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Key Considerations With Primary Repair Of Osteochondral Lesions

Is microfracture surgery worthwhile? Are marrow stimulation techniques effective? Can particulated juvenile allograft cartilage have an impact? Addressing these questions and more, the authors offer a thorough review of the literature and share pertinent insights on surgical treatment of osteochondral lesions. 

In order to properly repair cartilage defects, it is important that we understand the nature of these defects. Cartilage is smooth elastic tissue composed of glycosaminoglycans, proteoglycans, collagen fibers and elastin. It is both avascular and aneural, and protects the ends of bones at the joints. Cartilage has a very slow turnover of its extracellular matrix (ECM) and does not regenerate. It has limited repair capabilities because chondrocytes are bound in lacunae and cannot migrate to damaged areas. This causes much difficulty in healing any cartilage damage. Deposition of new matrix is slow because hyaline cartilage does not have a blood supply. Fibrocartilage scar tissue usually replaces damaged hyaline cartilage.1

Hyaline cartilage is the native cartilage on the joint surfaces of long bones in humans. Hyaline cartilage has fewer cells than elastic and fibrous cartilage, and more intercellular space. The layers of articular cartilage include hyaline cartilage, tidemark, calcified cartilage and subchondral bone. 

Hyaline cartilage in the talus is different than anywhere else in the human body. The cells and extracellular matrix components are identical, but it behaves differently with respect to response to injury and susceptibility to injury.2 Mean ankle joint articular cartilage thickness ranges from 1.0 to 1.7 mm thick in comparison to the articular cartilage in the knee that ranges from 1.5 to 6.0 mm in thickness depending on location.3,4 

Talar dome osteochondritis dessicans (OCD) classification includes constrained or unconstrained lesions, depending on whether the defect extends to breach the subchondral plate at either the medial or lateral shoulder of the talar dome.5 Constrained lesions have an intact margin of healthy bone and cartilage after debridement whereas unconstrained lesions tend to lack distinct margins, such as a shoulder lesion that extends into the gutter of the ankle or a lesion with an underlying cyst.5 Talar dome OCDs can also be laminated or delaminated. Chondral delamination is the separation of the articular cartilage from the underlying subchondral bone at the tidemark.6 Eighty percent of OCDs in the ankle are not delaminated and involve articular cartilage and subchondral bone.

Reports of these injuries suggest they are caused by shearing stress concentrated at the junction of non-calcified and calcified cartilage.6,8-10 The mechanism of injury associated with delamination injuries, acute shear forces, produces painful lesions. Cartilage delamination injuries can occur as an isolated chondral injury or in association with a second cartilage injury. 

Early identification of these injuries is important as they have a poor prognosis when they are unrecognized or untreated. Identification of these lesions preoperatively can alert the surgeon of the extent of the cartilage injury and the extent of debridement necessary to treat the lesion. Advanced imaging is necessary for detection of chondral delamination injuries. On magnetic resonance imaging (MRI), chondral delamination injuries show linear T2-weighted signal intensity of joint fluid at the interface of the articular cartilage and subchondral bone.

A long-standing debate among foot and ankle surgeons is why osteochondral lesions are so painful when cartilage lacks nerve innervation. Van Dijk and colleagues theorized that pain is caused by synovial fluid that is forced underneath cartilage and into subchondral bone, leading to subchondral cyst formation and increased pressure within the talus.11 

The outcome after an acute talar dome osteochondral impaction injury is variable. The chondral surface may remain intact and there may be resolution of the subchondral bone marrow edema without complication. On the other hand, the relatively poor, retrograde blood supply of the talar dome predisposes to incomplete healing and the development of focal areas of ischemic and devascularized subchondral bone. In this bone, there may be resorption of subchondral trabeculae, replacement with fibrotic tissue and successive development of cystic changes.12

In addition, any fissuring or break in the chondral surface and subchondral plate can lead to synovial fluid inflow into the subchondral bone. Bone marrow edema is usually evident within hours of injury and will generally persist for several months. Eriksen and Ringe suggest bone marrow lesions correspond with pain because they denote a recovery response to underlying traumatic injury and trabecular damage.12 Cystic change almost always develops at sites of preexisting bone marrow edema signal and can vary from a predominantly fibrotic appearance to fluid-filled content in talar dome osteochondral lesions.5

What Is The Role Of Microfracture In Cartilage Regeneration?

There is much controversy in the cartilage regeneration community regarding the efficacy of microfracture in recent years. The original theory behind microfracture is that subchondral penetration causes bone marrow stimulation, leading to the formation of fibrocartilage. While fibrocartilage is not as durable and effective as the original hyaline cartilage, researchers have noted the short-term efficacy of fibrocartilage as a temporary solution for pain caused by acute OCDs.13 Recent literature shows the lack of long-term efficacy surrounding microfracture, leading to a newer theory behind approaching acute lesions. 

