Cartilage restoration procedures in patellofemoral stabilization

Introduction

Cartilage defects in the knee are common injuries in active populations (1), and a significant number of cartilage lesions are present in the patellofemoral (PF) joint (2). Patellar instability can place a patient at greater risk for cartilage injury. Anatomic risk factors like trochlear dysplasia, coronal plane malalignment, and rotational abnormalities can contribute to patellar maltracking and instability, which in turn can result in chondral injury to the PF joint. When it comes to treatment of PF instability, the a la carte approach is widely used as an algorithm to address the many factors which may contribute to instability (3). While soft tissue procedures such as medial patellofemoral ligament (MPFL) reconstruction are necessary to restore tracking of the patella, there is a role for addressing the additional pathoanatomic factors contributing to instability with procedures such as tibial tubercle osteotomy (TTO) and trochleoplasty (4,5). Cartilage lesions of the PF joint have been shown to be associated with recurrent patellar instability. Nomura et al. studied patients with patellar instability and observed that up to 96% of patients had associated articular cartilage injuries (6,7). Franzone et al. evaluated the association between chronicity of patellar instability with the grade and location of chondral injury in patients undergoing MPFL reconstruction. The study concluded that there was a higher grade of PF chondral injury in patients with more chronic patellar instability (8). Similarly, a more recent study found that patients with more than 5 patellar dislocations had a 3-fold increased incidence and severity of trochlear cartilage lesions (9).

The characteristics of chondral injuries can vary based on the etiology of patellar instability (10). For instance, patellar instability resulting in a dislocation event will most often result in cartilage injury to the medial facet upon re-entry of the patella into the trochlear groove, as well as an impaction injury to the lateral aspect of the lateral femoral condyle. Alternatively, PF maltracking without instability tends to lead to lateral PF cartilage lesions and wear (11). PF lesions can be further complicated by the presence of valgus alignment and/or rotational abnormalities. It is important to consider the etiology and unique characteristics of cartilage defects as it relates to treatment goals and options. The biomechanical complexity of the PF joint offers a unique challenge to the management of cartilage lesions. We seek to outline the clinical evaluation, imaging, non-operative, and operative treatment options for cartilage restoration in PF stabilization and provide an overview of the current evidence for each technique.

Clinical evaluation

Workup for cartilage lesions in patients with PF instability should start with a thorough history and review of symptoms. Patients may report anterior knee pain with activities such as going up stairs or squats. Symptom onset can be gradual or acute after a traumatic patellar instability event. While obtaining a history, it is important to distinguish patellar dislocation from subluxation, determine if the patella reduced spontaneously or required formal reduction, and take note of how long the patella was dislocated before successful reduction. A full past medical history is crucial to determine prior dislocation events or other injuries to the knee. It may also reveal risk factors for ligamentous laxity, such as Ehlers-Danlos and Marfan syndrome. On physical exam, it is important to assess gait, standing alignment, and joint laxity with a Beighton Score (12). An evaluation of the patient’s rotational alignment may reveal certain risk factors for patellar instability, such as femoral anteversion and external tibial torsion, both of which can be evaluated with the patient lying prone. Standing alignment should also be assessed to evaluate for genu valgum. The knee should be assessed for effusion, crepitus, pain with palpation of the facets and medial and lateral retinaculum, apprehension with medial and lateral translation of the patella, and J sign with open chain extension (13,14). Obtaining radiographs, including bilateral standing anteroposterior, lateral, merchant, and weight-bearing full-length views, is important for evaluation of alignment, as well as the presence of joint space narrowing (Iwano Classification) (15). Advanced imaging plays a crucial role in the diagnosis and management of cartilage defects in the knee. Computed tomography of the knee is useful for evaluation of rotation and trochlear groove characteristics. Magnetic resonance imaging (MRI) is helpful to assess for the presence and degree of chondral injury, which can range from cartilage fissures to osteochondral fractures. The presence of subchondral edema, cysts, or any compromise of the subchondral architecture is important to take note of, as it may direct the surgeon toward osteochondral-based approaches. In the setting of PF instability, the diagnosis of concomitant chondral or osteochondral injury is critical to inform staging and timing of surgical treatment planning when necessary.

Non-operative treatment

There is a role for non-operative treatment in the management of PF instability. A first-time dislocator can undergo a trial of conservative management with a brief period of immobilization in a knee brace, physical therapy (PT), and nonsteroidal anti-inflammatory drugs (NSAIDs) for pain control. Immobilization and taping are thought to encourage healing of the medial soft tissue structures and promote stability (16). PT should entail closed-chain exercises with a focus on quadriceps strengthening, specifically the vastus medialis obliquus (17,18). Despite non-operative management with rehabilitation commonly being used as first-line treatment for PF instability, there are some limitations and drawbacks to its utility. For example, studies have shown an association with high redislocation rates (19,20). Atkin et al. prospectively studied 74 first-time dislocators who were treated with a standardized rehabilitation protocol and found that a majority of patients (58%) had limitations at 6-month follow-up (21). Additionally, Stefancin et al. did a systematic review of non-operative versus operative treatment of first-time traumatic patellar dislocations, and recommended that patients with loose bodies or osteochondral injury be indicated for surgical intervention (22). The risk of further instability events and progression of chondral injury highlights the appeal of operative intervention. We discuss several surgical approaches to addressing PF chondral injury in the setting of instability (Table 1).

