As the concept of femoroacetabular impingement (FAI) has become accepted , more hip problems are being treated with joint preservation surgeries [5, 46, 61]. These advances in hip preservation are fueled by better diagnostics and technical improvements in both hip arthroscopy and surgical hip dislocation. However, focal chondral and osteochondral defects in the hip remain a therapeutic challenge. Most cartilage repair techniques were introduced to treat lesions in the knee. These include arthroscopic débridement , bone marrow stimulation [21, 32, 52, 58], chondrocyte implantation , and autograft  or allograft transplantation . Second-generation techniques combine the use of scaffolds with bone marrow stimulation or chondrocyte implantation. Two of the more well-known second-generation techniques are autologous matrix-induced chondrogenesis (AMIC) [7, 31, 60], which combines a scaffold with bone marrow stimulation, and matrix-induced autologous chondrocyte implantation (MACI) , which combines a scaffold with chondrocyte implantation.
The majority of focal cartilage lesions caused by FAI are located on the acetabulum [23, 46, 62], although femoral head defects are not infrequent [40, 54]. Acetabular cartilage defects are often treated by débridement of loose flaps, rim trimming, and microfracture of the remaining defect. Improvements in the modified Harris hip score  at a minimum of 12 months’ followup have been reported with this strategy [29, 50]. Chondral and osteochondral lesions of the femoral head are more difficult to treat. Often, these are larger lesions with cystic or sclerotic subchondral bone located in a weightbearing area of the femoral head. Thus, simple types of bone marrow stimulation are not good treatment options and other cartilage restoration procedures should be considered .
Compared with the knee, the hip has more soft tissue coverage and more bony constraint, making hip arthroscopy and open approaches more technically complex and invasive than those for the knee. As such, cartilage restoration techniques that require a two-stage procedure (autologous chondrocyte implantation [ACI]) or an autogenous donor site are more invasive in the hip than in the knee. Osteochondral allograft is a potential option; however, it can be expensive and there are time constraints associated with the availability of a fresh allograft.
Although similar to ACI or MACI, AMIC is less expensive and is a one-stage procedure. AMIC involves application of a fibrin gel in a microfractured or drilled defect, with placement of a collagen Type I/III membrane over both the gel and defect. The addition of the fibrin and collagen membrane stabilizes the microfracture clot and promotes hyaline cartilage formation rather than reparative fibrocartilage [18, 59, 60, 64]. AMIC has been used routinely at our institution to treat large cartilage defects in the knee for more than 5 years. We reasoned it might be useful for treating larger cartilage lesions (> 2 cm2) in the hip and began using the technique in 2009. In another report , the potential etiology of the rare parafoveal femoral head lesions seen in three of our six patients was described in more detail.
However, it is unclear whether the approach relieves symptoms or provides a durable repair. We therefore describe the use of second-generation bone marrow stimulation (AMIC) for treating focal chondral and osteochondral lesions in the hip and present the results of short-term followup in a small series of patients.
The indications for AMIC were full-thickness chondral lesions larger than 2 cm2 or osteochondral lesions larger than 1 cm2 with a bony defect after débridement of necrotic bone in weightbearing regions of the acetabulum or femoral head that could not be unloaded by an osteotomy in patients younger than 35 years with symptoms despite at least 3 months of nonoperative management, including activity modification, physical therapy, medical management, and injections. Contraindications to AMIC were lesions smaller than 2 cm2 that could be adequately managed with microfracture, arthroscopic débridement, or redirectional osteotomies; patients who were unable or unwilling to comply with postoperative rehabilitation and weightbearing protocols; arthritis due to a systemic inflammatory disorder; substantially advanced arthritis involving the majority of both the femur and acetabulum; and lesions in patients older than 35 years. A lesion size of 2 cm2 or larger was chosen as the indication for AMIC because the results of microfracture in lesions beyond this size are less predictable [34, 37]. Analysis of focal cartilage defects in the knee also indicate shear stress on the adjacent cartilage increases for lesions larger 1 cm2 , increasing the risk of symptoms and further cartilage breakdown. Microfracture reportedly improves IKDC and International Cartilage Repair Society (ICRS) scores at 2-year followup when used for chondral lesions of this size [34, 42]. Because a stable bony base is required for microfracture to form fibrocartilage, we extended our indications for AMIC in the hip to osteochondral lesions larger than 1 cm2 as it is unlikely durable fibrocartilage will be produced when microfracture alone is performed for these lesions.