It does not make sense to damage subchondral and cancellous bone, since the body does not have the ability to heal insufficient bone. One can only use true microfracture on delaminated cartilage lesions. Many cases of ankle osteochondral lesions involve “failed” subchondral bone or bone cysts. Microfracture allows for fluid penetration below subchondral bone, which leads to increased intraosseous pressure. Bone is “soft” to begin with, and becomes softer by iatrogenic placement of additional holes into it. Unfortunately, the body is unable to recover from this, leading to failure of this treatment protocol. 

In a 2018 study, Solheim and colleagues investigated the survival of cartilage repair in the knee by comparing microfracture (119 patients) and mosaicplasty/osteochondral autograft transplantation (OAT) (84 patients).14 They found only a 60 percent survival rate for microfracture repair at three years and determined that mosaicplasty/osteochondral autograft transplantation were more durable. Solheim and coworkers concluded that microfracture articular cartilage repairs failed more often and earlier than the mosaicplasty/osteochondral autograft transplantation repairs, both in the whole cohort and in a subgroup of patients matched for age and size of treated lesions.14

Pertinent Imaging Pearls

The ultimate goals of imaging chondral and osteochondral lesions in the ankle are primarily detection, demonstration of position and extent, including status of the chondral surface, demonstration of any associated chondral delamination, assessment of the integrity of the subchondral plate and assessment of the cancellous subchondral bone for bone marrow edema-like signal, sclerosis, cystic change and for presence of an unstable osteochondral fragment.15

Plain film radiographs, computed tomography (CT) and bone scan may help in detection and characterization of these lesions. However, only magnetic resonance imaging (MRI) provides a comprehensive assessment of all these pathologies, making it the gold standard for assessment of OCDs.5 Magnetic resonance imaging reportedly has a sensitivity of 0.96 and a specificity of 0.96 in the diagnosis of these lesions.15 However, we advise caution that MRI can often overestimate the extent of the lesion and the only true way to assess the lesion is through direct visualization.

A Guide to Treatment Options and Techniques for Talar OCD

Early diagnosis of talar osteochondral lesions is imperative and leads to better patient outcomes.16 Clinically, patients with talar osteochondral lesions tend to present with low-grade aching ankle pain months after an ankle sprain or other ankle trauma. Patients typically describe an aching, deep pain and note ankle instability, catching or locking. Physical exam findings tend to include reduced or painful ankle joint range of motion, and mild non-pitting edema. Tenderness or pain with palpation may exist either medially or laterally on the ankle joint as well.16

Treatment depends on the location and size of the defect as well as the presence of secondary degenerative changes. At earlier stages, one should initiate non-surgical treatment options, including non–weightbearing and immobilization in a controlled ankle movement (CAM) boot or short leg cast, corticosteroid injections and/or physical therapy.16 It is best to exhaust conservative treatment options prior to surgical intervention. However, non-surgical treatment options for osteochondral lesions of the talus only have a reported success rate of 45 percent in the literature.15,17 

Surgeons can approach cartilage repair in the ankle joint arthroscopically or through an open or mini-arthrotomy. There are several advantages to the arthroscopic approach in comparison to the open approach. Arthroscopy is less invasive, requiring only two small stab incisions for portal access.18 This approach allows the surgeon and patient to avoid open arthrotomies and risky malleolar osteotomies. The arthroscopic approach can improve patient outcomes by allowing outpatient treatment, decreasing postoperative morbidity and permitting faster and more functional rehabilitation.18 The major disadvantage to the arthroscopic technique is its large learning curve. 

In some rare cases, with hard-to-reach osteochondral lesions, the open approach is necessary. The open approach provides full joint access, direct visualization of the ankle joint and is good for surgeons lacking confidence and/or experience in arthroscopy. Disadvantages to this approach include increased risk of infection and wound dehiscence, the possibility for increased surgical time, increased risk of neurovascular compromise, and longer recovery time.18

Several surgical treatment options are available for treatment of cartilaginous lesions, including excision and debridement, marrow stimulation techniques, osteochondral autografts, and osteochondral allografts. Marrow stimulation techniques are typically first-line treatment options due to their relative ease, quicker recovery time and ability to perform arthroscopically. This technique has fallen out of favor in recent literature due to the concept of bone marrow stimulation causing irreversible damage to the subchondral bone, leading to continued pain and procedural failure.19 

Seow and coworkers reviewed 17 animal studies with 520 chondral lesions for the purpose of clarifying the morphology of subchondral bone following bone marrow stimulation in preclinical, translational animal models.19 Their results demonstrated that the morphology of subchondral bone did not recover following bone marrow stimulation. In comparison with untreated chondral defects, bone marrow stimulation resulted in superior morphology of superficial subchondral bone and cartilage, but inferior morphology, specifically bone density, of the deep subchondral bone.19 

One should reserve true microfracture for delaminated cartilage lesions, which is difficult in the ankle since 80 percent involve the subchondral plate.7 Retrospective studies looking at the success rates of microfracture show good to excellent results in 39 to 96 percent of cases.20 This large variation in success sparked a lot of debate in the foot and ankle community regarding the efficacy of microfracture as a standard treatment option for cartilage repair. 

