Focal chondral defects ( FCDs ) constitute a common finding, with a reported incidence of 4.2% and 6.2% in the general population in patients younger than 40, resulting in more than 200,000 surgical procedures per year ( Fig. 22.1 ). , Furthermore, the prevalence is reported to be as high as 36% in athletes. Importantly, if these lesions are not addressed in a timely manner, they have been reported to worsen over time and may progress to more diffuse osteoarthritis (OA). The treatment of FCD remains a challenge because cartilage repair procedures have failed to reproduce native cartilage to date. ,
The cause of FCD is multifactorial. One well-known cause is osteochondritis dissecans (OCD), a condition in which the subchondral bone and overlying articular cartilage detach from the underlying bony surface, occasionally manifesting as multiple FCD. The incidence of OCD is between 15 and 29 per 100,000. More commonly, FCDs are the result of trauma. Indeed, injuries resulting in acute instability such as knee dislocation and subluxation may also result in the development of articular cartilage lesions. Approximately half of patellofemoral FCDs occur in the setting of a traumatic injury. Additionally, chronic degenerative changes predispose to articular lesions as the result of repetitive microtrauma.
Although cartilage research has grown exponentially, basic science and clinical studies focusing on its foundation, namely the subchondral bone, have not received the same attention. The subchondral bone provides mechanical and biological support for the overlying articular cartilage, and it undergoes constant adaptation in response to changes in the biomechanical environment of the joint. Consequently, subchondral bone lesions are commonly associated with cartilage lesions. An understanding of this anatomy is essential in cases in which the subchondral bone is compromised and recognition of the extent of the lesion may guide treatment and outcomes.
Treatment of FCD has traditionally been managed nonoperatively; however, the literature suggests that somewhere between 11% and 40% of all patients younger than 40 who underwent arthroscopic surgery for other reasons had identifiable and treatable chondral injuries that were unaddressed, which may improve outcomes. , , An emphasis on the surgical management of FCD has evolved with the advent of improved biotechnology and surgical techniques to address FCD. In particular, there has been a shift towards cartilage reparative and regenerative procedures in an effort to restore cartilage, prevent further cartilage degeneration, and reduce morbidity.
Several major procedures are considered when treating FCD. These procedures are associated with favourable, reproducible outcomes and include microfracture, osteochondral allograft transplantation (OCA), osteochondral autologous transplantation (OAT), matrix-induced autologous chondrocyte implantation (MACI, Sanofi, Boston, MA, USA), minced cartilage procedures (DeNovo Natural Tissue (NT), Zimmer Inc., Warsaw, IN, USA), viable osteochondral surface allografts (Cartiform, Osiris, Inc., Naples, FL, USA; and Prochondrix, AlloSource, Denver, CO, USA), extracellular matrix scaffolds (BioCartilage, Arthrex, Inc.) and single-stage autologous options (GraftNet, Arthrex, Inc.). Given the array of treatment options, the challenge lies in determining which intervention or combination of interventions is most appropriate given patient- and defect-specific characteristics. As these restorative techniques become more prevalent, it is imperative to provide an update on the outcomes and indications for these procedures to disseminate standards of treatment and to optimize patient outcomes.
The purpose of this chapter is to provide a comprehensive review of FCDs of the knee and provide the treating surgeon with a thorough understanding of concepts from diagnosis to rehabilitation. In particular, we provide treatment algorithms based on current practice and indications to help guide treatment. Conservative and surgical approaches to the treatment of these defects are described, as well as recommended postoperative rehabilitation. For each surgical approach, a discussion on clinical, radiographic, and outcome survivorship, when available, follow. Finally, future directions for the field of cartilage repair are discussed.
Microscopic Anatomy of Articular Cartilage
Articular cartilage consists of five different zones, which can be distinguished based on the morphology and orientation of collagen fibrils. In the superficial zone (zone 1), the collagen fibres are tangentially oriented into tightly packed parallel laminae that radiate vertically from the calcified zone. Zone 2, or the intermediate zone, contains randomly oriented collagen fibrils. Zone 3, which is also referred to as the radial zone, is the thickest layer with the highest concentration of proteoglycans and water. The tidemark serves as the junction between the calcified and uncalcified cartilage matrix (zone 4). Lastly the zone of calcification (zone 5) serves as an anchor to a complex network of collagen fibrils ( Fig. 22.2 ).