A surgical dislocation of the hip with a stepped trochanteric osteotomy, as has been described in detail elsewhere [19, 55], was used for all patients. After dislocation of the femoral head, the cartilage lesion was evaluated (Fig. 1A-B). Delaminated and unstable cartilage was removed until stable cartilage shoulders were obtained, and the bottom of the defect was débrided with a sharp curette to a stable base. In osteochondral defects, cysts and sclerotic bone were removed until healthy bleeding bone was observed. The base of the defect was drilled with an irrigated 1.6-mm Kirschner wire (instead of bone marrow stimulation performed with a microfracture awl). We chose to drill rather than microfracture as several recent animal studies have observed more anatomic subchondral bone structure and fibrocartilage with drilling [13-15]. Drill holes were placed 2 to 3 mm apart and drilled to a depth of at least 1 cm. Smaller bone bridges were avoided to maintain the mechanical integrity of the loaded subchondral bone. After the sclerotic floor of the defect was prepared, autologous cancellous bone harvested from the stable portion of the greater trochanter was impacted into the defect and secured with a commercially available fibrin glue (Tisseel®; Baxter Healthcare Corp, Deerfield, IL, USA) (Fig. 1C). Removal of the unhealthy bone from the base of the osteochondral defect creates the potential for a large height difference at the chondral surface. To avoid this, healthy autogenous bone graft was used to fill the defect to the chondral tidemark. This technique has been previously described in combination with ACI . The fibrin glue increases the mechanical stability of the local environment for the mesenchymal progenitor cells released from the bone marrow . In some patients, the defect may not be deep enough to require bone grafting. The lesion was then templated with aluminum foil (Fig. 1D). A dry collagen Type I/III membrane (Chondro-Gide®; Geistlich Pharma AG, Wolhusen, Switzerland) was cut slightly smaller than the template because, once the membrane was moistened, it increased in size by 10% to 20%. An overlap of the membrane on the cartilage edge was avoided because it causes increased shear forces on the membrane. The membrane was moistened and placed on the defect with the porous side to the bone. The membrane was sewn into the defect with absorbable fine suture (6-0 polydioxanone). Care was taken to place the knots on the membrane and not on the cartilage. Fibrin glue was then used to cover the knots and seal the edges of the defect (Fig. 1E). The combination of the collagen Type I/III membrane and fibrin glue over the sutures creates a smooth cartilage surface, which reduces friction over the fragile repair, and may encourage chondrocyte differentiation [59, 64].
Postoperatively, all patients remained toe-touch (15-kg) weightbearing with crutches and hip flexion limited to 90° for 6 to 8 weeks postoperatively to protect the healing cartilage and the trochanteric osteotomy. Passive motion using a standard passive motion machine for 6 to 8 hours daily with knee flexion from 0° to 70° was prescribed for the first 6 to 8 weeks. Once postoperative radiographs demonstrated healing of the intertrochanteric osteotomy, weightbearing was advanced, crutches were discontinued, and formal physical therapy was initiated for normalization of gait, ROM, and strength.
Patients and Methods
We retrospectively reviewed all six patients treated with surgical hip dislocation and AMIC for large (> 2-cm2) femoral head or acetabular chondral or osteochondral lesions between March 2009 and December 2010 (Table 1); five femoral head and one acetabular lesions were treated, one chondral and the other five osteochondral. Three of these six patients were also included in a report describing the etiology of the parafoveal femoral head chondral defect . At the request of that journal’s editors, the details of treatment and Tegner and Lysholm outcome scores at 1 year were included in that report although the purpose of the report was to describe the chondral lesion. All patients underwent preoperative MRI to assess the cartilage lesion and additional hip pathology; all were classified as ICRS (Table 2) Grade 3 or 4 lesions . Due to different underlying diagnoses, including FAI and epiphyseal dysplasia, patients underwent a combination of surgical procedures to address associated pathologic conditions. The patients were young, ranging in age from 15 to 31 years (Table 1). All patients participating in our study were educated in detail about the surgical technique, alternatives, advantages and disadvantages, and potential complications. A minimum of 1-year postoperative followup was obtained for four patients (range, 1-2.5 years). One patient was lost to followup and did not respond to repeated attempts at both written and telephone contact. One additional patient was not available for postoperative MRI and did not return the outcome questionnaire due to incarceration. At the time of surgery, all patients gave written consent to publish their outcomes. The study was performed in compliance with our institutional review board.
