胫骨骨折手术前后关节内炎症因子的变化分析
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摘要
目的探讨胫骨骨折手术前后关节液中炎症因子的变化情况。方法对2015年10月至2017年5月我院收治的胫骨平台骨折患者手术前后关节内的炎症因子进行分析,共纳入41例,其中男28例,女13例。年龄23～64岁,平均42.8岁。骨折按Schatzker分型:I型9例,II型7例,III型6例,IV型4例,V型7例,VI型8例。按受伤至手术时间不同分为两组,A组:36例,受伤至手术时间为3～7天,平均5.2天;B组:5例,受伤至手术时间为12～14天,平均12.6天。手术当天及术后4天收集关节腔积液,ELISA检测IL-1β、TNF-α、TRAP、IL-6的表达情况。结果 Schatzker III型骨折关节腔积液中IL-1β的表达较其它4型都低(P=0.001,P=0.000,P=0.001,P=0.000),与Schatzker IV型相比,差异无统计学意义(P=0.607)。TRAP的表达较其它4型都低(P=0.003,P=0.042,P=0.017,P=0.032),与Schatzker IV型相比,差异无统计学意义(P=0.173)。IL-6的表达较其它5型都低(P=0.000,P=0.000,P=0.001,P=0.000,P=0.000)。而TNF-α在各分型中的表达,差异无统计学意义(P=0.134)。IL-1β和IL-6在Schatzker II、VI型骨折关节腔积液中的表达量高于Schatzker III、IV型,差异有统计学意义(P=0.001,P=0.003,P=0.001,P=0.003;P=0.000,P=0.015,P=0.000,P=0.046)。A组和B组术后4天关节腔内IL-6的表达量均较术前增高(P=0.000,P=0.002),A组术后关节腔内IL-1β、TNF-α、TRAP的表达量较术前降低(P均为0.000),而B组术后反而增高(P=0.002,P=0.007,P=0.004)。结论受伤后7天内手术恢复骨折完整性,可降低关节内炎症因子的表达,而受伤后12天以上手术,炎症因子会再度升高。
Objective To investigate changes of pre-and post-operative intra-articular inflammatory factors of tibial plateau fracture. Methods From October 2015 to May 2017, 41 patients with tibial plateau fracture were enrolled. There were 28 males and 13 females with an average age of 42.8 years( range: 23-64 years). Schatzker type: I type 9 cases, II type 7 cases, III type 6 cases, IV type 4 cases, V type 7 cases, VI type 8 cases. They were divided into two groups according to the time from injury to operation. Group A: 36 cases; the time from injury to operation was 3-7 days, with an average of 5.2 days; Group B: 5 cases; the time from injury to operation was 12-14 days,with an average of 12.6 days. The joint effusion was collected on the day of operation and four days after operation.Expressions of IL-1 beta, TNF-alpha, TRAP and IL-6 were detected by ELISA. Results The expression of IL-1 beta in joint effusion of Schatzker III was lower than that in other 4 types( P = 0.001, P = 0.000, P = 0.001, P = 0.000),and there were no significant differences compared with Schatzker IV( P = 0.607). The expression of TRAP in joint effusion of Schatzker III was lower than that in other 4 types( P = 0.003, P = 0.042, P = 0.017, P = 0.032), and there were no significant differences compared with Schatzker IV( P = 0.173). The expression of IL-6 in joint effusion of Schatzker III was lower than that in other 5 types( P = 0.000, P = 0.000, P = 0.001, P = 0.000, P = 0.000). There were no significant differences in the expression of TNF-alpha among various Schatzker types( P = 0.134). Expressions of IL-1 beta and IL-6 in the joint effusion of Schatzker II and VI were higher than that in Schatzker III and IV, and differences were statistically significant( P = 0.001, P = 0.003, P = 0.001, P = 0.003; P = 0.000, P = 0.015, P = 0.000,P = 0.046). Expressions of IL-6 in the joint effusion of Group A and Group B on the 4 th day after operation were higher than that before operation( P = 0.000, P = 0.002). Expressions of IL-1 beta, TNF-alpha, IL-6 and TRAP in the joint effusion in Group A were lower( P = 0.000) than those before operation, while those in Group B were higher( P = 0.002, P = 0.007, P = 0.004). Conclusions Inflammatory response in the joint decreases as the integrity of the fracture is restored by the operation within 7 days after the injury, otherwise it will rise after 12 days of the injury.
