Osteointegration of PLLA/ß-TCP Biocomposite Anchors Used in Coracoid Transfer Procedures for Shoulder Instability: Quantitative Computed Tomography With a Minimum 2-Year Follow-up.

Background: Biocomposite anchors have been a popular choice for use in coracoid transfer procedures for shoulder instability and are hypothesized to allow bone ingrowth. Purpose: To quantitatively evaluate the osteointegration of 85% PLLA/15% ß-TCP biocomposite anchors used in the coracoid transfer procedure for shoulder instability. Study Design: Case series; Level of evidence, 4. Methods: We performed a retrospective case series of abstracted data from the records of 74 patients who underwent coracoid transfer procedures with biocomposite anchors. Computed tomography was performed at 24 months postoperatively. A total of 4 researchers independently reviewed the computed tomography images. The density (in Hounsfield unit [HU] values) of the anchor tunnels, glenoid, and subscapularis was assessed, and osteointegration of the anchor tunnels was evaluated with HU values, the quantitative ossification quality score (QOQS), and tunnel widening. Results: Included were 74 patients (58 male, 16 female), involving 76 shoulders and 124 biocomposite anchors. At ≥24-month follow-up, 72 of 124 (58.06%) anchor tunnels were classified as QOQS type 1, including 12 completely ossified tunnels and 60 almost completely ossified tunnels. Some degree of ossification (QOQS types 1-3) was observed in 118 (95.16%) anchor tunnels. Overall, 3 anchor tunnels were enlarged (QOQS type 5). The mean HU value of the anchor tunnels was 339.75, which was significantly higher than the preoperative HU value of the glenoid vault (262.19). Among the 124 anchor tunnels, 79 had HU values higher than their glenoid HU values, and 45 had lower HU values than their glenoid HU values. In the comparison of tunnel HU values at 12 versus ≥24 months, the HU value at ≥24 months was significantly higher. A total of 20 anchor tunnels widened. Conclusion: Among 124 anchor tunnels, 95.16% showed ossification, 58.06% were completely or nearly completely ossified, and 3 were enlarged. The HU value of the anchor tunnel increased over time.

Comparison of the TightRope system versus hook plate in acute acromioclavicular joint dislocations: a retrospective analysis.

This study compared the results of the minimally invasive coracoclavicular (CC) fixation with a single TightRope (MITR) procedure and the hook plate (HP) procedure for acute acromioclavicular (AC) joint dislocation treatment. Sixteen patients with a mean age of 44.9 ± 11 years were treated with the MITR procedure. Nineteen patients with a mean age of 40.2 ± 8.7 years were treated using the HP procedure. Clinical outcomes were evaluated with the Visual Analog Scale (VAS) for pain, Constant-Murley Score (CMS), and University of California at Los Angeles (UCLA) Shoulder score. Vertical displacement of the clavicle with reference to the height of the acromion was measured in standard anteroposterior radiographs. The mean follow-up was 27 months in the MITR group and 30 months in the HP group. No statistically significant differences were found between the MITR group and the HR group in terms of VAS score (0.4 ± 0.6 vs 0.7 ± 0.6, P = 0.138), UCLA Shoulder score (33.9 ± 2.5 vs 33.7 ± 1.5, P = 0.843), or CMS (95.7 ± 7.3 vs 93.7 ± 6.6, P = 0.400). No redislocation was identified in the HP group, while redislocation occurred in 1 of 16 (6.3%) patients in the MITR group. One patient in the HP group (5.3%) had acromial osteolysis, while no acromial osteolysis was found in the MITR group. No other adverse events, such as infections, tunnel widening, fractures, or implant-related complications, were observed. Both procedures provided satisfactory results. The HP procedure provided better reduction, while the MITR procedure provided a slightly lower tendency of pain. Long-term follow-up is needed to investigate the clinical outcomes and radiological outcomes of both groups.