Clinical and radiographic followups were scheduled at 6 weeks, 6 months, and 12 to 24 months after surgery. In November 2011, we obtained current Oxford Hip Scores and UCLA Activity Scores from the four patients who could be located [43, 44]. A followup MRI was performed 6 months postoperatively to assess lesion healing and resolution of bone marrow edema. All MRIs were performed with a 1.5-T system using a body matrix coil (MAGNETOM® Avanto or Espree; Siemens Medical Solutions, Erlangen, Germany). A single T2 slice 90° to the largest portion of the lesion was chosen for evaluation. Two of us (LMT, MRS) evaluated the quality of repair tissue in consensus, according to a modified magnetic resonance observation of cartilage repair tissue (MOCART) scoring system [38, 39]. The MOCART system is an evaluation of nine variables on a standard MRI comparing the morphology and signal intensity of articular cartilage repair tissue to the adjacent native cartilage (Table 3). The interobserver reliability of the MOCART system has previously been evaluated in a prospective cohort study of patients undergoing matrix-assisted cartilage transplantation for articular cartilage defects larger than 2 cm2 in the knee , with an intraclass correlation coefficient ranging from 0.76 to 1.0, depending on the variable. The score was modified from that originally reported because our institution does not routinely obtain a three-dimensional gradient echo sequence with fat suppression, which is used to evaluate the signal intensity of the repair tissue. A dual T2 fast spin echo sequence is part of our routine MRI protocol. This is also part of the validated MOCART scoring system and is used to determine the repair tissue signal intensity. One of the evaluators (LMT) was a hip preservation fellow who was not involved in any way in the treatment of the patients. The second evaluator (MRS) has extensive experience with cartilage restoration in the knee and provided technical assistance with the AMIC procedure at the time of surgery but was not otherwise involved with the patients’ care.
No intraoperative or immediate postoperative complications occurred. Oxford Hip Scores and UCLA Activity Scores improved for all five patients followed until 1 year (Table 4). Patient 4 was seen 7 months postoperatively with subjectively improved hip ROM and improvement in overall hip function, but due to incarceration, 1-year postoperative outcomes scores could not be obtained (Fig. 2). Patient 2 described groin pain that occurred during training for karate competitions; however, she was able to return to training and competition. On examination, pain was produced in deep flexion and with adduction and internal rotation. The ROM was, however, symmetric to the contralateral side. The patient also underwent an MR arthrogram, which showed possible adhesions . As she is able to train and compete and otherwise has no symptoms at rest or with activities of daily living, the patient elected to forego further evaluation or surgical management of the adhesions. She also had a kissing lesion on the acetabular cartilage. This was repaired but may contribute to her residual symptoms.
The four lesions evaluated by MRI appeared to be completely filled with complete integration of the border zone (Table 4). The quality of the repair tissue was variable. The structure of the repair tissue appeared inhomogeneous for three of four patients. The cartilage signal for two of four patients was isointense when compared to that of the surrounding cartilage and the surface of the repaired cartilage was intact for two of four patients. The surface of the repair tissue was normal for two patients, showed mild fibrillation (< 50%) for one patient, and was damaged in one patient. The subchondral lamina (the subchondral bone plate beneath the repair tissue) was intact for only one patient. The subchondral bone (the bone adjacent to the repair site) appeared normal for two of four patients. The subchondral bone of the other two patients appeared to consist partly of granulation tissue, but no edema, cystic changes, or sclerotic areas were observed. One patient (Patient 2) had possible ventral adhesions; this same patient underwent MR arthrogram, making it impossible to determine whether an effusion was also present. No other patient had an effusion.
The bony constraint and soft tissue coverage in the hip limit the options for repair of larger cartilage defects in the femoral head and acetabulum. AMIC is a second-generation bone marrow stimulation technique developed for the treatment of larger cartilage defects in the knee. We believe AMIC is a reasonable option for cartilage repair in the hip for our stated indications because it is a one-stage technique that is not limited by allograft availability and does not create autograft donor site morbidity. We assessed the short-term (1- to 2.5-year) clinical and radiographic (MRI) outcomes of focal chondral and osteochondral lesions in hips treated with AMIC and surgical hip dislocation.
