Management of bilateral osteochondritis dissecans of the trochlea in a skeletally immature patient

Abstract

Osteochondritis dissecans (OCD) lesions are injuries that occur more commonly in the skeletally immature population. In most cases, the aetiology is not well understood, but fortunately, many OCD lesions may heal on their own over time, particularly in skeletally immature patients with open physes. Conversely, if the lesion is considered unstable, surgical intervention may be required. This case demonstrates an especially rare presentation of bilateral OCD lesions within the lateral femoral trochlear facet. The lesions became symptomatic approximately 1 year apart without a specific injury. Non-operative treatment was not recommended in either case due to the size and instability of each lesion. The surgical treatment used an augmented microfracture technique. At 12 and 23 months after surgery, both knees remain asymptomatic and the patient has returned to their desired activities.

Background

Osteochondritis dissecans (OCD) lesions within the knee are typically idiopathic that occur at the subchondral bone. This injury is more common among adolescents as compared with adults.¹ Although the exact incidence of OCD in adolescence remains inconclusive, the literature estimates a range of 2.3/100 000 to 31.6/100 000.^2–4 Furthermore, the true prevalence of bilateral OCD in a skeletally immature population is unknown; however, more recent literature demonstrates a 29% incidence of bilateral disease.⁵ There are a wide range of locations within the knee in which OCD lesions can occur. The most common location of these lesions is the medial femoral condyle (77%); conversely, one of least common (1%), occur at the trochlear groove.⁶

Current literature suggests several possible modalities including both exogenous and endogenous causes of OCD.⁷ Endogenous causes can include genetic predispositions or abnormalities within the subchondral bone making the knee more susceptible to injury. Exogenous injuries include direct trauma to the bone or repetitive stress over time. As research on OCD continues, it has become evident that many lesions may be multifactorial in origin.

This case discusses a young male patient sustaining unstable, rare bilateral OCD lesions which were treated surgically.

Case presentation

A healthy 14-year-old boy presented to clinic having problem of left knee pain after participating in sports. The patient had no history of a prior knee injury or pertinent medical or family history. He did not have a defined trauma to the knee, but he reported a painful pop. The patient initially attempted rest, ice, compression and elevation along with non-steroidal anti-inflammatory drugs therapy. After no relief from symptoms, the patient visited a general orthopaedic surgeon who obtained knee radiographs which revealed open physis bilaterally but were otherwise unremarkable. MRI was ordered, and the patient was subsequently referred to a surgeon specialising in sports medicine.

The left knee examination revealed medial joint line tenderness, medial and lateral parapatellar tenderness, mild effusion and pain with flexion. Testing of the cruciate and collateral ligaments and menisci was unremarkable. There was a palpable loose body present at the lateral gutter. MRI revealed a joint effusion with a displaced osteochondral fracture present in the lateral trochlear groove. Due to the size and instability of the lesion, surgery was recommended. After a thorough discussion of the risk and benefits of surgery, the patient and family elected to proceed with a surgical treatment.

Approximately 1 year later, at the age of 15, the patient presented to clinic with a similar story. While playing sports, he suddenly began experiencing right knee pain. Radiographs were obtained, which demonstrated suprapatellar joint effusion and open physis. Physical examination revealed medial parapatellar tenderness and mild effusion but was otherwise normal. MRI was ordered and revealed an OCD lesion present at the lateral trochlear groove with an additional osseous body extruded into the lateral parapatellar recess. Due to the size and instability of the lesion, non-operative treatment was not recommended, and surgical intervention was agreed on by the patient and his family.

Investigations

Radiographs, MRI, physical examination and diagnostic arthroscopy were used to confirm the diagnosis for each separate injury. Based on the patient’s physical examination and previous radiographs, MRI of the left knee was ordered. The radiologist appreciated an osteochondral fracture of the lateral trochlear groove and a displaced osteochondral fragment present in the lateral joint process on the left knee MRI (figure 1). Diagnostic arthroscopy of the left knee confirmed the findings of the MRI (figure 2).

Figure 1.

