Risk factors for venous thromboembolism following knee arthroscopy: A systematic review and meta-analysis of observational studies.

Objectives: To evaluate the risk factors for increased risk of venous thrombosis after arthroscopic knee surgery. Methods: PubMed, EMBASE and Cochrane Library were searched from their inception to April 4, 2023. Observational studies investigated venous thrombosis following arthroscopic knee surgery were included. The Newcastle Ottawa Scale (NOS) was used to evaluate the methodological quality of included studies. The odd ratios (ORs) and 95% confidence intervals (CIs) pertaining to each risk factor were synthesized through a random effects model by STATA 14 software. Results: The protocol this meta-analysis has been registered on PROSPERO (CRD42023410283). A total of 22 observational studies were included in the systematic review, all of which were of moderate or high methodological quality. The results of the meta-analysis revealed that several factors were significantly associated with an elevated risk of venous thrombosis following arthroscopic knee surgery. These factors included age (mean age ≥30 years) [OR = 1.08, 95%CI (1.04, 1.13), P = 0.001], overweight or obesity [OR = 1.31, 95%CI (1.13, 1.52), P＜0.001], oral contraceptive use [OR = 1.90, 95%CI (1.52, 2.37), P＜0.001], and smoking history [OR = 1.35, 95%CI (1.06, 1.71), P = 0.014]. Furthermore, the subgroup analysis indicated that patients with an average age over 50 years [OR = 3.18, 95%CI (1.17, 8.66), P = 0.001] and those who underwent surgery with a tourniquet for ≥90 min [OR = 4.79, 95%CI (1.55, 14.81), P = 0.007] were at a significantly increased risk of venous thrombosis after knee arthroscopy. Conclusion: Age, obesity, oral contraceptives, smoking history, and prolonged tourniquet use may increase the risk of venous thrombosis after arthroscopic knee surgery. The incidence of venous thrombosis after knee arthroscopy is on a downward trend, but due to its severity, increasing awareness of risk factors and implementing effective prophylaxis are important tasks for clinicians to prevent the risk of venous thrombosis after knee arthroscopy.

Breakage risk of different sacroiliac screws in unilateral sacral fractures a finite element analysis.

OBJECTIVE: To compare the breakage risk of lengthened sacroiliac screws and ordinary sacroiliac screws to treat unilateral vertical sacral fractures and provide a reference for clinical application. METHODS: A finite element model of Tile C pelvic ring injury (unilateral type Denis II fracture of the sacrum) was produced. The sacral fractures were fixed with a lengthened sacroiliac screw and ordinary sacroiliac screw in 6 types of models. The maximal von Mises stresses and stress distributions of the two kinds of screws when standing on both feet were measured and compared. RESULTS: The maximal von Mises stress of the lengthened screw was less than that of the ordinary screw. Compared with ordinary screw, the stress distribution in the lengthened screw was more homogeneous. CONCLUSIONS: The breakage risk of screws fixed in double segments is lower than that of screws fixed in single segments, the breakage risk of lengthened screws is lower than that of ordinary screws, and the breakage risk of screws fixed in S2 segments is lower than that of screws fixed in S1 segments.

Anatomic relationship between S2 sacroiliac screws' entry points and pelvic external branches of superior gluteal artery.

OBJECTIVE: To study the relationship between the pelvic external branches of the superior gluteal artery and the entry area of the S2 sacroiliac screw to provide the anatomical basis and technical reference for avoiding the superior gluteal artery injury during the clinical screw placement. METHODS: CTA imaging of superior gluteal artery of 74 healthy adults (37 males and 37 females) was randomly selected. The safe bony entry area ('safe area' for abbreviation) of S2 sacroiliac screw in the standard lateral view of the pelvis three-dimensional reconstruction CT image was determined by the CT auxiliary measurement software. The relationship between the pelvic external branches of the superior gluteal artery and the safe area of S2 sacroiliac screw was observed, and the cases in which the artery intersected the safe area were counted. The distance between the safe area and the superior gluteal artery branches closest to it was measured for the cases in which the artery and the safe area did not intersect. RESULTS: 21 of the 74 cases did not have a bone channel of horizontal S2 sacroiliac screw, so they were excluded from this study. In the remaining 53 cases, 12 cases had the deep superior branch of the superior gluteal artery through the safe area of S2 screw (22.6%), and 16 cases had the superficial branch of the superior gluteal artery through the safe area of S2 screw (30.2%). There was no obvious overlap feature and law between the safe area and the superficial and deep superior branches. In 20 cases of the 53 cases, the safe area of S2 screw was located between the deep superior branch and the superficial branch of superior gluteal artery (37.7%), and in 5 cases, the safe area of S2 screw was located behind the superficial branch of superior gluteal artery (9.4%). In the cases where the superior gluteal artery did not intersect the screw entry bony safe area, the part of superior gluteal artery closest to the safe area was located in front or back of the widest part of the safe area. CONCLUSION: The risk of accidental injury of the deep superior branch and superficial branch of the superior gluteal artery is high during the process of S2 sacroiliac screw placement. Even if the screw entry point is located in the bony safe area, the absolute safety of screw placement cannot be guaranteed. We strongly suggest that a careful and thorough plan is needed before surgery.

Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway.

CONTEXT: The prevalence of gout has greatly increased, and it has become the most common inflammatory arthritis in men. Isovitexin possesses anti-inflammatory and antioxidant properties. OBJECTIVE: We explored the effects of isovitexin on rats with acute gouty arthritis (GA). MATERIALS AND METHODS: Fifty-four Sprague-Dawley rats were assigned to five groups: sham, model, positive (colchicine, 0.3 mg/kg), isovitexin (100 mg/kg), TLR4 inhibitor (TAK-242, 3 mg/kg) and isovitexin + TAK-242. The gait of rats and the ankle joint swelling index were monitored. The levels of tumour necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and IL-6, and pathological changes in the synovial tissues were determined. RESULTS: Isovitexin significantly reduced the ankle joint swelling index at day 7 compared to that in the model group (4.39 ± 1.01 vs. 6.09 ± 1.31). Moreover, isovitexin alleviated the infiltration of inflammatory cells and ameliorated the proliferation of synovial cells. The levels of TNF-α (93.42 ± 5.02 pg/mL), IL-1ß (25.46 ± 1.91 pg/mL) and IL-6 (194.71 ± 7.92 pg/mL) in the isovitexin group were significantly lower than in the model group (129.39 ± 5.43, 39.60 ± 2.71 and 223.77 ± 5.35 pg/mL). The expression of TLR4, MyD88 and p-NF-κB-p65 was remarkably decreased after isovitexin and colchicine treatment. The effect of isovitexin was similar to that colchicine. Furthermore, the combination of isovitexin and TAK-242 had better effect, and there was no significantly difference with colchicine treatment. DISCUSSION AND CONCLUSIONS: Isovitexin ameliorates joint inflammation in acute GA via the TLR4/MyD88/NF-κB pathway. Isovitexin may be a potential substitute medicine for GA.

Biomechanical comparison of three minimally invasive fixations for unilateral pubic rami fractures.

BACKGROUND: To compare the mechanical characteristics of a percutaneous superior pubic intramedullary screw, percutaneous bridging plate and percutaneous screw-rod system of the anterior ring for the treatment of unilateral vertical pubic fractures to provide a reference for clinical application. METHODS: A finite element model of pelvic anterior ring injury (unilateral vertical pubic fracture) was produced. The fractures were fixed with a percutaneous superior pubic intramedullary screw, percutaneous bridging plate and percutaneous screw-rod system of the anterior ring and their combinations in 5 types of models. The fracture stabilities under vertical, bilateral and anterior-posterior load were quantified and compared based on the displacement of the hip joints' midpoint as quantificational index of fracture stability. RESULTS: In the condition of bilateral and anterior-posterior load, the vertical, bilateral and anterior-posterior displacements of the hip joints' midpoint of different models were significantly different respectively. In general, the displacements of the 5 pelvic anterior ring fixations were ranked from maximum to minimum as follows: bridging plate, pelvic anterior screw-rod system, combination of bridging plate and pelvic anterior screw-rod system, superior pubic intramedullary screw and combination of superior pubic intramedullary screw and pelvic anterior screw-rod system. CONCLUSION: For the fixation in unilateral pubic fractures of pelvic ring injury, the percutaneous superior pubic intramedullary screw is optimal, the percutaneous pelvic anterior screw-rod system is the second choice, and percutaneous bridging plate ranks the third. The percutaneous pelvic anterior screw-rod system can significantly increase fixation stability of the percutaneous superior pubic intramedullary screw and the percutaneous bridging plate.

miR-296-5p inhibits IL-1ß-induced apoptosis and cartilage degradation in human chondrocytes by directly targeting TGF-ß1/CTGF/p38MAPK pathway.