There are several limitations to this study. First, we are reporting a small series consisting of our initial patients treated with this approach. Second, the followup is short. Third, we do not have preoperative Oxford Hip or UCLA Activity Scores, which would have allowed comparison with our postoperative data. Fourth, five of six patients underwent bone grafting over a drilled defect. Although bone grafting with ACI has been reported , bone grafting an osteochondral defect combined with bone marrow stimulation has not previously been described. The effect of the bone graft on the quality of the cartilage repair tissue is unknown. The effect of the cartilage repair on the surgical outcome is potentially confounded by the other surgical procedures performed at the same time. Similar to the treatment of cartilage defects in the knee, however, we believe the joint should be stabilized and any correctable mechanical abnormalities addressed surgically to protect the healing cartilage and prevent further damage from occurring. The cause of chondral and osteochondral defects occurring in FAI is subject to some debate. While most agree acetabular chondral delamination occurs as a result of shear forces created by the cam deformity [11, 23, 29, 40, 46, 50, 56, 62], the cause of defects occurring remotely to the cam or pincer deformity is subject to more speculation. Charbonnier et al.  demonstrated impingement and secondary femoral head subluxation in dancers with morphologically normal hips, and two studies have demonstrated decreased hip flexion and abduction in patients with FAI [33, 36]. It may be that patients participating in sports or vocations that require deeper, forceful, or repetitive hip flexion and rotation subject their cartilage to similar episodes of dynamic instability secondary to their impingement . To eliminate the potential cause of the chondral damage, we believe patients with impingement and an osteochondral defect should undergo concomitant treatment to address their bony pathomorphology. As such, femoral head osteoplasty or acetabular rim trimming and labral repair should be performed for patients with FAI, as indicated by the specific type of impingement.
We observed improved short-term function in these patients with imaging suggesting some healing after repair of these defects. It is important to remember these are complex cases in young adults with limited treatment options. Fontana et al.  recently reported the results of arthroscopic autologous chondrocyte transplantation (ACT) in the hip with the use of a scaffold. The study reported on patients with full-thickness chondral defects of a size (> 2 cm2) similar to those in our series and compared their outcomes with those of a matched cohort who had undergone arthroscopic débridement. The patients who underwent ACT had clearly better outcomes at 6 years as compared to the débridement group. In contrast to our series, all of their patients had acetabular lesions and no lesion involved the subchondral bone . In the discussion, the authors noted simple débridement for lesions larger than 2 cm2 was not efficacious as there was no change in outcome scores preoperatively to postoperatively. In addition, they mentioned future studies could potentially use microfracture in combination with a scaffold or compare the results of their technique with microfracture .
Most of the studies on AMIC have been published for the knee, although there is also a single case report of AMIC performed for a talar lesion . Gille et al.  reported their intermediate-term (2-year) results, with a stable functional result between 1 and 2 years. Knee-specific outcome and activity scores including the Lysholm, Cincinnati, Tegner, and IKDC scores all improved at 12 and 24 months. Nonetheless, the results were not flawless: three patients were not satisfied and two were referred for TKA. MRI obtained 2 years postoperatively showed bone marrow lesions, osseous hypertrophy, and intralesional osteophytes in some patients. However, 10 of 15 patients had greater than 50% defect filling. The authors did not attempt to correlate the functional results with the radiographic appearance of the lesion. Other smaller cohorts with a minimum of 1-year followup have reported improvement in knee-specific outcome scores [17, 49]. Dhollander et al.  observed intralesional osteophytes on MRI performed 1 to 2 years postoperatively in three of five patients.
Published outcomes of other cartilage repair or restoration procedures in the hip are limited (Table 5). A PubMed search using the terms “osteochondritis OR osteochondrosis OR osteochondral defect OR chondral defect AND hip[ti]” performed in March 2012 produced 339 results. Of these titles, 70 were published in English and pertained to humans. A review of these 70 abstracts revealed 35 were published in the last 30 years and three specifically described the outcome of a cartilage procedure in the hip [1, 3, 48], all of which were case reports of one or two patients. Nonetheless, there are some data regarding the treatment of cartilage lesions in the hip (Table 5). In addition to the series of patients treated with ACT mentioned earlier, there are some large series of patients who have had microfracture in the hip. The results for microfracture in the hip have been reported as part of the treatment for FAI [11, 29, 50]. Haviv et al.  reported their results of patients with FAI and chondral lesions. In their cohort, patients who had microfracture had better outcomes scores in short-term followup than historical control patients who had simple débridement .
Here we describe the use of second-generation bone marrow stimulation, AMIC, as an option for treating chondral and osteochondral defects larger than 2 cm2 in the hip. AMIC has not previously been described for the treatment of these lesions in the hip. The 1- to 2-year results for AMIC in the knee, however, are generally good, with high rates of patient satisfaction . Our short-term results indicate AMIC may be one practical treatment for large cartilage lesions in the hip. Nonetheless, the long-term results of AMIC, including the duration of symptom relief, durability of the repair cartilage, and potential to prevent subsequent osteoarthrosis, remain unknown. As with many other promising surgical techniques, studies with larger cohorts, longer followup, and prospective collection of pre-and postoperative outcomes scores are necessary to determine the answers to these questions and the efficacy of this technique.
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