Uni-compartment knee arthroplasty is an effective treatment for SONK. In this study, knee pain was alleviated and the function of the knee improved after UKA. SONK is a common condition that can be treated non-operatively or with joint-preserving surgical intervention [13, 14]. SONK can progress to articular collapse and end-stage joint osteoarthritis despite medical intervention. Knee arthroplasty for SONK includes both TKA and UKA approaches; however, it remains controversial which approach results in the best surgical outcome for SONK. The indications for UKA are much stricter than those of TKA for patients with osteonecrosis. UKA is utilized in single-compartment osteonecrosis without degenerative changes in other compartments. Intact ligament structures with virtually normal alignment are also required. Several previous studies reported that TKA gave better outcomes than UKA [14, 15]. However, using current surgical techniques, UKA can preserve the anterior cruciate ligament and non-involved cartilage in other knee compartments, all of which are sacrificed in TKA. As a result, UKA is considered a better option for SONK patients with only single compartment involvement. In previous studies, UKA had a higher risk of revision and worse clinical outcomes than TKA for single compartment osteoarthritis [16, 17]. Using a modern implant design and modified surgical techniques, Myers et al. found that inadequate patient selection and improper surgical indication wound resulted in high revision rates and poor clinical outcomes [7, 18, 19]. Kozinn et al. concluded that UKA was contraindicated in patients with inflammatory arthritis, tricompartmental knee arthritis, fixed varus deformity greater than 10°, fixed valgus deformity greater than 5°, flexion contracture greater than 15°, and knee instability without an intact anterior cruciate ligament .
A prospective study of SONK treated with UKA showed significant improvement in OKS post-operatively. UKA appears to be the treatment of choice with the advantage of minimizing bone stock destruction, decreasing the use of bone cement, and better preservation of knee function in comparison to outcomes following TKA .
Chalmers et al. found that the success rates of UKA without revision surgery at 5 and 10 years post-operatively were 89% and 76%, respectively. Three cases (7.1%) were converted to TKA, one for development of lateral osteonecrosis (secondary osteonecrosis due to steroid treatment) and two for lateral compartment degeneration . Secondary osteonecrosis of the knee can be caused by alcohol abuse, high-dose systemic corticosteroid use, or other direct cause . Misdiagnosed secondary osteonecrosis was a risk factor for UKA success and further revision surgery.
Polyethylene wear is another issue, and some studies reported that fixed-bearing UKA may produce substantial wear due to malposition. The incidence of polyethylene wear is rare in mobile-bearing UKA because this prosthesis preserves more of the natural kinematics of the knee. However, all of our cases were conducted with fixed-bearing prostheses, and none showed obvious signs of wear on follow-up radiographic images .
Because the precise etiology of SONK is currently unknown, effective management of the condition remains challenging for orthopedists. In the past, SONK was thought to result from focal ischemia that caused bone necrosis. Another hypothesis was that SONK may be caused by subchondral insufficiency fractures. Subchondral insufficiency fractures may produce fluid accumulation in the bone marrow, bringing on focal ischemia and ultimately necrosis [3, 24]. Subchondral insufficiency fractures may be attributed to pathological lesions, including osteoporosis, meniscus tear, or meniscectomy.
A recent study in support of this alternative hypothesis demonstrated that meniscus tears are related to cartilage destruction in the knee joint. Allaire et al. proposed that MMPRT may alter the knee’s natural biomechanics and increase the peak contact pressure in the joint. The authors even raised the possibility that the effect after MMPRT injury was comparable to the patients’ status-post total medial meniscectomy . The incidence of MRI-identified MMPRT was 69.6% (16/23 cases) in our study cohort. A retrospective analysis by Robertson et al. found a similar high incidence of MRI-identified MMPRT (80% of patients) in SONK. They proposed that femoral overload with increasing interosseous pressure by meniscal discontinuity is one of the causes of SONK . In comparison to patients with knee osteoarthritis, the incidence of MMPRT and the level of posterior tibia slope were higher in SONK patients. Yamagami et al. proposed that MMPRT and higher posterior tibia slope have a greater association with SONK development . Although the definite mechanism remains unknown, many studies have proposed that MMPRT has a key role in the development of SONK.
This study has limitations. First, we utilized a retrospective design with a small number of patients. Second, only short-term follow-up was available. No long-term radiographic outcomes or complication rates from polyethylene wear or implant loosening were available for assessment. Future long-term prospective studies are needed to fully understand the functional outcomes and complication rates.