immature with an intact lesion and no loose bodies. Non-operative management may include activity modification, protected weight bearing (partial or non-weight bearing), and immobilization. The goal of non-operative intervention is to promote healing in the subchondral bone and potentially prevent chondral collapse, subsequent fracture, and crater formation.[47]

Patients with OCD of the knee are immobilized for four to six weeks in a cylinder cast in extension to remove shear stress from the involved area, however, they are permitted to walk with weightbearing as tolerated. If the plain radiographs taken three months after the start of non-operative therapy reveal that the lesion has healed, then a gradual return to activities is instituted. Patients with some component of healing demonstrated by increased radiodensity in the subchondral region, or those patients whose lesions are unchanged, are candidates to repeat the above described three-month protocol until healing is noted.[49]

Surgical treatment

The choice of surgical verse non-surgical treatments for osteochondritis dissecans is still controversial.[50] Consequently, the type and extent of surgery necessary varies based on patient age, severity of the lesion, and personal bias of the treating surgeon—entailing an exhaustive list of suggested treatments. Thus, a variety of surgical options exist for the treatment of persistently symptomatic, intact, partially detached, and completely detached OCD lesions.[49]

Intact lesions

Schematic drawing illustrating two drilling techniques for OCD lesions.
(A) Retrograde drilling theoretically avoids the articular cartilage but technically more challenging. (B) Antegrade drilling.

If non-operative measures are unsuccessful in healing intact lesions, drilling may be considered to stimulate healing of the subchondral bone. Arthroscopic drilling may be performed by using an antegrade approach through the articular cartilage, or by using a retrograde approach, which is intended to avoid penetration of the articular cartilage. This has proven successful with positive results at one-year follow-up with antegrade drilling in 9 out of 11 patients with the juvenile form of OCD,[51] and in 18 of 20 skeletally immature patients (follow-up of five years) who had failed prior conservative programs.[52]

Hinged lesions

Pins and screws can be used to secure flap lesions. Pain relief is usually rapid (within days after operation), suggesting that the pain may be caused by increased pressure at the line of separation between the fragment and the epiphysis.[51][53][54] Options for securing hinged lesions include bone pegs, metallic pins and screws, as well as bioresorbable screws and pins.

Full thickness lesions

A variety of options exist for treating full thickness lesions. Three methods commonly used for full thickness lesions include arthroscopic drilling, abrasion with a high-speed burr, and microfracturing with a pick.

Using pluripotential cells from the marrow elements was established with the first surgical debridement of an OCD lesion in 1946 by Magnusson. The recruited cells differentiate mostly into fibrocartilage, which is principally type I collagen and rarely types II, VI, and IX (hyaline types). While small lesions can be effectively resurfaced, the repair tissue typically has less strength than normal hyaline articular cartilage and must be protected from high impact loading for 6 to 12 months. The results for large lesions usually diminish over time due to the decreased resilience, stiffness, and poor wear characteristics of the fibrocartilage.[55]

In attempts to address the weaker structure of the reparative fibrocartilage, new techniques have been designed to fill the defect with tissue that more closely simulates normal hyaline articular cartilage. One such technique is autologous chondrocyte implantation (ACI), which is useful for large, isolated femoral defects in younger patients. In this technique, chondrocytes are extracted arthroscopically from healthy articular surface and grown. The chondrocytes are then injected into the defect that has been covered by a periosteal patch. ACI surgery has reported good to excellent results for reduced swelling, pain and locking in clinical follow ups.[56][57] However, some physicians have preferred to use undifferentiated pluripotential cells, such as periosteal cells and bone marrow stem cells, as opposed to chondrocytes. These too have demonstrated the ability to regenerate both the cartilage and the underlying subchondral bone.[58]

Another method used to promote normal articular cartilage replacement is the technique of transplanting autologous osteochondral plugs. The plugs are taken from a relatively "non-weight-bearing region" of the knee, such as the area just above the intercondylar notch or the edge of the patellar groove, and inserted in the defect. OATS has reported good clinical results with plugs taken from the lateral facet of the patella when treating 10 patients with large femoral OCD lesions.[59] Limitations of this procedure include donor site morbidity, plug damage from percussive forces during insertion, and the technical challenge of placing the plug edges flush with the adjacent articular cartilage.