When undiagnosed or left untreated, FCD has the potential to progress towards further cartilage damage and, according to some studies, OA. , Once symptomatic, FCDs have a propensity for continued symptom progression over variable periods depending on comorbidities and patient-specific factors. Early management is important to restore normal joint congruity, pressure distribution and normal knee kinematics. A timely diagnosis allows for appropriate consideration of the various treatment options. Because outcomes are highly dependent on the underlying disease, the more precise a diagnosis is preoperatively, the better the algorithm can be tailored to successfully treat these injuries. FCD is diagnosed through a combination of patient history; physical examination; imaging, including plain radiographs and magnetic resonance imaging; biomarker analysis; and arthroscopy.
As in any diagnostic work-up, it is important to obtain a comprehensive history from any patient that complains of knee pain, particularly because of the overlapping symptoms of cartilage defects and intraarticular pathological conditions. Sports participation is the most common inciting event shared among those with a diagnosis of chondral lesions. Approximately half of patellofemoral FCDs occur in the setting of a traumatic injury. Patients with FCDs are usually young, active and able to carry out activities of daily living (ADLs), although they may complain of pain with specific activities, such as deep squats or cutting. Notably, an activity or ‘trauma’ may not necessarily cause the FCD but rather incite the onset of symptoms on a preexisting yet asymptomatic FCD, resulting from localised degeneration.
Pain is the most common presenting complaint for patients with FCDs. This can present acutely in the setting of injury or sudden load or insidiously in the case of repetitive microtrauma or OCD. This is classically reported with weightbearing and localised to the same compartment as the defect. Pain that worsens with flexion suggests a more posterior lesion. Patellofemoral articular defects typically present as anterior knee pain. However, it is not uncommon for patients to report pain located retropatellar, peripatellar or, in the instance of trochlear defects, posteriorly in the popliteal area. Considering that articular cartilage is aneural, the pain often originates from surrounding structures, including capsular or synovial irritation and overload of the subchondral bone resulting in loss of tissue homeostasis. Therefore, if a FCD is identified in the context of pain-free tissue homoeostasis, the structural cartilage defect may not be of clinical significance. If pain and loss of tissue homoeostasis are present, other causes of the pain must also remain on the differential despite a high clinical suspicion.
Activity-related swelling should raise suspicion for a possible FCDs. The presence of this finding in the absence of pain can help exclude other potential pathological conditions. For example, patellofemoral pain syndrome may also present as swelling with activity but is more often than not painful. Activity-related swelling and, in particular, joint effusion indicate more advanced disease. Diffuse cartilage damage more reliably presents with subtle decreases in range of motion, which has a predilection to limit flexion earlier than extension. These patients also present with diffuse rather than focal pain during activity. For the previously mentioned reasons, it is important to differentiate an isolated FCD from an ongoing osteoarthritic process that has patchy diffuse involvement of the cartilage and results in pain as a result of loss of generalised tissue homoeostasis.
To better understand the best course of treatment, it is critical to obtain a history of any previous treatments that the patient has received to the symptomatic knee, particularly previous injections (cortisone, hyaluronic acid, platelet-rich plasma (PRP)) and surgeries. Insufficient rehabilitation or inappropriately timed return to high-load activities after past surgeries is a common source of symptoms when a patient has already undergone an operation on the ipsilateral knee. This should be evaluated as a potential source of pain before considering a costly work-up or revision surgery.
The physical examination should begin with a gait analysis followed by evaluation of the symptomatic knee joint for effusion, deformity, contracture, malalignment and patellar maltracking. An OCD-derived FCD at the lateral aspect of the medial femoral condyle can cause the patient to ambulate with an antalgic gait or with the affected leg in obligate external rotation (Wilson sign) as a compensatory mechanism to avoid tibial spine impingement. In patellofemoral FCDs, gait abnormalities, such as in-toeing or hip abductor weakness, are commonly seen. Additionally, it is common to see femoral anteversion and valgus malalignment of the lower extremity. Patients with FCDs usually have normal range of motion and focal tenderness over palpable areas along the lateral or medial femoral condyles. Joint line tenderness is commonly elicited when the lesion affects the femoral condyle and tibial plateau. However, it must be recognised that neither a patient’s history nor physical examination are sensitive or specific for differentiating cartilage defects from other intraarticular derangements but may only raise clinical suspicion to pursue further work-up.