T-2 weighted axial (A) and sagittal (B) MRI views of the left knee demonstrating an osteochondral fracture of the lateral trochlear groove and displaced osteochondral fragment in the lateral joint process.

Figure 2.

Intraoperative arthroscopic images of the displaced osteochondral fragment present in the left knee (A) and removed fragment under gross examination (B).

Due to a history of an OCD lesion, physical examination and a similar story in the patient’s right knee, an MRI was obtained. The radiologist appreciated a high stage, unstable OCD lesion present in the lateral trochlear groove with a displaced fragment in the lateral parapatellar recess (figure 3). Diagnostic arthroscopy confirmed the pathology and location of the findings present in the MRI (figure 4).

Figure 3.

T-2 weighted axial (A) and sagittal (B) MRI views of the right knee demonstrating an unstable osteochondritis dissecans lesion in the lateral trochlear groove and displaced osteochondral fragment in the lateral parapatellar recess.

Figure 4.

Intraoperative arthroscopic images of the displaced osteochondral fragment present in the right knee.

Treatment

Several surgical options were discussed; however, the recommended surgery was an arthroscopic debridement, microfracture, osteochondral allograft and removal of loose bodies. The surgery occurred approximately 4 weeks after the symptoms appeared.

Both surgeries began with a diagnostic arthroscopy in which a thorough diagnostic arthroscopy was performed to rule out an additional meniscal, cruciate, or cartilage lesions. Then, the lesion and loose bodies consistent with diagnostic imaging were identified. The loose bodies were removed, and then the microfracture of the lesion was carried out with a curved awl. The damaged cartilage was minced by sucking it up multiple times using a double cut 3.8 mm shaver (Arthrex, Naples, Florida). The cartilage was harvested and captured with a GraftNet (Arthrex) device. A solution of platelet rich plasma mixed with BioCartilage (Arthrex) and the patient’s minced cartilage from the loose body was placed into the region and sealed with fibrin glue (figure 5). On the right side, a larger arthrotomy was used due to the size and location of the defect (figure 6).

Figure 5.

Intraoperative arthroscopic image of the left knee defect filled with a solution of platelet rich plasma mixed with BioCartilage and the patient’s minced cartilage from the loose body.

Figure 6.

Intraoperative arthroscopic image of the right knee after application of the solution of platelet rich plasma mixed with BioCartilage and the patient’s minced cartilage from the loose body.

The patient was at 50% weightbearing for 6 weeks postoperatively; thereafter, full weight bearing was gradually introduced. Formal physical therapy began within 5 days and continued until 12 weeks after surgery. Initial exercises included stretching, straight-leg raises and passive range of motion. Exercises progressed gradually through closed and open chain exercises to dynamic weight training.

Outcome and follow-up

No surgical complications occurred, and the patient successfully progressed through the postoperative physical therapy as directed. Appropriate recovery milestones were met, and the patient was transitioned back to full return of normal activities. At 12 and 23 months postoperative, the patient has been participating in sports without limitation.

Discussion

This case outlines a rare condition present at an uncommon location of the knee bilaterally. Current research is not sufficient to conclude the exact cause for development of OCD lesions; however, it has been observed that both biological and mechanical factors have been linked to the cause of development. Biological factors include genetic cause, deficits of ossification centres and alterations in endocrine factors such as vitamin D and human growth hormone deficiency.^{8 9} Another promising theory includes irregular vascular anatomy of the subchondral bone leading to local ischaemia making the area more susceptible to microtrauma or avascular necrosis. Mechanical factors include tibial spine impingement, discoid meniscus, other biomechanical alterations and traumatic injuries.^10–13 In a systemic review, Andriolo et al found that number of studies linking genetic disorders, followed by biomechanical alterations and injury/overuse as the cause of OCD.¹⁴ There are several theories postulating the simultaneous interplay between both biological and mechanical factors in a common foundation for development of OCD lesions. However, these theories are typically based on low levels of retrospective data and no strong conclusions have been made.

