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Subchondral Bone Plasty Versus Grafting For Osteochondral Talar Defects: Which Is Superior?

January 2022

PointValjee

Here the author outlines proper diagnostic and therapeutic pathways, including subchondral bone plasty, to treat osteochondral talar lesions. Sharing evidence from the literature and his experience, he contends that subchondral bone plasty is an effective, minimally invasive option that may allow earlier weight-bearing.

By Jashan Valjee, DPM, FACFAS

Osteochondral lesions of the talus include articular damage to the cartilage and underlying subchondral bone, which results in a variety of pathology from exposure and damage of the subchondral bone plate to delineation of the cartilage. The injury mechanism leading to cartilage damage is typically an ankle injury where the talus impacts the distal tibial plafond, thereby creating microfractures in the cartilage and subchondral bone plate.1,2 After further weight-bearing, synovial joint fluid infiltrates these microfractures due to increased pressure, resulting in expansion of the lesions and possibly cysts. These change the ankle joint congruency and biomechanical loading, causing pain. If left untreated, this can accelerate further ankle degeneration. Up to 75 percent of talar osteochondral lesions occur after traumatic injuries, such as ankle sprains and ankle fractures.3 Studies attribute up to 45 percent of athletic injuries to ankle sprains, and an estimated 28,000 ankle sprains occur daily.4 We can then establish solid treatment protocols because of this high number of cases. Advancements in imaging and arthroscopy have led to the improvement of treatment paradigms. Various factors influence decision making, including patient baseline activity level, lesion size, morphology, foot and/or ankle deformity, concomitant injuries, ankle instability, and primary or secondary lesions. In my practice, I use these protocols as a baseline and then try to individualize it for each patient.

Pertinent Pearls In Imaging And Conservative Treatment

Imaging is a crucial diagnostic tool in treatment planning for osteochondral lesions of the talus. Radiographs are still important despite their low accuracy for detecting OLTs.5 It can evaluate ankle alignment, talar tilt, and syndesmotic injury, especially with a weight-bearing film. Magnetic resonance imaging (MRI) and computed tomography (CT) are common diagnostic tools with high sensitivity and specificity. CT is preferable to assess the lesion size and bony morphology. It can also better assess the subchondral bone layer. MRI is best used to assess ankle cartilage, detect bone marrow edema, or diagnose concomitant soft tissue injuries of the ankle. To properly assess lesion size, CT is preferred, as MRI can overestimate lesion size when bone marrow edema is present.5

Conservative treatment is a must before any surgical intervention using the algorithms mentioned above and is usually a combination of efforts to reduce symptoms. The primary goal is to offload the ankle and reduce synovial fluid pushed into the subchondral defects. This will reduce the amount of damage to the lesion, the surrounding cartilage and the subchondral plate, in turn, decreasing pain and synovial fluid inflammation. Physical therapy can help strengthen the ankle joint and surrounding soft tissue structures. Bracing and orthotic support can help redistribute the weight-bearing ankle load.6 Injection therapy such as cortisone, hyaluronic acid, and platelet-rich plasma can help reduce inflammation of the joint. Activity modification and immobilization are also considerations. Surgical intervention is warranted if pain persists past three months after exhaustion of conservative treatment.6

Examining The Available Surgical Options

Two mainstays of treatment for talar osteochondral lesions are microfracture, stimulating bone marrow and, therefore, repairing the process, and autograft or allograft cartilage implantation. Newer techniques like subchondral bone plasty can offer another tool for treatment. Developed for the knee, this technique successfully fills subchondral cysts that typically develop at the tibial plateau.7 During the procedure, the surgeon injects a bone substitute material via a retrograde approach to fill the subchondral lesion.7 This minimally invasive technique usually takes place under fluoroscopic guidance using retrograde drilling and injecting the cement-like paste through a cannula. The exact material varies per vendor, but it is typically a calcium phosphate that mimics the makeup of cancellous bone with some proprietary agent. The material is essentially a bone graft substitute that will resorb and be replaced with new bone.6,7 It may be combined with additional arthroscopic treatments, such as microfracture, or with regenerative products like bone marrow aspirate. If there is a cartilaginous defect, I will usually choose microfracture and subchondral bone plasty in the presence of subchondral plate damage or cystic change. By drilling through the sclerotic bone, one disrupts interosseous or intraosseous blood vessels, forming a fibrin clot. This releases mesenchymal stem cells, stimulating revascularization and the formation of fibrin cartilage.8 Being inferior to native hyaline cartilage, I feel that if there is any subchondral pathology, it warrants attention.