Chondroplasty

One of the most commonly performed procedures for the treatment of chondral injuries in the knee is chondroplasty (23). This involves the mechanical debridement of a partial or full-thickness chondral lesion, usually measuring less than 1–2 cm² to create a more stable border along the lesion. Patients who may benefit from chondroplasty alone are those with evidence of isolated cartilage injury on MRI, which can range from signal heterogeneity within cartilage to partial or complete chondral loss. Patients may report catching or locking, and debridement of any frayed or fragmented cartilage may lead to relief of symptoms. Chondroplasty offers a treatment option for small chondral injuries, but because it is often used in conjunction with other procedures, there is a paucity of literature on outcomes of chondroplasty alone. Anderson et al. sought to assess the effect of arthroscopic chondroplasty performed on the knee in isolation (59% PF cartilage lesions), and found that patient-reported outcomes improved significantly in the cohort at an average of 32 months (24). Even when considering the PF joint specifically, isolated chondroplasty of grade 2 or worse cartilage lesions has been associated with an improvement in patient-reported outcomes. Similarly, a study of 36 patients who underwent isolated arthroscopic debridement for patellar chondromalacia found a significant improvement in Fulkerson-Shea Patellofemoral Joint Evaluation Scores (from 51.9 to 71.8) (25). While there is a scarcity of literature examining the use of isolated chondroplasty in the treatment of PF cartilage lesions in the setting of instability, Yi et al. studied functional outcomes in patients who underwent arthroscopic debridement and lateral retinacular release for PF arthrosis (26). The authors found a significant increase in postoperative functional scores, decrease in pain scores, and comparable results when compared to controls who had undergone arthroscopic PF debridement alone. Although patients with known history of patellar instability events were excluded from the study, lateral retinacular release was performed to address maltracking under direct visualization and reduce increased lateral PF compartmental pressures. Chondroplasty alone would not be sufficient to address PF instability, as it would risk complications such as persistent instability, maltracking, or unbalanced forces on the patella, but it offers an option to address PF cartilage lesions in this setting.

Microfracture

Microfracture is a technique which employs the use of awls to create perpendicular perforations in subchondral bone to stimulate bone marrow elements to fill a cartilage defect through a reparative process (27,28). It is used for full-thickness cartilage lesions and involves debridement of unstable cartilage from the margins to reveal a rim of healthy cartilage surrounding the defect. This is followed by microfractures made 3–4 mm apart to an adequate depth which is confirmed by the visualization of fat release from bone marrow (29). Isolated microfracture is reserved for patients with focal (2–4 cm²) full-thickness cartilage loss, and it should generally be avoided for bipolar PF lesions, in patients with malalignment, and higher-demand patients. Animal studies have shown increased tissue volume, type II collagen, and fibrous reparative tissue in defects after microfracture (30,31). Augments to microfracture, such as hyaluronic acid, growth factor, and chondrocyte augmentation have been developed with the goal of fostering an environment which would promote the differentiation of mesenchymal cells to reparative tissue that more closely reflects cartilage (32-34). For instance, microfracture with cell-free polymer-based augment has been shown to be associated with repair tissue rich in cartilaginous material and proteoglycans when compared to microfracture alone in a sheep model (35). Microfracture offers a cost-effective option for the treatment of chondral defects (36,37), and has been associated with patient satisfaction and improvement of symptoms in both the short- (38) and long-term (39). Despite support for microfracture in the literature, there has been a shift away from palliative and reparative procedures and towards restorative techniques for the treatment of chondral lesions of the knee (40). This is likely due to the variability in long-term outcomes of reparative procedures. A systematic review of microfracture for osteochondral defects in the knee found failure rates of 2.5% 2 years out from surgery and as high as 31% 5 years after surgery, suggesting lack of longevity of results (41). Kreuz et al. sought to assess outcomes in patients with full thickness cartilage defects of the knee who underwent microfracture alone and found there was a deterioration in clinical scores after 18 months, specifically for patients with PF defects (42). While microfracture is a cost-effective and relatively simple way to address cartilage injuries of the knee, it is no longer recommended in the PF joint. The lack of consistently reassuring long-term results has led to a shift towards other techniques for addressing PF chondral lesions.

Open reduction internal fixation (ORIF) of osteochondral fractures

ORIF is an option for the treatment of osteochondral fractures of the PF joint for fragments large enough to accommodate implants and with substantial, healthy subchondral bone attached. Various methods and materials can be used for fixation, including non-biodegradable or absorbable implants. Non-biodegradable options include plates, pins, or screws made from titanium, stainless steel, or polyether ether ketone (PEEK), whereas bioabsorbable options include polymer-based implants, absorbable suture fixation, or magnesium-based alloys (43). While treatment of osteochondral lesions was classically done with screw fixation, as it allows for compression across the fragment (44), this typically requires staged removal of hardware. Bioabsorbable screws on the other hand, not only provide compression, but also avoid the need for a second surgery (45). One retrospective study assessed the radiographic and functional outcomes in 9 patients who underwent arthroscopic bioabsorbable screw fixation of osteochondral lesions of the femoral condyle, and found that 7 of the patients had excellent outcomes and healed lesions on MRI at 33 months post-operatively (46). Studies have also assessed the use of bioabsorbable pins in the treatment of osteochondral fractures, with many showing excellent radiographic and functional outcomes in adolescent populations (47-49). Another option for the treatment of osteochondral fracture is suture fixation, a fragment preserving technique that avoids fixation through the articular cartilage. Vogel et al. described a technique for suture fixation of osteochondral fragments using knotless suture anchors and Vicryl suture, and an arthroscopic assessment at 10 weeks revealed healed fracture and resorption of suture (50). While ORIF of osteochondral fragments offers a great option to restore congruity of the articular surface, its narrow indications leave room for other techniques and therapies to be used in the treatment of PF cartilage defects.

Cell-based therapies

Autologous chondrocyte implantation (ACI)

Cell-based therapies can be utilized in cartilage injuries that do not contain any underlying subchondral or bony defects. They can be used for lesions of any size, typically ranging from 2–8 cm². One of the first cell-based techniques described was the ACI technique which involves two stages. The first procedure is done arthroscopically and includes harvesting cartilage cells from the patient’s knee. The grafted area is roughly 5 mm × 8 mm and can be harvested from the medial or lateral femoral trochlea or intercondylar notch. The harvested cartilage cells then undergo expansion for 4–6 weeks. Once the cells have sufficiently multiplied, they are then replanted in the patient’s knee during the second stage (51). The original ACI procedure included the use of a separate membrane that the surgeon would secure to the cells during the second stage of the surgery. It would then be implanted into the knee using suture fixation. This process was technically demanding and could cause damage to surrounding tissues in the knee. The third generation of the ACI procedure, matrix-induced autologous chondrocyte implantation (MACI), involves applying the cartilage cells to a porcine collagen membrane during the manufacturing process (52). The cells and membrane together are then applied to the cartilage defect using fibrin glue. The second implantation procedure is generally performed through an open or mini-open technique (Figure 1).