Hepcidin-induced reduction in iron content and PGC-1ß expression negatively regulates osteoclast differentiation to play a protective role in postmenopausal osteoporosis.

As a necessary trace element, iron is involved in many physiological processes. Clinical and basic studies have found that disturbances in iron metabolism, especially iron overload, might lead to bone loss and even be involved in postmenopausal osteoporosis. Hepcidin is a key regulator of iron homeostasis. However, the exact role of hepcidin in bone metabolism and the underlying mechanism remain unknown. In this study, we found that in postmenopausal osteoporosis cohort, the concentration of hepcidin in the serum was significantly reduced and positively correlated with bone mineral density. Ovariectomized (OVX) mice were then used to construct an osteoporosis model. Hepcidin overexpression in these mice significantly improved bone mass and rescued the phenotype of bone loss. Additionally, overexpression of hepcidin in OVX mice greatly reduced the number and differentiation of osteoclasts in vivo and in vitro. This study found that overexpression of hepcidin significantly inhibited ROS production, mitochondrial biogenesis, and PGC-1ß expression. These data showed that hepcidin protected osteoporosis by reducing iron levels in bone tissue, and in conjunction with PGC-1ß, reduced ROS production and the number of mitochondria, thus inhibiting osteoclast differentiation and bone absorption. Hepcidin could provide new targets for the clinical treatment of postmenopausal osteoporosis.

Identification of CIRBP and TRPV4 as Immune-Related Diagnostic Biomarkers in Osteoarthritis.

PURPOSE: Osteoarthritis (OA) is the most common chronic joint disorder in elderly individuals. This study aimed to identify immune-related diagnostic gene signatures for OA. METHODS: First, we performed single-sample gene set enrichment analysis (ssGSEA) to evaluate the infiltration of immune cells in OA expression data from the Gene Expression Omnibus (GEO) database. Then, weighted gene coexpression network analysis (WGCNA) was performed to identify hub modules and genes related to immune cell types with significant infiltration. Finally, we screened diagnostic markers from the differentially expressed genes (DEGs) in both the OA group and the hub module using least absolute shrinkage and selection operator (LASSO) logistic regression. RESULTS: Immune filtration analysis showed that immature B cells, mast cells, natural killer T cells, myeloid-derived suppressor cells (MDSCs), and type 2 T helper cells were dysregulated in OA samples. In WGCNA, a total of 120 genes were selected as hub genes associated with mast cell infiltration.The enrichment analysis showed that spliceosome, positive regulation of cell migration, and response to mechanical stimulus were mainly involved. The LASSO regression model for the GSE117999 dataset revealed 15 DEGs for predicting OA. Finally, two genes were obtained by intersection for further investigation. CONCLUSION: Cold-inducible RNA-binding protein (CIRBP) and transient receptor potential vanilloid 4 (TRPV4) were identified as diagnostic biomarkers for OA, and both were positively correlated with mast cell infiltration.

Rapamycin improves bone mass in high-turnover osteoporosis with iron accumulation through positive effects on osteogenesis and angiogenesis.

Iron accumulation is an independent risk factor for type I osteoporosis, but the molecular mechanisms of the phenomenon are not well defined, and effective therapy has not been reported. Here, we found that the level of mTOR was increased both in wild-type mouse models with iron accumulation and transgenic mouse models (Hepc-/-) of high-turnover osteoporosis with iron accumulation. We show that an increased level of mTOR can depress osteogenesis and angiogenesis by Cxcl9 both in bone and in vitro. Suppression of mTOR in mouse models by rapamycin and in vitro by siRNA transfection recovered both osteogenesis and angiogenesis. These findings revealed the role of mTOR in osteogenesis and angiogenesis in high-turnover osteoporosis with iron accumulation and showed that rapamycin targeting of mTOR ameliorates osteogenesis and angiogenesis to improve bone mass.

Methylation of bone SOST impairs SP7, RUNX2, and ERα transactivation in patients with postmenopausal osteoporosis.