First-line imaging for the approach to FCDs consists of conventional cartilage radiographs – in particular, bilateral standing anteroposterior (AP), 45-degree flexion weightbearing posteroanterior (PA; Rosenberg view), and nonweightbearing lateral and patella sunrise views (Merchant view). These views allow for evaluation of pathological joint conditions, such as degenerative changes in the tibiofemoral and patellofemoral joints, trochlear dysplasia, and abnormal patella height, tilt and subluxation. The Merchant view is useful to determine joint space narrowing in OA of the patellofemoral articulation. In most cases, FCDs will not be apparent on plain radiographs because most lesions are extraosseous; however, this imaging modality can detect lesions that involve subchondral bone and lead to FCD, such as OCD. The 45-degree flexion PA radiographs are particularly helpful to diagnose fairly large OCD lesions along the posterior femoral condyles. When OCD are suspected, contralateral knee radiographs can be considered given the high incidence of bilateral involvement. Radiographic findings consistent with an OCD include an area of osteosclerotic bone, with a high-intensity line between the defect and epiphysis. Radiographs should be assessed for radiolucencies, subchondral cysts, sclerosis, fragmentation, loose bodies, joint space narrowing and physeal status because these can affect the treatment algorithm. The long-leg axial alignment radiograph is the final view implicated in suspected FCD evaluation and is of utmost importance to determine the mechanical alignment in patients with known or suspected chondral defects. The benefit of this view is that it confers the ability to determine whether the symptomatic knee requires malalignment correction with a concomitant osteotomy. It is useful to obtain these images with a radiological marker alongside the knee to allow for correction of magnification and accurate determination of appropriately sized donor tissue if needed depending on surgical approach.
Magnetic resonance imaging (MRI) is an effective imaging modality for evaluating articular cartilage and the subchondral bed. Although determining the size of a lesion on imaging is helpful for prognostic and surgical planning purposes, MRI often underestimates lesion size by as much as 60%. Moreover, the appearance of cartilage lesions on MRI is often inconsistent with clinical symptoms and arthroscopic findings. Novel MRI techniques such as the delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) and T2 relaxation time mapping have shown great potential in the evaluation of articular cartilage, although these technologies are not widely available and not routinely used for clinical purposes. dGEMRIC tags glycosaminoglycan (GAG) content in cartilage and can be helpful in the diagnosis of early knee OA and cartilage health after ligament rupture. This imaging modality also allows for measurement of compressive stiffness after cartilage repair procedures. ,
T2 relaxation time mapping, an emerging MRI parameter that represents the internuclear reaction secondary to transverse relaxation of hydrogen ions, has demonstrated potential in measuring the collagen content of cartilage. The benefit of this test is the ability to evaluate cartilage degeneration from time of injury, thus providing information about optimal timing for surgical intervention. Such advances in imaging allows for the ascertainment of objective information, which helps to determine the optimal window and treatment methodology. However, because they are emerging technologies the authors of this chapter do not routinely use these MRI-based modalities in the evaluation of patients with FCD.
Cartilage biomarker analysis is a novel diagnostic tool for detecting the presence of chondral damage. Several type II collagen degradation markers, specifically neoepitope specific for type II collagen cleavage (C2C), cartilage oligomeric matrix protein precursor (COMP) and C-propeptide of type II procollagen (CPII), as well as type II collagen synthesis markers (serum PIIANP), have been identified as potential indicators of cartilage degradation. These precursor proteins are processed by proteases before incorporation into fibrils, thus releasing markers that are then detectable in serum and urine assays. The relative levels of collagen synthesis biomarkers and degradation products can be used to gauge the extent of cartilage turnover occurring at the articular surface.
A number of assays exist that are specifically designed to detect these propeptide levels. Although initial studies have reported promising results in the detection of osteoarthritic changes in the joint, there is a paucity of literature that affirms the efficacy of the use of these biomarkers in detection of FCDs. Future studies in this area are underway to validate these biochemical markers as a tool for early detection of morphological changes within the joint with the hopes to help guide the timing and nature of future treatment.