Figure 1 Intraoperative photos of a patella cartilage defect prepared and fixed using matrix-induced autologous chondrocyte implantation technique. Written informed consent for publication of these images was obtained from the patient.

The most common cartilage treatment procedure in the PF joint is the ACI/MACI procedure (53). This is in part due to the complex morphology of the PF joint when compared to the condyles or plateaus. The graft consists of the patient’s own cells, decreasing concern for disease transmission or host reaction. It can also be used for larger cartilage defect sizes than microfracture or osteochondral autograft transfer (OAT) procedures (2–4 cm²). The biggest drawbacks to the procedure are the necessity for two surgeries and the high costs associated with two surgeries and cell development in a lab (37,54).

Though original studies of the ACI procedure did initially show poor outcomes in the PF joint when compared to the tibiofemoral compartments (51), subsequent studies have shown improved results. A cohort study of 67 patients with PF defects treated with MACI was compared to 127 patients with lesions in the femoral condyle. Both groups had increased patient-reported outcome measures (PROMs) scores postoperatively and there was no difference in net increase score between the two groups (55). MRI composite score at 2 years had no difference between the groups with 3/4 of patients with good/excellent results. One multicenter study of 110 patients undergoing MACI procedure found improvement in International Knee Documentation Committee (IKDC) (40±14 to 69±20) and Cincinnati scores (3.2±1.2 to 6.2±1.8) at an average of 7.5 years postoperatively. They did not find any difference in outcomes for defect location, size, concomitant realignment procedures, or sex (56). Another study of 48 ACI procedures saw improved visual analogue scale (VAS) pain scores (6.4 to 4.5) and Modified Cincinnati scores (45.13 to 54.81) at an average of 3.3 years postoperatively. They found that lesions involving the medial facet had improved outcomes compared to lateral and diffuse lesions (57). Many studies included patients undergoing concomitant realignment surgeries of the PF joint including TTO and lateral retinacular release (58-63). Some studies showed improved outcomes in patients undergoing both procedures (63) while others showed no difference (62).

Multiple studies have also assessed postoperative MRI after MACI procedures and have found favorable results. One case study of 24 patients who underwent MACI procedures in the PF joint showed >50% infill of cartilage in 82% of patients 5 years postoperatively (64). Another case series of 95 patients who underwent MACI procedure in the PF joint saw 72% of patients had 50–100% graft infill 2 years postoperatively and had a 4.3% graft failure rate (65). At 10-year follow-up, they did not see any changes to the graft on MRI (55,66). MACI procedures show favorable clinical and MRI results for repair of cartilage lesions in the PF joint, though there are considerable drawbacks including high cost and the necessity for a two-stage approach.

Particulated juvenile articular cartilage (PJAC)

Another cell-based therapy used in cartilage lesion restoration is the PJAC procedure (Figure 2). This procedure includes using juvenile cartilage (donors age <13 years) as allograft. Juvenile chondrocytes were found to have increased levels of chordin-like 1 (CHRDL1) and microfibrillar-associated protein 4 (MFAP4) which can aid in survival and proliferation of bone-derived stem cells (67). During the procedure, the cartilage defect is prepared and a layer of fibrin glue is applied. Minced pieces of the donor cartilage are placed in the defect and another layer of fibrin glue is placed to cover the fragments. This is performed in a single surgery using a mini-open approach. The major benefits of the procedure are that it can be performed in one stage and the relative technical ease compared to other cell-based therapies. There is a cost associated with the cartilage allograft, but it is comparatively lower than in ACI procedures (68). There is no autologous harvesting during the procedure, so there is no concern for donor site morbidity.

Figure 2 Intraoperative photos of a patella cartilage defect treated with particulated juvenile articular cartilage. Written informed consent for publication of these images was obtained from the patient.

Research on PJAC is mostly limited to case series currently but initial data are promising. Multiple case series show improved clinical outcomes. A recent study of 65 patients (70 knees) that underwent PJAC for full-thickness PF lesions showed improvement in knee injury and osteoarthritis outcome score (KOOS), IKDC, and Kujala scores at >2-year follow-up. In this study, 98% of patients also underwent patellar stabilization or offloading procedure at the same time (69). A study of 13 PF lesions treated with PJAC showed statistically significant improvement in KOOS score (58.4±15.7 to 69.2±18.6) at an average of 8.2 (0.67–32.7) months postoperatively. No patients required reoperation (70). Another study of 27 patients undergoing PJAC for PF lesions showed statistically significant increases in postoperative IKDC and knee outcome survey activities of daily living scale (KOS-ADL) scores 2 years postoperatively. They did not see any effect of age, concomitant TTO, or lesion location on clinical outcomes (71). There were multiple studies that included MRI imaging postoperatively. One study of 15 PF lesions treated with PJAC showed 73% of patients had normal or nearly normal cartilage repair at 2 years. Two patients had gross hypertrophy of the graft and required arthroscopic debridement (72). Another prospective study including 30 PF lesions treated with PJAC showed >67% lesion fill in 69% of patients. No patients required further reoperation in their study (72). Another study of 36 PF lesions in patients under 21 showed 78% of patients with a majority of defects filled on MRI at 2 years postoperatively (73). One study found that most patients had more than 2/3 cartilage defect filling on MRI by 3 months postoperatively. They found, however, that PROM scores were not correlated with defect fill percentage in short-term follow-up (69).

