Cartilage Restoration Procedures of the Knee

Neal B. Naveen, BS

Taylor M. Southworth, BS

Alex Beletsky, BS

William M. Cregar, MD

Tracy M. Tauro, BS, BA

Kelechi R. Okoroha, MD

Toufic R. Jildeh, MD

Brian J. Cole, MD, MBA

Adam B. Yanke, MD, PhD

INTRODUCTION

Articular cartilage is a highly specialized unit of connective tissue that is paramount to the movement of joints by acting as a load-bearing structure and to minimize friction.¹,² The articular cartilage overlies the subchondral bone and is a thin layer between 2 and 4 mm composed of chondrocytes and an extracellular matrix (ECM). It is divided into four layers, each with distinct morphology, biochemical composition, and biomechanical properties (from deep to superficial): The calcified cartilage layer (CCL), deep, transitional, and superficial zone.³ The three cartilaginous zones range in collagen orientation and water composition, while the CCL is a thin layer that acts to offset the discontinuity in stiffness between the subchondral bone and cartilaginous layers, as well as securing the layers together.¹,⁴,⁵ Water is the largest component of the ECM, ranging from 65% in the deep zone of the osteochondral unit to almost 80% in the superficial zone, and serves to nourish the collagen network.⁶,⁷

The ECM is also composed of collagen fibers and proteoglycans, with a small component of other proteins and glycoproteins.⁷ There are over eight different types of collagen fibers present in hyaline cartilage, with over 90% of the fibers being type II collagen.⁸ The chondrocytes are of mesenchymal stem cell origin and are primarily responsible for the synthesis of the ECM. This complex framework of chondrocytes, macromolecules, and a collagen fibril mesh provides cartilage its tensile strength and unique structure.

Articular cartilage receives its nutritional supply and oxygen by diffusion through the surrounding synovial fluid and at times the subchondral bone.⁹ Therefore, injuries to hyaline cartilage that do not penetrate the subchondral bone cannot produce an inflammatory response and thus have a low capacity for healing.¹⁰,¹¹ Full-thickness cartilage injuries do undergo some degree of regeneration by initiating a typical inflammatory response, which consists of hematoma formation, mitogenic chondrocyte activity, and vascular ingrowth.¹²,¹³ Unfortunately, the fibrocartilage produced by this inflammatory response, as opposed to healthy hyaline cartilage, gradually deteriorates and leads to the progression of osteoarthritis (OA) due to its inferior biomechanical properties.¹¹,¹⁴,¹⁵,¹⁶

Thus, due to its avascular and aneural nature, articular cartilage has poor intrinsic healing capacity and is often susceptible to injury and degeneration into chondral lesions.⁶,¹⁷,¹⁸ Over time, the articular surface may become destabilized from the subchondral bone and resultant shear forces may wear away the resulting fragment in a process known as osteochondritis dissecans (OCD).¹⁹ Some causes for chondral lesions may include repetitive microtrauma, genetic predisposition, or vascular ischemia.²⁰ Left unmanaged, these lesions can be debilitating for active patients and lead to the early onset of OA. One of the challenges of developing an adequate treatment for defects lies in the complex structure and function of healthy hyaline cartilage, as the entire osteochondral unit must be restored rather than just the articular surface.¹¹,¹²

The prevalence of chondral defects is estimated at 15 to 30 per 100,000, the majority of which occur in the knee. Focal chondral defects have been reported in up to 89% of high-level athletes due to the repetitive load-bearing stresses that occur during activity.²¹,²²,²³,²⁴ However, these defects are not confined to solely athletes, as focal cartilage defects have been identified in over 60% of patients undergoing knee arthroscopies.³,²⁵,²⁶ Nearly 80% of the cases involve the medial femoral condyle (MFC), 15% involve the lateral femoral condyle, and 5% involve the patellofemoral region.²⁷,²⁸

Patients may typically complain of catching, pain, crepitus, and effusion, which often prevent these patients from participating in their usual daily activities, and larger lesions have a significant risk of progressing to OA.²⁹ The challenge has been finding a process that restores the joint surface congruity, controls the patient’s symptoms, is able to withstand the intra-articular forces of the knee over time, and prevents the progression of focal chondral injuries to end-stage OA. The treatment modality is largely contingent upon the stability of a lesion; patients having a short duration of symptoms and a stable lesion can be managed successfully with just a hiatus from sporting or high-impact activity. In the setting of an unstable lesion
or failure of nonsurgical management, there are a number of treatment modalities that can be used to repair the lesion and can be classified as either palliative, reparative, restorative, or reconstructive procedures.