Diagnostic arthroscopy remains the gold standard for the evaluation of intraarticular pathological conditions of the knee. This minimally invasive diagnostic procedure allows for direct identification and classification of FCDs, as well as detection of any concomitant injuries or additional articular cartilage pathological condition that may need to be addressed in place of or in addition to the FCD. A simple debridement during the procedure may help improve symptomatic lesions and delay treatment of FCDs in almost 60% of patients. During arthroscopy, the chondral defect size can be measured and graded according to standardised criteria systems: the Outerbridge or International Cartilage Repair Society (ICRS) criteria ( Table 22.1 ).
|Grade||Outerbridge Grading System||International Cartilage Rating Systems (ICRS)|
|I||Cartilage with softening and swelling||Superficial lesions, fissures, cracks, indentations|
|II||Partial-thickness defect with fissures on the surface that do not reach subchondral bone or exceed 1.5 cm in diameter||Fraying lesions extending down to <50% of cartilage depth|
|III||Defect extends to level of subchondral bone with a diameter of more than 1.5 cm||Partial loss of cartilage thickness, cartilage defects extending down >50% of cartilage depth|
|IV||Exposed subchondral bone head||Complete loss of cartilage thickness, bone only|
The size and location of the lesion play a large role in management; therefore it is important to directly document and probe these lesions during arthroscopy. Defect size, patient factors and subchondral bone involvement ultimately contribute to the treatment decision.
Nonsurgical management of symptomatic FCD of the knee has a limited role given the underlying mechanism of the defect and the biological nature of cartilage, which limits self-resolution. Nonsurgical management of these defects is incapable of restoring the loss of articular cartilage because of the poor intrinsic capacity for healing inherent in cartilage. This is especially true once the FCD is directly correlated as a symptom generator that impairs activity levels and causes sufficient pain or swelling. Alternatively, nonsurgical management, when successful, can lead to transient pain relief in patients with symptomatic focal FCD but is unlikely to provide long-term relief.
Nonsurgical management of FCD of the knee consists of a set of noninvasive options with the intention to maintain function and minimise pain. The use of nonsteroidal anti-inflammatory (NSAID) medications, chondroprotective agents (glucosamine, chondroitin phosphate), intraarticular injections (corticosteroids, hyaluronic acid, PRP), weight loss, physical therapy, activity modification and knee braces may all provide symptomatic benefit in these patients, depending on the severity and progression of the disease. However, it is important to note that these agents do not diminish the rate of progression of cartilage loss, nor do they restore the structural integrity of the articular cartilage.
The long-term results of conservative management are not well studied. In a prospective study of 28 athletes with isolated chondral defects confirmed radiographically, Messner and Maletius investigated the long-term outcomes of these patients to better understand prognosis. At 14-year follow-up, the majority of patients (78.6%) endorsed good or excellent knee function; however, more than 50% of these patients demonstrated interval increases of abnormal findings, with 12 patients demonstrating joint space reduction. The authors concluded that conservative treatment was not useful for modifying disease progression, despite maintaining self-perceived function.
Surgical Treatment Algorithm
An increasing body of evidence suggests that symptomatic FCDs need to be addressed surgically because of the potential for both worsening of associated symptoms and further progression of cartilage degeneration. , , Moreover, full-thickness FCDs have been associated with a greater risk of total knee arthroplasty (TKA) compared with moderate OA. Therefore it is imperative for the treating knee surgeon to understand indications and approaches for the surgical intervention of FCD.
The goal of treating symptomatic FCD is to restore the osteochondral unit in an anatomical fashion while maintaining the supporting subchondral bone and cartilage and minimizing the surgical burden on the patient. The expectation after management of these lesions is pain relief and return to previous level of activity without limitation. The algorithm for treatment of FCD is constantly evolving as different treatment techniques are developed and tested. Before addressing the FCD, the knee requires a comprehensive evaluation with particular attention to extrinsic factors that could contribute to the symptoms or affect the integrity of the planned intervention.
