Introduction

The success rate of anterior cruciate ligament (ACL) reconstructions is good to excellent, yet the increased number of ACL reconstructions leads inevitably to a rise in complications [1–4]. One of the common complications following ACL reconstruction is anterior knee pain (AKP) [1, 2]. AKP can interfere negatively with the post-operative rehabilitation program and may reduce patient satisfaction and be a cause for re-operation [5]. Identifying the underlying factors under this frequent complication, and finding the means to prevent or correct them can increase patient satisfaction, improve functional scores and reduce the need for re-admission [4–6]. The causes of AKP after ACL reconstruction are multifactorial, but key factors such as range-of-motion deficit due to tunnel malpositioning or Cyclops lesions, increased body mass index, older patient’s age, infrapatellar nerve injury and autograft type have been identified [4–6]. Other authors have failed to correlate AKP with previous epidemiologic studies and have recorded the same prevalence of AKP among patients of different age and sex [7]. This can be attributed to reasons other than patients’ age or donor-site morbidity in the persistence of AKP [5, 8].

AKP can be a challenging diagnosis and the differential is vast for other than post-operative ACL reconstruction. There are a group of patients with patellofemoral (PF) disorders who have underlying non-anatomic factors and they present with a wide range of symptoms from patellar dislocation to pain [9–12]. In these patients, AKP is the result of patellar maltracking, PF impingement and subsequent increased PF pressures or cartilaginous lesions [13]. The importance of extensor mechanism deficiency, lower-limb malalignment and soft-tissue imbalance has been studied extensively, but the most persistent anatomic findings in patients with PF disorders are trochlear dysplasia and patella alta [14–16]. Trochlear dysplasia is a developmental condition in which the distal femur loses its normal concave shape and turns to an abnormal flat or even convex geometry. Dejour has classified trochlear dysplasia in four distinctive types according to the presence of the crossing sign, the supratrochlear spur and/or the double-contour sign (Fig. 1) [17]. Trochlear dysplasia has been directly associated with both recurrent patellar dislocation [18–20] and AKP [21, 22] in patients with patellar instability, since it has been observed in 96 % of patients with PF disorders and in only 3 % of controls [15, 22]. The surgical correction of trochlear dysplasia is done with the sulcus-deepening trochleoplasty procedure, in which the elevated groove is eliminated and the abnormal sulcus is deepened [23–25]; this can also rarely be enriched by the addition of patellar osteotomy in order to achieve a better congruency between the two articulating bones [26]. Some authors have also suggested that trochlear dysplasia may extend more distally to the intercondylar notch and therefore could be more frequent in patients with ACL tears due to a reduced intercondylar notch size that predisposes to ACL injury (Fig. 2) [27].

Fig. 1
figure 1

Dejour’s classification of trochlear dysplasia in four types: type A with the crossing sign (the groove is flush with the facets), type B with the crossing sign and the supratrochlear spur (“bump”), type C with the crossing sign and the double-contour sign (medial hypoplastic condyle), and type D with all three signs

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Fig. 2
figure 2

Intra-operative view of the distal femur with a dysplastic trochlea, that may continue into the intercondylar notch

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Furthermore, patella alta has been biomechanically and clinically linked to increased incidence of AKP [28–31] and present in 30 % of patients with PF disorders and in 0 % of controls [15, 22]. There are also reports of a group of patients with ‘potential patellar instability’, in whom trochlear dysplasia and/or patella alta are present and causing AKP but with no history of patellar dislocation [15].

A potential increased prevalence of signs of PF anatomic anomalies could advise the surgeon to pre-operatively evaluate the PF joint in the ACL-deficient patient or identify an additional source of probable post-operative AKP. The purpose of the present epidemiologic study was to record the radiographic presence of trochlear dysplasia and patella alta in patients who undergo ACL reconstruction as a potential underlying factor for post-operative AKP. The authors tested the hypothesis that the imaging findings of trochlear dysplasia and abnormal patellar height are more frequent in ACL reconstruction patients than those previously recorded in the average population.