A few studies also looked at return to sport after PJAC (74,75). One study of 34 patients under the age of 21 years who underwent PJAC for PF lesions found a 100% return to sport rate (73). Another study of 41 patients who were treated with PJAC for PF lesions also showed a 100% return to sport rate (17/17 athletes) with an average follow-up of 2.5 years. They did find that 14.6% of their cohort required reoperation for complications relating to the procedure (74). PJAC shows promising clinical, MRI, and return to sport outcomes in the short- to mid-term and is a cost-effective, single-stage procedure for cartilage defects in the PF compartment.

Orthobiologics

Even with advancements in cartilage repair techniques in recent years, there are still significant limitations including cost, donor site morbidity, and overall success rates with the current options. New biologic agents are being developed to try to fill the need. There are limited data on their use and efficacy in chondral defects in the knee and minimal data on their use specifically on PF cartilage defects (68,75). Some techniques being looked at include an acellular scaffold from porcine type 1 collagen (Cartifill, Cellontech, Seoul, South Korea), an aragonite-based acellular scaffold (Agili-C, Smith & Nephew, Watford, UK), a cartilage allograft putty (CartiMax, CONMED, Largo, FL, USA), micronized cartilage extracellular matrix (Biocartilage, Arthrex, Naples, FL, USA) and a cryopreserved osteochondral allograft (Cartiform, Arthrex). Most biologic treatments are currently limited to short-term follow-up case series though some promising results have been seen. One case series with 2-year follow-up using agili-C on large chondral defects in the knee showed improved KOOS and IKDC scores. MRIs obtained showed 78.7% coverage after 2 years. The study had a 9% failure rate requiring revision surgery (76). There is another promising case series using Biocartilage with 2-year follow-up. Sixty-two patients were treated with the AutoCart system involving the use of the patient’s own cartilage mixed with Biocartilage. At two years, the patients had improved patient-reported outcomes and on average patients had good fill and integration of cartilage on MRI (77). More data are needed to determine the efficacy of any potential therapies especially for use in the PF joint.

Osteochondral-based approaches

OAT

Cartilage defects of the PF joint that compromise the subchondral bone require procedures that address both the chondral and subchondral defects. This includes OAT/mosaicplasty and osteochondral allograft transplantation (OCA). OAT/mosaicplasty is generally used for smaller cartilage defects (<2.5 cm²) in the knee (78) (Figure 3). The procedure involves harvesting donor cartilage with bone plugs from non weight-bearing or lower weight-bearing cartilage areas of the knee including the intercondylar notch. If the cartilage defect size requires multiple plugs, donor tissue can be taken from various sites and used together to fill the cartilage lesion (mosaicplasty). It can be performed through open, mini-open, or arthroscopic technique. This can be nuanced and difficult for PF lesions as a common donor site for condylar lesions has historically been the lateral trochlea but in patients with PF pathology this is often an area the surgeon would avoid harvesting from.

Figure 3 Intraoperative photos of a patella cartilage defect treated with osteochondral autograft transfer. Written informed consent for publication of these images was obtained from the patient.

Some of the challenges associated with OAT are that the PF joint has unique morphology and thickness compared to other cartilage-containing areas of the knee. Matching the donor site morphology to the defect can be challenging and can possibly cause early failure of the repair (79). Also, harvesting donor cartilage creates a second site of injury in the knee and can cause donor site morbidity for patients. In one study of young athletes undergoing mosaicplasty, it was found that 5% of patients had ongoing anterior donor site pain (80). However, the OAT procedure is performed in a single stage and does not require costly allografts or cell regeneration (37).

An early study of OAT in the PF joint found high rates of failure compared with the femoral condyle, possibly having to do with the size of defect, lack of concomitant offloading procedures, and early techniques (79). This has not been seen in newer studies of OAT in the PF joint (81-85). Multiple studies used MRI to assess the graft viability postoperatively. All of the studies found that a majority of patients had good cartilage fill (67–100%) (81-85) in the short and medium term. Multiple studies also found improved clinical outcomes postoperatively (81-85). One study included 22 patients at 2.3-year follow-up after OAT for PF lesions with an average lesion size of 165.6 mm². They found that IKDC scores improved from 47.2 to 74.4 and SF-36 scores improved from 64.0 to 79.4 on average (85). None of their patients required a secondary surgery. They did not find any differences in patients who had to undergo concomitant realignment procedures at the time of surgery. The OAT procedure can show promising outcomes for smaller lesions (<2.5 cm²) in the PF joint, but complex PF morphology, donor site morbidity and larger lesions can result in inferior results for patients.

OCA

OCA offers an option for larger chondral or osteochondral defects in the knee. The defect is reamed to a depth of 5–7 mm and then measured such that the allograft can be prepared to match those dimensions (Figure 4). The press-fit technique is used to place the allograft in the defect using a bone tamp with gentle force (86). Allograft can be fresh or stored through options including freezing and cryopreservation, each of which has an effect on the viability of graft and, in turn, may impact the longevity of favorable outcomes in patients undergoing transplantation. For instance, it has been shown in goat models that frozen allograft is associated with lower cartilage stiffness, matrix content, and cellularity when compared to fresh allograft (87). The use of osteochondral allograft for large PF and bipolar defects comes with a particular set of challenges and has been associated with worse outcomes than when compared to lesions of the femoral condyles or tibial plateau. In a systematic review of 19 papers with 1,036 patients undergoing OCA transplantation in the knee, Familiari et al. reported an overall 5-year survival rate of 89% and a 10-year survival rate of 79%. Outcomes were comparatively worse for patellar lesions, which had a survival rate of 78% at 5 and 10 years, and for bipolar lesions which had a survival rate of just 64% and 39% at 5 and 10 years, respectively (88). Another study assessed 2-year outcomes in patients who underwent fresh OCA transplantation and reported a success rate of 76%, but this dropped to 56% when only considering bipolar lesions (89). Despite inferior results, there are studies with promising outcomes for OCA in addressing PF cartilage defects. A retrospective study assessed the use of OCA transplantation for bipolar trochlear and patellar lesions in 17 patients with PF instability, and found that at an average of 33 months of follow-up, patients had improved pain, function, stability and activity level (90). In all patients, MPFL reconstruction or TTO was used to address PF instability, and no patient had recurrent instability at final follow-up. Despite higher failure rates than other cartilage restoration procedures, patients report high satisfaction after OCA transplantation, demonstrating its viability as an option for patients with large PF defects (91).

