Background: The tendon graft used in anterior cruciate ligament reconstruction (ACLR) undergoes “ligamentization” after implantation, and the reported length of this process varies from 6 to 48 months. Some grafts have ruptured at subsequent follow-up evaluations. Although the progress of graft ligamentization can be followed with postoperative magnetic resonance imaging (MRI) for reassessment, it is not known whether a delay in ligamentization (as reflected by a higher signal of the graft) is associated with an increased chance of subsequent graft rupture. Hypothesis: Signal intensity of the graft on reassessment MRI (signal-noise quotient [SNQ]) would be associated with the incidence of future graft rupture at subsequent follow-up. Study Design: Case-control study; Level of evidence, 3. Methods: A total of 565 ACLRs with intact graft on first-time reassessment MRI after surgery were followed for a mean period of 67 months. The rates of 1-year and 2-year follow-up were 99.5% and 84.5%, respectively. The signal intensity of the intact graft on the first-time reassessment MRI was evaluated (1) quantitatively by the SNQ and (2) qualitatively with the modified Ahn classification. Among the 565 ACLRs, 23 additional graft ruptures developed during a time interval of 7 months to 9 years after the surgery. Results: Higher SNQ was associated with increased chance of subsequent graft rupture (SNQ 7.3 ± 6 for subsequent graft rupture vs 4.4 ± 4 for grafts without subsequent rupture; P = .004, Mann-Whitney U test). The other important confounders that were associated with increased chance of graft rupture were younger age at the time of ACLR ( P < .001) and longer follow-up time ( P = .002). Multiple linear regression showed that all 3 factors (higher SNQ, younger age, and longer follow-up) were independent predictors of graft rupture (SNQ, P = .03; age, P < .001; follow-up, P = .012). When the reassessment MRI was performed in the second year after ACLR, the odds ratio of future graft rupture of a heterogeneous hyperintense graft when compared with a homogeneous hypointense graft was 12.1 (95% CI = 2.8 to 52.6) P < .001, Fisher exact test). Conclusion: Higher signal intensity of the intact graft on reassessment MRI (higher SNQ and heterogeneous hyperintense graft) was associated with increased chance of subsequent graft rupture.

Background: The effect of smoking on graft rupture after anterior cruciate ligament (ACL) reconstruction is not well understood. Hypothesis: It was hypothesized that there will be no relationship between tobacco use and graft rupture after ACL reconstruction, as reflected by postoperative magnetic resonance imaging (MRI) and arthroscopic examination. Study Design: Cohort study; Level of evidence, 3. Methods: Included were 233 patients who received primary ACL reconstruction with hamstring tendon autograft between January 1, 2013, and December 31, 2019, and who underwent MRI evaluation at 20.2 ± 1.9 months postoperatively. The patients were categorized by smoking history into 2 groups: 39 smokers and 194 nonsmokers. The 2 groups did not differ significantly in age, sex, operative technique, preinjury Tegner score, or mean time until postoperative MRI. The primary outcome was graft rupture rate, with rupture confirmed by either arthroscopic assessment or postoperative MRI diagnosis. The secondary outcome measure was degree of graft ligamentization, evaluated by measuring the signal-to-noise quotient (SNQ) of the graft. Results: The overall ACL graft rupture rate was 6.0%. The rupture rate was significantly higher in smokers than in nonsmokers (12.8% vs 4.6%, respectively; P = .0498). Smokers also had a significantly higher whole-graft SNQ compared with nonsmokers (4.7 ± 4.4 vs 3.3 ± 3.7, respectively; P = .028), suggesting less satisfactory ligamentization in smokers. Conclusion: Smoking was associated with a higher risk of graft rupture of ACL reconstruction and a higher SNQ of the intact graft as shown on postoperative MRI.