Materials and methods

All consecutive cases of skeletally-mature ACL-deficient knees that would undergo ACL reconstruction in three different hospitals were prospectively included from January 2012 to May 2012. Inclusion criteria were: acute and sub-acute (less than six months) ACL injury with no previous ipsilateral knee operation. Patients with chronic ACL tears, prior-to-ACL-injury history of patellar instability or other PF disorders were excluded from the study.

In every case, AP and axial views at 30° flexion were performed while the sagittal weight bearing views were done under fluoroscopy with the posterior femoral condyles superimposed. The presence of trochlear dysplasia was rated using the Dejour’s classification in four distinct types, A to D [17] with the use of true lateral knee X-rays. Patellar height was measured with the use of Caton-Deschamps index on lateral knee X-rays, where values over 1.2 are indicative of patella alta (Fig. 3) [32]. The three chief surgeons who performed the ACL reconstructions and three independent examiners evaluated the X-rays for the diagnosis of trochlear dysplasia and the measurement of patellar height. The type of ACL injury was diagnosed both clinically and subsequently confirmed during arthroscopy to categorize them to full or partial tears.

Fig. 3
figure 3

The Caton-Deschamps index for the evaluation of patellar height is the ratio of AT:AP and has a normal value range of 0.6–1.2. Values less than 0.6 are indicative of patella infera and values greater than 1.2 are indicative of patella alta

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Statistical analysis included the use of chi-square test for qualitative parameters (trochlear dysplasia type) and the use of Mann–Whitney for quantitative parameters (Caton-Deschamps index). Level of statistical significance was set to p < 0.05.

Results

Two hundred sixty-four patients (299 knees) were included throughout the study period. Mean age was 32 ± ten years (range, 17–56). Female to male ratio was 0.4. Thirty-five patients (13.2 %) had bilateral ACL injury. Two hundred seventy-eight (92.9 %) knees had isolated ACL tear. Among them, 254 (84.9 %) had a complete ACL injury and 24 (8.0 %) had a partial ACL tear, which was confirmed during arthroscopy. In 21 cases (7.1 %) there was a concomitant collateral ligament injury.

The evaluation of lateral X-rays for trochlear dysplasia revealed the following findings: 44 (14.7 %) knees had a positive ‘crossing sign’ in the lateral X-rays and 255 (85.3 %) had no sign of trochlear dysplasia (p < 0.01). Among the cases with trochlear dysplasia, 41 (93 %) had type A trochlear dysplasia with the presence only of the ‘crossing sign’ and three (7 %) had type C trochlear dysplasia. There was no significant correlation between the cases with trochlear dysplasia and bilateral ACL injury (p = 0.35).

Patellar height results in the study group included mean Caton-Deschamps index of 1.0 ± 0.14 (range, 0.5–1.4). Twenty (6.6 %) knees had an index of less than 0.8 and two (0.6 %) knees had an index less than 0.6. In contrast, 15 (5.0 %) knees had an abnormal value of more than 1.2, indicating patella alta. The correlation between Caton-Deschamps index > 1.2 and the presence of trochlear dysplasia was non-significant (p = 0.48).

Discussion

The present study records some pre-operative epidemiologic data of patients with ACL injury with emphasis on the imaging of the PF joint. The most important finding of the study is the increased prevalence of trochlear dysplasia in patients with ACL injury, when compared to the incidence of trochlear dysplasia in the general population in the literature.

The prevalence of trochlear dysplasia and patella alta in the control population have been documented before. Dejour et al. showed that trochlear dysplasia with a positive ‘crossing sign’ is present in 96 % of patients with PF disorders, while they recorded it only in 3 % of 194 controls [15]. More recently, Keser et al. studied the occurrence of trochlear dysplasia using the lateral trochlea inclination index of Carrillion [18], in patients with AKP with no apparent aetiology, and found that it was present in 16.5 % of the 109 cases and in 2.7 % of the control group, which consisted of patients for meniscal pathology [21]. In this study, the authors recorded the same prevalence of trochlea dysplasia in controls with the study of Dejour, which was published 14 years ago. Botchu et al. evaluated the presence of trochlear dysplasia in patients with ‘knee pathology’, and found 58 out of 95 cases with trochlear dysplasia [27]. Although the authors confirm that this high prevalence of dysplasia does not correspond to the general population, and that their study population was biased, they found an 8.8-fold increased risk for ACL tear in patients with Dejour type A dysplasia than in patients without dysplasia [27].