Following surgery, I recommend non-weight-bearing for a total of six weeks, but I do start earlier at four weeks if patient is pain-free. I then transition into a supportive, ASO-style lace-up ankle brace and start physical therapy for six weeks. Of note, I recommend my patients start early, non-weight-bearing range of motion exercises at two weeks postop. Patients typically return to full activity at three months.9

A Closer Look At Subchondral Bone Plasty

The most significant advantage of subchondral bone plasty is the minimally invasive technique, with mostly stab incisions and the typically outpatient setting. Even when paired with arthroscopy for the talus, the procedure time is prompt. Compared to large incisions, exposure of the joint, and osteotomies of medial malleolus, this is by far a less aggressive procedure. The other main benefit of subchondral bone plasty is that in most cases, you may perform additional more invasive revisions if subnchondral bone plasty fails or if the condition progresses in the years to come. If autograft or allograft procedures fail, surgical revision can be quite complex. Subchondral bone plasty does have its limitations, primarily regarding the size of the lesion. If it is greater than 1.5 to 2.0cm,10 then subchondral bone plasty may be inadequate, and I will typically favor a more invasive technique.

A prospective study using nine patients and subchondral bone plasty demonstrated good results.11 The mean lesion size as measured on preoperative MRI was 1.3 x 1.4 cm (range, one x 0.8 cm to two x 2.3 cm). A mean 1.7 cc (range, 1.5 to two cc) of calcium paste was injected in the subchondral bone at the lesion level, under arthroscopic visualization to debride any calcium paste leakage. All outcome measures demonstrated marked improvement from baseline to final follow-up. The mean weight-bearing visual analog pain score improved from mean 7.8 (range 6 to 9) to 0.5 (range, 0 to 1); the mean total FAOS improved from mean 67.1 (range, 55 to 79) to mean 90.6 (range, 87 to 95). At the one-year postoperative visit, all patients declared that they would have the procedure again.11

A recent comprehensive review included 17 studies, of which 13 were of the knee and four on the foot and ankle. All but one study were level IV evidence; the mean MINORS score was 9 ± 2. There were 756 patients included, 45.1 percent were female, and the mean age was 54 years (range 20-85). Thirteen studies investigated the effect Subchondroplasty® (Zimmer-Biomet) to the knee, while four studied the impact on the foot and ankle. The median length of follow-up was 12 months. The most common indication for Subchondroplasty was joint pain with corresponding bone marrow lesion. Major contraindications to Subchondroplasty included severe osteoarthritis, joint instability, and malalignment.12

Mean pain score on visual analog scale prior to Subchondroplasty was 7.8 ± 0.6, but decreased to 3.4 ± 0.7 postoperatively. All studies investigating functional scores reported improvement following Subchondroplasty (IKDC 31.7 ± 1.9-54.0 ± 4.2 and KOOS 38.1 ± 0.6-70.0 ± 4.1). There were consistently high levels of patient satisfaction; 87 ± 8 percent of patients would be willing to undergo the procedure again. They reported seven cases of complications, most seriously osteomyelitis and avascular necrosis. Admittedly there are low-quality studies on subchondral bone plasty to the talus, but evidence points to this procedure playing a role in resolving minor lesions and delaying more invasive and expensive procedures in patients with bone marrow lesions.12

Concluding Thoughts

In conclusion, I contend that the literature and my experience supports that subchondral bone plasty is a novel procedure that can help patients with talar osteochondral lesions return to early weight-bearing activity with a safe, minimally invasive technique. It addresses subchondral bone pathology by restoring it to healthy native cancellous bone. In addition, I encourage more investigation of the benefits of this procedure and its expansion of use in the foot and ankle. 

Dr. Valjee is a Diplomate of the American Board of Foot and Ankle Surgery and a Fellow of the American College of Foot and Ankle Surgeons. He is in practice in Glen Burnie, MD.