Figure 4 Intraoperative photos of a patella cartilage defect treated with osteochondral allograft transplantation. Written informed consent for publication of these images was obtained from the patient.

Conclusions

Cartilage lesions of the PF joint in the setting of instability pose a specific problem for surgeons and patients due to the unique morphology and biomechanics of the joint. MPFL reconstruction, trochleoplasty, and TTO are some of the procedures that can be implemented to address PF instability, but cartilage restoration is also critical to stabilizing the PF joint and addressing pain. The OAT procedure has shown improved clinical outcomes but requires taking a donor graft from the knee and is reserved for smaller lesions (<2.5 cm²). On the other hand, OCA can be used on larger cartilaginous lesions, and the allograft can often better match the PF joint morphology. It does not require a second site of injury in the knee, and thus there is no risk of donor site morbidity. OCA is our recommended method when osteochondral or bony injury is involved, and pre-operative MRI is critical to assess for subchondral edema or cysts to accurately indicate a patient for this procedure. Cell-based therapies can be used to repair larger cartilage lesions. ACI/MACI is the most widely used cell-based therapy with good clinical results, but is costly and requires two surgeries for the patient. PJAC is a single surgery cell-based repair using allograft with impressive short to mid-term clinical and MRI outcomes. Newer orthobiologic therapies are being developed and tested but more data are needed to assess their efficacy in PF lesions.

Acknowledgments

We would like to thank Dr. Aruna Seneviratne for his support with this project.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editor (Ting Cong) for the series “Current Concepts and Techniques in Soft Tissue Repair and Joint Preservation” published in Annals of Joint. The article has undergone external peer review.

