BACKGROUND:Compared with total knee arthroplasty,unicondylar knee arthroplasty has such advantages as quick recovery,low cost and good proprioception,but its high revision rate after operation is also a problem that cannot be ignored.At present,the reasons for the high revision rate after unicondylar knee arthroplasty are not completely clear.Therefore,preoperative strict control of surgical indication may be crucial to improve postoperative outcome and reduce revision rate after unicondylar knee arthroplasty.As an index commonly used in the measurement of imaging,the evaluation of joint space width may have important clinical reference value in the selection of indications for unicondylar knee arthroplasty. OBJECTIVE:To review the measurement of joint space width and its effect on the curative effect and outcome of medial unicondylar knee arthroplasty. METHODS:WanFang and PubMed were used to search the relevant literature published from January 1,1950 to June 1,2023 on the evaluation factors of curative effect of unicondylar knee arthroplasty and the influence of joint space width on the curative effect of unicondylar knee arthroplasty.By summarizing and analyzing the literature,the measurement methods of joint space width,the influence of preoperative medial compartment joint space width on the curative effect of medial compartment joint space width,and the influence of postoperative lateral compartment joint space width on the outcome were reviewed. RESULTS AND CONCLUSION:(1)Although many methods have been used to study and measure knee joint space width,X-ray measurement of joint space width under weight-bearing position is still a common method in daily orthopedic practice to assess the progression of osteoarthritis,and it can moderately reflect the thickness of cartilage.(2)Preoperative medial compartment joint space width of knee joint can affect the efficacy of medial movable platform after unicondylar knee arthroplasty.Patients with knee osteoarthritis whose medial joint space width/lateral joint space width ratio is<40%or medial joint space width≤2 mm may be more suitable for medial movable platform unicondylar knee arthroplasty.(3)Changes in lateral compartment joint space width after medial unicondylar knee arthroplasty also have a certain impact on outcome.Improving the joint matching degree of lateral compartment after surgery can delay the progression of lateral compartment joint degeneration and reduce the prosthesis revision rate.However,relevant clinical studies are still lacking.In conclusion,the imaging measurement of joint space width has important clinical reference value for evaluating the postoperative efficacy and prognosis of medial unicondylar knee arthroplasty.

Objective To explore the effect of primary exchange reamed nailing (ERN) and augmentation compression plating (ACP) combined with autogenous bone grafting (ABG) on health-related quality of life in patients with dystrophic or atrophic nonunion of femoral shaft after intramedullary nailing. Methods The study used a prospective study method. Sixty- two patients with femoral shaft nonunion after intramedullary nailing from August 2010 to October 2016 were selected, and the patients were divided into ERN group (group A, 32 cases) and ACP group (group B, 30 cases) by random digits table method. In group A, isthmus nonunion was in 18 cases (56.2％), and non-isthmus nonunion in 14 cases (43.8％); in group B, isthmus nonunion was in 16 cases (53.3％), and non-isthmus nonunion in 14 cases (46.7％ ). The health- related quality of life was compared between 2 groups, including physical component summary (PCS) and mental component summary (MCS) in the- 12- item short form health survey (SF- 12), brief pain inventory- severity (BPI- S) and brief pain inventory- interference (BPI- I). Results Fifty-four patients were followed-up for more than 1 year, and the mean follow-up time was 18.3 (13 to 37) months. All patients successfully achieved bone union, and the mean time was 5.8 (4 to 8) months. Significant improvements in terms of SF-12 PCS and SF-12 MCS score were noted after operation for patients with isthmus nonunion in both groups (t=3.148, 2.156, 2.456 and 2.559; P < 0.05), but there were no significant differences before and after operation in group A with non-isthmus nonunion (P >0.05). At the last follow-up, SF-12 PCS and SF-12 MCS in group B were significantly improved compared with those in group A: (45.2 ± 5.8) scores vs. (33.6 ± 4.7) scores and (48.8 ± 6.5) scores vs. (39.4 ± 5.6) scores, and there were statistical difference (P<0.05); SF-12 BPI-S and BPI-I showed obvious relief: (4.6 ± 2.1) scores vs. (6.2 ± 2.5) scores and (5.2 ± 1.9) scores vs. (6.8 ± 2.7) scores, and there were statistical differences (P<0.05); however there were no statistical difference in SF-12 PCS, SF-12 MCS, BPI-S and BPI- I between 2 groups (P>0.05). Conclusions Compared with ERN combined with ABG, ACP combined with ABG can significantly improve the quality of life in patients with dystrophic or atrophic nonunion of femoral shaft after intramedullary nailing. It has greater advantage on the improvement of health-related quality of life, especially for patients with non-isthmus nonunion.