 

CounterpointSebag

This author points out the significant complexity of determining the best surgical course for patients with osteochondral talar defects. However, in his presentation of his experience and evidence from the literature, he contends that grafting is generally a superior choice to subchondral bone plasty.

By Joshua Sebag, DPM, AACFAS

In general, surgeons prefer autogenous grafting material, with well-documented benefits.1 Multiple devices and safe techniques exist for bone procurement for osteochondral lesions of the talus. Dowel harvesters, suction-aided curettes, and traditional window access techniques allow ample harvest to place within lesion sites.2 Bone procurement does add to operative time, however, minimally and with good reason. In the event of a concomitant cartilaginous lesion which is either large, unstable, or not amenable to conservative measures, lesion grafting in addition to chondral replacement may be warranted. The most challenging lesions I experience are frequently large and unstable at the shoulders of the talar dome in young patients, particularly the anterolateral aspect.

How Does Imaging Contribute?

No substantial evidence exists supporting any one advanced imaging modality as superior and no gold standard in imaging for osteochondral lesions of the talus is present. However, there is support that magnetic resonance imaging (MRI) and computed tomography (CT) differ when estimating lesion size.3,4 Further, CT may better reveal additional architectural abnormalities of the talus. For evaluation and diagnosis, Vergagen and team prospectively showed higher sensitivity with MRI compared to CT.3

In some cases, an MRI may overestimate severity and lesion size.4 However, on MRI, one can frequently visualize other peritalar pathology, like collateral ligament involvement and extrinsic tendon pathology. In my experience, given that a lesion’s depth and complexity, size, bone marrow edema, and location contribute to the treatment path, an MRI over-read is essential. If one suspects an osteochondral lesion, CT evaluation can better approximate lesion size when considering surgery. For bipolar lesions, evidence of moderate-to-severe ankle arthrosis, or advanced body mass index (BMI) and age, it is prudent to manage patient expectations. Preop discussion of risk is key in these populations, as failure rates are increased.

Bone marrow edema (BME) refers to high-signal intensity changes on MRI fluid-sensitive sequences. One can attribute bone marrow edema to many pathologies, and in many instances to ankle injury. Regardless of cause, I find physiologic remodeling of the subchondral bone can become limited because of increased focalization of stress, ongoing abnormal joint forces, and reduced healing capacity of the subchondral bone. Bone marrow edema is a known prognostic factor associated with pain, dysfunction, and progressive cartilage damage.

I’ve observed subchondral bone plasty popularized as a minimally invasive technique to allow focal decompression and accurate placement of calcium phosphate via a trocar cannula system attempting to decrease symptomatic subchondral lesions frequently seen on advanced imaging as BME. Treatment is therefore indicated in symptomatic patients, but is not without drawbacks.

How Does One Choose An Approach?

Talar osteochondral injury can be challenging. Often such injury may occur after an otherwise benign ankle sprain. Inherently, the damaged articular cartilage has poor intrinsic reparative capability. Further, tenuous vascular supply and highly congruous trochlear articulations subject the talus to increased force, shear, and potential development of osteochondral lesions. We might expect a future increase in ankle injury and subsequent osteochondral talar lesions as high-impact sporting activities increase in acceptance and more youths participating.5 Talar osteochondral lesions may present as bone marrow cystic lesions, cartilage damage, and frequently components of both, often at the talar shoulder.6 It is generally accepted that the larger the lesion’s size, the more challenging to treat.

Operative arthroscopy remains the gold standard in evaluating and grading these lesions. It allows direct visualization and probing to accurately assess the lesion and cartilage stability.7 The Ferkel classification and method of intraarticular evaluation is relatively easy to master and similar to other classifications, describing intraoperative findings in six stages using a probe: A: soft, smooth cartilage; B: rough cartilage; C: fissures; D: cartilage flap with exposed bone; E: loose non-displaced fragment; and F: displaced fragment.8

Although core decompression of subcartilaginous cystic lesions can adequately treat some bone marrow edema, other authors show bone marrow edema and abnormal bone morphology.9 Newer research suggests careful placement of bone void fillers, avoiding subchondral bone plasty overfill. Concerns following core decompression and subchondral bone plasty increased with reports of talar avascular necrosis (AVN) after introducing bone cement into the talar lesion.8,9

