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BackgroundTo evaluate the clinical results of arthroscopic repair with or without platelet-rich plasma (PRP) for tears of the discoid lateral meniscus (DLM).MethodsTwenty-nine patients with DLM tears within a stable knee were arthroscopically treated with meniscal suture repair. Of those, 14 were augmented with platelet-rich plasma (PRP), and 15 were performed without PRP augmentation. Patients were evaluated at baseline (the day before surgery) and then 12 and 24 months after the last injection. Evaluation included the Lysholm score, and Ikeuchi grade, Visual analogue score (VAS) for pain and failure rate. Failure was defined by patients developing symptoms of joint line pain, locking, swelling or requiring repeat arthroscopy.ResultsThere was no difference in the failure rate in the PRP group (1 of 14) compared with the non-PRP group (2 of 15) (P = 0.58). Statistically significant improvement in Lysholm score, Ikeuchi grade and VAS for pain was documented at the last follow-up compared with baseline in both PRP and non-PRP group. No significantly difference was found between the PRP group and non-PRP group on Lysholm score, Ikeuchi grade and VAS for pain at the last follow-up. In the univariate analysis of each variable, younger age (P = 0.036) and longer follow-up duration (P = 0.043) were statistically associated with a better function improvement. Whereas in multivariate analysis, only younger age (P = 0.004) was significantly associated with a better function improvement.ConclusionWith regard to clinical evaluations in arthroscopic repair for DLM tears, PRP group had similar effect in pain relief and functional improvement to non-PRP group at mid-term follow-up. Future larger prospective studies with a longer follow-up are needed to determine whether PRP should be used with DLM repair.

Background: The best type of autograft for anterior cruciate ligament (ACL) reconstruction remains debatable. Hypothesis: Compared with bone–patellar tendon–bone (BPTB) and hamstring tendon (HT) autografts, the quadriceps tendon (QT) autograft has comparable graft survival as well as clinical function and pain outcomes. Study Design: Meta-analysis; Level of evidence, 4. Methods: A systematic literature search was conducted in PubMed, Embase, Scopus, and the Cochrane Library to July 2020. Randomized controlled trials (RCTs) and observational studies reporting comparisons of QT versus BPTB or HT autografts for ACL reconstruction were included. All analyses were stratified according to study design: RCTs or observational studies. Results: A total of 24 studies were included: 7 RCTs and 17 observational studies. The 7 RCTs included 388 patients, and the 17 observational studies included 19,196 patients. No significant differences in graft failure ( P = .36), the International Knee Documentation Committee (IKDC) subjective score ( P = .39), or the side-to-side difference in stability ( P = .60) were noted between QT and BPTB autografts. However, a significant reduction in donor site morbidity was noted in the QT group compared with the BPTB group (risk ratio [RR], 0.17 [95% CI, 0.09-0.33]; P < .001). No significant differences in graft failure ( P = .57), the IKDC subjective score ( P = .25), or the side-to-side stability difference ( P = .98) were noted between QT and HT autografts. However, the QT autograft was associated with a significantly lower rate of donor site morbidity than the HT autograft (RR, 0.60 [95% CI, 0.39-0.93]; P = .02). A similar graft failure rate between the QT and control groups was observed after both early and late full weightbearing, after early and late full range of motion, and after using the QT autograft with a bone plug and all soft tissue QT grafts. However, a significantly lower rate of donor site morbidity was observed in the QT group compared with the control group after both early and late full weightbearing, after early and late full range of motion, and after using the QT autograft with a bone plug and all soft tissue QT grafts. No difference in effect estimates was seen between RCTs and observational studies. Conclusion: The QT autograft had comparable graft survival, functional outcomes, and stability outcomes compared with BPTB and HT autografts. However, donor site morbidity was significantly worse with the QT autograft than with BPTB and HT autografts.

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3D bioprinting is a promising strategy to develop heterogeneous constructs that mimic osteochondral tissue. However, conventional bioprinted hydrogels suffer from intrinsically weak mechanical strength, limited cell adaptability, and no sustained release of biochemical drugs, restraining their use as bioinks to emulate native osteochondral extra cellular matrix. Herein, a novel host-guest modulated dynamic hydrogel is developed for 3D bioprinting heterogeneous cell-laden constructs for osteochondral regeneration. Apart from gelatin methacryloyl (GelMA), this bioink consists of dopamine-functionalized GelMA and acrylate β-cyclodextrin and is crosslinked by host-guest interaction to develop the dynamic network for obtaining promoted cell adaptability, enhanced cell adhesion, reinforced mechanical strength, and tunable modulus. Moreover, based on the sustained drug release provided by the cavity of β-cyclodextrin, a heterogeneous construct is constructed by employing kartogenin (a chondrogenic factor) into the upper zone with lower Young's modulus and melatonin (an osteogenic factor) into the bottom zone with higher modulus to mimic the osteochondral microenvironment. With the favorable regeneration results in vitro and in vivo, a broad application of this bioink in 3D bioprinting for tissues engineering is expected.

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Risk for Atrial Fibrillation (AF), the most common human arrhythmia, has a major genetic component. The T-box transcription factor TBX5 influences human AF risk, and adult-specific Tbx5-mutant mice demonstrate spontaneous AF. We report that TBX5 is critical for cellular Ca2+ homeostasis, providing a molecular mechanism underlying the genetic implication of TBX5 in AF. We show that cardiomyocyte action potential (AP) abnormalities in Tbx5-deficient atrial cardiomyocytes are caused by a decreased sarcoplasmic reticulum (SR) Ca2+ ATPase (SERCA2)-mediated SR calcium uptake which was balanced by enhanced trans-sarcolemmal calcium fluxes (calcium current and sodium/calcium exchanger), providing mechanisms for triggered activity. The AP defects, cardiomyocyte ectopy, and AF caused by TBX5 deficiency were rescued by phospholamban removal, which normalized SERCA function. These results directly link transcriptional control of SERCA2 activity, depressed SR Ca2+ sequestration, enhanced trans-sarcolemmal calcium fluxes, and AF, establishing a mechanism underlying the genetic basis for a Ca2+-dependent pathway for AF risk.