Osteoarthritis (OA) is characterized by apoptosis of chondrocytes and an imbalance of extracellular matrix (ECM) synthesis and catabolism. Emerging evidence has demonstrated that miRNAs are involved in OA pathologies, but the role of miR-296-5p in OA remains unclear. The present study proposes to reveal the functions and mechanisms of miR-296-5p in a cell model of OA. In this study, human chondrocytes were treated with 5 ml interleukin-1 beta (IL-1ß) to induce apoptosis and cartilage degradation. Our results showed that miR-296-5p was downregulated in chondrocytes stimulated with IL-1ß. Overexpressed miR-296-5p enhanced cell proliferation and inhibited apoptosis and matrix degrading enzyme expression in response to IL-1ß stimulation, and knockdown of miR-296-5p showed the opposite effect. Further, we found that miR-296-5p directly targeted the 3'-untranslated region (3'-UTR) of TGF-ß1 mRNA, and miR-296-5p inactivated the TGF-ß1/CTGF/p38MAPK signaling pathway. Overexpression of TGF-ß1 alleviated the inhibition of miR-296-5p on chondrocyte apoptosis and cartilage degradation. In conclusion, miR-296-5p inhibited the progression of OA through the CTGF/p38MAPK pathway by directly targeting TGF-ß1.

The Effects of MiR-214-3p and Irisin/FNDC5 on the Biological Behavior of Osteosarcoma Cells.

Background: Irisin/fibronectin type III domain-containing protein 5 (FNDC5) has important effects on breast cancer and liver cancer, however, its role in osteosarcoma is poorly understood. This study explored the effects of irisin/FNDC5 in osteosarcoma cells, aiming to provide a direction for treating osteosarcoma. Material and Methods: The expression levels of irisin/FNDC5 in serums and tissues of osteosarcoma patients and the expression characteristics of FNDC5 in osteosarcoma cell lines were measured. The effects of irisin, at different concentrations (0, 25, 50, 100, and 200 ng/mL), and FNDC5 on the viability, migration, and invasion of U2OS cells were analyzed. The target gene regulating FNDC5 was predicted, and its effects on irisin/FNDC5 and osteosarcoma cells were further explored. Results: The authors found that irisin/FNDC5 was significantly downregulated in the serums and tissues of osteosarcoma patients, and FNDC5 was also lowly expressed in osteosarcoma cell lines, especially in U2OS cells. Irisin/FNDC5 could not only inhibit the viability of U2OS cell in a concentration- and time-dependent manner but could also suppress cell migration and invasion. Furthermore, miR-214-3p inhibited the expression of irisin/FNDC5, and promoted the migration, invasion, and epithelial/mesenchymal transition (EMT) of U2OS cell through targeting FNDC5. Conclusions: Irisin/FNDC5 could inhibit the viability, migration, invasion, and EMT of osteosarcoma cells, and miR-214-3p could target FNDC5 to release its antitumor effects. Thus, irisin/FNDC5 and miR-214-3p might become a new direction for the treatment of osteosarcoma patients in the future.

Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway.

BACKGROUND AND OBJECTIVE: Endometrial carcinoma (EC) is one of the most frequently diagnosed malignancies in females. Dysregulation of lncRNA TDRG1 has been widely documented in several cancers, including EC. However, the mechanism of this lncRNA involving in EC progression remains to be further elucidated. MATERIALS AND METHODS: The enrichment levels of TDRG1 in EC tissues and cell lines were examined by RT-qPCR. Flow cytometry, cell counting kit-8 (CCK-8), transwell, and Western blot assays were conducted to assess whether TDRG1 knockdown could affect cell cycle arrest, proliferation, migration, invasion, and apoptosis of EC cells. The phosphorylation levels of mTOR, AKT and PI3K that associated with PI3K/Akt/mTOR pathway were determined by Western blot assay. RESULTS: TDRG1 expression was markedly upregulated in EC tissues and cell lines. Knockdown of TDRG1 significantly induced cell cycle arrest and apoptosis, inhibited cell proliferation, restrained the invasion and migration abilities in EC cells. Moreover, TDRG1 silencing decreased the protein levels of p-AKT, p-PI3K, and p-mTOR of EC cells. CONCLUSION: Our data underlined the implication of TDRG1 in EC progression, proposing that targeting TDRG1 might be a potential therapeutic avenue in EC.