Microfracture involves drilling through the subchondral bone, allowing bone marrow substrates to leave the subchondral bone and fill the defect.13 This process leads to angiogenesis and the production of a clot primarily composed of fibrocartilage, which provides high tensile strength and support. Marrow stimulation procedures do not promote the excretion of growth factors or extracellular matrix proteins necessary for repair and regeneration of healthy hyaline cartilage, making it a short-term solution.13 

Recent literature has shown long-term failure of microfracture, with researchers noting recurrence of pain and joint stiffness.21 The study authors prefer abrasion chondroplasty with implantation of juvenile allograft cartilage, which is supported in the literature.21 

Emerging Advanced Modalities For Cartilage Restoration

In many cases, marrow stimulation procedures may not be adequate, leaving the patient with continued pain, requiring more advanced cartilage restoration techniques. There are multiple options for cartilage restoration including cartilage replacements, biological cartilage scaffolds and pluripotent cells.20

Cartilage replacement allografts provide donor allografts for repair of OCDs and allow the ability for hyaline cartilage regeneration in a single-staged procedure. In addition, osteochondral allografts have increased healing potential since they are more metabolically active, have a denser concentration of chondrocytes and initiate less of an immune response.20,22,23

Our preferred technique includes the use of particulated juvenile allograft cartilage (PJAC), comprised of morselized cartilage fragments from cadaveric donors under the age of 13 since higher levels of type II collagen and proteoglycan production typically exist in cartilage donors from this age group in comparison to adults.24 The juvenile allograft cartilage is chondroinductive, chondroconductive and chondrogenic, making it an ideal graft option for cartilage regeneration.25 Juvenile chondrocytes have the ability to migrate from the extracellular matrix and proliferate to form neocartilage that integrates with surrounding native articular cartilage.25-29 With particulated juvenile allograft cartilage, there is a minimal amount of manipulation and processing, thereby increasing the risk of disease transmission that comes with its use.27

The current literature shows that particulated juvenile allograft cartilage is effective for large and small osteochondral lesions, and as an index procedure to treat the lesion.30 Contraindications for particulated juvenile allograft cartilage include degenerative arthritic changes and history of infection. Surgeons often treat large cystic lesions with cancellous chips, structural bone graft or flowable calcium phosphate injections, followed by placement of particulated juvenile allograft cartilage over the top of the cartilage defect.31 

Hatic and Berlet first described the technique for particulated juvenile allograft cartilage placement in 2010, performing this procedure with an open ankle joint arthrotomy.32 

In 2012, Kruse and team, including the senior author, published a more efficient and non-invasive technique for performing the particulated juvenile articular cartilage graft technique arthroscopically.22 After induction of anesthesia and ensuring a sterile field in the usual aseptic manner, one applies a non-invasive ankle distractor and obtains standard anteromedial and anterolateral arthroscopic portals. The surgeon identifies the osteochondral lesion of the talus and debrides down to healthy subchondral bone using arthroscopic shavers and curettes, taking care to ensure a sharp line of transition of healthy cartilage around the lesion.

In cases in which the subchondral bone is not intact, the first layer of fibrin glue, one applies, prevents bleeding of the cancellous bone, allowing the implant to adhere to the adhesive surface. To prepare the ankle joint for implantation, the surgeon dries the joint with an abdominal insufflator and normal arthroscopic suction. Utilizing the insufflator allows for maintenance of joint distension and prevents the joint from overheating. One directly dries the osteochondral bed with cotton tip applicators prior to glue placement. Once the subchondral bone of the osteochondral lesion of the talus is dry, one inserts the cartilage graft through a 10-gauge catheter in the anteromedial portal onto a layer of fibrin glue. Then the surgeon applies a second layer of fibrin glue over the cartilage to fill the remaining defect. The insufflator is then once again employed to ensure that the fibrin glue is dry to the touch before closing the arthroscopic portals.13 Studies show that chondrocytes have the ability to migrate through fibrin glue within two weeks.33,34

In the aforementioned work by Kruse and colleagues, the authors utilized particulated juvenile articular cartilage graft in the arthroscopic repair of a full-thickness, posteromedial 7 x 5 mm osteochondral lesion of the talus in a 30-year-old woman.22 At a two-year follow-up, the patient presented pain-free at full activity with no restrictions. 

