When Should Patients Bear Weight After Microfracture Surgery?

Osteochondral lesions of the talus result in a spectrum of pathology from delamination of cartilage to exposure of the subchondral bone plate. There are various methods of treatment, the main two being bone marrow stimulation through microfracture surgery or cartilage implantation through allograft or autograft methods.

The microfracture procedure results in the surgeon debriding the lesion, often arthroscopically, and then placing multiple holes in the cartilage and subchondral bone plate. The goal of this is to stimulate the release of a blood clot that contains undifferentiated mesenchymal stem cells and growth factors.¹ Under the influences of the growth factors, mesenchymal stem cells maturate into chondrocytes and osteoblasts for cartilage and subchondral bone plate repair respectively.¹ This ultimately results in the formation of a type-1 fibrocartilage tissue in the site of the defect, replacing the damaged type-2 hyaline cartilage.²

After explaining this procedure to patients, one of the first questions is often “How long will I be off my feet?” Various authors cite ranges of non-weightbearing from one week to three months after microfracture surgery to the talus.^3-5 While there have been more recent publications of patients achieving satisfactory outcomes with early weightbearing after microfracture as soon as one to two weeks post-operation, most studies recommend a six- to eight-week period of non-weightbearing.^3–5

I always learned in residency and fellowship, and therefore assumed the standard of care was four to six weeks non-weightbearing. Reasons for a delay in weightbearing included the notion that the quality and volume of repaired tissue is affected by postoperative joint loading with excess loads weakening or destroying the repair tissue.⁴ Axial weightbearing pressure may also cause edge loading around the debrided lesion, decreasing repair tissue adherence and inadvertently increasing lesion size.^2,4

I began to consider the procedure of microfracture as an iatrogenic osteochondral lesion of the talus. I had been researching this as it pertains to Subchondroplasty^® (Zimmer/Biomet) and bone marrow lesions, and the histopathology and mechanics behind bone marrow lesion development. This often traumatically induced lesion results in some spectrum of cartilage damage from sheer/scuffing to bruising, softening and cracking, all the way to fracture to and through the subchondral bone plate beneath.⁶ When the subchondral bone plate is harmed, there is potential for subchondral bone plate cysts or bone marrow lesion formation.

Additionally, an abnormal subchondral bone plate is one major factor pertaining to cartilage repair and arthritis formation. Bone marrow lesion development is associated with subchondral bone plate attrition, localized inflammation, bone turnover and cartilage loss.⁷ Furthermore, a weak foundation (damage to subchondral bone plate or presence of bone marrow lesions) is unable to support overlying cartilage.^8,9

During weightbearing, axial loading between the tibia and talus results in pressure that theoretically forces joint fluid (and the contained inflammatory markers) into the path of least resistance. In normal situations, the intact cartilage keeps the fluid within the joint and it is unable to enter the subchondral bone plate or deeper tissues.⁶ However, when abnormal pathology is present, a pathway may exist to or through the cartilage, subchondral bone plate and into the trabecular bone beneath.^6,9 In a post-microfracture patient, this could be through those sites of subchondral bone plate penetration by the instrumentation.

Researchers have cited that intermittent or continuous high local pressure interferes with bone perfusion, which may lead to osteonecrosis, bone resorption and formation of lytic regions.⁶ Sources of this pressure include mechanical forces, gravity, compression, fluid stress and hydrostatic pressure exchanges as a repetitive cycle of fluid exchange during activities such as weightbearing.^1,6 With each step, synovial fluid travels under high pressure from the joint space through the subchondral bone plate, into the bone and back out again. This results in a vicious cycle, which over time can lead to subchondral bone plate cyst formation.^6,9 Also, both pain through subchondral bone plate nerve endings and joint degeneration are associated with intra-osseous pressures, which can be induced by the transfer of fluid (synovial) between the joint and subchondral bone plate by the aforementioned mechanisms.⁶

It takes a minimum of two weeks for fibrocartilage tissue characteristics to appear at the repair site while chondrogenesis in the defect takes months to mature.¹ Mesenchymal stem cell conversion to bone cells and the beginning repair of the subchondral bone plate start 14 days after injury. Both of these histopathologic factors dictate a need for protection while maturation of repair tissues occurs and reaches a safe level for the external forces of weightbearing. This is why in traumatic induced osteochondral lesions of the talus (Berndt-Hardy 1,2 and medial/small 3), the non-operative treatment is protection, often non-weightbearing, for four to six weeks.^9,10

So why don’t we abide by this plan for iatrogenic-induced osteochondral lesions of the talus? Due to the aforementioned rationale, I will stick with a longer period of four to most likely six weeks non-weightbearing after microfracture repair to allow protection and maturation of the fibrocartilage at the site of the defect.

Questions for discussion: What is your normal weightbearing progression for patients having microfracture repair of the talus? Is there any rationale to this treatment program? Do you find yourself performing fewer microfractures with greater utilization of newer biocartilage type products on the market?

Dr. Hood is a fellowship-trained foot and ankle surgeon. Follow him on Twitter at @crhoodjrdpm.

Dr. Hood has no financial disclosures related to this blog.

References

1.      Madry H, van Dijk CN, Mueller-Gerbl M. The basic science of the subchondral bone. Knee Surgery, Sport Traumatol Arthrosc. 2010;18(4):419-433.

2.      Hannon CP, Smyth NA, Murawski CD, et al. Osteochondral lesions of the talus: aspects of current management. Bone Jt J. 2014;96 B(2):164-171.

3.      Shuyuan L, Hongliang L, Yujie L, Junliang W, Chang L. Clinical outcomes of early weight-bearing after arthroscopic microfracture during the treatment of osteochondral lesions of the talus. Chinese Med J. 2014;127(13):2470-2474.

4.      Lee D-H, Lee K-B, Jung S-T, Seon J-K, Kim M-S, Sung I-H. Comparison of early versus delayed weightbearing outcomes after microfracture for small to midsized osteochondral lesions of the talus. Am J Sports Med. 2012;40(9):2023-2028.

5.      Lundeen GA, Dunaway LJ. Immediate unrestricted postoperative weightbearing and mobilization after bone marrow stimulation of large osteochondral lesions of the talus. Cartilage. 2016:1-7.

6.      van Dijk CN, Reilingh ML, Zengerink M, van Bergen CJA. Osteochondral defects in the ankle: Why painful? Knee Surgery, Sport Traumatol Arthrosc. 2010;18(5):570-580.

7.      Cohen SB, Sharkey PF. Subchondroplasty for treating bone marrow lesions. J Knee Surg. 2015.

8.      McCollum GA, van den Bekerom MPJ, Kerkhoffs GMMJ, Calder JDF, van Dijk CN. Syndesmosis and deltoid ligament injuries in the athlete. Knee Surgery, Sport Traumatol Arthrosc. 2013;21(6):1328-1337.

9.      Wodicka R, Ferkel E, Ferkel R. Osteochondral lesions of the ankle. Foot Ankle Int. 2016:1-12.

10.    Badekas T, Takvorian M, Souras N. Treatment principles for osteochondral lesions in foot and ankle. Int Orthop. 2013;37:1697-1706.