In a different study, Dejour et al. reported the prevalence of the ‘crossing sign’ in 18 % of people with ‘potential patellar instability’ [15, 22] who had AKP but no history of patellar dislocation [22]. Our findings suggest that the radiographic prevalence of trochlear dysplasia in ACL-deficient patients (14.7 %) is higher than the one recorded in control groups in different studies (3 % and 2.7 %) and similar to the increased prevalence found in patients with ‘potential patellar instability’ (18 %). On the other hand, patella alta is present in 30 % of patients with ‘objective patellar instability’ with a history of true patellar dislocation, yet in 0 % of controls with no AKP and no PF instability [15, 22]. In the present study, the authors documented the presence of patella alta in 5 % of patients with ACL tears and no history of PF disorders.

The evaluation of the PF joint before ACL reconstruction is not routinely included in the everyday clinical practice and, furthermore, the diagnosis of trochlear dysplasia on X-rays requires specifically true lateral views [33]. If the lateral X-rays have not absolutely superimposed posterior femoral condyles, even small rotation of the femur up to 5° can result in significant under-estimation of the dysplasia [34]. Additionally, the presence of trochlear dysplasia should be evaluated on the sagittal plane (lateral X-rays) or transverse MRI slices rather than axial views of the patella [17, 33]. This is because dysplasia occurs in the most proximal part of the femoral trochlea [15], and the axial views of the patella in 30° of knee flexion, or more, show the tangent view of the more distal part of the trochlea which is usually deep and normal, even in knees with dysplasia [15, 17, 35, 36]. The femoral trochlear can deepen quickly for proximal to distal and therefore, axial patella views may give false-negative results of trochlear dysplasia.

There are patient-related or intrinsic factors affecting the incidence of AKP after ACL reconstruction and surgery-related or extrinsic factors. According to the literature, the most important extrinsic factors affecting AKP after ACL reconstruction are the type of autograft, pathology of the patellar tendon (e.g. ‘tendinitis’ and donor-site morbidity from BPTB harvesting), infrapatellar nerve injury, range-of-motion deficit (e.g. Cyclop’s lesion), aggressive rehabilitation protocols and pre-existing patellofemoral cartilage injuries [3, 5, 8, 37]. These sources of AKP are often a matter of controversy in literature. Some authors document a higher prevalence of AKP after reconstruction with bone-patellar tendon-bone (BPTB) grafts, especially in the early post-operative period, while others record a similar long-term prevalence of AKP among BPTB and hamstring tendon autografts [8, 37, 38]. A recent multicentric study showed that AKP is more frequent among patients treated with BPTB grafts when compared with hamstrings, but the level and the intensity of recorded pain measured in a visual analogue scale, is higher in patients receiving a hamstrings autograft [39].

In general these factors can be a cause of early AKP after ACL reconstruction. On the other hand, important intrinsic factors are increased body mass index, female gender and increased age [40, 41]. Additional intrinsic factors of AKP could be potentially the presence of trochlear dysplasia and patella alta, which in the present study showed an increased incidence among patients undergoing ACL reconstruction.

Post-operative AKP is very often attributed to patellar tendon tendinitis. The authors’ belief is that such a diagnosis should not be made lightly, because ‘tendinitis’ is in fact a diagnosis with specific histological findings and not only clinical symptoms of pain over the patellar tendon. There is not always an easy correlation to the graft used. Some articles report that AKP may occur from 42.0 % to 62 % in the early post-operative period [5, 42] and can remain in up to 20 % of these patients in the long-term, even in cases where the hamstrings were harvested [5, 43, 44]. Most authors agree that the long-term incidence of AKP is not crucially dependent on donor-site-morbidity [45]. BPTB harvesting results in higher AKP, mostly in the early post-operative period [37, 38]. Feller et al. compared the presence of AKP between BPTP and hamstring autografts and found the same incidence at two months post-operatively, but more pain and a significant quadriceps deficit in the BPTB group at four months [42]. This quadriceps muscle deficit and especially the lack of co-ordination between anterior and posterior thigh muscles has been associated with AKP by other authors. Shelbourne et al. recorded the same AKP between ACL reconstruction patients with BPTP and controls when they followed a rehabilitation program focused on quadriceps strengthening and early full extension [46]. They attributed the source of AKP not in donor side morbidity but in flexion contracture and quadriceps muscle weakness. On the other hand, Condouret et al. recorded the same incidence of AKP between BPTB and hamstrings grafts, while finding greater muscle deficit at two years post-operatively in hamstrings (17 %) compared to quadriceps (3 %) [47].

