Biomechanical Properties and Kinematics of Medial Patellofemoral Ligament Reconstruction: A Systematic Review.

Background: While the biomechanical properties of the native medial patellofemoral ligament (MPFL) have been well studied, there is no comprehensive summary of the biomechanics of MPFL reconstruction (MPFLR). An accurate understanding of the kinematic properties and functional behavior of current techniques used in MPFLR is imperative to restoring native biomechanics and improving outcomes. Purpose: To provide a comprehensive review of the biomechanical effects of variations in MPFLR, specifically to determine the effect of graft choice and reconstruction technique. Study Design: Systematic review. Methods: A systematic review was performed in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A total of 32 studies met inclusion criteria: (1) using ≥8 human cadaveric specimens, (2) reporting on a component of MPFLR, and (3) having multiple comparison groups. Results: Gracilis, semitendinosus, and quadriceps grafts demonstrated an ultimate load to failure (N) of 206.2, 102.8, and 190.0 to 205.0 and stiffness (N/mm) of 20.4, 8.5, and 21.4 to 33.6, respectively. Single-bundle and double-bundle techniques produced an ultimate load to failure (N) of 171 and 213 and stiffness (N/mm) of 13.9 and 17.1, respectively. Anchors placed centrally and superomedially in the patella produced the smallest degree of length changes throughout range of motion in contrast to anchors placed more proximally. Sutures, suture anchors, and transosseous tunnels all produced similar ultimate load to failure, stiffness, and elongation data. Femoral tunnel malpositioning resulted in significant increases in contact pressures, patellar translation, tilt, and graft tightening or loosening. Low tension grafts (2 N) most closely restored the patellofemoral contact pressures, translation, and tilt. Graft fixation angles variably and inconsistently altered contact pressures, and patellar translation and tilt. Conclusion: Data demonstrated that placement of the MPFLR femoral tunnel at the Schöttle point is critical to success. Femoral tunnel diameter should be ≥2 mm greater than graft diameter to limit graft advancement and overtensioning. Graft fixation, regardless of graft choice or fixation angle, is optimally performed under minimal tension with patellar fixation at the medial and superomedial patella. However, lower fixation angles may reduce graft strain, and higher fixation angles may exacerbate anisometry and length changes if femoral tunnel placement is nonanatomic.

Suture Anchor-Based Quadriceps Tendon Repair May Result in Improved Patient-Reported Outcomes but Similar Failure Rates Compared to the Transosseous Tunnel Technique.

PURPOSE: The purpose of this study was to compare failure rates and patient-reported outcomes between transosseus (TO) suture and suture anchor (SA) quadriceps tendon repairs. METHODS: Following institutional review board approval, patients who underwent primary repair for quadriceps tendon rupture with TO or SA techniques between January 2009 and August 2018 were identified from an institutional database and retrospectively reviewed. Patients were contacted for satisfaction (1-10 scale), current function (0-100 scale), failure (retear), and revision surgeries; International Knee Documentation Committee (IKDC) score and Knee Injury and Osteoarthritis Outcomes Score (KOOS) were also collected to achieve a minimum of 2-year follow-up. RESULTS: Sixty-four patients (34 SA, 30 TO) were available by phone or e-mail at a mean of 4.81 ± 2.60 years postoperatively. There were 10 failures, for an overall failure rate of 15.6%. Failure incidence did not significantly differ between treatment groups (P = .83). Twenty-seven patients (47% of nonfailed patients) had completed patient-reported outcomes. The SA group reported higher subjective function (SA: 90 [85-100] vs TO: 85 [60-93], 95% CI of difference: -19.9 to -2.1 × 10-5, P = .042), final IKDC (79.6 [50.0-93.6] vs 62.1 [44.3-65.5], 95% CI of difference: -33.0 to -0.48, P = .048), KOOS Pain (97.2 [84.7-97.2] vs 73.6 [50.7-88.2], 95% CI of difference: -36.1 to -3.6 × 10-5, P = .037), Quality of Life (81.3 [56.3-93.8] vs 50.0 [23.4-56.3], 95% CI of difference: -50.0 to -6.2, P = .026), and Sport (75.0 [52.5-90.0] vs 47.5 [31.3-67.5], 95% CI of the difference: -45.0 to -4.1 × 10-5, P = .048). CONCLUSIONS: There is no significant difference in failure rate between transosseus and suture anchor repairs for quadriceps tendon ruptures (P = .83). Most failures occur secondary to a traumatic reinjury within the first year postoperatively. Despite the lack of difference in failure rates, at final follow-up, patients who undergo suture anchor repair may report significantly greater subjective function and final IKDC, KOOS Pain, Quality of Life, and Sport scores. LEVEL OF EVIDENCE: III, retrospective cohort study.

HOIL1 Is Essential for the Induction of Type I and III Interferons by MDA5 and Regulates Persistent Murine Norovirus Infection.

The linear ubiquitin chain assembly complex (LUBAC), composed of heme-oxidized IRP2 ubiquitin ligase 1 (HOIL1), HOIL1-interacting protein (HOIP), and SHANK-associated RH domain-interacting protein (SHARPIN), is a crucial regulator of multiple immune signaling pathways. In humans, HOIL1 or HOIP deficiency is associated with an immune disorder involving autoinflammation, immunodeficiency, and inflammatory bowel disease (IBD)-like symptoms. During viral infection, LUBAC is reported to inhibit the induction of interferon (IFN) by the cytosolic RNA sensor retinoic acid-inducible gene I (RIG-I). Surprisingly, we found that HOIL1 is essential for the induction of both type I and type III IFNs, as well as the phosphorylation of IFN regulatory factor 3 (IRF3), during murine norovirus (MNoV) infection in cultured dendritic cells. The RIG-I-like receptor, melanoma differentiation-associated protein 5 (MDA5), is also required for IFN induction and IRF3 phosphorylation during MNoV infection. Furthermore, HOIL1 and MDA5 were required for IFN induction after Theiler's murine encephalomyelitis virus infection and poly(I·C) transfection, but not Sendai virus or vesicular stomatitis virus infection, indicating that HOIL1 and LUBAC are required selectively for MDA5 signaling. Moreover, Hoil1-/- mice exhibited defective control of acute and persistent murine norovirus infection and defective regulation of MNoV persistence by the microbiome as also observed previously for mice deficient in interferon lambda (IFN-λ) receptor, signal transducer and activator of transcription factor 1 (STAT1), and IRF3. These data indicate that LUBAC plays a critical role in IFN induction to control RNA viruses sensed by MDA5.IMPORTANCE Human noroviruses are a leading cause of gastroenteritis throughout the world but are challenging to study in vivo and in vitro Murine norovirus (MNoV) provides a tractable genetic and small-animal model to study norovirus biology and immune responses. Interferons are critical mediators of antiviral immunity, but excessive expression can dysregulate the immune system. IFN-λ plays an important role at mucosal surfaces, including the gastrointestinal tract, and both IFN-λ and commensal enteric bacteria are important modulators of persistent MNoV infection. LUBAC, of which HOIL1 is a component, is reported to inhibit type I IFN induction after RIG-I stimulation. We show, in contrast, that HOIL1 is critical for type I and III IFN induction during infection with MNoV, a virus that preferentially activates MDA5. Moreover, HOIL1 regulates MNoV infection in vivo These data reveal distinct functions for LUBAC in these closely related signaling pathways and in modulation of IFN expression.