Predictive factors for new onset or progression of knee osteoarthritis one year after trauma: MRI follow-up in general practice

We evaluated prognostic factors, including initial MRI findings after knee trauma, for new onset or progression of OA of the femorotibial joint, as assessed by follow-up MRI after one year. Unlike previously published studies on this subject, we conducted this study in the general practice population as most patients with traumatic knee injury are managed in a primary care setting in our country. In the univariate logistic regression analysis, higher age (>50 years), higher body mass index (>25 kg/m2), and bone marrow oedema were associated with new or progressive osteoarthritic changes of the femorotibial joint one year after trauma. In multivariate logistic regression analysis, however, only bone marrow oedema was statistically significant and it was found to be a strong predictor. Whereas previously published studies focused on the long-term (2 years and more) risk of developing OA after knee injury, we focused on the risk of developing MRI signs of OA during the first year following trauma [7, 8, 24].

Both higher age and higher body mass index were identified as risk factors for progression of knee osteoarthritis in previous case control studies and population based studies [2, 4, 25]. Although we only found this association in univariate logistic regression analysis, we kept these variables in the model, as these are established risk factors for osteoarthritis. It is possible that the number of patients was too small to demonstrate significance. Apparently bone marrow oedema is more important in the onset or progression of knee osteoarthritis than the other two risk factors.

Our findings are consistent with other reports on bone marrow oedema. In the Pond-Nuki dog model of OA, bone marrow lesions were considered a very early sign of OA [10]. In a longitudinal study by Felson et al. bone marrow oedema was suggested to be a powerful predictor of disease progression in non-traumatically injured patients with symptomatic OA of the knee [9]. Kubota et al. recently found a relationship between bone marrow abnormalities and the progression of knee OA [26].

Histopathologically, bone marrow oedema after traumatic knee injury (also referred to as bone bruise) is thought to be the result of microfractures and haemorrhage in the subcortical trabecular bone. Bone bruise-related cartilage changes are reported to be the result of chondrocyte degeneration with proteoglycan loss [27]. As damage to the articular cartilage is thought to be an important factor in the development of OA, this may explain the relationship between traumatic bone marrow oedema and early progression of OA.

In a previous study, we found that the median healing time of post-traumatic bone bruises in our study group was 42.1 weeks [28]. The present study suggests that although the bone bruise itself is healed within a year, a long-term effect may be initiated by this lesion, i.e. the development of osteoarthritic change of the knee joint.

Our study has several limitations. We only evaluated the femorotibial joint because there were too few patients (n = 4) with new onset or progressive patellofemoral OA to justify a separate logistic regression analysis. We considered that a pooled analysis of these joints would be meaningless, because the pathogenesis of femorotibial and patellofemoral OA and the effect of trauma is probably different. In recent MRI-based studies on OA, the Whole Organ Magnetic Resonance Imaging Score (WORMS) and Knee Osteoarthritis Scoring System (KOSS) have been used to evaluate the severity of degenerative change [15, 18]. At the time of the baseline MRI performed in our study (2002–2003), these semi-quantitative scoring systems had not been introduced, although the items scored were almost identical to KOSS. For reasons of comparability and to avoid interfering with the prospective study design, we used the KOSS items for the evaluation of progression of OA, but we continued using the adapted Kellgren and Lawrence system for grading OA on the 1-year follow-up MRI [19]. The outcome was defined as any increase on the Kellgren and Lawrence scale. We acknowledge that this refers to a heterogeneous group of patients including those with new onset OA and those with progression of pre-existing osteoarthritic changes. Most patients with progression of OA on MRI, however, had no OA initially, indicating that the results of this study were largely based on patients who developed new onset degenerative change within one year of trauma. Most of these patients developed mild degenerative change of Kellgren and Lawrence grade 1–2 severity. As the contralateral knee was not imaged, we cannot exclude that degeneration as part of the natural history explains part of our findings. Furthermore, which proportion of osteoarthritic change is attributable to trauma is unknown, but whether or not the OA is attributable to the trauma, although interesting pathophysiologically, is clinically less relevant. The important point is that in a patient with knee injury, bone marrow oedema predicts the development of early OA.

We performed our study in the primary care setting, and consequently patients with more severe traumatic knee injuries were not included because they were referred to secondary care immediately. This may explain the relatively limited number of meniscal injuries and cruciate ligament injuries in our patient population, which implied a limited power to demonstrate a statistically significant association between these lesions and early progression of OA. The true extent to which meniscal damage and cruciate ligament injuries predict early progression of OA may be underestimated in our study, as both types of lesions have been reported to be risk factors for progression of OA [6‐8].

As it was not the aim of the study to evaluate treatment for traumatic knee lesions, we did not record in detail what procedure was performed in the operated patients. To explore the consequences of this limitation, we performed a sensitivity analysis excluding the operated patients. The same prognostic factor with a similar odds ratio was found, indicating that the results of the analysis were not influenced by the type of treatment, underscoring the robustness of the model.

We found a significant association between new onset or progression of femorotibial OA at follow-up MRI and clinical outcome as measured by perceived recovery. All patients in our study sustained a knee injury resulting in acute trauma-related symptoms. One year after trauma the expected natural healing course would be complete recovery or at least strong improvement. As the disabling symptoms in the initial stage after trauma are no longer present one year after trauma, a perceived recovery less than “strong improvement” in all likelihood reflects the effect of new onset or progressive OA. In light of our results, this stresses the importance of identifying those patients with bone bruise in the initial stage after trauma and those with no or minor improvement of clinical outcome after trauma, as these patients are at high risk of developing new onset OA. In the future these patients may benefit from the development of treatment strategies targeting bone bruises.

In conclusion, the results of this study demonstrate that bone marrow oedema on initial MRI after knee trauma is a strong predictor, and in multivariable analysis the only predictor, of new onset and progression of knee osteoarthritis on 1-year follow-up MRI, which is reflected in the clinical outcome.