Sclerostin (SOST), a glycoprotein predominantly secreted by bone tissue osteocytes, is an important regulator of bone formation, and loss of SOST results in Van Buchem disease. DNA methylation regulates SOST expression in human osteocytes, although the detailed underlying mechanisms remain unknown. In this study, we compared 12 patients with bone fractures and postmenopausal osteoporosis with eight patients without postmenopausal osteoporosis to understand the mechanisms via which SOST methylation affects osteoporosis. Serum and bone SOST expression was reduced in patients with osteoporosis. Bisulfite sequencing polymerase chain reaction revealed that the methylation rate was higher in patients with osteoporosis. We identified osterix (SP7), Runt-related transcription factor 2 (RUNX2), and estrogen receptor α (ERα) as candidate transcription factors activating SOST expression. Increased SOST methylation impaired the transactivation function of SP7, RUNX2, and ERα in MG-63 cells. AzadC treatment and SOST overexpression in MG-63 cells altered cell proliferation and apoptosis. Chromatin immunoprecipitation showed that higher methylation was associated with reduced SP7, RUNX2, and ERα binding to the SOST promoter in patients with osteoporosis. Our studies provide new insight into the role of SOST methylation in osteoporosis.

Iron Accumulation Leads to Bone Loss by Inducing Mesenchymal Stem Cell Apoptosis Through the Activation of Caspase3.

Osteoporosis (OP) is a disease associated with bone loss and microstructure degradation. Recent studies have shown that iron accumulation may be a risk factor for OP. Bone marrow mesenchymal stem cells (MSCs) are multipotent cells and precursors to osteoblasts. MSCs play an important role in OP. Therefore, we evaluated the correlation between MSCs and OP in an environment of iron accumulation. Serum P1NP was decreased in iron accumulation mice. Micro-CT revealed that iron accumulation decreased bone mineral density and spatial structural parameters. Iron accumulation inhibited MSC quantity in bone marrow. However, the iron chelator deferoxamine (DFO) rescued the suppression. Iron accumulation also changed the MSC cell cycle. Iron elevated MSC cell ROS level and NOX4 protein expression. MSC apoptosis was increased, and more caspase3 was cleaved after iron intervention. Our data suggests that iron accumulation inhibits MSC quantity and induces MSC apoptosis. Bone loss from iron accumulation may correlate with the inhibition of MSCs.

GOLM1 Stimulation of Glutamine Metabolism Promotes Osteoporosis via Inhibiting Osteogenic Differentiation of BMSCs.

BACKGROUND/AIMS: Bone marrow mesenchymal stem cells (BMSCs) play an essential role in osteoporosis. However, the molecular mechanisms and the involvement of glutamine metabolism in osteogenic BMSCs differentiation and osteoporosis remain largely unclear. In this study, we investigated the role of Golgi membrane protein 1 (GOLM1) and glutamine metabolism in BMSCs differentiation and osteoporosis. METHODS: Osteogenic differentiation-inducing media (Odi) was used to induce the osteogenic differentiation of BMSCs. The mRNA expression of GOLM1, ALP, Runx2, Osx, BSP and OCN was determined by qRT-PCR assay. Western blot assay was used to analyze GOLM1, p-mTOR, mTOR, p-S6 and S6 abundance in GOLM1 silencing and over-expressed BMSCs. Glutamine uptake, intracellular glutamine, glutamate and α-KG level was detected using indicated Kits. GOLM1 antibody, glutamine metabolism inhibitors EGCG and BPTES were used to treat ovariectomy (OVX)-induced osteoporosis. Bone mineral density and bone volume relative to tissue volume (%) were analyzed by micro-CT. Serum was collected from osteoporosis patients and healthy participants and subjected to GOLM1 determination using ELISA Kit. RESULTS: GOLM1 expression and glutamine metabolism were suppressed by Odi. GOLM1 blockage or inhibition of glutamine metabolism promoted the osteogenic differentiation of BMSCs induced by Odi. GOLM1 activated glutamine metabolism depending on the mTOR signaling pathway. In vivo, GOLM1 antibody or combination of glutamine inhibitor EGCG and BPTES rescued the osteoporosis in an OVX-operated mouse model. Serum GOLM1 level was increased in the patients of osteoporosis compared with healthy people. CONCLUSION: GOLM1 stimulates glutamine metabolism to suppress the osteogenic differentiation of BMSCs and to promote osteoporosis. Therefore, GOLM1 activation of glutamine metabolism is a potential target for osteoporosis.