Objective To analyze the related risk factors of re-nonunion after primary revision for femoral shaft nonunion subsequent to failed intramedullary nailing. Methods A retrospective study was performed in 61 patients with femoral shaft nonunion subsequent to failed intramedullary nailing from June 2008 to June.All patients were divided into re-nonunion group(22 cases)and non-re-nonunion group (39 cases) according to diagnostic criteria of bone re-nonunion. Univariate analysis was used to analyze 14 factors that may lead to the occurrence of re-nonunion after revision for femoral shaft nonunion subsequent to failed intramedullary nailing including age, gender, body mass index (BMI), smoking, alcohol abuse, injury reason, fracture types, intramedullary nail types, locking screws technology for intramedullary nail, bone nonunion sites, bone nonunion time, pathological types of bone nonunion, primary revision methods and autologous bone graft or not, and multi-factor logistic regression analysis was performed on the factors showing a significant difference. Results Univariate analysis showed significant difference in smoking (χ2= 6.564, P = 0.036), BMI (χ2= 6.783, P = 0.021), bone nonunion sites(χ2=7.316,P=0.011),primary revision methods(χ2=8.069,P=0.003)and autologous bone graft or not(χ 2=6.668,P=0.027).Logistic regression analysis showed that primary revision methods(OR=1.027,95% CI 0.028-0.463,P<0.05)and autologous bone graft or not(OR=1.024,95% CI 0.006-0.363, P < 0.05) were independent risk factors for re-nonunion after revision of femoral shaft nonunion subsequent to failed intramedullary nailing. Conclusions Primary revision methods and autologous bone graft or not are independent risk factors for re-nonunion after revision of femoral shaft nonunion subsequent to failed intramedullary nailing.By strictly controlling the surgical indications and combining with autogenous bone grafting,it is possible to reduce the occurrence of nonunion after primary revision of the femoral shaft nonunion subsequent to failed intramedullary nailing.

BACKGROUND:Lisfranc injury is a concealed or low-energy damage in the athletic population. The optimal treatment strategies for Lisfranc injury in the athletes, especial y for high-level or professional athletes, remain controversial. Improvement and development in treatment for Lisfranc injury are ongoing. OBJECTIVE:To summarize the diagnostic and therapeutic strategies and problems in surgery in Lisfranc injuries in the athletic population. METHODS:A computer-based online search was conducted in PubMed and Web of science databases from June 1909 to June 2014 to screen the relevant articles regarding the diagnostic and therapeutic strategies for Lisfranc injury using the key words“Lisfranc, injury, athletes”. The irrelevant and duplicate articles were excluded, and final y 43 articles were reviewed. RESULTS AND CONCLUSION:With the improvement and development in the therapeutic methods for Lisfranc injury, suture button fixation and bioabsorbable screw technology, as novel treatment strategies, have the potential to help restore and/or preserve stability at the tarsometatarsal joints, to avoid the potential risk for internal fixation irritation or the need for removal of hardware after fixation. However, more multi-center, prospective, randomized control ed clinical trials are required for seeking the optimal treatment for Lisfranc injury. For the athletes with Lisfranc injury, the best treatment option, removal timing of internal fixation devices, and the proper postoperative function exercise performed according the conditions of patients are vital for restoring the professional sports level.