LncRNA LOC730101 promotes osteosarcoma cell survival under energy stress.

Long non-coding RNAs have been proved in tumorigenesis of various cancers, including osteosarcoma. However, the role of LOC730101 in cancer is rare to be reported, not mention to osteosarcoma. In current study, quantitative real-time PCR, was applied to evaluate the expression of LOC730101 under energy stress. The roles of LOC730101 in cell viability, apoptosis and tumor development under energy stress were analyzed by cell biological assays in vitro and in vivo. AMPK CA (continuously active) and Compound C (AMPK inhibitor) were employed to investigate the mechanism. And we further confirmed that compared with adjacent tissues, LOC730101 is remarkably increased in osteosarcoma in our fresh tissues. In addition, cellular function assays demonstrated that LOC730101 promotes cell viability, tumor development, and deficiency of LOC730101 promotes cell apoptosis under energy stress. Furthermore, we validated that up-regulated LOC730101 enhances cell viability through AMPK under energy stress. Taken together, our findings enlarged the knowledge about the roles of LOC730101 in osteosarcoma progression.

Irisin reverses the IL-6 induced epithelial-mesenchymal transition in osteosarcoma cell migration and invasion through the STAT3/Snail signaling pathway.

As a novel discovered myokine, irisin is considered to be a promising candidate for the treatment of metabolic disorders and cancer. However, little is known about the anti-metastasic effect of irisin on osteosarcoma cells and its underlying mechanisms. In the present study, we aimed to explore the effect of irisin on the migration and invasion of osteosarcoma cells and the underlying mechanisms involved. Viability and proliferation of osteosarcoma cells were examined by MTT assay. Then, by using scratch wound healing assay and Transwell assays, we evaluated migratory and invasive ability of the cells, respectively. Moreover, the expression of epithelial-to-mesenchymal transition (EMT) markers were determined by qPCR, western blot and immunofluorescence staining after treatment with IL-6 and irisin. Furthermore, the expression of ERK, p38, STAT3 and Snail were detected by western blot analysis. Finally, an inhibitor of STAT3, WP1066 was applied to testify the effect of irisin on the expression of EMT markers and Snail. It was found that irisin treatment significantly suppressed the proliferation, migration and invasion of osteosarcoma cells. Furthermore, irisin reversed the IL-6-induced epithelial­mesenchymal transition (EMT) in osteosarcoma cells by regulating the expression of E-cadherin, N-cadherin, vimentin, fibronectin, MMP-2, MMP-7 and MMP-9. In addition, irisin suppressed the IL-6-activated phosphorylation of STAT3 and the expression of Snail in osteosarcoma cells. Finally, blockade of STAT3 by WP1066 (a STAT3 inhibitor) further enhanced the effect of irisin on the EMT and Snail expression in osteosarcoma cells. Collectively, our findings revealed that irisin may play a critical role in the IL-6-induced EMT of osteosarcoma cells via the STAT3/Snail signaling pathway.

Paris saponin VII suppresses osteosarcoma cell migration and invasion by inhibiting MMP­2/9 production via the p38 MAPK signaling pathway.

