This study was a retrospective analysis of 23 hips patients (39 affected hip joints) with osteonecrosis of the femoral head with stage II of the disease, based on the Ficat-Arlet classification system, underwent core decompression. The main goal was to evaluate the prognostic factors of core decompression surgery in SLE patients suffering from ONHF. Our results revealed that 54% of the joints had increased exacerbation of radiographic deterioration. Hip joint replacement surgery was performed on 33% of the joints. The factors affecting joint prognosis following core decompression revealed that a positive antiphospholipid antibody accelerates the deterioration of the joint radiograph, and the consumption of alendronate (bisphosphonate) has a significant positive effect on patient satisfaction. The cumulative steroid dose (prednisolone) and its continuing treatment following core decompression did not affect the prognosis of the patients.
The incidence of asymptomatic ONFH in SLE is up to 34–44% [16]. In a cross-sectional study that examined 31 hip joints with AVN in 18 patients with lupus in a period of 4 to 18 years (average 12 years), 21 joints (68%) required a total hip replacement [17]. In our study, out of the 39 hip joints, 33.3% of the hip joints underwent total hip arthroplasty at a minimum of 1 year and a maximum of 5 years (average of 3.5 years) from core decompression. The higher percentage of THA (almost 2 times) in that study compared to our study might have been due to the longer follow-up period in that study.
In our study, out of the 39 joints examined, 53.8% of the affected joints showed signs of radiographic deterioration in the follow-up imaging at least 2 years and at most 6 years (average 4.97 years) after core decompression. In a study on 26 joints (19 patients) with osteonecrosis of the femoral head with grade I or II involvement, which underwent core decompression surgery, 17 joints (4.65%) had very good or good results using Ficat criteria. 8 joints (8.3%) required further surgery (hip arthroplasty for 7 joints and osteotomy for 1 joint) [11].
In our study, patients who had abnormal aPL levels were 10.3 times more likely to develop osteonecrosis of the femoral head than patients with normal aPL levels, indicating that high levels of anti-phospholipid antibodies (particularly IgG anti-cardiolipin) play an important role in the development of AVN in SLE patients [18–20]. There have been few studies on the effect of AVN risk factors on its progression in SLE patients. In one study by Mont et al., 18 SLE patients (31 hip joints) with AVN were compared to 48 hip joints in 32 patients with various causes of femoral head AVN. In this study, they stated that core decompression, high levels of anti-phospholipid antibodies, and other AVN risk factors did not affect the progression of AVN deterioration in 18 SLE patients (18 cases with 31 hip joints) [17]. Another cross-sectional study of SLE patients with AVN of the femoral head indicated that the involvement severity of the articular surface of the femoral head was the most important prognostic factor of core decompression, while other factors like corticosteroid consumption and high levels of anti-phospholipid antibodies had no statistically significant effect on the prognosis of core decompression in these diseases [21].
In this study, we have explored the relationship between patients' satisfaction with joint function following core decompression and the taking of bisphosphonate family medicines for the first time. SLE patients with femoral head osteonecrosis who had core decompression surgery and a history of bisphosphonate consumption were 83.2% less dissatisfied with joint function than patients who had no history of taking this medication (P < 0.02). Bisphosphonates (alendronate) have been shown in animal experiments to improve trabecular ossification and microcirculation in the femoral head, as well as to prevent corticosteroid-induced AVN of the femoral head [22]. In addition, an association between osteopenia and AVN has been shown in kidney transplant recipients [23]. There is currently no information on the protective role of bisphosphonates in humans; however, there are few evidence-based studies that bisphosphonates may play a role in ameliorative the symptoms of patients with non-femoral head AVN and delaying the onset of the disease.
In SLE, the most common cause of AVN is corticosteroid usage. Although the pathogenesis of CS-related osteonecrosis is unknown, ischemia is the main cause of AVN. Some of the pathogenic processes of AVN caused by high corticosteroid regimens include fat embolism, increased intraosseous pressure (IOP) due to adipocyte hypertrophy, vasoconstriction, and decreased mesenchymal stem cells (MSC) [24]. According to a meta-analysis study, the mean daily dose, instead of the cumulative dose, was related to the severity of AVN [25]. A cross-sectional study depict that, in a one-year follow-up examination of the hip joint MRI, osteonecrosis was considerably higher in SLE patients than in non-SLE patients taking corticosteroids [26]. In our study, the mean daily dose of corticosteroid (oral prednisolone) before and after core decompression did not have a significant relationship with hip joint prognostic factors.
Other than cyclophosphamide, immunosuppressive medicines including MMF, azathioprine, and methotrexate are linked to an increased incidence of AVN in SLE patients [18]. In patients with bone marrow transplants has been demonstrated that MMF and calcineurin inhibitor consumption increases the incidence of AVN [27]. There is no evidence of the effect of these medicines on the prognosis of joint survival with AVN following core decompression. The result of our study demonstrated that, after core decompression, patients who had high-dose azathioprine therapy were more likely to develop radiographic deterioration of the affected joint and the requirement for total hip replacement. However, independent of other variables impacting the study, azathioprine was unable to sustain a significant relationship with prognostic indicators. To support these findings, we can point out that azathioprine is prescribed for more severe SLE patients. The poor prognosis in azathioprine-treated patients could be attributable to the severity of the underlying disease and administration of higher doses of prednisolone; however, there is no link between azathioprine and AVN exacerbation. According to our findings and other studies, more investigation is required on the role of azathioprine in the survival of AVN joints following core decompression.