The GDF11-FTO-PPARγ axis controls the shift of osteoporotic MSC fate to adipocyte and inhibits bone formation during osteoporosis.

During osteoporosis, the shift of bone mesenchymal stem cell (BMSC) lineage commitment to adipocyte leads to the imbalance between bone mass and fat, which increases the risk of fracture. The mechanism underlying this process is not fully understood. Fat mass and obesity-associated protein (FTO) is an RNA demethylase that demethylates various methylated nucleic acids and participates in various physiological and pathological processes. Here we identified FTO as a regulator for BMSC fate determination during osteoporosis. FTO was up-regulated in bone marrow during aging or osteoporosis in human and mice in a GDF11(growth differentiation factor 11)-C/EBPα-dependent mechanism. The expression of FTO was also up-regulated during adipocyte differentiation of BMSCs whereas its expression was down-regulated during osteoblast differentiation. Gain-of-function and loss-of-function experiments showed that FTO favored the BMSCs to differentiate to adipocytes rather than osteoblasts. Further mechanism study demonstrated that FTO bound and demethylated the mRNA of the Peroxisome proliferator-activated receptor gamma (Pparg), leading to the increase in the expression of Pparg mRNA. Reversely, Pparg knockdown blocked the function of GDF11-FTO during osteoblast differentiation of BMSCs. Furthermore, conditionally genetic knockout of Fto in osteoblasts inhibited the development of osteopenia in mice. Collectively, our findings demonstrated that GDF11-FTO-Pparg axis promoted the shift of osteoporotic BMSC fate to adipocyte and inhibited bone formation during osteoporosis.

Human type H vessels are a sensitive biomarker of bone mass.

Vascularization is fundamental for bone formation and bone tissue homeostasis. However, in human subjects, a direct molecular relationship has not been identified between angiogenesis and agents that promote bone disease or factors related to age. Osteopenia is a condition in which bone mineral density is lower than normal, and it represents a sign of normal aging. Here we tested whether the type H vessel, which was recently identified as strongly positive for CD31 and Endomucin (CD31hiEmcnhi) in mice, is an important indicator of aging and osteopenia in human subjects. We found that age-dependent losses of type H vessels in human bone sections conform to the observations in aged mice. The abundance of human type H vessels and osteoprogenitors may be relevant to changes in the skeletal microarchitecture and advanced osteopenia. Furthermore, ovariectomized mice, a widely used model for postmenopausal osteoporosis, exhibited significantly reduced type H vessels accompanied by reduced osteoprogenitors, which is consistent with impaired bone microarchitecture and osteoporosis, suggesting that this feature is an indicator of bone mass independent of aging. More importantly, administration of desferrioxamine led to significantly increased bone mass via enhanced angiogenesis and increased type H vessels in ovariectomized mice. Altogether, these data represent a novel finding that type H vessels are regulated in aged and osteopenia subjects. The abundance of human type H vessels is an early marker of bone loss and represents a potential target for improving bone quality via the induction of type H vessels.

Local bone interaction between renin-angiotensin system and kallikrein-kinin system in diabetic rat.