Palliative approaches may include loose body removal or débridement which may provide short-term symptom relief.³⁰,³¹,³²,³³ Reparative procedures may include microfracture/marrow stimulation or drilling, which stimulates the defect to be filled with fibrocartilage.³⁴ The resulting hyalinelike cartilage from restorative procedures such as autologous chondrocyte implantation (ACI) may provide better long-term durability than fibrocartilage due to its superior viscoelastic and force distribution properties.³⁴,³⁵ Finally, reconstructive procedures place a preformed osteochondral unit directly into the defect area and include osteochondral allograft (OCA) or autograft. Each procedure comes with its own indications and contraindications—age, lesion characteristics, level of activity, and patient expectations are just a few factors that must be considered in order to choose the best treatment modality for a patient. The purpose of this chapter is to explore outcomes, discuss the general indications and contraindications, and postoperative management for each of these techniques.

More recently, the role of different techniques has been further defined with respect to lesion location, lesion size, and specific patient demands.³⁶ Although primary repair is preferred for any cartilage injury that is amenable to fixation in a natural position, microfracture is indicated in the case of moderate symptoms, small-to middle-sized lesions (i.e., <2-3 cm in size), and grade III/IV (modified Outerbridge classification) OA.³⁷,³⁸ Microfracture represents an optimal treatment for femoral condyle lesions <2 to 3 cm in size in both low-demand patients but results can deteriorate in high-demand patients, patellofemoral lesions, or large (i.e., >2-3 cm) lesions.³⁶ Treatment decisions are more complex in patients with large femoral condyle lesions. OCA transplantation or ACI is the preferred treatment option in patients with high demands; however, in moderate demand patients, microfracture may be a reasonable alternative. Prior surgical treatment may also guide indications as patients with a history of failed microfracture treatment for the lesion in question may be best suited for a reconstructive option.³⁶ Lesion depth should also be considered, as deeper lesions often involve significant bone and are best treated with OCA³⁹ (Fig. 25-1).

FIGURE 25-1 Indications for cartilage treatment: an overview. ACI, autologous chondrocyte implantation; OCA, osteochondral allograft; MFX,Microfracture; OAT, osteochondral autograft.

OVERALL CARTILAGE INDICATIONS

General indications for cartilage treatment beyond débridement include full-thickness cartilage defects, unstable cartilage defects overlying subchondral bone, and unstable partial-thickness defects.⁴⁰ Concurrent angular deformity of the knee also needs to be addressed in these patients at the time of cartilage treatment.⁴¹ Other important considerations include ligamentous insufficiency (i.e., anterior cruciate ligament [ACL], posterior cruciate ligament [PCL]) and meniscal deficiency, which may require concurrent treatment.⁴²,⁴³ Partial
meniscectomy is considered in patients with meniscal injury, although outcomes in those with severe chondral damage have demonstrated elevated rates of subsequent OA following meniscectomy.⁴⁴ Additionally, the role of anteromedialization procedures, particularly in the case of lateral patellofemoral lesions, is emerging.³⁶,⁴⁵

Contraindications for cartilage treatment include systemic diseases that may predispose to arthritis (i.e., posttraumatic, postinfectious), diseases altering the therapeutic release of marrow factors (i.e., systemic, immune-mediated disease), or primary cartilage diseases that may alter the functionality of the articular cartilage (i.e., polychondritis, OCD). Global degenerative osteoarthrosis, capsular contraction, synovitis, partial-thickness defects, or scarring of the anterior interval has previously been identified as contraindications.⁴⁶ Cartilage procedures should not be performed in patients unable to tolerate weight-bearing on the contralateral leg or unable to follow postoperative rehabilitation protocols.⁴⁶ When considering the defect location, overall alignment, defect size, and patient demands, one can understand the best treatment option available to the patient (Fig. 25-1).

MICROFRACTURE

Microfracture was originally designed as a surgical intervention for patients with posttraumatic cartilage lesions which progressed to full-thickness cartilage defects.⁴⁶ The procedure relies on an influx of marrow factors (i.e., mesenchymal stem cells, growth factors), formation of a fibrin clot, and subsequent remodeling into fibrocartilage.⁴⁷ Due to the advancement of more involved cartilage techniques (i.e., ACI, matrix-associated chondrocyte implantation [MACI]) as well as limited outcomes, microfracture has taken a lesser role in treatment of cartilage defects.⁴⁸,⁴⁹ Due to its ease of implementation, microfracture has been utilized in settings that differ from large restorative or reconstructive options. Specifically, indications for correcting meniscal deficiency, alignment, and postoperative weight-bearing have not been as stringent as with other cartilage procedures. Current evidence suggests that optimal outcomes are seen in patients with lesions <2 to 3 cm², no prior cartilage surgery, and age <30 years old. Femoral condyle lesions also have better outcomes than the patella and other options should be considered in this region.

