Objective To investigate the feasibility and effect of human amniotic membrane in prevention of tendon adhension after tendon sheat defect repair. Methods The amniotic membrane in size of 1.5 cm × 1.0 cm was harvested from human placenta which was voluntary donated from maternal after cesarean. Forty healthy male Leghorn chicken (aged 3-6 months) were selected, weighing (1.86 ± 0.04) kg. The model of flexor digitorum profundus tendon and tendon sheath defects was established at the third toe. After repair of the flexor digitorum profundus tendon, the human amniotic membrane was used to repair the tendon sheath defect in the right foot (group A), but tendon sheath defect was not repaired in the left foot (group B) . At 1, 2, 4, and 6 weeks after operation, the gross and histological observations were done; the degree of tendon adhesions was graded according to Tang’s tendon adhesion general observation grading standards; and the biomechanical properties (tendon slip length and total flexion angle) were tested. Results All animals survived after operation and incisions healed. Gross and histological observations showed that the new tendon sheath formed with time passing after operation in groups A and B; new tendon sheath was more maturer and smoother in group A than in group B. The degree of tendon adhesions in group A was significantly less than that in group B (P lt; 0.05) at 1 and 6 weeks after operation. The biomechanical test results showed there was no significant difference in the tendon slip length between 2 groups at 1 and 2 weeks after operation (P gt; 0.05), but the tendon slip length of group A was significantly longer than that of group B at 4 and 6 weeks after operation (P lt; 0.05). The total flexion angle of group A was significantly smaller than that of group B at 1, 2, 4, and 6 weeks after operation (P lt; 0.05). Conclusion It is effective in the prevention of tendon adhesion to use the amniotic membrane for repairing the tendon sheath defect, which is beneficial to recovery of the tendon sliding function.
Objective To compare the effect of decimeter wave with sodium hyaluronate product (SHP) on preventing and treating peritendinous adhesion and promoting tendon heal ing. Methods Totally 96 healthy male white 6-month-old Leghorn chickens weighing (2.24 ± 0.07) kg were randomized into group A ( decimeter wave therapy group, n=32),in which decimeter wave therapy was appl ied 1 to 21 days after operation at a frequency of 915 MHz, a power of 8 W, radiation distance of 10 cm, for 10 minutes once per day; group B (SHP group, n=32), in which 5 mL and 1.2% SHP was appl ied; and group C (control group, n=32), in which injury received no treatment. The III and IV toes of left feet of all chickens were made into tendon injury model. The general condition of animal was observed after operation; gross and histological observations were made 7, 10, 14, 18, 21 and 28 days after operation, and the biomechanical analysis was done 14 and 28 days after operation. Results Operative incision healed well, no infection and death occurred. Peritendinous adhesions in groups A, B were looser, and tendon heal ing was better than that of group C 14 and 28 days after operation. More fibroblasts with active metabol ism and more collagen formation in groups A, B than that in group C. The Pmax of group A was better than that of group B 14 and 28 days after operation (P lt; 0.05); the δmax of group A was better than that of group B 18 and 21 days after operation (P lt; 0.05), and the W0 of group A was better than that of group B 18, 21 and 28 days after operation (P lt; 0.05). There was no significant difference between group A and group B at the other time points. Conclusion Topical decimeter wave therapy and appl ication of SHP after flexor tendon repair can promote intrinsic heal ing, meanwhile they can prevent the adhesion of tendon and reduce extrinsic heal ing. Decimeter wave therapy can improve the qual ities of tendon’s wound heal ing.