OBJECTIVE: This study was performed to investigate bone deteriorations and the involvement of skeletal renin-angiotensin system (RAS) and kallikrein-kinin system (KKS) of male rat in response to the hyperglycemia. METHODS: The biomarkers in serum and urine were measured by ELISA kit, and tibias were taken for the measurement on gene, protein expression and histological analysis, femurs were taken for the measurement on biomechanical parameters and micro-CT. RESULTS: The DM1 showed the decreased level of osteocalcin, testosterone and FGF-23, and the increased level of serum CTX as compared to those of vehicle group. The H&E staining showed remarkable bone deteriorations, including increased disconnections and separation of trabecular bone among growth plate and joint cartilage in DM1 group. Biomechanically, the maximum load, maximum stress, and strain parameter of DM1 group was significantly lower than control group. Type 1 diabetic mice displayed bone loss shown the reduction of bone volume/total volume, trabecular number, trabecular thickness and bone mineral density. The STZ injection significantly up-regulated mRNA expression of AT1R, AGT, renin, renin-receptor, and ACE, and the expression of AT2R, B1R and B2R were down-regulated in tibia of rat in hyperglycemia group. The protein expression of renin, ACE and Ang II were significantly up-regulated, and AT2R, B1R and B2R were down-regulated in DM1 group. CONCLUSIONS: The treatment of hyperglycemia was detrimental to bone as compared to the vehicle group, and the underlying mechanism was mediated, at least partially, through down-regulation of KSS activity and up-regulation of RAS activity in local bone.

Sirt3-MnSOD axis represses nicotine-induced mitochondrial oxidative stress and mtDNA damage in osteoblasts.

Increasing evidence has suggested an important role played by reactive oxygen species in the pathogenesis of osteoporosis. Tobacco smoking is an important risk factor for the development of osteoporosis, and nicotine is one of the major components in tobacco. However, the mechanism by which nicotine promotes osteoporosis is not fully understood. Here, in this study, we found that nicotine-induced mitochondrial oxidative stress and mitochondrial DNA (mtDNA) damage in osteoblasts differentiated from mouse mesenchymal stem cell. The activity of MnSOD, one of the mitochondrial anti-oxidative enzymes, was significantly reduced by nicotine due to the reduced level of Sirt3. Moreover, it was also found that Sirt3 could promote MnSOD activity by deacetylating MnSOD. Finally, Mn(III)tetrakis (4-benzoic acid) porphyrin (MnTBAP, a MnSOD mimetic) was found to markedly reduce the effect of nicotine on osteoblasts. In summary, Sirt3-MnSOD axis was identified as a negative component in nicotine-induced mitochondrial oxidative stress and mtDNA damage, and MnTBAP may serve as a potential therapeutic drug for osteoporosis.

[Comparative evaluation of the techniques and effects of RetroButton and Interference Screw in anterior cruciate ligament reconstruction].

OBJECTIVE: To evaluate the difference between RetroButton and Interference Screw in Anterior Cruciate Ligament (ACL) Reconstruction. METHODS: Ninety-seven patients with ACL rupture were treated by arthroscopic reconstruction with RetroButton and Interference Screw from June 2008 to December 2011. There were 54 males and 43 females with an average age of 27.5 years (range, 18-53 years). The preoperative magnetic resonance imaging (MRI) of all injured knees revealed the rupture of ACL. The average time from injury to surgery was 13.1 days (range, 6-20 days). All the patients were randomly divided into RetroButton group and Interference Screw group. And all the operations were performed under arthroscopy. Patients were instructed to walk with crutches and weight-bearing 4 weeks after operation. Walk without crutches was allowed 6 to 8 weeks after reconstruction and normal daily activities were gradually resumed. RESULTS: The average follow-up was 54.6 months (range 48-60 months). No adverse biological reactions or infection ever occurred. There was no spontaneous rupture or laxity of graft. The average Lysholm knee score[(56.1 ± 7.9) vs (93.1 ± 6.1); (55.3 ± 8.5) vs (93.2 ± 5.7)], KT-1000 examination [(9.2 ± 1.8) vs (2.1 ± 1.4); (9.5 ± 1.7) vs (2.1 ± 1.5)], International Knee Documentation Committee (IKDC) subjective and objective score [(49.7 ± 5.9) vs (91.7 ± 5.0); (50.2 ± 6.3) vs (91.0 ± 6.1)] were improved significantly in both two groups (all P<0.01), and there was no significant difference between the two groups [(93.1 ± 6.1) vs (93.2 ± 5.7), P>0.05]. CONCLUSIONS: ACL reconstruction using RetroButton and Interference Screw are simple and effective, and can lead to good ligamentous stability and knee function. The two kinds of fixation methods have no significant difference in short and medium term effect. Long-term follow-up should be performed to confirm the durable stability of the knee.