Extrinsic factors that must be considered include malalignment, concomitant meniscal deficiency, ligament insufficiency and knee instability. If present, these concomitant extrinsic factors can be treated with the appropriate intervention simultaneously ( Fig. 22.3 ): for malalignment, a simultaneous or staged osteotomy (high tibial, distal femoral or tibial tuberosity); for meniscal deficiency, a meniscal repair or meniscal allograft transplantation; for ligament insufficiency and knee instability, a ligament reconstruction or repair, respectively. It is imperative to both identify and address the existence of these pathological conditions because failure to do so will compromise the outcomes of FCD treatment.
Extrinsic Factor I: Malalignment
Malalignment of the tibiofemoral joint can predispose the affected compartment to undue mechanical stress that accelerates the development and progression of intraarticular pathological conditions. If varus malalignment is present in the setting of medial femoral condyle disease, a valgus-producing proximal tibial osteotomy (PTO) should be performed to unload the articular surface and repair the site. Similarly, valgus malalignment can be addressed with a distal femoral osteotomy, a closing wedge PTO (CWPTO) or proximal lateral opening tibial varus osteotomy to off-load the lateral compartment. Failure to correct malalignment has been reported to lead to inferior outcomes after FCD treatment. Moreover, improved functional status and symptom relief have been reported in combined osteotomy and cartilage surgery. Kahlenberg et al. reported on 827 patients who underwent high tibial osteotomies (HTOs) and cartilage repair or restoration surgery with 2-year follow-up and demonstrated improved clinical outcomes with low rates of complications (10.3%). Malalignment should be corrected in conjunction with FCD treatment to avoid subjecting the treated lesion to inappropriate mechanical stress.
Extrinsic Factor II: Meniscal Pathological Conditions
Cartilage structure and meniscal integrity are closely intertwined. Failure to address either defect during surgery can potentiate the progression of disease. For example, if cartilage procedures are performed in patients who are meniscus deficient, increased contact pressure on the implanted cartilage, graft or developing fibrocartilage may ensue and jeopardise the procedure. In cases where the damaged meniscus is not amenable to repair or has been previously removed in a subtotal meniscectomy, a meniscus allograft transplantation (MAT) in addition to addressing the chondral defect is a viable surgical solution. Success with MAT has been demonstrated with judicious selection criteria; however, meniscal insufficiency in the setting of a FCD, typically on the femoral side, is one of the most challenging pathological conditions to treat. When performed in combination, our preferred technique for addressing the meniscus is through an arthroscopic technique, and the cartilage restoration procedure is then performed using an appropriate technique for the indicated procedure (i.e., arthroscopic for microfracture, OAT or MACI versus open for OCA). A systematic review evaluating six studies including 110 patients at a mean follow-up of 36 months found that combined MAT and cartilage restoration or repair had similar outcomes to isolated cartilage repair as determined by the Lysholm Knee Questionnaire, Knee Injury and Osteoarthritis Outcome Score (KOOS), International Knee Documentation Committee (IKDC), Tegner Activity Scale, Modified Hospital for Special Surgery (HSS) Knee Rating Scale and 36-item Short Form Health Survey (SF-36); however, a higher reoperation rate was observed with the combined procedure. The available clinical studies reporting outcomes after combined meniscus and femoral OCA are encouraging as a viable and predictable joint preservation strategy. ,
Extrinsic Factor III: Ligamentous Insufficiency and Knee Instability
Ligamentous insufficiency and instability of the knee necessitates ligament reconstruction or repair to avoid suboptimal outcomes after FCD treatment. Failure to address concomitant instability or ligamentous insufficiency may result in jeopardisation of the restored chondral surface through abnormal joint kinematics, further osteochondral damage, and predisposition to advanced progression of OA. Accordingly, we recommend performing primary ligamentous reconstruction, addressing the chondral defect and, if only the subchondral surface is jeopardised, adding bone marrow aspirate concentrate (BMAC) (see Fig. 22.3 ). Addressing ligament deficiencies in addition to FCD has been shown to be safe and efficacious. A retrospective comparative study of 75 patients undergoing OAT who had either anterior cruciate ligament (ACL)-intact or ACL-reconstructed knees demonstrated statistically similar failure rates and clinical outcomes at a minimum of 2 years follow-up.