Objective To study the status quo ofthe methods and materials for accelerating the tendon healing and preventing the tendon adhesion as to provide an essential reference for future research and clinical application. Methods The recent articles on methods of accelerating tendon healing and preventing tendon adhesion were extensively reviewed. Results Tendon healing was decided by the co-effects of both endogenous and exogenous ways, and the former was more important. It was affected by the tendon sheath, vincula tendinum and synovial fluid as well. Tendon adhesion was mostly caused by excessive participation of exogenous healing factors and serious damage of the situations around the tendon. Tendon healing was accelerated by methods like repairing, reconstruction of peri-tendon tissues, electric stimulation, physiotherapy, adding herbs or growth factors,and gene intervention. Tendon adhesion was reduced or prevented by methods likethe restoration of tendon sheath, using substitutions, adding herbs/ drugs, andimproving suturing techniques. Conclusion Via the appropriate methods and techniques combining the Chinese traditional and modern medicine, tendon healing can be accelerated and the quality of tendon healing can be improved.
Objective To study the effect of decorin in the suppression of postoperative flexor tendon adhesion. Methods Eighteen Japanese large ear white rabbits underwent complete transection of the Ⅱ digit flexor digitorum profundus tendon in zone Ⅱ and defects immediately were repaired using the modified Kessler technique with -0 nonabsorbable monofilament suture. The site of the right repaired tendon was then injected with 100 μl of decorin(0.25mg/ml) as test toe, the site of the left repaired tendon with 100 μl of PBS as control toe. Inevery group, rabbits were killed and the feet were prepared for biomechanical testing, macroscopic examination and histological inspection. Results In every group, biomechanical testing demonstrates that the sliding distances and the rangs of motion significantly increased in the test toe compared with the control toe(Plt;0.05); macroscopic examination demonstrated that the tendon adhesions of the test toe were significantly reduced when compared with the control toe. In the tese toe, hematoxylin and eosin staining revealed that the hyperplasia of fibroblast was significantly delayed and the collagen fibrils arranged regularly and hadthe normal diameters. Conclusion Decorin can significantly reduce the flexor tendon adhesion formation, adjust collagen fibrillogenesis and promote the tendon healing.
Objective To study the adhesion-preventing effect of basic fibroblast growth factor(bFGF) combined slow-releasing degradable membrane.Methods The bFGF combined slow-releasing degradable membrane was made from bFGF and the reagent which could promote fibrinogen synthesize. Sixty-six SD rats were divided into groups A,B,C randomly (22 rats each group). In group A, sutured achilles tendon were encapsulated with bFGF combined slow-releasing degradable membrane;in group B, sutured achilles tendon were encapsulated with degradable membrane without any drug; in group C, achilles tendon were only sutured. Ninety days later, light-microscope, electronmicroscopoe, figureanalysing, hydroxyproline content, extent of peritendon adhesion and biomechanic test were evaluated.Results ①The amount of fibroblast and fibrinogen inside the sutured tendon in group A was larger than that inits peripheral connective tissue and in groups B and C (P＜0.05). Thecontent of hydroxyproline and the ultimate tensile strength in group A was higher than those in groups B and C(P＜0.01).② The peripheral tissue in group A almostremains the formal loose connective tissue, but it became dense connective tissue in groups B and C and grew into the tendon. Moreover, the extent of adhesion in group A was lesser than that in groups B, C according to the mensuration of peritendon adhesion.Conclusion The bFGF combined slow-releasing degradable membrane can make the intrinsic healing of tendon faster than peripheral
lfty white Leghorn hens were used,and 10 were randomly grouped as control,the other 40received the operation.A half of the profundus tendons of the second and third fore-toes of both sideswere cut.After the oporation,no Way immobiliZation was used.The oporated toes on one side wererandomly chosen as the treatment group,another side the oporated toes on the other side were served asthe control group. The toes having the injured tendons in the tratment group were irradiated for twentyminut...