Peer Review File: Available at https://aoj.amegroups.com/article/view/10.21037/aoj-25-57/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aoj.amegroups.com/article/view/10.21037/aoj-25-57/coif). The series “Current Concepts and Techniques in Soft Tissue Repair and Joint Preservation” was commissioned by the editorial office without any funding or sponsorship. J.N.G. reports that he is a consultant and speaker for various subjects for JnJ Medtech. E.D. reports that she is a consultant for CONMED, on the ISAKOS Diversity Advisory Board, ISAKOS Program Committee, and the AOSSM Education Committee. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. Written informed consent for publication of this article and accompanying images was obtained from all the patients.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Curl WW, Krome J, Gordon ES, et al. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997;13:456-60. [Crossref] [PubMed]
2. Hjelle K, Solheim E, Strand T, et al. Articular cartilage defects in 1,000 knee arthroscopies. Arthroscopy 2002;18:730-4. [Crossref] [PubMed]
3. Pineda T, Dejour DH. ‘À la carte’ treatment algorithm for patellofemoral instability. Rev Esp Cir Ortop Traumatol 2025;S1888-4415(25)00018-9.
4. Hiemstra LA, Kerslake S, Kupfer N, et al. Patellofemoral Stabilization: Postoperative Redislocation and Risk Factors Following Surgery. Orthop J Sports Med 2019;7:2325967119852627. [Crossref] [PubMed]
5. Levy BJ, Tanaka MJ, Fulkerson JP. Current Concepts Regarding Patellofemoral Trochlear Dysplasia. Am J Sports Med 2021;49:1642-50. [Crossref] [PubMed]
6. Nomura E, Inoue M. Cartilage lesions of the patella in recurrent patellar dislocation. Am J Sports Med 2004;32:498-502. [Crossref] [PubMed]
7. Nomura E, Inoue M, Kurimura M. Chondral and osteochondral injuries associated with acute patellar dislocation. Arthroscopy 2003;19:717-21. [Crossref] [PubMed]
8. Franzone JM, Vitale MA, Shubin Stein BE, et al. Is there an association between chronicity of patellar instability and patellofemoral cartilage lesions? An arthroscopic assessment of chondral injury. J Knee Surg 2012;25:411-6. [Crossref] [PubMed]
9. Bram JT, Lijesen E, Green DW, et al. The Number of Patellar Dislocation Events Is Associated With Increased Chondral Damage of the Trochlea. Am J Sports Med 2024;52:2541-6. [Crossref] [PubMed]
10. Chilelli BJ, Cole BJ, Farr J, et al. The Four Most Common Types of Knee Cartilage Damage Encountered in Practice: How and Why Orthopaedic Surgeons Manage Them. Instr Course Lect 2017;66:507-30.
11. Hinckel BB, Gomoll AH, Farr J 2nd. Cartilage Restoration in the Patellofemoral Joint. Am J Orthop (Belle Mead NJ) 2017;46:217-22.
12. Beighton P, Solomon L, Soskolne CL. Articular mobility in an African population. Ann Rheum Dis 1973;32:413-8. [Crossref] [PubMed]
13. Dennis ER, Gruber S, Marmor WA, et al. Evaluation and management of patellar instability. Ann Jt 2022;7:2. [Crossref] [PubMed]
14. Gomoll AH, Minas T, Farr J, et al. Treatment of chondral defects in the patellofemoral joint. J Knee Surg 2006;19:285-95. [Crossref] [PubMed]
15. Strauss EJ, Galos DK. The evaluation and management of cartilage lesions affecting the patellofemoral joint. Curr Rev Musculoskelet Med 2013;6:141-9. [Crossref] [PubMed]
16. McConnell J. Rehabilitation and nonoperative treatment of patellar instability. Sports Med Arthrosc Rev 2007;15:95-104. [Crossref] [PubMed]
17. Weber AE, Nathani A, Dines JS, et al. An Algorithmic Approach to the Management of Recurrent Lateral Patellar Dislocation. J Bone Joint Surg Am 2016;98:417-27. [Crossref] [PubMed]
18. Clark D, Metcalfe A, Wogan C, et al. Adolescent patellar instability: current concepts review. Bone Joint J 2017;99-B:159-70. [Crossref] [PubMed]
19. Alshaban RM, Ghaddaf AA, Alghamdi DM, et al. Operative versus non-operative management of primary patellar dislocation: A systematic review and network meta-analysis. Injury 2023;54:110926. [Crossref] [PubMed]
20. Moiz M, Smith N, Smith TO, et al. Clinical Outcomes After the Nonoperative Management of Lateral Patellar Dislocations: A Systematic Review. Orthop J Sports Med 2018;6:2325967118766275. [Crossref] [PubMed]
21. Atkin DM, Fithian DC, Marangi KS, et al. Characteristics of patients with primary acute lateral patellar dislocation and their recovery within the first 6 months of injury. Am J Sports Med 2000;28:472-9. [Crossref] [PubMed]
22. Stefancin JJ, Parker RD. First-time traumatic patellar dislocation: a systematic review. Clin Orthop Relat Res 2007;93-101. [Crossref] [PubMed]
23. McCormick F, Harris JD, Abrams GD, et al. Trends in the surgical treatment of articular cartilage lesions in the United States: an analysis of a large private-payer database over a period of 8 years. Arthroscopy 2014;30:222-6. [Crossref] [PubMed]
24. Anderson DE, Rose MB, Wille AJ, et al. Arthroscopic Mechanical Chondroplasty of the Knee Is Beneficial for Treatment of Focal Cartilage Lesions in the Absence of Concurrent Pathology. Orthop J Sports Med 2017;5:2325967117707213. [Crossref] [PubMed]
25. Federico DJ, Reider B. Results of isolated patellar debridement for patellofemoral pain in patients with normal patellar alignment. Am J Sports Med 1997;25:663-9. [Crossref] [PubMed]
26. Yi N, Yuan H, Zhang YK, et al. Arthroscopic release of lateral patellar retinaculum for patellofemoral arthrosis. BMC Surg 2025;25:164. [Crossref] [PubMed]
27. Steadman JR, Rodkey WG, Briggs KK. Microfracture to treat full-thickness chondral defects: surgical technique, rehabilitation, and outcomes. J Knee Surg 2002;15:170-6.
28. Steadman JR, Rodkey WG, Rodrigo JJ. Microfracture: surgical technique and rehabilitation to treat chondral defects. Clin Orthop Relat Res 2001;S362-9. [Crossref] [PubMed]
29. Erggelet C, Vavken P. Microfracture for the treatment of cartilage defects in the knee joint - A golden standard? J Clin Orthop Trauma 2016;7:145-52. [Crossref] [PubMed]
30. Frisbie DD, Trotter GW, Powers BE, et al. Arthroscopic subchondral bone plate microfracture technique augments healing of large chondral defects in the radial carpal bone and medial femoral condyle of horses. Vet Surg 1999;28:242-55. [Crossref] [PubMed]