Furthermore, it has been suggested that multiple extrinsic factors, if present, can be addressed simultaneously with good outcomes. Schuster et al. reported on 23 knees that underwent combined ACL reconstruction, PTO and chondral abrasion or microfracture and found significant improvements in the IKDC score at 5-year follow-up. They noted that only four ACL grafts were insufficient at final follow-up. Therefore the surgeon should not be hesitant to address all deficiencies to best restore the anatomy and to provide the patient with the best chance for an excellent outcome.
After extrinsic causes of FCD progression have been addressed, attention can be turned to the FCD itself. Generally these management options can be grouped into three categories: palliative (debridement), reparative (marrow stimulation techniques), and restorative (osteochondral grafting, chondrocyte implantation and cellular techniques). All these techniques have been shown to provide therapeutic benefit. The challenge is determining which intervention is most appropriate given the clinical presentation and chondral defect characteristics. This decision-making process requires a patient-specific focus and consideration of multiple factors that often extend beyond the realm of obvious pathological conditions. These include age, body mass index, presentation (weightbearing pain, nonweightbearing pain, swelling, catching, clicking and aggravating manoeuvres such as stair climbing or descending), occupation, risk aversion (willingness to pursue other surgical options should the primary therapy fail), surgical history and compliance with previous interventions.
Specific characteristics of the defect also need to be understood in order to offer the correct treatment options. Size, location, number, depth and geometry are all defect-specific variables that need to be considered before selecting an appropriate intervention. The condition of subchondral bone and surrounding cartilage and the degree of containment should also be noted. The quality of cartilage on the opposing surface is another important factor that is often overlooked. Even minimal articular wear can have implications on the outcome of these interventions. A good understanding of each variable and how they will be addressed will help ensure a good prognosis for the patient.
Patellofemoral lesions can be addressed with simultaneous realignment procedures to unload the patellofemoral compartment and protect the cartilage repair site. Traditional anteromedialisation of the tibial tuberosity is an effective treatment option when the FCD is on the inferolateral aspect of the patellofemoral joint. Medial patellofemoral lesions are treated with a more vertically oriented anteromedialisation or isolated anteriorisation. For a more detailed description of patellofemoral joint disease and treatment options, please refer to the corresponding chapter in this book.
The treatment algorithm for chondral lesions is typically guided by the presence or absence of comorbid extrinsic factors, lesion size, location of the lesion and activity level of the patient. Primary repair is the standard of care for any chondral injury that is amenable to fixation. These include any acute osteochondral fragments and any unstable or in situ OCD lesions. It is essential to fix large fragments (more than 1 cm 2 ) of the weightbearing portion of the femoral condyles. A primary repair is carried out through several steps: (1) elevation of the unstable fragment; (2) debridement of the fibrous base and possible microfracture using drilling, rather than awls, if necessary to stimulate healing via bone marrow product consolidation; (3) bone grafting of areas of cystic changes or bone loss; and finally (4) rigid fixation of the fragment under compression. The author’s preferred technique is to use headless differentially pitched metallic compression screws that are removed after a period of 8 to 10 weeks of protected weightbearing to ensure healing and to prevent the screws from becoming prominent should the osteochondral fragment subside over time. Second-look arthroscopy for hardware removal just before a transition to full weight bearing for tibiofemoral lesions can be used to examine the osteochondral defect and evaluate the success of the procedure. This can help guide future recommendations regarding the timing and extent of return to sport.
When a lesion is not appropriate for primary repair, a treatment algorithm has been developed that relies on a graduated surgical plan, addressing the pathological condition while minimising iatrogenic damage (see Fig. 22.3 ). The more invasive salvage options are reserved for when these first-line treatments fail.
First-line treatment typically consists of debridement, abrasion arthroplasty or marrow stimulation techniques, the most common being microfracture. Debridement involves an arthroscopically performed technique where unstable damaged articular cartilage is debrided, potentially reducing the biological burden to the joint and reducing mechanical symptoms caused by flaps of articular cartilage. Abrasion arthroplasty, a more extensive debridement of the cartilage defect, can additionally be performed with the intent of exposing the microvasculature of the subchondral bone in order to stimulate fibrocartilage repair. Microfracture largely replaced abrasion chondroplasty and is considered the gold standard for isolated articular lesions smaller than 2 cm 2 . This technique is similar to debridement with the addition of subchondral drilling to encourage chondrocyte and bone marrow cell recruitment and repair at the defect site. This technique is minimally invasive, single stage, low cost and technically easier than other treatments. However, the fibrocartilaginous repair tissue that fills the FCD, primarily composed of type I and III collagen with abnormal proteoglycans, lacks the intrinsic biochemical and viscoelastic properties of normal hyaline cartilage. Moreover, the destruction of the subchondral plate carries concern for subchondral cyst formation and devitalisation of subchondral anatomy.