[Antagonistic effects of estrogen on iron-induced bone resorption and its mechanism].

OBJECTIVE: To explore the antagonistic effect of estrogen on iron-induced bone resorption and the role of oxidative stress. METHODS: In vivo, 8-week-old female imprinting control region mice were randomly divided into 3 groups of ferritin (F), ovariectomy (OVX) and F+OVX. Intervention was made by ferric ammonium citrate (FAC) and OVX. Serum levels of ferritin, malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. The expression changes of TRAP, CTR, matrix metallopeptidase 9 (MMP9) and CTK derived from murine bilateral tibia were detected by reverse transcription-polymerase chain reaction (RT-PCR). A high-resolution micro-computed tomography was utilized for scanning distal femur. In vitro, RAW264.7 cells were used and intervened by FAC and estradiol. Tartrate resistant acid phosphatase (TRAP) staining was performed and wine-red TRAP positive cells were counted. ROS level was detected by 2', 7'-dichloro-dihydrofluorescein diacetate (DCFH-DA) with a multi-detection reader. RESULTS: The serum ferritin were heightened in F and F+OVX groups [(335.30 ± 44.10) vs (41.38 ± 5.56) µg/L, (324.80 ± 38.60) vs (41.38 ± 5.56) µg/L respectively, P < 0.01]. The trend of MDA level was F+OVX>OVX>F while SOD level was quite opposite. Body mass density of F+OVX group was lower than that of OVX group (0.114 ± 0.013 vs 0.187 ± 0.029 mg/mm³, P < 0.05) or F group (0.114 ± 0.013 vs 0.902 ± 0.064 mg/mm³, P < 0.05). RT-PCR: TRAP and CTK gene expression of OVX group was lower than that of F+OVX group. However, TRAP, CTR and CTK gene expression of F+OVX group was higher than that of F group. TRAP staining: FAC increased the number of TRAP positive cells (41.7 ± 5.5 vs 20.0 ± 4.0, P < 0.05) while estradiol decreased it (14.8 ± 5.1 vs 41.7 ± 5.5, P < 0.05). DCFH-DA test show that reactive oxygen species was elevated by FAC (160% ± 8% vs 100% ± 9%, P < 0.05) and reduced by estradiol (53% ± 13% vs 160% ± 8%, P < 0.05). CONCLUSION: The antagonistic effect of estrogen on iron-induced bone resorption is probably regulated by oxidative stress.

Angiotensin II induces mitochondrial oxidative stress and mtDNA damage in osteoblasts by inhibiting SIRT1­FoxO3a­MnSOD pathway.

Previous report showed that angiotensin II accelerates osteoporosis, and recent clinical studies suggest that several antihypertensive drugs, especially angiotensin-converting enzyme inhibitors, reduced bone fractures. However, the underling mechanism by which angiotensin II induces bone dysfunction is largely unknown. Here in this study, we show that angiotensin II induces mitochondrial oxidative stress and mitochondrial DNA (mtDNA) damage. We find that the protein and RNA levels of mitochondrial catalase and manganese superoxide dismutase (MnSOD) are decreased in osteoblasts in the presence of angiotensin II. Further, we show that angiotensin II inhibits the protein level of SIRT1, but not SIRT3, which results in the hyperacetylation of the forkhead box O3a (FoxO3a) and inhibition of the expression of catalase and MnSOD. Finally, we show that SRT3025 (Sirt1 activator) and Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP, a MnSOD mimetics) can markedly reduce mitochondrial oxidative stress and mtDNA damage. In summary, we identify a novel SIRT1­FoxO3a­MnSOD axis in angiotensin II-induced mitochondrial oxidative stress and mtDNA damage in osteoblasts.