Utilizing the validated Foot and Ankle Outcome Score (FAOS) in a retrospective review, Chopra and colleagues reviewed clinical outcomes in patients treated with an arthroscopic implantation of particulated juvenile articular cartilage graft between 2008 and 2016.35 They evaluated 32 patients with mean age of 40.7 years and a mean follow-up time of 24 months. The researchers noted that 28 out of 32 patients (88 percent) scored a good or excellent result in activities of daily living. They found that 26/32 (81 percent) patients had at least good results in both pain and symptoms and 25/32 (78 percent) patients had at least a fair result for functional sports and quality of life. 

The study authors concluded that although particulated juvenile articular cartilage graft implantation for repair of OCDs is a fairly new line of treatment, their study results provide strong evidence of the potential effectiveness of this procedure.35 The use of juvenile cartilage increases the number of immature chondrocytes, which are more metabolically active and capable of spontaneous repair, giving them the ability to differentiate into hyaline-like cartilage instead of fibrocartilage.22,36 

Can Synthetic Calcium Phosphate Have An Impact? 

There is much debate surrounding the question of why some osteochondral lesions are painful and others are not. One new theory questions whether pain stems from the chondral lesion itself or is initiated more by underlying bone marrow edema. There is a prevailing belief that intra-articular pressure forces synovial fluid through microfissures in the subchondral plate, causing subchondral cysts and the formation of bone marrow lesions. 

A new technique involves injecting flowable synthetic calcium phosphate directly into the bone marrow lesion. In our experience, this technique buttresses the internal architecture of the bone marrow lesion, providing stability and allowing healing with internal support. 

The technique involves standard arthroscopy followed by identification, visualization and fluoroscopic assistance for triangulation of the location of the osteochondral defect to make sure placement is accurate. One then places the injectable synthetic calcium phosphate directly into the bone marrow lesion under fluoroscopic and/or arthroscopic guidance. Using fluoroscopy and the original MRI as reference, one inserts a cannula into the area of the bone marrow lesion, taking care to correlate and triangulate positioning on true AP and lateral fluoroscopic views. Injection is under thumb pressure only, in order to flow into the area of insufficient bone. Leakage into the joint often occurs and is easy to remove with an arthroscopic shaver. Leakage into the joint may be a sign of accurate placement. Another indication of proper placement includes the extrusion of fat bubbles from the osteochondral lesion. 

Essential Post-Op Principles

Correct, pathology-specific, procedure selection is imperative for providing the best chance of repair; however, postoperative protocol is just as important. 

Marrow stimulation procedures such as excision and debridement, microfracture and abrasion chondroplasty all have a similar typical postoperative course. The senior author’s typical protocol involves patients remaining in a fracture boot for four weeks with early range of motion at week two, subsequent transition into an ankle brace and continued physical therapy. Full return to activity without restrictions is expected around three months. If pain should persist at six months, the senior author recommends MRI to evaluate for failure of subchondral bone and failure to heal the marrow stimulation site.

The postoperative course following particulated juvenile articular cartilage graft includes non–weightbearing for four weeks in a fracture boot with range of motion starting at two weeks. These range of motion exercises should include ankle dorsiflexion and plantarflexion without inversion or eversion. Patients should start physical therapy with no axial loading to the ankle and no single leg exercises at four weeks. At eight weeks, patients may begin non-impact exercises (biking, swimming, rowing) with no axial impact (running, stairs, hopping) for four months. 

The senior author advises against obtaining MRI too early in the postoperative course since the particulated juvenile articular cartilage graft will be hydrophilic for up to 18 months. This could lead to MRI reports stating that the OCD is still present. From the senior author’s experience, after second looks at months four, six, 12 and 18 months, stable cartilage is evident at month four, with full incorporation of cartilage at around 18 months. If pain and stiffness persist at four to six months postoperatively, the senior author recommends considering repeat arthroscopy to clean out arthrofibrosis that one may see with overgrowth of the repair site. 

In Conclusion

Significant improvements and advancements have emerged in cartilage restoration techniques over the last decade. Ask yourself if you are using a technique that has fallen out of favor or one that has proven ineffective in the long term. We owe it to our patients to stay current on the most progressive, evidence-based techniques available. By taking the time to understand what makes these lesions so painful, we can address the true pathology and improve patient outcomes. 

Dr. Ng is a fellowship-trained foot and ankle surgeon who is in private practice in Denver, CO. He is the Director of the Rocky Mountain Reconstructive Foot & Ankle Fellowship in Denver, CO. He is a board member and Fellow of the American College of Foot and Ankle Surgeons, and a Past President of the American Board of Foot and Ankle Surgery.

Dr. Rao is a Reconstructive Foot and Ankle Surgery Fellow at the Silicon Valley Reconstructive Foot & Ankle Fellowship, Palo Alto Medical Foundation in Mountain View, Calif

Features
By Alan Ng, DPM, FACFAS and Nilin M. Rao, DPM, PhD
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