31. Breinan HA, Martin SD, Hsu HP, et al. Healing of canine articular cartilage defects treated with microfracture, a type-II collagen matrix, or cultured autologous chondrocytes. J Orthop Res 2000;18:781-9. [Crossref] [PubMed]
32. Legović D, Zorihić S, Gulan G, et al. Microfracture technique in combination with intraarticular hyaluronic acid injection in articular cartilage defect regeneration in rabbit model. Coll Antropol 2009;33:619-23.
33. Kuo AC, Rodrigo JJ, Reddi AH, et al. Microfracture and bone morphogenetic protein 7 (BMP-7) synergistically stimulate articular cartilage repair. Osteoarthritis Cartilage 2006;14:1126-35. [Crossref] [PubMed]
34. Dorotka R, Windberger U, Macfelda K, et al. Repair of articular cartilage defects treated by microfracture and a three-dimensional collagen matrix. Biomaterials 2005;26:3617-29. [Crossref] [PubMed]
35. Erggelet C, Endres M, Neumann K, et al. Formation of cartilage repair tissue in articular cartilage defects pretreated with microfracture and covered with cell-free polymer-based implants. J Orthop Res 2009;27:1353-60. [Crossref] [PubMed]
36. Aae TF, Randsborg PH, Lurås H, et al. Microfracture is more cost-effective than autologous chondrocyte implantation: a review of level 1 and level 2 studies with 5 year follow-up. Knee Surg Sports Traumatol Arthrosc 2018;26:1044-52. [Crossref] [PubMed]
37. Schrock JB, Kraeutler MJ, Houck DA, et al. A Cost-Effectiveness Analysis of Surgical Treatment Modalities for Chondral Lesions of the Knee: Microfracture, Osteochondral Autograft Transplantation, and Autologous Chondrocyte Implantation. Orthop J Sports Med 2017;5:2325967117704634. [Crossref] [PubMed]
38. Miller BS, Steadman JR, Briggs KK, et al. Patient satisfaction and outcome after microfracture of the degenerative knee. J Knee Surg 2004;17:13-7. [Crossref] [PubMed]
39. Steadman JR, Briggs KK, Rodrigo JJ, et al. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy 2003;19:477-84. [Crossref] [PubMed]
40. Gowd AK, Cvetanovich GL, Liu JN, et al. Management of Chondral Lesions of the Knee: Analysis of Trends and Short-Term Complications Using the National Surgical Quality Improvement Program Database. Arthroscopy 2019;35:138-46. [Crossref] [PubMed]
41. Mithoefer K, McAdams T, Williams RJ, et al. Clinical efficacy of the microfracture technique for articular cartilage repair in the knee: an evidence-based systematic analysis. Am J Sports Med 2009;37:2053-63. [Crossref] [PubMed]
42. Kreuz PC, Steinwachs MR, Erggelet C, et al. Results after microfracture of full-thickness chondral defects in different compartments in the knee. Osteoarthritis Cartilage 2006;14:1119-25. [Crossref] [PubMed]
43. Cordunianu MA, Antoniac I, Niculescu M, et al. Treatment of Knee Osteochondral Fractures. Healthcare (Basel) 2022;10:1061. [Crossref] [PubMed]
44. Lewis PL, Foster BK. Herbert screw fixation of osteochondral fractures about the knee. Aust N Z J Surg 1990;60:511-3. [Crossref] [PubMed]
45. Nuelle CW, Nuelle JAV, Balldin BC. Open Reduction Internal Fixation of a Traumatic Osteochondral Lesion of the Patella With Bioabsorbable Screw Fixation. Arthrosc Tech 2019;8:e1361-5. [Crossref] [PubMed]
46. Dines JS, Fealy S, Potter HG, et al. Outcomes of osteochondral lesions of the knee repaired with a bioabsorbable device. Arthroscopy 2008;24:62-8. [Crossref] [PubMed]
47. Matsusue Y, Nakamura T, Suzuki S, et al. Biodegradable pin fixation of osteochondral fragments of the knee. Clin Orthop Relat Res 1996;166-73.
48. Walsh SJ, Boyle MJ, Morganti V. Large osteochondral fractures of the lateral femoral condyle in the adolescent: outcome of bioabsorbable pin fixation. J Bone Joint Surg Am 2008;90:1473-8. [Crossref] [PubMed]
49. Gkiokas A, Morassi LG, Kohl S, et al. Bioabsorbable pins for treatment of osteochondral fractures of the knee after acute patella dislocation in children and young adolescents. Adv Orthop 2012;2012:249687. [Crossref] [PubMed]
50. Vogel LA, Fitzsimmons KP, Lee Pace J. Osteochondral Fracture Fixation With Fragment Preserving Suture Technique. Arthrosc Tech 2020;9:e761-7. [Crossref] [PubMed]
51. Brittberg M, Lindahl A, Nilsson A, et al. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 1994;331:889-95. [Crossref] [PubMed]
52. Wood D, Zheng MH. Matrix-Induced Autologous Chondrocyte Implantation. In: Williams RJ, editor. Cartilage Repair Strategies. Totowa, NJ: Humana Press; 2007:193-206.
53. Mouzopoulos G, Borbon C, Siebold R. Patellar chondral defects: a review of a challenging entity. Knee Surg Sports Traumatol Arthrosc 2011;19:1990-2001. [Crossref] [PubMed]
54. Everhart JS, Campbell AB, Abouljoud MM, et al. Cost-efficacy of Knee Cartilage Defect Treatments in the United States. Am J Sports Med 2020;48:242-51. [Crossref] [PubMed]
55. Ebert JR, Schneider A, Fallon M, et al. A Comparison of 2-Year Outcomes in Patients Undergoing Tibiofemoral or Patellofemoral Matrix-Induced Autologous Chondrocyte Implantation. Am J Sports Med 2017;45:3243-53. [Crossref] [PubMed]
56. Gomoll AH, Gillogly SD, Cole BJ, et al. Autologous chondrocyte implantation in the patella: a multicenter experience. Am J Sports Med 2014;42:1074-81. [Crossref] [PubMed]
57. Macmull S, Jaiswal PK, Bentley G, et al. The role of autologous chondrocyte implantation in the treatment of symptomatic chondromalacia patellae. Int Orthop 2012;36:1371-7. [Crossref] [PubMed]
58. Andrade R, Nunes J, Hinckel BB, et al. Cartilage Restoration of Patellofemoral Lesions: A Systematic Review. Cartilage 2021;13:57S-73S. [Crossref] [PubMed]
59. Henderson IJ, Lavigne P. Periosteal autologous chondrocyte implantation for patellar chondral defect in patients with normal and abnormal patellar tracking. Knee 2006;13:274-9. [Crossref] [PubMed]
60. Mandelbaum B, Browne JE, Fu F, et al. Treatment outcomes of autologous chondrocyte implantation for full-thickness articular cartilage defects of the trochlea. Am J Sports Med 2007;35:915-21. [Crossref] [PubMed]
61. Farr J. Autologous chondrocyte implantation improves patellofemoral cartilage treatment outcomes. Clin Orthop Relat Res 2007;187-94.
62. Vanlauwe JJ, Claes T, Van Assche D, et al. Characterized chondrocyte implantation in the patellofemoral joint: an up to 4-year follow-up of a prospective cohort of 38 patients. Am J Sports Med 2012;40:1799-807. [Crossref] [PubMed]