Fresh osteoarticular allografts have also been used for the treatment of OCD defects. In a study of 126 patients with OCD of the knee, Ghazavi et al reported an 85% success rate at 7.5 years after osteochondral allograft transplantation. This procedure may be an option when other treatments have failed and symptoms persist.[60]

Unstable lesions

Some methods of fixation for unstable lesions include countersunk compression screws and Herbert screws or pins made of stainless steel or bioresorbable materials. If loose bodies are present, they are removed. Although each case is unique, ACI is generally performed on large defects in skeletally mature patients.

Epidemiology

OCD is a relatively rare disorder with an estimated occurrence of 15 to 30 cases per 100,000 persons.[13][61] Although rare, OCD is noted as an important cause of joint pain in active adolescents. The juvenile form of the disease occurs in children with open growth plates, usually between the ages 5 and 15 years and occurs more commonly in males than females, with a ratio between 2:1 and 3:1.[20] [62] The adult form, which occurs in those who have reached skeletal maturity, is most commonly found in patients of ages 16 to 50 years. However, OCD has become more common among adolescent females as they become more active in sports.[63]

The knee is the most commonly involved joint, as the ratio of knee lesions to all other areas combined, including the talus, capitellum, and wrist, is 3:1.[20]

The most commonly affected areas of the knee are:

Less frequent locations include:[66][67]

History

In 1887, Francis König[6] published a paper on the cause of loose bodies in the joint with three conclusions:

  1. "That trauma had to be very severe to break off parts of the joint surface."
  2. "That lesser degrees of trauma might contuse the bone to cause an area of necrosis which might then separate."
  3. "That in some cases, the absence of trauma worth mentioning made it likely that there existed some spontaneous cause of separation."

König named the disease "osteochondritis dissecans," [7] describing it as a subchondral inflammatory process of the knee, resulting in a loose fragment of cartilage from the femoral condyle. In 1922, Kappis[68] described this process in the ankle joint. On the basis of a review of all literature describing transchondral fractures of the talus, Berndt and Harty developed a classification system for "radiographic staging of osteochondral lesions of the talus (OLTs)."[18] The term osteochondritis dissecans has persisted and since been broadened to describe a similar process occurring in many other joints, including the knee, hip, elbow, and metatarsophalangeal joints.[20][62][69][70]

Veterinary aspects

In animals, OCD is considered a developmental and metabolic disorder related to cartilage growth and endochondral ossification. Osteochondritis itself signifies the disturbance of the usual growth process of cartilage, and OCD is the term used when this affects joint cartilage causing a fragment to become loose.[71] OCD in animals is "well recognized but poorly understood".

According to the Columbia Animal Hospital the frequency of affected animals is "Dogs, humans, pigs, horses, cattle, chickens, and turkeys", and in dogs "The most commonly affected breeds include the German Shepherd, Golden and Labrador Retriever, Rottweiler, Great Dane, Bernese Mountain Dog, and Saint Bernard."[14] Whilst any joint may be affected, the joints commonly affected by OCD in the dog are: shoulder (often bilaterally), elbow, knee and tarsal (hock).[14]

The problem develops in puppyhood although often subclinically, and there may be pain or stiffness, discomfort on extension, or other compensating characteristics. Diagnosis is via scans such as X-ray, arthroscopy, or MRI, and treatment is often surgical although the best method remains open to debate.

Because an animal may compensate for painful forelegs by misuse of rear legs, there is a possibility that this condition can be masked by other skeletal and joint conditions such as hip dysplasia.