Arthroscopic posterior cruciate ligament reconstruction using LARS artificial ligament: a retrospective study.

BACKGROUND: The aims of this study were to analyze the preliminary clinical effects of arthroscopic reconstruction of posterior cruciate ligament (PCL) using Ligament Advanced Reinforcement System (LARS) artificial ligament. It is hypothesized that LARS artificial ligament is a safe and effective choice for PCL reconstruction, providing good knee stability. MATERIALS AND METHODS: Forty-one patients who underwent PCL reconstruction using LARS artificial ligament were enrolled in this retrospective study. Average age at time of surgery was 34 y (range, 23-57 y). Average time from injury to surgery was 15 d (range, 5-45 d). Average follow-up period was 44 mo (range, 36-54 months). Follow-up examinations included the Lysholm Knee Score and the International Knee Documentation Committee (IKDC) score. RESULTS: The average Lysholm knee score was 64.9 ± 8.8 preoperatively (range, 47-75) versus 92.1 ± 3.3 three years after operation (range, 79-100). Thirty-six of 41 patients (88%) showed good or excellent results at final assessment. The final IKDC score at 3 y postoperatively rated as normal in 21 patients (51%), nearly normal in 17 patients (42%), abnormal in three patients (7%). CONCLUSIONS: The results shows that LARS artificial ligament appears to be an effective device for PCL reconstruction leading to good ligamentous stability and knee function. Long-term follow-up should be performed to confirm the durable stability of the knee and the tolerance of the knee to the LARS artificial ligament.

[A clinical report on arthroscopic reconstruction of posterior cruciate ligament using ligament advanced reinforcement system].

OBJECTIVE: To explore the operative techniques and preliminary clinical effect of arthroscopic reconstruction of posterior cruciate ligament (PCL) using ligament advanced reinforcement system (LARS). METHODS: From June 2006 to July 2007, 9 patients with PCL rupture were treated with LARS under arthroscopic observation. There were 8 males and 1 female, aged 23-49 years old. The left knee was involved in 3 cases and the right knee in 6 cases. The main causes of injuries were sports in 5 cases, falling in 1 case and traffic accident in 3 cases. The time from injury to reconstruction was 6-20 days (13.6 days on average). There were 2 cases with associated medial meniscus injury and 1 with lateral meniscus injury. X-ray films showed no avulsion fracture of tibial plateau was found. The preoperative Lysholm score was 40-55 (50 on average). According to the preoperative international knee documentation committee (IKDC) grading, 1 case was graded as C and 8 as D. The Lachman test showed that there was 1 case (+), 6 cases (++) and 2 cases (+++). The operation was performed under arthroscopic observation. The tibial isometric point and tunnel were drilled with the help of a drill bit guide, while the femoral isometric point and tunnel were drilled under the C-arm X-ray machine. The diameter of the bone tunnels was 6 mm, while the diameters of LARS artificial ligaments and cannulated interference screws were 7 mm. RESULTS: All the patients were regularly followed up for 8-16 months (10.5 months on average). The postoperative Lysholm score was 70-95 (85 on average). There were 5 cases of excellent, 3 of good and 1 of fair, with the choiceness rate of 88%. The postoperative IKDC grading showed that 7 cases were graded as A and 2 as B. The Lachman test showed that no case was positive. Complications such as infection, spontaneous rupture or laxity of graft were not observed. CONCLUSION: PCL arthroscopic reconstruction with the use of LARS artificial ligaments leads to a good anatomic reconstruction and knee function with minor injury, rapid recovery and satisfactory clinical effect.