The location of the lesions presented in this case displays an especially uncommon finding. It is known that OCD occurs most commonly in the lateral aspect of the medial femoral condyle.⁶ As previously stated, OCD lesions present at the trochlea are rare, leading to an especially limited selection for literature, and no gold standard for treatment options. Treatment of OCD is guided by clinical and diagnostic imaging to determine the stability of the lesion. Although there are no clear definitions of stability, Wall et al defined a stable OCD lesion as ‘one showing no breach in the articular or the subchondral bone-lesion interface’ and these constructs are commonly used throughout the specialty.¹⁵ According to the most recent guideline summary published by the American Academy for Orthopaedic Surgeons in 2011, current indications for surgical interventions include failure of conservative treatment, presence of loose bodies and detachment of the lesion.¹⁶ Most stable OCD lesions can be successfully treated non-operatively which include immobilisation, as well as restrictions on weight-bearing activity for approximately 3–9 months.⁴ Conversely, it has been shown that unstable OCD lesions left untreated are correlated with early onset of osteoarthritis within the knee.¹⁷ Samora et al conducted a retrospective study looking at the predictors of lesion stability and found that lesions in atypical locations of the knee, such as non-weight-bearing surfaces, are more likely to be unstable and are associated with lower rates of healing when treated non-operatively.¹⁸ The OCD lesions outlined in this case was more advanced, and unstable, which led to the decision of surgical intervention versus non-operative treatment. Leaving these lesions untreated would likely lead to further damage of articular surfaces, likely early onset of osteoarthritis, as well as significant discomfort preventing the patient from participating in desired activities, such as sports.

When surgery is deemed appropriate, controversy arises as there are no gold standard techniques for surgical intervention of OCD lesions. In this case, skeletal immaturity, lesion location and stage of pathogenesis were the main proponents that directed the decision to treat the OCD lesion with an augmented microfracture. Due to the rarity of OCD lesions present at the trochlea, there is limited scientific literature available demonstrating clear optimal techniques in surgical intervention.

The option of only removing the loose body and leaving the cartilage defect alone was recommended against due to the size and location of the lesion. Fixation with a bioabsorbable or metal screw was decided against due to the very thin layer of bone attached to the lesion as seen on MRI. Intraoperative, this was confirmed as well as the remaining bone was quite friable and cracked. An osteochondral allograft plug was decided against due to the location of the underlying physes which would have to be reamed out during recipient site preparation with resulting physeal disruption with angular growth abnormalities. Although microfracture alone of chondral lesions have been shown to be successful at returning patients back to physical activity, the long-term data outcome data remain sparse.¹⁹ Solheim et al conducted a prospective study regarding the long-term outcomes of microfracture procedure in 110 patients with lesions present at various locations of the knee. Researchers found a relatively high rate of reoperation, including conversion to knee arthroplasty at a median follow-up of 12 years.²⁰ Current literature demonstrates that an augmented microfracture is a promising treatment option in cartilaginous defects.²¹ In the case previously described, marrow stimulation (microfracture) and biological scaffolds combined with minced allograft cartilage (BioCartilage), autologous platelet rich plasma were used to fill the defect. The purpose of this technique is to supply a scaffold of native extracellular matrix, including additional cartilaginous growth factors, to improve the degree and quality of healing within the articular defect. This novel technique continues to display favourable results for a less invasive and a potentially more cost-effective way to treat injuries of the articular cartilage. Although short-term outcomes are encouraging, it is unclear regarding the long-term outcomes of this technique.

There is a limited capacity for regeneration of the articular cartilage; thus, it is important to appropriately diagnose and treat this injury to prevent early onset of degenerative joint disease. This case is unique in that a bilateral OCD lesion developed in almost identical positions of each knee. Further research is warranted in this area to fully understand the aetiology and determine a gold standard for treatment.

Learning points.

• Juvenile osteochondritis lesions can be a challenging pathology to treat, and it is important to consider many factors when deciding on the appropriate treatment plan.

• There is no gold standard surgical treatment for unstable osteochondritis dissecans lesions.

• Augmented microfracture technique may be a favourable technique in the treatment of osteochondritis dissecans.