See also

References

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  2. ↑ 2.0 2.1 Pappas AM (1981). "Osteochondrosis dissecans". Clin. Orthop. Relat. Res. (158): 59–69. PMID 7273527.
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  33. ↑ 33.0 33.1 Kocher MS, Tucker R, Ganley TJ, Flynn JM (2006). "Management of osteochondritis dissecans of the knee: current concepts review". Am J Sports Med. 34 (7): 1181–91. doi:10.1177/0363546506290127. PMID 16794036. Unknown parameter |month= ignored (help)
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  35. ↑ J. N. Wilson (1967). "A diagnostic sign in osteochondritis dissecans of the knee" (PDF). J Bone Joint Surg Am. 49 (3): 477–80. PMID 6022357. Unknown parameter |month= ignored (help)
  36. ↑ Harding WG 3rd. (1977). "Diagnosis of ostechondritis dissecans of the femoral condyles: the value of the lateral x-ray view". Clin Orthop Relat Res. 123: 25–6. PMID 852179. Unknown parameter |month= ignored (help)
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  38. ↑ Cahill BR. (1995). "Osteochondritis dissecans of the knee: Treatment of juvenile and adult forms". J Am Acad Orthop Surg. 3 (4): 237–47. PMID 10795030. Unknown parameter |month= ignored (help)
  39. ↑ De Smet AA, Fisher DR, Graf BK, Lange RH (1991). "Characterizing osteochondral lesions by magnetic resonance imaging" (PDF). Arthoscopy. 7 (1): 101–4. PMID 2117355.
  40. ↑ 40.0 40.1 Dipaola JD, Nelson DW, Colville MR (1990). "Osteochondritis dissecans of the knee: value of MR imaging in determining lesion stability and the presence of articular cartilage defects". AJR Am J Roentgenol. 155 (2): 549–53. PMID 2009106. Unknown parameter |month= ignored (help)
  41. ↑ Bui-Mansfield LT, Kline M, Chew FS, Rogers LF, Lenchik L (2000). "Osteochondritis dissecans of the tibial plafond: imaging characteristics and a review of the literature". AJR Am J Roentgenol. 175 (5): 1305–8. PMID 11044029. Unknown parameter |month= ignored (help)
  42. ↑ Cahill BR, Berg BC (1983). "99m-Technetium phosphate compound joint scintigraphy in the management of juvenile osteochondritis dissecans of the femoral condyles". Am J Sports Med. 11 (5): 329–35. PMID 6638247.
  43. ↑ "Adolescent Osteochondritis Dissecans of the Elbow". Text " eOrthopod.com " ignored (help)
  44. ↑ Cooper, Grant. "Osteochondritis Dissecans". eMedicine. Retrieved 2008-09-18.
  45. ↑ 45.0 45.1 Bradley J, Dandy DJ (1989). "Osteochondritis dissecans and other lesions of the femoral condyles" (PDF). J Bone Joint Surg Br. 71 (3): 518–22. PMID 2722949. Unknown parameter |month= ignored (help)
  46. ↑ Lützner J, Mettelsiefen J, Günther KP, Thielemann F (2007). "[Treatment of osteochondritis dissecans of the knee joint]". Orthopade (in German). 36 (9): 871–9, quiz 880. doi:10.1007/s00132-007-1130-3. PMID 17680233. Unknown parameter |month= ignored (help)
  47. ↑ 47.0 47.1 Smillie I. (1957). "Treatment of osteochondritis dissecans" (PDF). J Bone Joint Surg. 39 (2): 248–260. PMID 13438964.
  48. ↑ "Autologous Chondrocyte Transplantation". Retrieved 2008-09-17.
  49. ↑ 49.0 49.1 Stephan G. Pill, Theodore J. Ganley, John M. Flynn, R. Alden Milam, Paul J. King, John R. Gregg (2001). "Osteochondritis Dissecans of the Knee: Experiences at The Children's Hospital of Philadelphia and a Review of Literature". Unv. Penn. Ortho. J. 14 (1): 25–34.
  50. ↑ Nobuta S, Ogawa K, Sato K, Nakagawa T, Hatori M, Itoi E (2008). "Clinical outcome of fragment fixation for osteochondritis dissecans of the elbow" (PDF). Ups. J. Med. Sci. 113 (2): 201–8. PMID 18509814.
  51. ↑ 51.0 51.1 Bradley J, Dandy DJ (1989). "Results of drilling osteochondritis dissecans before skeletal maturity" (PDF). J Bone Joint Surg Br. 71 (4): 642–4. PMID 2768313. Unknown parameter |month= ignored (help)
  52. ↑ Anderson AF, Richards DB, Pagnani MJ, Hovis WD (1997). "Antegrade drilling for osteochondritis dissecans of the knee". Arthroscopy. 13 (3): 319–24. PMID 9195028. Unknown parameter |month= ignored (help)