【Abstract】 Objective To explore the preventing effects of TGF-β1 antibody (TGF-β1Ab) compounded with fibringlue (FG) on postoperative adhesions of flexor tendon. Methods Seventy-two Leghorn chickens were randomly divided into 4 groups (groups A, B, C and D), 18 chickens for each group, and the long flexor tendons of the 3rd and 4th toes in zone Ⅱ of all chickens were transversed and sutured with the 4-strand cruciate repair technique to make defect models. In group A, 0.2 mL TGF-β1 Ab was appl ied at repair site. In group B, 0.2 mL FG was appl ied at repair site. In group C, 0.2 mL TGF-β1Ab and FG was appl ied at repair site. In group D, 0.2 mL normal sodium was appl ied at repair site. At 1, 3 and 8 weeks after operation, the tendons of 6 chickens in each group were harvested for morphological and histological evaluation. Six specimens of each group were obtained for biomechanical test at 3 and 8 weeks. Results The gross observation showed that the differences ingrading of tendon adhesion were not significant among 4 groups at 1 week after operation (P gt; 0.05), but the differences were significant between groups A, B, D and group C at 3 and 8 weeks after operation (P lt; 0.05). Histological observation showed that collagen fibers arranged irregularly in groups A, B and D, but arranged regularly in group C at 3 and 8 weeks after operation. At 3 weeks after operation the gl iding excursion ratio of the tendon in groups A, B, C and D were 0.45 ± 0.05, 0.40 ± 0.10, 0.79 ± 0.09 and 0.25 ± 0.07 respectively ; the simulated active flexion ratio were 0.61 ± 0.02, 0.67 ± 0.03, 0.91 ± 0.03 and 0.53 ± 0.04 respectively; the work of flexion were(18.00 ± 0.77), (17.80 ± 1.13), (27.60 ± 1.73) and (15.60 ± 1.27)?/N respectively. There were significant differences between group C and other three groups (P lt; 0.05). The tendon anastomosis breaking strengthwere (14.2 ± 1.9), (15.2 ± 2.2), (16.0 ± 2.2) and (14.7 ± 2.7) N, showing no significant differences among 4 groups (P gt; 0.05).At 8 weeks after operation, the gl iding excursion ratio of the tendon in groups A, B, C and D were 0.45 ± 0.07, 0.43 ± 0.08, 0.80 ± 0.09 and 0.29 ± 0.05 respectively; the simulated active flexion ratio were 0.61 ± 0.02, 0.63 ± 0.03, 0.92 ± 0.03 and 0.53 ± 0.03 respectively, the work of flexion were (18.30 ± 0.84), (18.60 ± 0.80), (27.90 ± 1.24) and (15.30 ± 0.75) ?/N respectively. There were significant differences between group C and other three groups (P lt; 0.05). The tendon anastomosis breaking strength were(51.9 ± 3.0), (51.4 ± 1.4), (53.3 ± 1.3) and (52.3 ± 2.2) N, showing no significant differences among 4 groups (P gt; 0.05). Conclusion TGF- β1Ab compounded with FG could significantly prohibit the formation of fibrous adhesions without interfering with the heal ing process.
To investigate the preventive effect of TGF-β1 neutral izing antibody on collagen production and adhesion formation of flexor tendon. Methods Tendon fibroblasts, epitenon tenocytes, and endotenon tenocytes were obtained from 6 New Zealand rabbit flexor tendons. Each cell culture was supplemented with 1 ng/mL of TGF-β along with increasing dose of TGF-β1 neutral izing antibody. Col I production was measured by enzyme-l inked immunoabsorbent assay after 3 days. Eighty-four adult New Zealand White rabbits forepaws underwent sharp transection of middle digit flexor digitorumprofundus and immediate repair. Then the rabbits were divided into three groups: the normal saline (NS group, n=36), 1.0 µg/ mL TGF-β1neutral izing antibody (1.0 µg/mL TGF-β1group, n=36) and 2.0 µg/mL TGF-β1 neutral izing antibody (2.0 µg/mL TGF-β1 group, n=12) were injected in tendon sheath respectively. Tendons were harvested at 4 and 8 weeks for biomechanics testing, histological evaluation and scanning electron microscope observation. Tendons were harvested at 1, 2, 4 and 8 weeks to determine the mRNA expression of TGF-β1 and Col I by in situ hybridization. Results ELISA exhibed that TGF-β1 enhanced Col I production and