Osteochondritis dissecans, or OCD for short, is not uncommon in clinical practice and is distinguished between primary and secondary. Most believe that it is caused by traumatic osteochondral fractures or repeated mild trauma resulting in impaired blood flow and necrotic detachment of osteochondral bone, while bacterial emboli or fat embolism of the terminal artery and familial inheritance have also been proposed. The fragment consists of cartilage and the bone beneath it.
The fragment is attached to the parent bone with or without a fibrous tip. There is fibrous tissue or fibrocartilage covering the severed surface of the parent bone and fragment and a small amount of new bone formation. Completely free fragments are growing in size as the free body absorbs synovial nutrients. The free body varies in size and number, and joint strangulation may occur. Tip fracture leads to intra-articular hematoma, and joint wear produces proliferative arthritis.
1.Etiology
The cause of this disease is still unclear, there are two theories as follows.
(1) Trauma theory: Frequent and continuous trauma can cause irreparable damage to bone and cartilage, resulting in degeneration, exfoliation or freeing of osteochondral bone. This understanding can explain why the disease is prevalent in athletes or people with high activity levels.
(2) Endocrine and genetic factors theory: The disease can also occur in people who do not exercise much and do not suffer from trauma frequently, so obviously trauma theory is difficult to explain this group of cases.
2.Clinical manifestations
It is common in males between the ages of 16 and 25, and is seen in the knee and elbow joints, but also in the hip, shoulder, ankle or metatarsophalangeal joints. It usually erodes one joint and has no systemic symptoms. There may be dull pain in the joint, aggravated by activity, reduced by rest, and light swelling of the joint. Free bodies may present with joint locking, hematoma, and traumatic arthritis. Joint swelling, effusion, pressure pain, and palpable masses may be detected, and twisting sounds may be heard with restricted movement. Muscle atrophy. The medial and lateral femoral condyles, patellofemoral articular surface, humeral epicondyle, radial tuberosity, and the internal superior talus of the ankle joint can develop, and pressure pain can be induced.
3.Examination and diagnosis
(1) X-ray examination: the typical injury is characterized by limited subchondral bone sclerosis with a clear outline, complete exfoliation and displacement with the surrounding normal bone separation. A translucent defect area can be seen in the femoral condyles, and free bodies can be seen in the joint cavity. Although X-rays are commonly used for this disease, they are of limited diagnostic value for OCD because they do not directly show cartilage and often miss small intraosseous lesions or bony lesions that have not yet been stripped, i.e., they do not allow early detection of the lesion and do not facilitate staging of the lesion.
(MRI is an effective method for early diagnosis and staging of exfoliative osteochondritis, as it can clearly show the morphology and signal changes in the articular cartilage and subchondral bone without damage to the joint.
(3) Arthroscopy: As a less invasive surgical procedure, it has been considered the “gold standard” for evaluating articular cartilage, but in clinical use, arthroscopy has been found to have certain shortcomings compared to MRI. Arthroscopy cannot detect early osteochondral lesions that have not undergone gross morphologic changes, thus causing a discrepancy in the recognition of MRI versus arthroscopy. This is particularly true in type I OCD lesions, and the ability of MRI to reflect cartilage surface contours and thickness challenges the “gold standard” status of arthroscopy.
4. Staging of exfoliative osteochondritis
Stage I: Subchondral bone necrosis followed by involvement of the cartilage in the joint manifestations. The cartilage becomes slightly softer and loses its luster.
Stage II: A part of the cartilage of the articular surface together with a small piece of cancellous bone under it gradually separates from the surrounding normal tissue due to ischemia and necrosis.
Stage III: Further cartilage loss, bone depression at the exfoliation, with fibrous tissue at the bottom, and crater-like changes at the edges.
5.Treatment
(1) Treatment of OCD in children
OCD in children is mostly negative on physical examination, and it is generally believed that the epiphysis has not yet healed. Treatment only requires braking to reduce pain and other symptoms and to prevent fretting. If the swelling and interlocking of the joint is progressively worse, it can be fixed in a tubular cast with the knee flexed at 30°, and activity should be performed as soon as the symptoms disappear, and the healing time can be advanced by 6-12 months by increasing the amount of activity on the X-ray. In recent years, it has been suggested that the failure rate of conservative treatment in children is as high as 50% and that surgery should be performed if conservative treatment fails or if symptoms do not disappear after 3 months.
(2) Treatment of OCD in adults
At present, it is internationally popular to treat OCD by arthroscopic cartilage chipping and drilling, and to treat OCD by cartilage grafting with autologous and allogeneic cartilage, which is also a fashionable treatment method. However, long-term clinical outcomes and a large number of clinical cases have not been reported.