The juvenile and adult forms of OCD have different symptoms and modes of treatment [14]. In the juvenile form, the primary complaints include non-specific pain, mild effusion, atrophy of the quadriceps muscle, external rotation of tibia while walking [14] and episodes of ‘catching’ or locking of the knee [4].

The adult form of presentation is the knee ‘giving way’ after an episode of significant trauma [14]. In both juvenile and adult forms, when the medial condyle of the knee if involved, the primary complaint is pain and difficulty in extending the leg [14]. The pain is poorly localized and characteristically worsens with weight bearing [4].

On examination, the patient is found to have crepitus [2], joint effusions [2], and joint line tenderness [10]. Patients with knee involvement usually walk with external tibial rotation and a positive Wilson’s sign is seen [1]. This sign can be elicited by flexion of knee to 90 ninety degree and then extending slowly, looking for any painful response from the patient [3].

• Knee Pain

  Prompt recognition of osteochondritis dissecans is important, as this entity is a treatable cause of knee pain. [ncbi.nlm.nih.gov]

• Knee Effusion

  Review Topic QID: 2914 1 Arthroscopic micro-fracture 4 Arthroscopic reduction and fixation ML 1 Select Answer to see Preferred Response PREFERRED RESPONSE 2 (OBQ06.200) An 11-year-old boy presents with recurrent knee effusions and discomfort with athletic [orthobullets.com]

  Sagittal T2-weighted image 1 year after injury reveals a subchondral cyst (arrow), an articular defect in the lateral tibial plateau, and a large knee effusion (arrowhead). Coronal T1-weighted image 2 weeks after injury is unremarkable. [emedicine.com]

• Bone Disorder

  Genetic predisposition is a less likely factor, although inherited bone disorders may be mistaken for OCD. 3 Clinical Presentation Patients are typically 12 to 20 years of age and active in gymnastics, baseball or other organized sports. [aafp.org]

  Osteochondritis dissecans (OCD), osteochondritis deformans (Perthes disease) and tibial tubercle avulsion fracture were described as part of the symptom complex in some heritable bone disorders [ 15 – 20 ]. [ped-rheum.biomedcentral.com]

• Incontinence

  Author Coauthor(s) Guy W Fried, MD Professor, Department of Rehabilitation Medicine, Jefferson Medical College of Thomas Jefferson University; Chief Medical Officer, Outpatient Medical Director, Medical Director of Incontinence and Respiratory Care Programs [emedicine.com]

As with most joint disorders, OCD is a radiologic diagnosis [10]. In patients with knee symptoms, X-rays with anteroposterior, lateral, sunrise or Merchant, and tunnel views are recommended [9]. If anteroposterior view alone is performed then there are greater chances of missing a lesion on the posterior aspect of the medial femoral condyle [1]. Once a lesion has been noticed, it is preferable that the contralateral knee must also be examined [10].

Once the lesion has been identified on X-ray, MRI must be carried out to stage the lesion for stability, as it is the most accurate method for staging lesions [12] [13] [9], studies have shown that MRI has a 97 percent sensitivity for detecting unstable lesions [12]. The presence of high signal changes on T2 images indicates the presence of fluid between the fragment and underlying bone [10]. MRI is also a strong indication if there is accompanying pathology involving the menisci, anterior cruciate ligament or articular cartilage [9]. If the plain radiographs are negative then other causes should be considered and OD can be ruled out safely [10].

Stages I and II involve lesions which are stable and stages III and IV show unstable lesions which have infringed upon the cartilage [10]. It is imperative to distinguish between stage II and stage III in order to plan the surgery [13]. If the MRI shows unstable lesions of stage III or IV, the arthroscopy should be performed to evaluate the extent of involvement of the cartilage [10]. Other radiographic modalities such as computed tomography, arthrography and nuclear bone scans have also been used to evaluate stability and prognosis, however they have their limitations [6].

Staging of the lesions is absolutely necessary before deciding the mode of treatment. While stable lesions are managed conservatively, unstable lesions are an indication for surgery [10], followed by post-operative physical therapy [9].

Juvenile OCD must be treated before epiphyseal closure in order to ensure full recovery [10]. In cases of the adult form, the therapy aims to preserve function of the joint and prevent onset of degenerative osteoarthritis [3].

Conservative management includes observation. It also requires the patients to avoid competitive sports for a minimum of six to eight weeks [10]. The aim of this type of therapy is to enable the patient to be symptom free [1]. Physical therapy including stretching, conditioning and quadriceps strengthening are also helpful [10].

If symptoms do not resolve with conservative measures, then the development of a loose body must be suspected and arthroscopic evaluation must be carried out [1].

According to recent trends, in cases where surgical intervention is required, there are five main surgical techniques which have yielded favorable results, these include osteochondral autologous transplantation, autologous chondrocyte implantation with bone graft, biomimetic nanostructured osteochondral scaffold implantation, bone-cartilage paste graft, "one-step" bone-marrow-derived cell transplantation technique [8].

The overall prognosis is good as patients usually recover. However, factors favoring a poorer prognosis include large size of the lesion and occurrence on a weight bearing area. Prognosis also worsens with increased age and physis closure [10].

Girls ages 11 years and less and boys aged 13 years and less have remarkable chances of resolution, whereas those affected over the age of 20 years have worse outcomes [1]. Stage III and IV lesions which are unstable and occurring in patients with a closed physis, have a particularly poor prognosis [10].

