High Incidence of Recurrent Patellofemoral Crepitus in Total Knee Arthroplasty Patients Following Arthroscopic Debridement.

Background: Patellofemoral crepitus is an unfavorable complication following total knee arthroplasty (TKA) with a posterior-stabilized (PS) implant. The purpose of this study was to study patellar crepitus recurrence and reoperation rates following arthroscopic debridement in patients with a PS-TKA. Methods: Our institution database was used to identify patients with a PS-TKA who underwent arthroscopic debridement for patellofemoral crepitus at our institution. Patients must have had a resurfaced patella and minimum 2 years clinical follow-up from the arthroscopic debridement to be included in the study. Recurrence of patellar crepitus, subsequent operations, and any adverse events were documented. Results: We identified 35 patients who met inclusion criteria with an average follow-up of 8.0 years (range 2.1 to 18.4 years) from their arthroscopic debridement. Nineteen patients (54.3%) had history of a nonarthroplasty knee surgery prior to their TKA. The mean time interval between TKA and arthroscopic debridement for patellar crepitus was 1.6 years (range 0.2 to 5.0 years). Overall, 16 patients (45.7%) developed recurrent crepitus (8 asymptomatic and 8 symptomatic). Six of the symptomatic patients (17.1% of the entire cohort) underwent a repeat surgery for recurrent patellofemoral crepitus. Of theses 6 patients, 3 developed recurrent crepitus but only 1 patient had a third surgical procedure. No postoperative complications were noted following any surgical procedure. The mean knee range of motion following arthroscopic debridement did not change (126.9° preoperatively vs 127.0° postoperatively). Conclusions: Patients experienced high rates of recurrent patellofemoral crepitus following arthroscopic debridement. One-sixth of the patient cohort required a second surgical intervention for recurrent crepitus.

EHD2 modulates Dll4 endocytosis during blood vessel development.

OBJECTIVE: Despite the absolute requirement of Delta/Notch signaling to activate lateral inhibition during early blood vessel development, many mechanisms remain unclear about how this system is regulated. Our objective was to determine the involvement of Epsin 15 Homology Domain Containing 2 (EHD2) in delta-like ligand 4 (Dll4) endocytosis during Notch activation. APPROACH AND RESULTS: Using both in vivo and in vitro models, we demonstrate that EHD2 is a novel modulator of Notch activation in endothelial cells through controlling endocytosis of Dll4. In vitro, EHD2 localized to plasma membrane-bound Dll4 and caveolae. Chemical disruption of caveolae complexes resulted in EHD2 failing to organize around Dll4 as well as loss of Dll4 internalization. Reduced Dll4 internalization blunted Notch activation in endothelial cells. In vivo, EHD2 is primarily expressed in the vasculature, colocalizing with junctional marker VE-cadherin and Dll4. Knockout of EHD2 in zebrafish produced a significant increase in dysmorphic sprouts in zebrafish intersomitic vessels during development and a reduction in downstream Notch signaling. CONCLUSIONS: Overall, we demonstrate that EHD2 is necessary for Dll4 transcytosis and downstream Notch activation.