Objective To investigate changes of pre-and post-operative intra-articular inflammatory factors of tibial plateau fracture. Methods From October 2015 to May 2017, 41 patients with tibial plateau fracture were enrolled. There were 28 males and 13 females with an average age of 42.8 years( range: 23-64 years). Schatzker type: I type 9 cases, II type 7 cases, III type 6 cases, IV type 4 cases, V type 7 cases, VI type 8 cases. They were divided into two groups according to the time from injury to operation. Group A: 36 cases; the time from injury to operation was 3-7 days, with an average of 5.2 days; Group B: 5 cases; the time from injury to operation was 12-14 days,with an average of 12.6 days. The joint effusion was collected on the day of operation and four days after operation.Expressions of IL-1 beta, TNF-alpha, TRAP and IL-6 were detected by ELISA. Results The expression of IL-1 beta in joint effusion of Schatzker III was lower than that in other 4 types( P = 0.001, P = 0.000, P = 0.001, P = 0.000),and there were no significant differences compared with Schatzker IV( P = 0.607). The expression of TRAP in joint effusion of Schatzker III was lower than that in other 4 types( P = 0.003, P = 0.042, P = 0.017, P = 0.032), and there were no significant differences compared with Schatzker IV( P = 0.173). The expression of IL-6 in joint effusion of Schatzker III was lower than that in other 5 types( P = 0.000, P = 0.000, P = 0.001, P = 0.000, P = 0.000). There were no significant differences in the expression of TNF-alpha among various Schatzker types( P = 0.134). Expressions of IL-1 beta and IL-6 in the joint effusion of Schatzker II and VI were higher than that in Schatzker III and IV, and differences were statistically significant( P = 0.001, P = 0.003, P = 0.001, P = 0.003; P = 0.000, P = 0.015, P = 0.000,P = 0.046). Expressions of IL-6 in the joint effusion of Group A and Group B on the 4 th day after operation were higher than that before operation( P = 0.000, P = 0.002). Expressions of IL-1 beta, TNF-alpha, IL-6 and TRAP in the joint effusion in Group A were lower( P = 0.000) than those before operation, while those in Group B were higher( P = 0.002, P = 0.007, P = 0.004). Conclusions Inflammatory response in the joint decreases as the integrity of the fracture is restored by the operation within 7 days after the injury, otherwise it will rise after 12 days of the injury.
引文
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[19]Hwang YS,Lee SK,Park KK,et al.Secretion of IL-6 and IL-8 from lysophosphatidic acid-stimulated oral squamous cell carcinoma promotes osteoclastogenesis and bone resorption[J].Oral Oncol,2012,48(1):40-48.
[20]Adams SB,Leimer EM,Setton LA,et al.Inflammatory microenvironment persists after bone healing in intra-articular ankle fractures[J].Foot Ankle Int,2017,38(5):479-484.
[21]Schett G,Gravallese E.Bone erosion in rheumatoid arthritis:mechanisms,diagnosis and treatment[J].Nat Rev Rheumatol,2012,8(11):656-664.
[22]Tsuboi H,Matsui Y,Hayashida K,et al.Tartrate resistant acid phosphatase(TRAP)positive cells in rheumatoid synovium may induce the destruction of articular cartilage[J].Ann Rheum Dis,2003,62(3):196-203.
[23]Bertuglia A,Lacourt M,Girard C,et al.Osteoclasts are recruited to the subchondral bone in naturally occurring posttraumatic equine carpal osteoarthritis and may contribute to cartilage degradation[J].Osteoarthritis Cartilage,2016,24(3):555-566.
[2]Schenker ML,Mauck RL,Ahn J,et al.Pathogenesis and prevention of posttraumatic osteoarthritis after intra-articular fracture[J].J Am Acad Orthop Surg,2014,22(1):20-28.
[3]Haller JM,Mcfadden M,Kubiak EN,et al.Inflammatory cytokine response following acute tibial plateau fracture[J].J Bone Joint Surg Am,2015,97(6):478-483.
[4]Stove J,Huch K,Gunther KP,et al.Interleukin-1beta induces different gene expression of stromelysin,aggrecan and tumornecrosis-factor-stimulated gene 6 in human osteoarthritic chondrocytes in vitro[J].Pathobiology,2000,68(3):144-149.
