Microfracture

Armando F. Vidal, MD

Rebecca Griffith, MD

Dr. Vidal or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of Smith & Nephew; serves as a paid consultant to or is an employee of Smith & Nephew and Stryker; has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-research-related funding (such as paid travel) from Smith & Nephew and Stryker; and serves as a board member, owner, officer, or committee member of the American Orthopaedic Society for Sports Medicine. Neither Dr. Griffith nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.

This chapter is adapted from Vidal AF, FitzPatrick J: Microfracture, in Flatow E, Colvin AC, eds: Atlas of Essential Orthopaedic Procedures. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2013, pp 76-83.

INTRODUCTION

Chondral lesions of the knee are frequently encountered during arthroscopic procedures and can commonly be a source of pain and recurrent effusions. In the young patient, the presence of chondral pathology can be complicated by instability, malalignment, and meniscal insufficiency. It has been known for decades that articular cartilage has limited intrinsic healing capacity; therefore, various different cartilage repair strategies have been developed. Broadly, these strategies have included marrow-stimulating techniques such as microfracture, autologous and allograft osteochondral transplants, and autologous chondrocyte implantation in the case of femoral condyle lesions.

Microfracture remains an excellent option for the treatment of chondral defects that require surgical intervention for symptomatic relief. It is a single-stage procedure that has been proven to be a cost-effective management strategy in the appropriate setting with correct indications.¹ Marrow-stimulating techniques rely on perforation of the subchondral plate, which allows pluripotential mesenchymal cells to fill the defect and create a hybrid fibrocartilage repair. Recent technological advances have focused on augmentation of the microfracture procedure using biologic acellular scaffolds with the goal to retain the mesenchymal cells and growth factors in a concentrated fashion at the site of the defect. Furthermore, multiple groups are now looking at augmenting the factors themselves with intra-articular injections at time of microfracture including hyaluronic acid, mesenchymal stem cells, and platelet-rich plasma.²^,³ Although these techniques may appear promising, they lack long-term results at this time and their application will not be addressed in this chapter.

Patient Selection

For many patients, the microfracture technique is the first-line treatment of full-thickness cartilage lesions (Outer-bridge grade IV) because of its success, relative ease, and cost effectiveness. In addition, when unsuccessful, it generally does not preclude the use of other cartilage restoration techniques as subsequent treatment options. The selection criteria for a successful outcome are very specific, however.

Indications

Clinically important parameters when considering the suitability of a patient for microfracture include size, location, and containment of the articular cartilage lesion; status of the meniscus; age of the patient; and body mass index. Although there is some controversy as to the maximum size of the lesion, many describe the “ideal” lesion as less than 2 cm² and not exceeding an area of 4 cm². Additionally, the lesion should be unipolar and well contained. Microfracture is not indicated for degenerative, bipolar lesions. Femoral condylar lesions are ideal; however, microfracture can be performed on any articular surface. Generally, the results are less favorable for lesions in the patellofemoral compartment. Additionally, the ability of these pluripotential cells to differentiate into cartilage is influenced by age. Several authors have shown better results in younger patients who are less than 40 years old and those with isolated lesions.⁴^,⁵

Contraindications

Contraindications to microfracture include bipolar lesions, diffuse degenerative joint disease, uncorrected malalignment, significant loss of meniscal tissue, and patients who will not be able to fulfill or comply with the
required postoperative protocol. Bipolar lesions preclude the appropriate healing environment because there are two incongruent surfaces in contact with one another.⁶ Lesions with subchondral bone loss and uncontained lesions are not amenable to microfracture for similar reasons (eg, osteochondral defect). Uncorrected malalignment will cause abnormal mechanics, which will place increased loads on the microfractured surface.⁷^,⁸ Longer duration of preoperative symptoms, patellofemoral osteochondral lesions, and a body mass index greater than 30 kg/m² may also have an association with poorer outcomes.⁴^,⁸^,⁹

PREOPERATIVE IMAGING

The diagnostic imaging begins with plain radiographs. A standard series includes four views: weight-bearing AP, weight-bearing 45° PA, lateral, and Merchant. In patients with chronic or degenerative conditions, these views can help determine if the degree of arthrosis is too severe or diffuse to consider microfracture as a viable option. In an acute injury, these four views may reveal a donor site and a loose body consistent with an osteochondral fragment. When any cartilage repair technique is being considered, including microfracture, long leg alignment radiographs must also be obtained to evaluate for any angular deformity that may require concomitant treatment. Focal cartilage lesions that satisfy these criteria in the setting of varus malalignment or patellar instability can be treated successfully with combined microfracture and high tibial osteotomy or microfracture and patellar stabilization procedure.⁷^,⁸

MRI also has become a standard diagnostic imaging technique. Cartilage-specific MRI sequences can accurately diagnose cartilage injury (Figure 1). Standard sequences include proton density-weighted fast spin-echo imaging with or without fat saturation, T2-weighted fast spin-echo imaging with or without fat saturation, and T1-weighted gradient-echo imaging with fat suppression. There are some newer sequences that have been validated to look at cartilage based on its biology including delayed gadolinium-enhanced MRI and sodium MRI sequences.¹⁰ In addition to the chondral injury, MRI will reveal any concomitant meniscal or ligamentous pathology that may need to be addressed.

FIGURE 1 Cartilage-specific MRI sequences. A, Transaxial proton-density fast spin-echo fat-saturation MRI demonstrates a posterior femoral condyle lesion. B, Coronal proton density-weighted fat-saturation MRI demonstrates a medial tibial plateau lesion.