Metastasis is the primary cause of mortality in osteosarcoma. Targeting metastasis is a major strategy in osteosarcoma treatment. As a traditional Chinese medicine, Trillium tschonoskii Maxim has been widely used in the therapy of various diseases, including cancer. However, currently there is no evidence regarding the anti­metastasic effect of Paris saponin VII (PS VII), which is extracted from Trillium tschonoskii Maxim, on osteosarcoma cells and its underling mechanisms. The present study aimed to examine the effect of PS VII on the migration and invasion of osteosarcoma cells. Viability and proliferation of osteosarcoma cells were examined by MTT assay. Migration and invasion of osteosarcoma cells was then detected using scratch wound healing assays and Transwell assays, respectively. Additionally, the expression of matrix metalloproteinase (MMP)­2 and ­9 was determined at the mRNA and protein level following treatment with PS VII. Mitogen­activated protein kinase (MAPK) expression was also detected by western blot analysis. Finally, an inhibitor of p38 MAPK was used to verify the effect of PS VII on the expression of MMP­2 and ­9, as well as the migration and invasion osteosarcoma cells. This demonstrated that the proliferation, migration and invasion of the osteosarcoma cells were suppressed following treatment with PS VII. PS VII downregulated the expression of MMP­2 and ­9 in a dose­ and time­dependent manner. PS VII also exerted its ability to downregulate the phosphorylation of p38 MAPKs. Furthermore, by using a p38 inhibitor, SB203580, the role of PS VII in MMP­2 and ­9 expression and osteosarcoma cell invasion was revealed. Taken together, these results demonstrated that PS VII suppresses the migration and invasion of osteosarcoma cells via the p38 MAPK signaling pathway.

The role of matrix metalloproteinase 14 polymorphisms in susceptibility to intervertebral disc degeneration in the Chinese Han population.

INTRODUCTION: Matrix metalloproteinase 14 (MMP14) plays an important role in the pathophysiology of intervertebral disc degeneration (IVDD). The present study aimed to determine whether two single nucleotide polymorphisms (-378 T/C and -364 G/T) of MMP14 were associated with the risk and severity of IVDD in the Chinese Han population. MATERIAL AND METHODS: A total of 908 patients with IVDD and 906 healthy controls were enrolled in this study. The grade of disc degeneration was determined according to Schneiderman's classification for magnetic resonance imaging. The polymorphisms of MMP14 were genotyped using polymerase chain reaction and direct sequencing. RESULTS: The genotype distribution of -364G/T did not show a significant difference between IVDD patients and healthy controls. The frequencies of the -378T/C and CC genotypes were significantly lower among IVDD patients compared with healthy controls (p < 0.001); unconditional logistic regression analysis revealed that the CT and CC genotypes were significantly associated with a decreased risk of IVDD compared with the TT genotype (p < 0.001). Patients with IVDD showed significantly higher frequencies of the T allele at -378T/C than healthy controls (p < 0.001). In addition, the -375 CC genotype, as well as the C allele, was associated with lower degenerative grades of IVDD compared with the TT genotype and the T allele, respectively (both p < 0.001). CONCLUSIONS: The -378T/C polymorphism of MMP14 may be associated with the risk and severity of IVDD in the Chinese Han population. It shows potential to become a biomarker to predict risk and severity of IVDD.

Visfatin promotes osteosarcoma cell migration and invasion via induction of epithelial-mesenchymal transition.

Visfatin is considered to be a biomarker in various types of cancers. However, no evidence has been reported for the direct effect of visfatin on osteosarcoma cell metastasis. The aims of the present study were to investigate the influence of visfatin on the migration and invasion of osteosarcoma cells and clarify the underlying mechanism. The expression levels of epithelial-mesenchymal transition (EMT) markers, as well as the transcriptional factor Snail-1, were first detected at both the protein and mRNA levels in U2OS osteosarcoma cells after stimulation of visfatin. Then the expression of NF-κB (p65) was detected by western blot analysis, and siRNA of Snail-1 and inhibitor of NF-κB were used to investigate the effect of visfatin. Finally, migration and invasion of the cells were detected respectively by scratch wound healing and transwell assays. Visfatin downregulated E-cadherin and upregulated N-cadherin in concentration- and time-dependent manners at the protein and mRNA levels. The expression of Snail-1 was also upregulated. Moreover, visfatin also promoted the nuclear translocation of the NF-κB pathway. Administration of siRNA of Snail-1 and the inhibitor BAY11-7082 validated the roles of Snail-1 and NF-κB in the visfatin-induced regulation of EMT markers. Migration and invasion of U2OS osteosarcoma cells were promoted following the application of visfatin. These results demonstrated that visfatin enhances the migration and invasion of osteosarcoma cells via the NF-κB/Snail-1/EMT pathway.

Arthroscopic posterior cruciate ligament reconstruction with allograft versus autograft.