[5]Chadjichristos C,Ghayor C,Kypriotou M,et al.Sp1 and Sp3transcription factors mediate interleukin-1 beta down-regulation of human type II collagen gene expression in articular chondrocytes[J].J Biol Chem,2003,278(41):39762-39772.
[6]Seguin CA,Bernier SM.TNFalpha suppresses link protein and type II collagen expression in chondrocytes:Role of MEK1/2and NF-kappaB signaling pathways[J].J Cell Physiol,2003,197(3):356-369.
[7]Punzi L,Galozzi P,Luisetto R,et al.Post-traumatic arthritis:overview on pathogenic mechanisms and role of inflammation[J].RMD Open,2016,2(2):e279.
[8]Bondeson J,Blom AB,Wainwright S,et al.The role of synovial macrophages and macrophage-produced mediators in driving inflammatory and destructive responses in osteoarthritis[J].Arthritis Rheum,2010,62(3):647-657.
[9]Lieberthal J,Sambamurthy N,Scanzello CR.Inflammation in joint injury and post-traumatic osteoarthritis[J].Osteoarthritis Cartilage,2015,23(11):1825-1834.
[10]Lewis JS,Hembree WC,Furman BD,et al.Acute joint pathology and synovial inflammation is associated with increased intra-articular fracture severity in the mouse knee[J].Osteoarthritis Cartilage,2011,19(7):864-873.
[11]Huebner KD,Shrive NG,Frank CB.New surgical model of post-traumatic osteoarthritis:isolated intra-articular bone injury in the rabbit[J].J Orthop Res,2013,31(6):914-920.
[12]Sward P,Frobell R,Englund M,et al.Cartilage and bone markers and inflammatory cytokines are increased in synovial fluid in the acute phase of knee injury(hemarthrosis)--a cross-sectional analysis[J].Osteoarthritis Cartilage,2012,20(11):1302-1308.
[13]Sward P,Struglics A,Englund M,et al.Soft tissue knee injury with concomitant osteochondral fracture is associated with higher degree of acute joint inflammation[J].Am J Sports Med,2014,42(5):1096-1102.
[14]Shimpo H,Sakai T,Kondo S,et al.Regulation of prostaglandin E(2)synthesis in cells derived from chondrocytes of patients with osteoarthritis[J].J Orthop Sci,2009,14(5):611-617.
[15]Liang DY,Li X,Li WW,et al.Caspase-1 modulates incisional sensitization and inflammation[J].Anesthesiology,2010,113(4):945-956.
[16]Yoshida Y,Tanaka T.Interleukin 6 and rheumatoid arthritis[J].Biomed Res Int,2014,11(1214):495-507.
[17]Hashizume M,Mihara M.The roles of interleukin-6 in the pathogenesis of rheumatoid arthritis[J].Arthritis,2011,10(15):624-632.
[18]Gabay C.Interleukin-6 and chronic inflammation[J].Arthritis Res Ther,2006,8(Suppl 2):S3-9.
[19]Hwang YS,Lee SK,Park KK,et al.Secretion of IL-6 and IL-8 from lysophosphatidic acid-stimulated oral squamous cell carcinoma promotes osteoclastogenesis and bone resorption[J].Oral Oncol,2012,48(1):40-48.
[20]Adams SB,Leimer EM,Setton LA,et al.Inflammatory microenvironment persists after bone healing in intra-articular ankle fractures[J].Foot Ankle Int,2017,38(5):479-484.
[21]Schett G,Gravallese E.Bone erosion in rheumatoid arthritis:mechanisms,diagnosis and treatment[J].Nat Rev Rheumatol,2012,8(11):656-664.
[22]Tsuboi H,Matsui Y,Hayashida K,et al.Tartrate resistant acid phosphatase(TRAP)positive cells in rheumatoid synovium may induce the destruction of articular cartilage[J].Ann Rheum Dis,2003,62(3):196-203.
[23]Bertuglia A,Lacourt M,Girard C,et al.Osteoclasts are recruited to the subchondral bone in naturally occurring posttraumatic equine carpal osteoarthritis and may contribute to cartilage degradation[J].Osteoarthritis Cartilage,2016,24(3):555-566.