the neutral izing antibody significantly inhibited TGF-β1-induced Col I production in all 3 cell culture with a dose-dependent. At 4 and 8 weeks after operation the gl iding excursion of the tendon and the simulated active flexion in NS group were less than that of 1.0 µg/mL TGF-β1 group and 2.0 µ g/mL TGF-β1 group. There was significant difference between NS group and 1.0 µ g/mL TGF-β1 group, 2.0 µ g/mL TGF-β1 group (P lt; 0.05). The tendon anastomosis breaking strength showed no significant differences among three groups (P gt; 0.05). Scanning electron microscope and histological observation showed that collagen fibers arranged irregularly in NS group, but arranged regularly in 1.0 µ g/mL TGF-β1 group and 2.0 µ g/mL TGF-β1group at 4 and 8 weeks after operation. The in situ hybridization results revealed that TGF-β1 and Col I mRNA expression in 1.0 µ g/mL TGF-β1 group was lower than that in NS group at each time. There was significant difference between two groups (P lt; 0.05). Conclusion TGF-β1neutral izing antibody can inhibit the function of the TGF-β1 effectively and prevent adhesion formation after the flexor tendon injured and repaired.
In order to prevent tendon adhesion following operation, autogenous great saphenous vein graft was used to reconstruct the tendon sheath. The operation was performed under microsurgical technique. This method was used to repair 23 tendons and 17 tendon sheaths. The early functional exercises were carried out after operation. Follow up from 10 months to 4 years, the prognosis was good except in 3 fingers, in which, the wounds were infected resulting the necrosis of the grafted veins and exposure of the repaired tendons. The details of the operation were introduced. It was emphasized that non-traumatic handling of the tissues was essential in preventing tendon from adhesion.
ObjectiveTo investigate the effect of Smad4 on the fibrosis of tendon derived fibroblasts (TDFs) induced by transforming growth factor β1(TGF-β1) by targeted regulation of miRNA219-5P (miR219-5P). MethodsThe tendons donated by the volunteers were harvested to isolate and culture TDFs. The 3rd generation cells were used for experiment. Chemically synthesized miR219-5P mimics, miR219-5P inhibitor, and negative control sequences were transfected into TDFs. The gene expression of miR219-5P in TDFs was detected by real-time PCR, and the protein expression of Smad4 in TDFs was detected by Western blot at 48 hours after transfection. The combining sites of miR219-5P and Smad4 in 3'UTR district were predicted by informatics software. Wild type and mutant type reporter gene expression vectors were constructed and then targeted verification was carried out by the luciferase reporter gene test. Transfected TDFs were then induced by TGF-β1. The proliferation activity of the cells were measured by the cell counting kit 8 after culturing for 24, 48, and 72 hours. The expressions of fibrosis related proteins in TDFs were detected by Western blot at 72 hours. ResultsAfter TDFs were transfected by miR219-5P mimics, miR219-5P expression was significantly up-regulated, but the expressions of Smad4 was decreased subsequently (P<0.05). Intracellular expression of miR219-5P was inhibited by miR219-5P mimics inhibitor, however, the protein expression of Smad4 was significantly increased (P<0.05). Luciferase reporter gene test showed that luciferase activities were significantly decreased in pGL3-WT-Smad4+mimics group, but were significantly increased in pGL3-WT-Smad4+inhibitor group when compared with pGL3-WT-Smad4 transfected group (P<0.05), but no significant difference was found between GL3-MT-Smad4+mimics and pGL3-MT-Smad4+inhibitor groups (P>0.05). Cell proliferation and the fibrosis related proteins were increased in TGF-β1 induced TDFs, however, decreased in TGF-β1 induced TDFs after transfected by miR219-5P inhibitor (P<0.01). ConclusionmiR219-5P can significantly inhibit fibrosis of TDFs induced by TGF-β1 by down-regulating Smad4 expression.