Hanselman and team reviewed seven cases of talar AVN radiograph at an average of 23 months postop from index subchondral bone plasty. All studied were symptomatic.10 In a separate paper one year later, the authors shared their experience with subchondral bone plasty, finding what they called “iatrogenic talar AVN after undergoing SCP for talar BMLs.”8 Moreover, I’ve observed industry proponents and manufacturers advocating modifications in the technique and recommending careful attention to avoid overfill. Therefore, I believe it is advisable to utilize autografts or demineralized bone matrices over synthetic or cement compounds. Frequently PRP may be an option in combination with autografts or demineralized bone matrices over synthetic or cement compounds, versus the calcium phosphate bone void fillers previously popularized. Our practice’s preference is bone marrow aspirate concentrate (BMAC) and autogenous bone graft (ABG) from the ipsilateral calcaneus or tibia. One can mix and inject this similarly to subchondral bone plasty with ease, given modern instrumentation. The viscosity of the injectable material is easily fine-tuned to ensure flow through cannulated trocars or syringes. The benefits of autografting mated with subchondral bone marrow edema/cystic lesion decompression and trocar injection of BMAC in place of subchondral bone plasty is a safe alternative, in my experience. There may be baseline AVN in patients with known talar OCD, and the direct causation from subchondral bone plasty is not well shown - a significant opportunity for future research. That said, avoiding potentially noxious injectables with even a low risk of interval AVN development makes good sense. Repercussions of AVN within the talar body and functional sequelae can prove catastrophic. One should note that alternatives which may decrease this likelihood are readily available.

Kohring and colleagues additionally reviewed two patients concurrently who developed talar AVN following introduction of subchondral bone plasty material. This article concluded that given a paucity of long-term follow-up and high-level literature support and the catastrophic sequalae of talar AVN, one should use subchondral bone plasty sparingly, if at all, when treating osteochondral lesions within the talus.9

Various authors describe the “sandwich technique” to accommodate full-thickness cartilage lesions with concurrent subchondral defect components.11,12 There is extensive discussion of this technique in the knee with longer follow-up. Multiple treatments are emerging in talar OCD treatment, much of it based on experience within the knee literature. Historically, Jones and Peterson developed and presented cases of an autologous chondrocyte implantation (ACI) “sandwich” technique nearly 20 years ago.11 They described it as an operative procedure to reconstruct end-stage femoral condyle OCD pathology involving autologous bone grafting and ACI. In this technique, one separates cultured chondrocytes from the autologous bone graft and marrow space by “sandwiching” the cells between periosteal membranes on the surface of the osteochondral unit.11

This same clinical idea/technique is gaining popularity for complex osteochondral talar lesion. Sadlik and team followed 10 patients over an average of 46 months with a modified “sandwich” technique for symptomatic talar dome lesions. Midterm results found a significant increase in mean AOFAS scores and reduction in mean VAS. Interestingly, the radiologic magnetic resonance observation of cartilage repair tissue score was 69.5 percent (±16.7) at final follow-up.12

In Conclusion

Grafting using juvenile particulate cartilage, cartilage substitutes, ABG and BMAC ± PRP are modern techniques for talar osteochondral lesions. The gold standard in orthopedic bone repair remains autogenous grafting. When viable procurement is possible and donor site morbidity low, the risk/reward ratio of autografting remains superior in my experience. Anecdotally, the space for synthetic, mined, or other forms of injectable cement in this setting is waning in popularity. Industry and evidence-based medicine support this shift to alternative graft techniques to decrease the possibility of iatrogenic talar AVN. 

Dr. Sebag is an Associate of the American College of Foot and Ankle Surgeons and is in practice in Port St. Lucie, FL.

Point References

1. Kerkhoffs GMMJ, Karlsson J. Osteochondral lesions of the talus. Knee Surg Sports Traumatol Arthrosc. 2019;27(9):2719–2720.

2. van Dijk CN, Reilingh ML, Zengerink M, van Bergen CJA. Osteochondral defects in the ankle: why painful? Knee Surg Sports Traumatol Arthrosc. 2010;18(5):570–580.

3. Hintermann B, Boss A, Schäfer D. Arthroscopic findings in patients with chronic ankle instability. Am J Sports Med. 2002;30(3):402-409.