  53. ↑ Johnson LL, Uitvlugt G, Austin MD, Detrisac DA, Johnson C (1990). "Osteochondritis dissecans of the knee: arthroscopic compression screw fixation". Arthroscopy. 6 (3): 179–89. PMID 2206180.
  54. ↑ Thomson NL (1987). "Osteochondritis dissecans and osteochondral fragments managed by Herbert compression screw fixation". Clin. Orthop. Relat. Res. (224): 71–8. PMID 3665256. Unknown parameter |month= ignored (help)
  55. ↑ Mandelbaum BR, Browne JE, Fu F; et al. (1998). "Articular cartilage lesions of the knee". Am J Sports Med. 26 (6): 853–61. PMID 9850792. Retrieved 2008-09-17.
  56. ↑ Brittberg M, Lindahl A, Nilsson A, Ohlsson C, Isaksson O, Peterson L (1994). "Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation". N. Engl. J. Med. 331 (14): 889–95. PMID 8078550. Retrieved 2008-09-17. Unknown parameter |month= ignored (help)
  57. ↑ Peterson L, Minas T, Brittberg M, Nilsson A, Sjögren-Jansson E, Lindahl A (2000). "Two- to 9-year outcome after autologous chondrocyte transplantation of the knee". Clin. Orthop. Relat. Res. (374): 212–34. PMID 10818982. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  58. ↑ O'Driscoll SW (1998). "The healing and regeneration of articular cartilage" (PDF). J Bone Joint Surg Am. 80 (12): 1795–812. PMID 9875939. Unknown parameter |month= ignored (help)
  59. ↑ Outerbridge HK, Outerbridge AR, Outerbridge RE (1995). "The use of a lateral patellar autologous graft for the repair of a large osteochondral defect in the knee". J Bone Joint Surg Am. 77 (1): 65–72. PMID 7822357. Unknown parameter |month= ignored (help)
  60. ↑ Ghazavi MT, Pritzker KP, Davis AM, Gross AE (1997). "Fresh osteochondral allografts for post-traumatic osteochondral defects of the knee". J Bone Joint Surg Br. 79 (6): 1008–13. PMID 9393922. Unknown parameter |month= ignored (help)
  61. ↑ Hughston JC, Hergenroeder PT, Courtenay BG (1984). "Osteochondritis dissecans of the femoral condyles" (PDF). J Bone Joint Surg Am. 66 (9): 1340–8. PMID 6501330. Unknown parameter |month= ignored (help)
  62. ↑ 62.0 62.1 Nagura S. (1960). "The so-called osteochondritis dissecans of Konig". Clin Orthop. 18: 100–121.
  63. ↑ Williamson LR, Albright JP (1996). "Bilateral osteochondritis dissecans of the elbow in a female pitcher". J Fam Pract. 43 (5): 489–93. PMID 8917149. Unknown parameter |month= ignored (help)
  64. ↑ Aichroth P (1971). "Osteochondritis dissecans of the knee. A clinical survey" (PDF). J Bone Joint Surg Br. 53 (3): 440–7. PMID 5562371. Unknown parameter |month= ignored (help)
  65. ↑ Lindén B (1976). "The incidence of osteochondritis dissecans in the condyles of the femur". Acta Orthop Scand. 47 (6): 664–7. PMID 1015263. Unknown parameter |month= ignored (help)
  66. ↑ Green WT, Banks HH (1953). "Osteochondritis dissecans in children". J Bone Joint Surg Am. 35-A (1): 26–47. PMID 13022705. Unknown parameter |month= ignored (help)
  67. ↑ Tuite MJ, DeSmet AA (1994). "MRI of selected sports injuries: muscle tears, groin pain, and osteochondritis dissecans". Semin Ultrasound CT MR. 15 (5): 318–40. PMID 7803070. Unknown parameter |month= ignored (help)
  68. ↑ Kappis M (1922). "Weitere beitrage zur traumatisch-mechanischen entstehung der "spontanen" knorpela biosungen". Dtsch Z Chir. 171: 13–29.
  69. ↑ Template:Harv
  70. ↑ Template:Harv
  71. ↑ Berzon JL (1979). "Osteochondritis dissecans in the dog: diagnosis and therapy". J. Am. Vet. Med. Assoc. 175 (8): 796–9. PMID 393676.

Additional Resources

  • Geor, Raymond J.; Kobluk, Calvin N.; Ames, Trevor R. (1994). The Horse: diseases & clinical management. Philadelphia, PA: W.B. Saunders Company. ISBN 0-443-08777-6.
  • Morrey, Bernard F. (2000). The Elbow and Its Disorders. Philadelphia, PA: W.B. Saunders Company. pp. 250–60. ISBN 0-7216-7752-5.
  • Walzer, Janet; Pappas, Arthur M. (1995). Upper extremity injuries in the athlete. Edinburgh, UK: Churchill Livingstone. p. 132. ISBN 0-443-08836-5.
  • Pettrone, FA (1986). American Academy of Orthopaedic Surgeons Symposium on Upper Extremity Injuries in Athletes. St. Louis, Mo: CV Mosby. pp. 193–232.


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