Although most cases of OCD are said to be of unknown nature [3], certain etiologies responsible for OCD include environmental [10], hereditary, recent or recurrent episodes of trauma, abnormalities of epiphyseal ossification, endocrine abnormalities and avascular necrosis factors [14].

The current incidence of OCD is approximately 15 to 30 cases per 100,000 persons [1] [5]. Although the conventional population affected by OCD includes young males between ages 10 and 20 years [10], the recent trend shows that it is increasingly affecting women [2] and children [1]. The sites most affected include the femoral condyles, talar dome and capitellum of humerus [6]. The knee is involved in 75 percent of the cases [3], specifically the non-weight bearing medial femoral condyle [7].

The mechanism of injury which is common to all etiologies is constant and recurrent shear and compression forces affecting the joint [10]. Majority of the patients with a classical picture OCD have a history of repeated incidents of micro-trauma rather than a single incident of trauma [1]. The fact that OCD is often bilateral and affects non-weight bearing areas, make it more likely that causes other than trauma are responsible for the insult [10].

Mechanisms thought to be involved in cutting off the blood supply to the joint include ischemia due to vascular spasm, emboli of fat and thrombosis or infection [1] [3]. Children are more susceptible to mild trauma during growth spurts because of the increased porosity bones and open epiphyseal plates during this period [11]. Certain abnormal ossification centers, common in rapidly growing children, are said to be responsible for starting the disease process [1].

There is no guideline for the prevention of OCD.

Osteochondritis dissecans (OCD) is a disease affecting the joints, in which the bone and some of the adjacent cartilage undergo necrosis as a result of loss of blood supply. The affected area is a focal of segment of bone undergoing necrosis [10]; the resultant necrosis of the cartilage is due to resorption of bone and the loss of supporting structure of the cartilage [2]. As a result, there is an outgrowth of bone into the empty space [10].

OCD can be classified in to two basic types: The juvenile form, occurring before epiphyseal closure, and the adult form, occurring after epiphysis closure [3].

Osteochondritis dissecans (OCD) is a disease of the joints in which a part of bone of cartilage (or both) loses blood supply and dies. This may be consequent to an injury or due to overuse as occurs in certain types of activities such as competitive sports.
The onset of the disease may be painless or may cause a sudden or gradual onset of symptoms. Sometimes, OCD is diagnosed ‘accidentally’ when as X-ray is being performed for some other reason.

The presenting symptoms can include pain, swelling, sensation of grinding within the joint, decreased range of movement or complete locking of the joint. Younger patients have a better prognosis as their growth plates have not fused as yet, whereas older patients have poorer outcomes. The prognosis also depends on the type and stage of the lesion with stages I and II having favorable outcomes and stages III and IV having more serious sequelae.

Treatment again depends on the staging of the disease; the first two stages can be managed with simple bed rest and physiotherapy and stages III and IV require surgical intervention.

1. Obedian RS, Grelsamer RP. Osteochondritis dissecans of the distal femur and patella. Clin Sports Med. 1997;16:157–74.
2. Williamson LR, Albright JP. Bilateral osteochondritis dissecans of the elbow in a female pitcher. J Fam Pract. 1996;43:489–93.
3. Clanton TO, DeLee JC. Osteochondritis dissecans: history, pathophysiology and current treatment concepts. Clin Orthop. 1982;167:50–64.
4. Schenck RC Jr, Goodnight JM. Osteochondritis dissecans. J Bone Joint Surg [Am ]. 1996;78:439–56.
5. Hughston JC, Hergenroeder PT, Courtenay BG. Osteochondritis dissecans of the femoral condyles. J Bone Joint Surg [Am]. 1984;66:1340–8.
6. Fisher DR, DeSmet AA. Radiologic analysis of osteochondritis dissecans and related osteochondral lesions. Contemp Diag Rad. 1993;16:1–5.
7. Aichroth PA. Osteochondritis dissecans of the knee. A clinical survey. J Bone Joint Surg [Br]. 1971;53:440–7.
8. Kon E, Vannini F, Buda R et.al, How to treat osteochondritis dissecans of the knee: surgical techniques and new trends: AAOS exhibit selection. J Bone Joint Surg Am. 2012 Jan 4;94(1):e1(1-8).
9. American Academy of Orthopaedic Surgeons Clinical Practice Guideline on the Diagnosis and Treatment of Osteochondritis Dissecans Rosemont (IL): American Academy of Orthopaedic Surgeons (AAOS); 2010
10. Allen L. Hixon, M.D., and Lisa M. Gibbs, M.D. Osteochondritis Dissecans: A diagnosis not to miss. Am Fam Physician. 2000 Jan 1;61(1):151-156.
11. Saperstein AL, Nicholas SJ. Pediatric and adolescent sports medicine. Pediatr Clin North Am. 1996;43:1013–33.
12. De Smet AA, Ilahi OA, Graf BK. Reassessment of the MR criteria for stability of osteochondritis dissecans in the knee and ankle. Skeletal Radiol. 1996;25:159–63.
13. Dipaola JD, Nelson DW, Colville MR. Characterizing osteochondral lesions by magnetic resonance imaging. Arthroscopy. 1991;7:101–4.
14. Matthew E. Sailors. Recognition and Treatment of Osteochondritis Dissecans of the Femoral Condyles. J Athl Train. Dec 1994; 29(4): 302, 304, 306.