4. Kerkhoffs, GMMJ, Kennedy, J.G., Calder, J.D.F. et al. There is no simple lateral ankle sprain. Knee Surg Sports Traumatol Arthrosc. 2016;24(4):941–943.

5. van Bergen CJ, Gerards RM, Opdam KT, et al. Diagnosing, planning and evaluating osteochondral ankle defects with imaging modalities. World J Orthop. 2015;6(11):944-953.

6. Rikken QGH, Kerkhoffs GMMJ. Osteochondral lesions of the talus: an individualized treatment paradigm from the Amsterdam perspective. Foot Ankle Clin. 2021;26(1):121-136.

7. Miller JR, Dunn KW. Subchondroplasty of the ankle: a novel technique. Foot Ankle Online J. 2015;8(1):7.

8. Dombrowski ME, Yasui Y, Murawski CD, et al. Conservative management and biological treatment strategies: proceedings of the International Consensus Meeting on Cartilage Repair of the Ankle. Foot Ankle Int. 2018;39(1_suppl):9S-15S.

9. ÜCuttica DJ, Smith WB, Hyer CF, Philbin TM, Berlet GC. Osteochondral lesions of the talus: predictors of clinical out- come. Foot Ankle Int. 2011;32(11):1045-1051.

10. ÜBaums MH, Schultz W, Kostuj T, Klinger HM. Cartilage repair techniques of the talus: an update. World J Orthop. 2014;5(3):171-179

11. Nairn LN, Subramaniam M, Ekhtiari S, Axelrod DE, Grant JA, Khan M. Safety and early results of Subchondroplasty® for the treatment of bone marrow lesions in osteoarthritis: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2021;29(11):3599-3607.

 

Counterpoint References

1. Lareau CR, Deren ME, Fantry A, et al. Does autogenous bone graft work? A logistic regression analysis of data from 159 papers in the foot and ankle literature. Foot Ankle Surg. 2015;21(3);150–159.

2. Fitzgibbons TC, Hawks MA, McMullen ST, Inda DJ. Bone grafting in surgery about the foot and ankle: indications and techniques. Am Acad Orthop Surg. 2011;19(2):112–120.

3. Jones D, Peterson L. Autologous chondrocyte implantation. Instr Course Lect. 2007;56:429–445.

4. Sadlik B, Kolodziej L, Blasiak A, Szymczak M, Warchal B. Biological reconstruction of large osteochondral lesions of the talar dome with a modified “sandwich” technique—midterm results. Foot Ankle Surg. 2017;23(4):290–295.

5. Delahunt E, Remus A. Risk factors for lateral ankle sprains and chronic ankle instability. J Athlet Train. 2019;54(6):611-616.

6. Togher CJ, Sahli H, Butterfield J, Sebag J, Shane AM, Reeves CL. Incidence of talar Osteochondral lesions after acute ankle fracture: A retrospective analysis. J Foot Ankle Surg. 2021;60(6):1184-1187.

7. Kohring, JM, Oh I, Baumhauer JF. Talar avascular necrosis after calcium phosphate injection treatment of talar bone marrow lesions. JBJS Case Connector. 2020;10(2):e1900389.

8. Hanselman AE, Cody EA, Easley ME, Adams SB, Parekh SG. Avascular necrosis of the talus after Subchondroplasty. Foot Ankle Int. 2021;42(9):1138-1143.

9. Savage-Elliott I, Ross KA, Smyth NA, Murawski CD, Kennedy JG. Osteochondral lesions of the talus. Foot Ankle Spec, 2014;7(5):414422.

10. Laffenêtre, O. Osteochondral lesions of the talus: current concept. Orthop Traumatol Surg Res. 2010;96(5):554-566.

11. Verhagen RA, Maas M, Dijkgraaf MG, Tol JL, Krips R, van Dijk CN. Prospective study on diagnostic strategies in osteochondral lesions of the talus: is MRI superior to helical CT? J Bone Joint Surg Br. 2005;87(1):41-46.

12. Easle MA, Latt LA, Santangelo JR, Merian- Genast M, Nunley JA. Osteochondral lesions of the talus. J Am Acad Orthop Surg. 2010;18(10):616-630.

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