Technique

After general anesthesia allows for appropriate muscle relaxation, an examination under anesthesia is performed to confirm the absence of ligamentous laxity or possible mechanical symptoms suggestive of a possible meniscal injury. The patient is most commonly positioned supine. A posterior lesion can necessitate knee hyperflexion that should be accounted for prior to initiation of arthroscopy.

Diagnostic arthroscopy requires a standard three-portal system with an anteromedial, anterolateral, and optional proximal outflow portal. Tourniquet use is not required, and arthroscopic pump pressure is varied to optimize viewing. A complete diagnostic workup includes inspection of the suprapatellar pouch, gutters (i.e., medial, lateral), the intercondylar notch, and both the patellofemoral and tibiofemoral (i.e., medial, lateral compartment) joints. A graduated probe can be utilized to inspect tears of the inferior aspect of the meniscus. The intercondylar notch must be inspected to ensure ligamentous stability of the ACL and PCL. Unstable chondral lesions should be marginally debrided to create an appropriately stable chondral border, devoid of loose bodies. The final, clean, stable lesion should provide a perpendicular surface of healthy, viable cartilage to ensure appropriate clot creation and proliferation.⁴⁶,⁴⁰ Chronic lesions can present a unique technical challenge due chronic cartilage degeneration, bony sclerosis, and subchondral thickening. In these scenarios, it becomes important to create a stable chondral surface with punctate bleeding uniformly over the cartilage surface to ensure appropriate propensity toward clot formation.⁴⁰ A degenerative knee may also warrant surgical release of the anterior interval via the intermeniscal interval, particularly if scarring is identified during the diagnostic portion of the procedure. Typically, if these procedures are necessary, the patient is poorly indicated for microfracture.

The microfracture is classically performed as the final intra-articular procedure of a case with the hopes of optimizing marrow release and fibrin clot formation.⁴⁰ Two important variations exist with respect to this instrumentation. Traditional methods utilize a microfracture awl to create perpendicular perforations in subchondral bone at depths of 2 to 4 mm.⁴⁰ More recent techniques utilizing microdrilling result in limiting bony compaction⁵⁰; however, there are concerns of thermal necrosis⁴⁶ (Fig. 25-2A and B). Using the preferred instrumentation, subchondral bone is perforated beginning at the lesion periphery and ending with the central site of microfracture. Careful distances between perforations are approximated such that fracture across the subchondral bone plate is appropriately avoided (i.e., 2-4 mm).³⁶ Fat droplets are commonly visualized at the bony fracture site, and bony bleeding can be utilized to gauge appropriate depth of penetration. Intra-articular drains are generally avoided due to concerns of limiting efficient marrow factor release to propagating of a fibrin clot.⁴⁶ The fibrocartilage clot has previous been described by Cole and associates as a “superclot,” due to the pluripotent nature of mesenchymal stem cells released from the marrow in the formation of fibrocartilage structure.³⁶ The microfracture can also be filled with micronized allogeneic cartilage which can help to act as a scaffold for the creation of hyalinelike cartilage. This allogeneic cartilage is typically mixed with platelet-rich plasma and applied in smaller defects and then sealed with a fibrin glue (Fig. 25-2C and D).⁵¹

FIGURE 25-2 Microdrilling and application of biocartilage to the trochlea and lateral tibial plateau. A and B: Osteochondritis dissecans (OCD) lesion is debrided and the bone is microdrilled several times to release marrow elements. C: A mixture of platelet-rich plasma and allogeneic cartilage is applied to the site of the microfracture. D: A thin layer of fibrin glue is applied to the surface of the filled defect.

Outcomes

There are numerous results published in the literature detailing outcomes following microfracture with varying results.⁵²,⁵³,⁵⁴,⁵⁵,⁵⁶,⁵⁷,⁵⁸ Table 25-1 summarizes the results of these previous studies.

Early investigations of microfracture generally demonstrated positive short-term outcomes.

Steadman and associated detailed clinical outcomes in 24 patients who underwent microfracture with a 24-month follow-up (61). Patients in their study were an average age of 38 years and injury date ranged from 1 day to 10 years. The author’s reported that at 3 years postoperatively, 75% of patients (152 of 203) had less pain; 19% had unchanged pain; and 6% felt worse. Additionally, the authors found negative predictors of postoperative outcomes to include preoperative joint space narrowing, age >30 years, chronicity of lesions, isolated defects, and non-CPM (continuous passive motion) use postoperatively. Outcomes in this study were not affected by lesion size, and survivability of the procedure demonstrated a small decline over 7 years (95% at 4 years, 92% at 7 years).