63. Pascual-Garrido C, Slabaugh MA, L’Heureux DR, et al. Recommendations and treatment outcomes for patellofemoral articular cartilage defects with autologous chondrocyte implantation: prospective evaluation at average 4-year follow-up. Am J Sports Med 2009;37:33S-41S. [Crossref] [PubMed]
64. Meyerkort D, Ebert JR, Ackland TR, et al. Matrix-induced autologous chondrocyte implantation (MACI) for chondral defects in the patellofemoral joint. Knee Surg Sports Traumatol Arthrosc 2014;22:2522-30. [Crossref] [PubMed]
65. Ebert JR, Fallon M, Smith A, et al. Prospective clinical and radiologic evaluation of patellofemoral matrix-induced autologous chondrocyte implantation. Am J Sports Med 2015;43:1362-72. [Crossref] [PubMed]
66. Ebert JR, Klinken S, Fallon M, et al. Clinical and Radiological Outcomes at ≥10-Year Follow-up After Matrix-induced Autologous Chondrocyte Implantation in the Patellofemoral Joint. Am J Sports Med 2024;52:2532-40. [Crossref] [PubMed]
67. Taylor SE, Lee J, Smeriglio P, et al. Identification of Human Juvenile Chondrocyte-Specific Factors that Stimulate Stem Cell Growth. Tissue Eng Part A 2016;22:645-53. [Crossref] [PubMed]
68. Dean RS, Hinckel BB, Omari A, et al. Treatment of Focal Cartilage Defects of the Knee: Classic and New Procedures. In: Sherman SL, Chahla J, Rodeo SA, et al. editors. Knee Arthroscopy and Knee Preservation Surgery. Cham: Springer International Publishing; 2023:1-18.
69. Marmor WA, Dennis ER, Buza SS, et al. Outcomes of Particulated Juvenile Articular Cartilage and Association With Defect Fill in Patients With Full-Thickness Patellar Chondral Lesions. Orthop J Sports Med 2024;12:23259671241249121. [Crossref] [PubMed]
70. Buckwalter JA, Bowman GN, Albright JP, et al. Clinical outcomes of patellar chondral lesions treated with juvenile particulated cartilage allografts. Iowa Orthop J 2014;34:44-9.
71. Wang T, Belkin NS, Burge AJ, et al. Patellofemoral Cartilage Lesions Treated With Particulated Juvenile Allograft Cartilage: A Prospective Study With Minimum 2-Year Clinical and Magnetic Resonance Imaging Outcomes. Arthroscopy 2018;34:1498-505. [Crossref] [PubMed]
72. Tompkins M, Hamann JC, Diduch DR, et al. Preliminary results of a novel single-stage cartilage restoration technique: particulated juvenile articular cartilage allograft for chondral defects of the patella. Arthroscopy 2013;29:1661-70. [Crossref] [PubMed]
73. Dawkins BJ, Shubin Stein BE, Mintz DN, et al. Patellofemoral joint cartilage restoration with particulated juvenile allograft in patients under 21 years old. Knee 2022;36:120-9. [Crossref] [PubMed]
74. Pearsall C, Chen AZ, Reynolds AW, et al. Particulated Juvenile Articular Cartilage Allograft Transplantation for Patellofemoral Defects Shows Favorable Return-to-Sport Rates and Patient-Reported Outcomes. Arthroscopy 2024;40:2875-83. [Crossref] [PubMed]
75. Debieux P, Mameri ES, Medina G, et al. Acellular scaffolds, cellular therapy and next generation approaches for knee cartilage repair. J Cartil Jt Preserv 2024;4:100180.
76. Kon E, Di Matteo B, Verdonk P, et al. Aragonite-Based Scaffold for the Treatment of Joint Surface Lesions in Mild to Moderate Osteoarthritic Knees: Results of a 2-Year Multicenter Prospective Study. Am J Sports Med 2021;49:588-98. [Crossref] [PubMed]
77. Schneider S, Ossendorff R, Walter SG, et al. Arthroscopic Autologous Minced Cartilage Implantation of Cartilage Defects in the Knee: A 2-Year Follow-up of 62 Patients. Orthop J Sports Med 2024;12:23259671241297970. [Crossref] [PubMed]
78. Angele P, Zellner J, Schröter S, et al. Biological Reconstruction of Localized Full-Thickness Cartilage Defects of the Knee: A Systematic Review of Level 1 Studies with a Minimum Follow-Up of 5 Years. Cartilage 2022;13:5-18. [Crossref] [PubMed]
79. Bentley G, Biant LC, Carrington RW, et al. A prospective, randomised comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee. J Bone Joint Surg Br 2003;85:223-30. [Crossref] [PubMed]
80. Hangody L, Dobos J, Baló E, et al. Clinical experiences with autologous osteochondral mosaicplasty in an athletic population: a 17-year prospective multicenter study. Am J Sports Med 2010;38:1125-33. [Crossref] [PubMed]
81. Emre TY, Atbasi Z, Demircioglu DT, et al. Autologous osteochondral transplantation (mosaicplasty) in articular cartilage defects of the patellofemoral joint: retrospective analysis of 33 cases. Musculoskelet Surg 2017;101:133-8. [Crossref] [PubMed]
82. Astur DC, Arliani GG, Binz M, et al. Autologous osteochondral transplantation for treating patellar chondral injuries: evaluation, treatment, and outcomes of a two-year follow-up study. J Bone Joint Surg Am 2014;96:816-23. [Crossref] [PubMed]
83. Figueroa D, Meleán P, Calvo R, et al. Osteochondral autografts in full thickness patella cartilage lesions. Knee 2011;18:220-3. [Crossref] [PubMed]
84. Figueroa D, Calvo Rodriguez R, Donoso R, et al. High-Grade Patellar Chondral Defects: Promising Results From Management With Osteochondral Autografts. Orthop J Sports Med 2020;8:2325967120933138. [Crossref] [PubMed]
85. Nho SJ, Foo LF, Green DM, et al. Magnetic resonance imaging and clinical evaluation of patellar resurfacing with press-fit osteochondral autograft plugs. Am J Sports Med 2008;36:1101-9. [Crossref] [PubMed]
86. Bugbee W, Cavallo M, Giannini S. Osteochondral allograft transplantation in the knee. J Knee Surg 2012;25:109-16. [Crossref] [PubMed]
87. Pallante AL, Görtz S, Chen AC, et al. Treatment of articular cartilage defects in the goat with frozen versus fresh osteochondral allografts: effects on cartilage stiffness, zonal composition, and structure at six months. J Bone Joint Surg Am 2012;94:1984-95. [Crossref] [PubMed]
88. Familiari F, Cinque ME, Chahla J, et al. Clinical Outcomes and Failure Rates of Osteochondral Allograft Transplantation in the Knee: A Systematic Review. Am J Sports Med 2018;46:3541-9. [Crossref] [PubMed]
89. Convery FR, Botte MJ, Akeson WH, et al. Chondral defects of the knee. Contemp Orthop 1994;28:101-7.
90. Mirzayan R, Charles MD, Batech M, et al. Bipolar Osteochondral Allograft Transplantation of the Patella and Trochlea. Cartilage 2020;11:431-40. [Crossref] [PubMed]
91. Gracitelli GC, Meric G, Pulido PA, et al. Fresh osteochondral allograft transplantation for isolated patellar cartilage injury. Am J Sports Med 2015;43:879-84. [Crossref] [PubMed]