Although microfracture remains the most popular treatment option for small chondral defects, reports suggest that abrasion chondroplasty carries similar outcomes without compromising the subchondral plate. Independent of the specific method used to stimulate fibrocartilage repair, strict adherence to essential principles, including uniform elimination of the calcified layer, creation of vertical walls at the transition of the defect adjacent to the normal articular cartilage and immediate low- or no-load range of motion for a period of 6 to 8 weeks, ensures the greatest likelihood of a successful reduction of symptoms.
Moreover, there appears to be a role for benign neglect in management of these incidental articular cartilage lesions. Ulstein et al. prospectively reported on 5-year outcomes of 368 patients who underwent primary ACL reconstruction who were found to have a concomitant full-thickness cartilage lesion. The authors found no difference in outcomes between chondral defects that were left unaddressed and those treated with debridement or microfracture, supporting the hypothesis that asymptomatic FCDs do not need to be routinely treated.
Lesion size and depth are important factors to consider when determining appropriate treatment. High-demand patients with small lesions or patients who have failed marrow stimulation are candidates for OAT. Larger lesions are better addressed with OCA or autologous chondrocyte implantation (ACI), which is commonly used in conjunction with a scaffold, termed matrix-induced ACI, because of durability and defect-filling capabilities. ACI/MACI is more appropriate for surface lesions with uninvolved or healthy subchondral bone, particularly in the patellofemoral joint. This technique does not violate the subchondral bone and does not limit the option for future treatments with other techniques, such as OAT or OCA. The condition of the subchondral plate is important for guiding therapy. If the plate is compromised, OAT or OCA are often indicated because these replace the entire osteochondral unit. The size of the lesion dictates which technique would be most appropriate. For example, larger, deeper lesions are more appropriately addressed with OCA because of lower donor site morbidity relative to OAT.
Location of the chondral defect helps dictate treatment as well. Femoral condyle lesions are the most common symptomatic chondral defect in the knee, followed by lesions in the tibial and patellofemoral compartments. OCA consistently allows for reproducible and accurate anatomical restoration when used for femoral condyle lesions. ACI/MACI also has an excellent outcome profile for lesions of the femoral condyle, especially as a first-line restoration technique with healthy subchondral bone. ACI/MACI and newer surface allografts (Cartiform or DeNovo NT) are also used to address lesions of the patellofemoral joint because the varying anatomical surface topography makes structural grafts more difficult to properly position.
The tibial articular surface is a difficult location to treat. A tibial articular lesion identified at the time of articular cartilage repair of the femoral condyle is usually treated with marrow stimulation techniques such as microfracture alone or with biological augmentation (i.e., BioCartilage). Another option for the treatment of these tibial articular chondral defects is OAT placed in a retrograde manner with a cannulated reamer system. For treatment of larger lesions of the tibial plateau with preservation of meniscus, there has been success reported with OCA or tibial resurfacing and concomitant realignment. This is particularly effective in the setting of fracture and development of secondary arthritis, with graft survival rates up to 65% at 15 years.
Several techniques have been developed to address FCD. These can be classified as palliative (debridement with or without abrasion arthroplasty), reparative (microfracture with or without a biological adjunct) or restorative (osteochondral transplantation, osteochondral allografts and MACI).
Debridement refers to the smoothing of degenerative cartilage and stabilisation of unstable cartilage flaps commonly seen in FCD. This technique is performed arthroscopically with a set of curettes and shavers ( Fig. 22.4 ). Low suction should be used on the shaver to remove diseased tissue that is resected while preserving intraarticular pressure to limit bleeding. The goal of this procedure is to remove any calcified cartilage within the defect while taking caution to preserve the subchondral bone and healthy surrounding cartilage.