In 2000, Passler reported on subjective results on 162 of his patients who received microfracture (74). Seventy-eight percent of patients receiving a microfracture reported reduced pain, 18% reported no change, and 4% reported they were worse at a mean follow-up of 4.4 years (range, 3-6 years).

TABLE 25-1 Clinical and Functional Outcomes Following Microfracture

Study	Technique	Number of Patients	Outcome Measures	Results	Findings
Dzioba⁵⁵ (1-y follow-up)	Drilling	48	Pain	69% pain free; 31% had persistent pain and/or effusions
Rodrigo et al⁵⁸	Microfracture	77	Lesion appearance (second-look arthroscopy)	Better defect filling when CPM used postoperatively (P = .003)	Extent of filling did not correlate with functional outcome
Levy et al⁵³ (1-y follow-up)	Débridement of calcified cartilage layer only	15 soccer players	Brittberg scoring system	6 excellent; 9 good; 0 fair; 0 poor	High-demand population
Steadman et al⁵⁴ (5-y follow-up)	Microfracture		Subjective questionnaire, pain, ADLs, work, sports participation	Pain: 75% improved; 20% unchanged; 5% worse. ADLs and work: 67% improved; 20% unchanged; 13% worse. Sports: 65% improved
Blevins et al⁵²	Microfracture	38 “high-level” athletes and 140 recreational athletes	Subjective questionnaire: pain, swelling, giving way, locking. Lesion appearance (second-look arthroscopy)	All functional parameters were significantly improved in both groups after surgery. Grading of lesion improved in both groups (P > .05)	Numerous associated diagnoses and concomitant procedures
Passler⁵⁶ (3- to 6-y follow-up)	Microfracture	162	Subjective questionnaire: pain	78% improved; 18% unchanged; 4% worse
Steadman et al⁵⁷ (3-y follow-up)	Microfracture	203	Subjective questionnaire: pain	75% improved; 19% unchanged; 6% worse	Negative predictors:
Steadman et al⁵⁷ (3-y follow-up)	Microfracture	203	Subjective questionnaire: pain	75% improved; 19% unchanged; 6% worse		Age >30 y Chronicity Isolated defect No CPM Size >300 mm² was not a negative predictor
ADL, activities of daily living; CPM, continuous passive motion.

Though early outcomes were encouraging, there is growing concern that these results may not be maintained. Mithoefer et al performed a systematic review of 3122 microfracture procedures with extended follow-up.⁵⁹ The author’s reported a significant improvement in knee function postoperatively with a short-term clinical improvement rate of 75% to 100% at 24 months postoperatively. However, after 24 months, 47% to 80% of patients reported a subjective decline in functional outcomes. Other studies have corroborated the regression of positive outcomes at long-term follow-up.⁶⁰,⁶¹,⁶² More recently Solheim and colleagues reported on long-term (>15 years) outcomes following a randomized controlled trial comparing microfracture to mosaicplasty.⁶³ The author’s found a significant improvement in all patients at 15-year follow-up. However, there was a clinically significant difference in Lysholm knee scores at all time points postoperatively with mosaicplasty demonstrating more beneficial outcomes. Patient characteristics including greater BMI (>30 kg/m²), larger defects (>2.5 cm²), and higher physical activity level have been correlated with decreased outcomes following microfracture.⁶⁴,⁶⁵,⁶⁶,⁶⁷ Kraeutler and associates performed a systematic review of three level 1 studies and two level 2 studies reporting 5-year outcomes following microfracture or ACI.⁶⁸ The authors found no difference in treatment failure at an average of 7 years postoperatively. Additionally, Lysholm score and Knee injury and Osteoarthritis Outcome Score (KOOS) were found to improve for both groups across studies, without a significant difference in improvement between the groups. In professional athletes including those in the National Basketball Association (NBA), there is a high rate of failure to return to sport (21%)⁶⁶,⁶⁷. In these high-level athletes, microfracture was correlated
with decrease player efficiency, minutes per game, and points per game. It is evident that the induction of marrow stimulation to produce fibrocartilage does not recreate the natural structure and strength of hyaline articular cartilage. This renders the surface less durable and more prone to wearing out over time, especially when enduring high-impact activities. It should be noted that in more recent studies which have shown regression in outcomes with follow-up, the procedure was performed with an awl and impaction technique which has potential limitations in cartilage defect treatment. Current techniques of marrow stimulation utilize microdrilling which has been theorized to limit bony compaction and facilitate greater delivery of mesenchymal cells into the defect. Future studies should employ randomized controlled trials and prospective studies comparing long-term outcomes of newer generation microfracture techniques compared to alternative resurfacing techniques.

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