Objective To analyze the related risk factors for Lisfranc injury resulting from low energy violence.Methods A retrospective study was performed for 61 cases (35 males,26 females) with low-energy foot injury hospitalized from June 2008 to June 2014.Mean age was 36.7 years (range,16-57 years).Fall injuries were noted in 24 cases,sports injuries in 21 cases,and twist injuries in 16 cases.The cases were divided into Lisfranc injury group(n =23) and non-Lisfranc injury group (n =38) according to the different diagnosis.Univariate analysis and multi-factor logistic regression analysis were used to identify the factors that may lead to the occurrence of Lisfranc injury including age,gender,body mass index,operation history,smoking,alcohol abuse,injury reason,medial depth of the mortise/ second metatarsal length (b/a),lateral depth of the mortise/ second metatarsal length (c/a),first metatarsal-to-talus angle,first intermetatarsal angle,second metatarsal length/foot length(a/g),calcaneal inclination angle and cuboid-navicular overlap/cuboid vertical height (e/e + f).Results Univariate analysis showed between-group differences were significant in age (x2 =7.385,P ＜0.05),injury reason (x2 =8.663,P ＜ 0.05),calcaneal inclination angle (t =3.958,P ＜ 0.05),b/a (t =5.051,P ＜ 0.05) and a/g(t =4.618,P ＜ 0.05).Logistic regression analysis identified b/a(OR =1.036,95 ％ CI 0.018-0.450,P ＜ 0.01) and a/g(OR =1.013,95％ CI 0.005-0.374,P ＜ 0.01) as independent risk factors for low-energy Lisfranc injury.Conclusion Low-energy Lisfranc injury is independently associated with b/a and a/g,and may relate to the decreased medial depth of the mortise and increased foot length.

BACKGROUND:Semaphorin7A (Sema7A) is a kind of cel surface protein, which can promote the fusion of osteoclasts and the migration of osteoblasts at the same time, affecting the dynamic balance of the bone. It is speculated that Sema7A siRNA may inhibit osteoblast apoptosis induced by titanium particles. OBJECTIVE:To study the effect of Sema7A on the preosteoblast activity inhibited by titanium particles. METHODS:Mouse MC3T3-E1 preosteoblasts at passages 6 and 7 were divided into four groups: in blank control group, MC3T3-E1 cels were cultured alone; in standard control group, cel were cultured with titanium particles; in experimental groups 1 and 2, the cels were cultured with titanium particles+Sema7A overexpression plasmids and titanium particles+Sema7A siRNA, respectively. Apoptotic rate of MC3T3-E1 cels was detected by flow cytometry; the mRNA expression of bone sialoprotein, osteocalcin and type I colagen was detected by Q-PCR; western blot assay was adopted to detect the protein expression of bone sialoprotein, osteocalcin and type I colagen; alizarin red calcium nodule staining was taken to detect the degree of osteoblast mineralization. RESULTS AND CONCLUSION:The expressions of bone sialoprotein, osteocalcin and type I colagen were decreased in the standard control group and experimental group 1, but these expression were significantly increased in the experimental group 2 compared with the standard control group (P < 0.05). Flow cytometry results suggested that the apoptotic rate of osteoblasts in the experimental group 1 was significantly higher than that in the other groups (P < 0.05), and the apoptotic rate in the experimental group 2 was lower than that in the standard control group (P < 0.05). Alizarin red staining showed that there were no obvious mineralized nodules in the experimental group 1, but mineralized nodules formed in the experimental group 2. In brief, the genetic interference technique that inhibits the activity of Sema7A can interfere the process of mouse MC3T3-E1 preosteoblast differentiation inhibited by titanium particles, and thus provide a feasible way for the clinical treatment of wear particles-induced osteolysis using biotechnology.

