Clinical Outcomes After ACL Reconstruction in Soccer (Football, Futbol) Players: A Systematic Review and Meta-Analysis.

CONTEXT: The risk factors for anterior cruciate ligament (ACL) tear for athletes participating in pivoting sports includes young age and female sex. A previous meta-analysis has reported a reinjury rate of 15% after ACL reconstruction (ACLR) for athletes across all sports. To the best of the authors' knowledge, this is the first systematic review and meta-analysis of available literature reporting outcomes after ACLR in soccer players. OBJECTIVE: To review and aggregate soccer-specific outcomes data after ACLR found in current literature to help guide a more tailored discussion regarding expectations and prognosis for soccer players seeking operative management of ACL injuries. DATA SOURCES: A comprehensive search of publications was performed using PubMed, EMBASE, Cochrane Central Register of Controlled Trials, and SPORTDiscus databases. STUDY SELECTION: Inclusion criteria consisted of original studies, level of evidence 1 to 4, studies reporting clinical and patient-reported outcomes (PROs) after primary ACLR in soccer players at all follow-up length. STUDY DESIGN: The primary outcomes of interest were graft failure/reoperation rates, ACL injury in contralateral knee, return to soccer time, and PROs. LEVEL OF EVIDENCE: Level 4. DATA EXTRACTION: Search of literature yielded 32 studies for inclusion that involved 3112 soccer players after ACLR. RESULTS: The overall graft failure/reoperation rate ranged between 3.0% and 24.8% (mean follow-up range, 2.3-10 years) and the combined ACL graft failure and contralateral ACL injury rate after initial ACLR was 1.0% to 16.7% (mean follow-up range, 3-10 years); a subgroup analysis for female and male players revealed a secondary ACL injury incidence rate of 27%, 95% CI (22%, 32%) and 10%, 95% CI (6%, 15%), respectively. Soccer players were able to return to play between 6.1 and 11.1 months and the majority of PROs showed favorable scores at medium-term follow-up. CONCLUSION: Soccer players experience high ACL injury rates after primary ACLR and demonstrated similar reinjury rates as found in previous literature of athletes who participate in high-demand pivoting sports.

Inhibiting tumor necrosis factor-alpha at time of induced intervertebral disc injury limits long-term pain and degeneration in a rat model.

BACKGROUND: Painful intervertebral disc (IVD) degeneration has tremendous societal costs and few effective therapies. Intradiscal tumor necrosis factor-alpha (TNFα) is commonly associated with low back pain, but the direct relationship remains unclear. PURPOSE: Treatment strategies for low back pain require improved understanding of the complex relationships between pain, intradiscal pro-inflammatory cytokines, and structural IVD degeneration. A rat in vivo lumbar IVD puncture model was used to 1) determine the role of TNFα in initiating painful IVD degeneration, and 2) identify statistical relationships between painful behavior, IVD degeneration, and intradiscal pro-inflammatory cytokine expression. METHODS: Lumbar IVDs were punctured anteriorly and injected with TNFα, anti-TNFα, or saline and compared with sham and naive controls. Hindpaw mechanical hyperalgesia was assayed weekly to determine pain over time. 6-weeks post-surgery, animals were sacrificed, and IVD degeneration, IVD height, and intradiscal TNFα and interleukin-1 beta (IL-1ß) expressions were assayed. RESULTS: Intradiscal TNFα injection increased pain and IVD degeneration whereas anti-TNFα alleviated pain to sham level. Multivariate step-wise linear regression identified pain threshold was predicted by IVD degeneration and intradiscal TNFα expression. Pain threshold was also linearly associated with IVD height loss and IL-1ß. DISCUSSION: The significant associations between IVD degeneration, height loss, inflammation, and painful behavior highlight the multifactorial nature of painful IVD degeneration and the challenges to diagnose and treat a specific underlying factor. We concluded that TNFα is an initiator of painful IVD degeneration and its early inhibition can mitigate pain and degeneration. Intradiscal TNFα inhibition following IVD injury may warrant investigation for its potential to alter downstream painful IVD degeneration processes.