ERS3003. Infrapatellar Fat Pad Injury and Cartilage Degradation in the Setting of ACL Tear
Authors * Denotes Presenting Author
  1. Richard Wang *; Jackson Memorial Hospital; University of Miami
  2. Daniel Quintero; University of Miami
  3. Sean Maloney; Jackson Memorial Hospital; University of Miami
  4. Nikhil Patel; University of Miami
  5. Griffin Harris; University of Miami
  6. Thomas Best; Jackson Memorial Hospital; University of Miami
  7. Jean Jose; Jackson Memorial Hospital; University of Miami
The infrapatellar fat pad (IFP), also known as Hoffa’s fat pad, has become a structure of increased interest in recent years. It serves as a reservoir and source of mesenchymal stem cells (MSCs), which have the potential to differentiate into chondrocytes, adipocytes, and other mesenchymal tissues, while also producing trophic factors that protect against apoptosis and fibrosis. Mechanically, the IFP plays a role in absorbing compressive loads and facilitating the distribution of synovial fluid. In the setting of anterior cruciate ligament (ACL) injury, there is commonly concomitant injury to the IFP. Notably, the patellofemoral compartment (PFC) articular cartilage is often relatively preserved at the time of the initial ACL injury. The primary objective of this study was to examine the relationship between the degree of initial injury to the IFP and the future development of PFC chondrosis in the setting of acute ACL tear necessitating ACL reconstruction surgery.

Materials and Methods:
In this IRB-approved retrospective study, all adult participants ages 18-45 years old who presented to our tertiary care university-based sports medicine clinic with MRI findings of acute ACL tears between January 2009 and October 2022 were included. All participants underwent ACL reconstruction at our institution and had subsequent follow-up MRIs within 3 years of surgery. Initial and subsequent MRI findings of PFC chondrosis were graded as per the modified Outerbridge criteria. Initial IFP injury was qualitatively graded as follows: no edema (grade 0), edema without architectural distortion (grade 1), edema with architectural distortion (grade 2), and edema with laceration/tear of the fat pad (grade 3). The Pearson correlation coefficient and Mann-Whitney U test were used.

A total of 111 participants met the inclusion criteria with a mean age of 28 years old. At the time of injury, 3 participants had no edema at the IFP, 58 participants had edema without architectural distortion, 23 participants had edema with architectural distortion, and 27 participants had edema with tearing of the fat pad. There was no correlation between the degree of initial IFP injury and initial PFC chondrosis (r = 0.01, p = 0.9372). There was a positive correlation between the degree of initial IFP injury and future progression of PFC chondrosis (r = 0.53, p<0.0001). There was a difference in the future progression of PFC chondrosis when comparing grade 1 and grade 2 IFP injuries (p= 0.0003). There was no difference when comparing grade 2 and grade 3 IFP injuries (p=0.2611).

Our study reinforces the importance of the IFP in maintaining cartilage homeostasis, demonstrates an association between IFP injury and the future development of knee osteoarthritis, and may provide a useful MRI classification system that can effectively diagnose the presence and severity of IFP injuries. Further investigations are needed to better understand the underlying mechanism and develop new strategies to prevent the development of knee osteoarthritis in the setting of IFP injuries and ACL tears.