BACKGROUND:Bone formation is a dynamic process, and osteoclasts and osteoblasts are involved in this dynamic process. Semaphorins were found first as axonal growth cone guidance molecules, which express in many different tissues and regulate many physiological processes. Recently, Semaphorins are confirmed to play an important role in the regulation of osteoclasts and osteoblasts. OBJECTIVE:To summarize the role of Semaphorins in bone homeostasis. METHODS: A computer-based search of PubMed and Web of Science was performed for articles related to the effect of Semaphorins in regulation of bone metabolism published from June 1993 to January 2014 using the keywords of “semaphorin, sema”. Irrelevant articles or duplicate content articles were excluded, and finaly 48 articles were reviewed. RESULTS AND CONCLUSION:Semaphorins act as a new class of regulatory molecules in the aspect of bone cytobiology. Studies have show semaphorins are actively involved in bone remodeling through some special mechanisms, and semaphorin proteins are crucial for bone homeostasis, which provides a new method and therapeutic target for the treatment of osteoporosis, bone sclerosis, osteolysis adjacent to joint prosthesis and other bone diseases.

BACKGROUND:Sema7A is a kind of cel surface protein, which can promote the fusion of osteoclasts and the migration of osteoblast at the same time, affecting the dynamic balance of bone. OBJECTIVE:To investigate whether Sema7A siRNA has ainhibitory effect on the osteoclast activation in the process of osteolysis which induced by titanium particles. METHODS:The precursor osteoclasts with the concentration of 4×109 RESULTS AND CONCLUSION:At 7 days of culture, the expression levels of interleukin-1, interleukin-1β, tumor necrosis factor α, matrix metaloproteinase-9 and the receptor activator of nuclear factor-κB in the positive control, /L were seeded on 96-wel plates containing glass cover slips, and divided into four groups: blank control, positive control, experiment and negative control groups. The cel culture medium was added into the control group. 20 μL un-transfected siRNA supernatant was added into the positive control group. 20 μL transfected Sema7A siRNA supernatant was added into the experiment group. 20 μL transfected control siRNA supernatant was added into the negative control group. The supernatant was obtained through the co-culture between titanium particles solution and monocyte-macrophage cel line RAW264.7of mouse for 24 hours. siRNA was transfected into mononuclear macrophage cel lines RAW264.7 of mice. negative control and experiment groups were higher than those in the control group (P < 0.05). The expression level of each factor in the experiment group was lower than that in the positive control and negative control groups (P < 0.05). At 8 days of culture, the proliferation activity of osteoclasts and the number of positive cels stained by tartrate-resistant acid phosphatase in the positive control, negative control and experiment groups were higher than those in the control group (P < 0.05). The proliferation activity of osteoclasts and the number of positive cels stained by tartrate-resistant acid phosphatase in the experiment group were lower than those in the control and negative groups (P < 0.05). These results demonstrate that Sema7A siRNA has a certain inhibitory effect on the osteoclast activation induced by titanium particles.