The increased prevalence of trochlear dysplasia in patients with ACL injury that the authors recorded in the present study is considered as an intrinsic factor for which the course cannot be altered by ACL surgery. In this study, the authors did not evaluate the correlation between post-operative AKP and trochlear dysplasia, and therefore safe conclusions for the aetiology of AKP in ACL-deficient patients with dysplasia cannot be made. The rationale of the study was rather an epidemiologic documentation of a sign that is usually found in patients with PF disorders like trochlear dysplasia, in a different group of ACL-deficient patients.

But both the presence of trochlear dysplasia and ACL surgery have been directly or indirectly correlated to the long-term progression to PF arthritis, whose chief complaint is AKP. More specifically, PF arthritis presents constantly with AKP, and other authors have documented that patients with established PF arthritis that required surgical treatment had a history of significantly higher AKP than controls (22 % vs 6 %, p < 0.001) [48]. The risk of long-term arthritis after ACL reconstruction has been questioned in the literature, and the possibility of PF arthritis following ACL reconstruction has been recently re-emphasized [49–51]. Järvelä et al. documented mild to severe PF osteoarthritis in 88.6 % of their patients seven years after ACL reconstruction [49] and also correlated the increased incidence of AKP in this group but, unfortunately, without evaluating for the presence of trochlear dysplasia in these patients [6]. Oiestad et al. documented 26 % of established PF arthritis 12 years after ACL reconstruction, again without checking for the pre-operative presence of similar radiological findings such as trochlear dysplasia [51]. Most recently, Culvenor et al. reviewed the increased incidence of PF arthritis with ACL reconstruction and recommended prevention and treatment strategies with attention to rehabilitation protocols and quadriceps and hamstring muscles coordination in order to minimize this complication [50]. Trochlear dysplasia has been found to be a strong associating factor for future PF arthritis [12, 52–54]. Many authors document the increased incidence of PF arthritis after high-grade dysplasia that may lead to patellar dislocation. But the risk of future PF arthritis from even low-grade dysplasia that does not necessarily lead to patellar dislocation cannot be under-estimated [55, 56]. Further studies that evaluate the correlation of post-operative AKP and future PF arthritis after ACL reconstruction with the presence of trochlear dysplasia, that seems to be increased in these patients, are required.

The clinical importance from the previous data lies on the possible association between post-operative AKP in ACL-deficient patients and the increased presence of trochlear dysplasia. The pre-operative evaluation of the PF joint with true lateral X-rays with attention to the presence of trochlear dysplasia is advised in the ACL-deficient patient. Post-operative AKP should not be dogmatically attributed to ‘tendinitis’, or aggressive rehabilitation. Trochlear dysplasia could probably be an additional risk for post-operative AKP, but cannot weaken the significance of other well-documented concomitant factors of AKP. The presence of dysplasia may adjust the rehabilitation protocols with emphasis on the conservative treatment of PF disorders, in order to attenuate the risk of AKP in the early post-operative period.

Limitations of the study include that there was no control group but we compared our results with previously published data about the prevalence of trochlea dysplasia in controls. Furthermore, there is no correlation between the presence of trochlea dysplasia and AKP, but this is just an epidemiologic study on the prevalence of radiographic signs of trochlear dysplasia in patients undergoing ACL reconstruction.

Conclusions

The most important finding of the study is the increased prevalence of trochlear dysplasia and patella alta in patients with ACL injury, when compared to the incidence of trochlear dysplasia and patella alta in the general population in the literature. This finding could sound as an alert of a possible additional risk factor for post-operative anterior knee pain after ACL reconstruction.