INTRODUCTION: The aim of the study was to compare and analyze retrospectively the outcomes of arthroscopic posterior cruciate ligament reconstruction with autograft versus allograft. MATERIAL AND METHODS: Seventy-one patients who underwent arthroscopic posterior cruciate ligament reconstruction with an autograft or allograft met our inclusion criteria. There were 36 patients in the autograft group and 35 patients in the allograft group. All the patients were evaluated by physical examination and a functional ligament test. Comparative analysis was done in terms of operation time, incision length, fever time, postoperative infection rate, incidence of numbness and dysesthesia around the incision, as well as a routine blood test. RESULTS: The average follow-up of the autograft group was 3.2 ±0.2 years and that of the allograft group was 3.3 ±0.6 years; there was no significant difference (p > 0.05). No differences existed in knee range of motion, Lysholm scores, International Knee Documentation Committee standard evaluation form and Tegner activity score at final follow-up (p > 0.05), except that patients in the allograft group had a shorter operation time and incision length and a longer fever time (p < 0.05). We found a difference in posterior drawer test and KT-2000 arthrometer assessment (p < 0.05). The posterior tibia displacement averaged 3.8 ±1.5 mm in the autograft group and 4.8 ±1.7 mm in the allograft group (p < 0.05). The incidence of numbness and dysesthesia around the incision in the autograft group was higher than that in the allograft group (p < 0.05). There was no infection postoperatively. The white blood cells and neutrophils in the allograft group increased more than those in the autograft group postoperatively (p < 0.05). CONCLUSIONS: Both groups of patients had satisfactory outcomes after the operation. However, in the instrumented posterior laxity test, the autograft gave better results than the allograft. No differences in functional scores were found.

[Prospective comparative study of arthroscopic anterior cruciate ligament construction with autograft and allograft].

OBJECTIVE: To study the clinical effect of arthroscopic anterior cruciate ligament (ACL) construction with different transplants. METHODS: From March 2006 to April 2009, 86 patients including 60 male and 26 female undergoing arthroscopic ACL reconstruction were prospectively randomized consecutively into autograft group (44 patients, using autogeneic hamstring tendons) and allograft group (42 patients, using allogenic lower extremity tendons). The age of those patients were 22 - 56 years, averaging (32 ± 7) years. The operations were made by the same doctor with the standard technology. The postoperative effects were assessed by the range of motion and tibia forward distance, Lachman test, pivot shift test, Daniel test, IKDC scores systems, Lysholm-Tegner scores. RESULTS: Seventy-nine patients were followed up, 41 patients in autograft groups averaged 39.6 months and 38 patients in allograft group averaged 37.4 months. The operation time of autograft group was (87 ± 11) minutes, that of allograft group was (55 ± 10) minutes (t = 15.732, P < 0.05). The time of postoperative fever of autograft group was (3.2 ± 1.4) days, that of allograft groups was (7.6 ± 5.3) days (t = 5.740, P < 0.05). The Lysholm scores of autograft group was 42 ± 7 before operation, and 89 ± 8 at final follow-up. The Lysholm scores of allograft group was 44 ± 6 before operation, and 87 ± 9 at final follow-up. There was statistic difference in both groups between before operation and final follow-up (t = 13.534 and 17.768, P < 0.05).But no statistic difference existed between the two groups (P > 0.05). The Tegner scores of autograft group was 2.9 ± 2.1 before operation, and 7.7 ± 1.2 at final follow-up. The Tegner scores of allograft group was 2.7 ± 1.4 before operation, and 7.1 ± 1.6 at final follow-up. There was statistic difference in both groups between before operation and final follow-up (t = 16.004 and 12.338, P < 0.05).No statistic difference existed between the two groups (P > 0.05). The KT2000 results showed that the anterior displacement of autograft groups was (10.7 ± 3.5) mm before operation and (5.0 ± 2.7) mm at final follow-up, the anterior displacement of allograft groups was (10.9 ± 2.9) mm before operation and (6.5 ± 2.4) mm at final follow-up, there was statistic difference between before and after operation in anterior displacement in two groups (t = 16.354 and 13.296 P < 0.05). There was no difference between two groups before operation and at final follow-up. Compared to before operation, the IKDC scores were improved greatly after operation (P < 0.05). CONCLUSION: The clinical effect of arthroscopic ACL construction with allograft transplants is near to autograft.