BACKGROUND:Previous studies have indicated that ulinastatin can inhibit RANKL-induced osteoclastogenesis on RAW264.7 cells and also lower matrix metal oproteinase-9 expression and activity. However, it remains be unclear whether ulinastatin has the intervention effect on polymethyl methacrylate (PMMA)-induced MC3T3-E1 mouse preosteoblast apoptosis or not. ＜br> OBJECTIVE:To explore the intervention role of ulinastatin on the PMMA-induced MC3T3-E1 mouse preosteoblast apoptosis and its effects on type I col agen, osteocalcin, matrix metal oproteinase-2 mRNA expression. ＜br> METHODS:MC3T3-E1 mouse preosteoblasts at passages 6 and 7 were divided into four groups:blank group (only cultured MC3T3-E1 mouse preosteoblast), PMMA-induced group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension), low dose ulinastatin group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension+500 U/mL ulinastatin) and high dose ulinastatin group (MC3T3-E1 mouse preosteoblast+1 g/L PMMA bone cement suspension+5 000 U/mL ulinastatin). MTT method was adopted to detect the proliferation activity of proliferative activity of MC3T3-E1 mouse preosteoblast;alizarin red staining method was used to observe mineralization nodules of MC3T3-E1 mouse preosteoblast among different groups;the change of apoptosis rate for MC3T3-E1 cells was detected by flow cytometry analysis;semi-quantitative RT-PCR was taken to analyze type I col agen, osteocalcin, matrix metal oproteinase-2 mRNA expression level in MC3T3-E1 mouse preosteoblasts among different groups. ＜br> RESULTS AND CONCLUSION:Compared with the blank group, PMMA significantly inhibited the proliferation activity of MC3T3-E1 mouse preosteoblast (P＜0.05), and however significantly promoted cells apoptosis (P＜0.05). After addition of different concentrations of ulinastatin (500, 5 000 U/mL), the proliferation activity of MC3T3-E1 mouse preosteoblasts significantly raised (P＜0.05), and cells apoptosis rate significantly decreased (P＜0.05), showing the dose and time-dependent relation. Type I col agen and osteocalcin mRNA expression levels both significantly decreased after co-culture in PMMA group compared with the blank group (P＜0.05), matrix metal oproteinase-2 mRNA expression level, however, significantly increased (P＜0.05). After intervention with 5000 U/mL ulinastatin, type I col agen and osteocalcin mRNA expression levels both significantly increased, while matrix metal oproteinase-2 mRNA expression level significantly decreased (P＜0.05). PMMA group showed no obvious mineralization nodules. Yet, mineralization nodules were formed in the blank group, high and low dose ulinastatin groups. These results indicate that ulinastatin could have the inhibitory effect on the PMMA-induced MC3T3-E1 mouse preosteoblast apoptosis, and it could promote type I col agen and osteocalcin mRNA expression and yet suppress matrix metal oproteinase-2 mRNA expression.

BACKGROUND:It is presumed that urinary trypsin inhibitor could have protective effects on local and systemic tissues and could inhibit osteoclast proliferation and activation under long-term chronic inflammation conditions and in ischemic and anoxic environment which was induced by prosthetic wear. OBJECTIVE:To investigate the inhibitory effect of ulinastatin on receptor activator for nuclear factor-κb ligand-induced differentiation, proliferation and osteoclastogenesis of RAW264.7 cells and its effects on matrix metal oproteinase-2, matrix metal oproteinase-9 expression level and activity. METHODS:Mouse monocyte/macrophage cellline RAW264.7 was treated with different concentrations of urinary trypsin inhibitor (0, 500, 5 000 U/mL) for 24, 48 and 72 hours. Experiments were divided into four groups:the blank group (RAW264.7 cells), receptor activator for nuclear factor-κb ligand-induced group (0 U/mL ulinastatin), 500 U/mL ulinastatin group and 5 000 U/mL ulinastatin group. RESULTS AND CONCLUSION:(1) MTT results indicated that there was no significant difference on the proliferation of RAW264.7 cells treated with urinary trypsin inhibitor at 0-5 000 U/mL (P>0.05) (2) Tartrate-resistant acid phosphatase staining results revealed that compared with receptor activator for nuclear factor-κb ligand-induced group, the number of tartrate-resistant acid phosphatase-positive cells was significantly less in the ulinastatin group (P<0.05), showing a time-dose dependent manner. (3) Immunohistochemisical results found that compared with receptor activator for nuclear factor-κb ligand-induced group, the percentage of matrix metal oproteinase-9-positive cells was apparently lower in the ulinastatin group. (4) Western blot assay results demonstrated that matrix metal oproteinase-9 expression was low in the RAW264.7 cells alone. At 48 hours after addition of receptor activator for nuclear factor-κb ligand, matrix metal oproteinase-9 protein expression was large. At 72 hours after culture in the 5 000 U/mL ulinastatin group, matrix metal oproteinase-9 protein expression was evidently reduced. (5) Gelatin zymography results showed that compared with the receptor activator for nuclear factor-κb ligand-induced group, matrix metal oproteinase-9 expression was significantly lower in the 5 000 U/mL ulinastatin group (P<0.05). Results suggested that urinary trypsin inhibitor inhibited receptor activator for nuclear factor-κb ligand-induced osteoclastogenesis and diminished matrix metal oproteinase-9 expression and activity.