Abstract
Category:
Ankle Arthritis; Basic Sciences/Biologics
Introduction/Purpose:
Recent advancements in prosthesis design and surgical techniques have improved the clinical outcomes of total ankle arthroplasty (TAA) for end-stage ankle arthritis, leading to pain relief and better function. However, some patients experience complications such as impingement, peri-implant cysts and osteolysis, and implant subsidence and loosening, ultimately necessitating reoperation or revision TAA (exchange or removal of one or both metal components). The purpose of this study is to investigate the underlying causes of revision for TAA failure by analyzing the clinical, radiographic, and pathologic features. We hypothesized that adverse tissue reactions to metal and polyethylene particles would degrade bone-implant interface bone quality, contributing significantly to the majority of failed ankle replacements.
Methods:
This is a single-institution series of patients obtained from a registry of patients undergoing primary TAA with any implant. Five surgeons contributed patients. Patients who underwent revision TAA (years 2016-2023) were eligible for study inclusion. Standard clinical, demographic, and radiographic data were collected. Reason for revision or reoperation were noted. At the time of reoperation or revision, intraoperative bone and soft tissue samples were obtained according to the discretion of the surgeon. Of 52 revision TARs identified, 42 patients had histologic specimens from the revision available and were included in analysis. Histologic slides were reviewed by two pathologists with expertise in musculoskeletal tissue and periprosthetic joint tissue. Pathologic findings were compared to the clinical impression, based off clinical examination, history, radiologic findings, and intraoperative assessment of implants.
Results:
42 revision TAA patients were included (mean age 61.2 +/- 9.4 years, 64% male (n= 27), mean BMI 30.2 +/- 6.5 kg/m2, mean time from primary to revision TAA 2.3 +/- 2.2 years). There were 2 cases (4.8%) with periprosthetic joint infection, 3 (7.1%) with calcium pyrophosphate deposition disease, 2 (4.8%) with immunologic reaction, and 8 (19.0%) with fibrosis. 27 revisions (64.3%) had foreign body giant cell and foamy macrophage reaction to metal and polyethylene materials (Figure). Of those with bone sent as specimen, there were macrophage infiltrates along the trabecular bone cavities. These pathologic findings were consistent with clinical loosening and radiographic lucency: 19 of the 27 patients had tibial and/or talar component loosening, 5 component subsidence, 2 concomitant PJI, and 1 gross osteolysis.
Conclusion:
This study demonstrated correlations between clinical, intraoperative, and pathologic findings for failed TAA. Failed TAAs showed characteristic pathologic findings of macrophage reactions to metal and polyethylene particles within the periprosthetic tissues. These reactions were found either in the capsule or the tibial or talar bone at the bone-implant interface. This may reduce the subchondral bone quality, ultimately causing osteolysis, loosening, and implant subsidence. It is still unclear why some failed TAAs are associated with this macrophage reaction, while others are associated with fibrosis. This emphasizes the importance of pathologic tissue evaluation for understanding the underlying etiologies of TAA failure.
Figure. Case of a 67-year-old male who underwent primary TAA for post-traumatic arthritis from chronic instability.
At 1 year after his TAA, he had progressive pain and swelling and had tibial component loosening with posterior subsidence (A). He underwent revision TAA at 1.8 years post-index. Pathologic examination of the peri-implant tissues taken from the revision are shown at 0.5x (B), 5x (C), and 40x (D) magnification, showing body giant cell and foamy macrophage reaction to metal particles and to polyethylene materials (E).