Complications After Treatment of Flexor Tendon Injuries

S, Lilly; Messer, Terry M.

doi:10.5435/00124635-200607000-00001

Cited by 87 publications

(79 citation statements)

References 56 publications

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“…3,[15][16][17][18] Other studies have focused on molecular treatment of the flexor tendon injury to provide adhesion-free healing via the delivery of anti-scarring adjuvants that inhibit the effects of TGF-b and bFGF among other factors. [19][20][21][22][23] Despite their promise, these approaches remain experimental and have yet to yield a clinical application, 3 largely because our understanding of the molecular mechanisms involved in the formation of adhesions after flexor tendon injury and grafting remains incomplete. The novel mouse model of FDL tendon grafts offers a quantitative tool to not only examine the biomechanical aspects of flexor tendon grafts, but also to potentially elucidate the molecular events involved in repair and subsequent adhesion formation via the use of transgenic mouse models of gain and loss of function.…”

Section: Discussionmentioning

confidence: 99%

“…Live autografts likely heal via intrinsic and extrinsic mechanisms that involve the graft tenocytes as well as the influx of synovial fibroblasts, precursor cells, and inflammatory cells, respectively. 3,26 As a result, autografts underwent extensive remodeling that negatively affected the rate of accrual of biomechanical strength over time as has been reported for flexor tendon gap defects. 25 By contrast, the acellular allografts can only heal by extrinsic mechanisms.…”

mentioning

confidence: 95%

“…3 Second, we hypothesized that the marked increase in the expression of Gdf5 and Vegfa mRNA might be involved in the improvements in joint flexion after 28 days. Whether this increased mRNA expression translates into increased GDF5 and VEGF protein synthesis at the repair site after 28 days remains to be verified in future experiments using immunohistochemistry.…”

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confidence: 99%

“…1 Adhesions are especially exacerbated in injuries involving flexor digitorum profundus (FDP) and flexor digitorum superficialis (FDS) tendons in Bunnell's ''no man's land'' or zone II of the hand, which to date remain unsolved clinical problems. 2,3 As an alternative to primary repair, which still represents the standard of care for these injuries, 3 surgeons often use a live tendon autograft especially when primary repair has been neglected or delayed because of infection, or in revision surgery when primary repair had failed. 4 Unfortunately, flexor tendon grafting procedures also experience post-operative adhesions that limit joint flexion or cause joint contracture.…”

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confidence: 99%

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Adhesions in a murine flexor tendon graft model: Autograft versus allograft reconstruction

Hasslund

Jacobson

Dadali

et al. 2008

Journal Orthopaedic Research

120

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Reconstruction of flexor tendons often results in adhesions that compromise joint flexion. Little is known about the factors involved in the formation of flexor tendon graft adhesions. In this study, we developed and characterized a novel mouse model of flexor digitorum longus (FDL) tendon reconstruction with live autografts or reconstituted freeze-dried allografts. Grafted tendons were evaluated at multiple time points up to 84 days post-reconstruction. To assess the flexion range of the metatarsophalangeal joint, we developed a quantitative outcome measure proportional to the resistance to tendon gliding due to adhesions, which we termed the Gliding Coefficient. At 14 days post-grafting, the Gliding Coefficient was 29-and 26-fold greater than normal FDL tendon for both autografts and allografts, respectively (p < 0.001), and subsequently doubled for 28-day autografts. Interestingly, there were no significant differences in maximum tensile force or stiffness between live autograft and freeze-dried allograft repairs over time. Histologically, autograft healing was characterized by extensive remodeling and exuberant scarring around both the ends and the body of the graft, whereas allograft scarring was abundant only near the graft-host junctions. Gene expression of GDF-5 and VEGF were significantly increased in 28-day autografts compared to allografts and to normal tendons. These results suggest that the biomechanical advantages for tendon reconstruction using live autografts over devitalized allografts are minimal. This mouse model can be useful in elucidating the molecular mechanisms in tendon repair and can aid in preliminary screening of molecular treatments of flexor tendon adhesions. ß

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Adhesions in a murine flexor tendon graft model: Autograft versus allograft reconstruction

Hasslund

Jacobson

Dadali

et al. 2008

Journal Orthopaedic Research

120

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“…Injury to the joint or tendon often causes restrictive fibrosis or adhesions, which severely restricts functional recovery (1,2). Adhesions occur following abdominal and pelvic surgery, often causing the serious complications of intestinal obstruction, chronic pain, and infertility in women (3).…”

Section: Introductionmentioning

confidence: 99%

Celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting ERK1/2 and SMAD2/3 phosphorylation

Fan

Zeng

et al. 2011

Mol Med Report

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Abstract. This study aimed to investigate whether celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting extracellular signal-regulated kinase 1/2 (ERK1/2) and SMAD2/3 phosphorylation. Celecoxib was added to NIH/3T3 fibroblasts stimulated by fibroblast growth factor-2 (FGF-2) or transforming growth factor-β1 (TGF-β1). NIH/3T3 fibroblast proliferation and viability were assessed by MTT assays; ERK1/2 expression and SMAD2/3 expression were assessed by quantitative RT-PCR and Western blot analysis. The results indicated that celecoxib suppressed cell proliferation (IC 50 FGF + group, 75±1.9 µmol/l) stimulated by FGF-2, and also inhibited cell viability (IC 50 FGF -group, 252±2.3 µmol/l) by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. In addition, celecoxib treatment led to the apoptosis of NIH/3T3 fibroblasts (IC 50 FGF -group, 35±1.4 µmol/l). Celecoxib also suppressed collagen expression (0.35-fold COL3 and 0.43-fold COL1 with 320 µmol/l celecoxib relative to the untreated group following stimulation for 3 h, p<0.01) when stimulated by TGF-β1, by inhibiting SMAD2/3 phosphorylation but not SMAD2/3 expression. Celecoxib is capable of inhibiting ERK1/2 and SMAD2/3 phosphorylation, which is responsible for NIH/3T3 fibroblast proliferation and collagen expression.

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