Flexor Tendon Entrapment of the Index Finger After Monteggia Fracture in a Pediatric Patient.

The present case report describes a pediatric patient who presented with flexor digitorum profundus (FDP) entrapment after a forearm fracture. The patient was diagnosed with a Bado type I Monteggia fracture. The fracture was reduced using closed reduction under fluoroscopy followed by Kirschner's wire fixation. This case is unique because the FDP was found entrapped in the fracture site 2 weeks post-operation and was managed using conservative therapy. FDP entrapment is typically managed by surgical intervention, and there have been no previous reports of conservative management. The FDP was released using passive extension of the index finger under general anesthesia, and no irreversible damage to the tendon or muscle was found. This case report demonstrates the potential for conservative therapy in the management of FDP entrapment after forearm fractures.

Upregulated expression of inducible nitric oxide synthase plays a key role in early apoptosis after anterior cruciate ligament injury.

The reason that the anterior cruciate ligament (ACL) has a very poor healing potential after injury is not well understood. In this study, we investigated the role of nitric oxide (NO) in the apoptotic cell death of ACL cells using a rabbit model and in vitro cell culture. The apoptosis of ACL cells in vivo was analyzed by TUNEL assay and electron microscopy. NO synthase (NOS) expression was observed by immunohistochemical analysis. ACL cells were cultured and the susceptibility to NO-induced apoptosis was tested. Inducible NOS (iNOS) expression after treatment with cytokines was examined by immunohistochemical and RT-PCR analyses. Mitogen-activated protein kinase (MAPK) inhibitors were used for the analysis of downstream signals. A significant number of apoptotic cells were observed on days 1 to 3 after injury; the apoptotic rate returned to the control level by day 7. Upregulation of iNOS in the ACL remnant was observed at day 1. Intraarticular injection of NOS inhibitor suppressed the apoptotic rate. Isolated ACL cells showed much higher susceptibility to NO-induced apoptosis than did medial collateral ligament cells. IL-1beta stimulated ACL cells to upregulate iNOS mRNA and increase NO production. p38 MAPK inhibitor decreased NO-induced apoptosis. Rapid iNOS induction after injury contributes to the high apoptotic rate of ACL cells, and this may partly account for the poor healing capacity of this ligament. iNOS and NO production is suggested to be stimulated by IL-1beta, and NO activates the p38 MAPK pathway and triggers an apoptotic signal in ACL cells.

Anterior cruciate reconstruction with bioactive Leeds-Keio ligament (LKII): preliminary report.

The scaffold type Leeds-Keio artificial ligament (LK) for ligament reconstruction of the knee provides sufficient strength to require minimal sacrifice of autogenous tissue. This implant works not only as prosthesis but also as scaffold onto which natural tissue grows from the synovium. LK has been in clinical use for anterior cruciate ligament (ACL) reconstruction since 1982, although the operative procedure has been modified and has undergone significant development since that time. Recently, we developed radio frequency-generated glow discharge (RFGGD)-treated LK ligament (LKII, previously indicated as Bio-LK) to improve tissue induction and reported that cell proliferation and cell attachment to artificial fibers increased considerably with this hydrophilic treatment. In this study, we report the findings of reconstructed ACL using LKII, which has been in clinical use since 2003. At reconstruction, LKII was covered with the remnant of the original ACL as much as possible in order to preserve the nerve ending system. Thirteen cases with over 12 months' postoperative history were reviewed. Knee stability was regained after reconstruction without any complications such as joint effusion and chronic synovitis. In one case, postoperative arthroscopy showed that the reconstructed ACL was completely covered with newly formed tissue at 8 weeks postoperatively. Biopsy revealed abundant fibroblasts, collagenous fibers, and vessels around the artificial fibers without marked inflammatory findings. Transmission electron microscope study showed abundant thin collagen fibers, which demonstrated regular orientation to some extent. Fibroblasts were observed with extensive amount of rough endoplasmic reticulum. According to these results, we consider LKII to be superior to LK in tissue induction and maturation.

Differential sensitivity to NO-induced apoptosis between anterior cruciate and medial collateral ligament cells.

It is well known that the anterior cruciate ligament (ACL) of the knee joint has poorer healing responses than the medial collateral ligament (MCL). Nitric oxide (NO) induces free radicals and plays a key role in the induction of apoptosis in various wound-healing models. We hypothesized that the poor healing response of the ACL may be ascribed to high susceptibility to apoptosis, and we investigated the difference in susceptibility to apoptosis between ACL and MCL cells after treatment with sodium nitroprusside, a NO donor. Apoptosis was evaluated by phase contrast microscopy, electron microscopy, DNA gel electrophoresis, and flow cytometric analysis. Although morphological changes and DNA ladders were observed in both ACL and MCL cells after 2 mM sodium nitroprusside treatment, ACL cells were more prone to apoptosis at 1 mM. Based on flow cytometric analysis, DNA fragmentation at 1 mM sodium nitroprusside was significantly greater in ACL cells than in MCL cells (58.6% +/- 1.6% vs. 11.9% +/- 2.2%). Caspase-3 inhibitor (Ac-Asp-Glu-Val-Asp-CHO) and caspase-9 inhibitor (Ac-Leu-Glu-His-Asp-CHO) completely inhibited this DNA fragmentation. In conclusion, the ACL and MCL cells exhibit essential differences, and the differential sensitivity to NO-induced apoptosis between the ACL and MCL cells may be a reflection of these differences.

The effect of hyperbaric oxygen therapy on the bout of treatment for soft tissue infections.

OBJECTIVES: Hyperbaric oxygen (HBO) therapy is often combined with antibiotic therapy for infections such as gas gangrene and osteomyelitis. Although numerous investigations have been undertaken to assess the effect of adjunctive HBO therapy on the treatment of infections, the bout of treatment has not been referred in the previous investigations. The purpose of this retrospective study was to evaluate the efficacy of HBO therapy on the bout of treatment for soft tissue infections. PATIENTS AND METHODS: In the period between 1994 and 2001, we treated 23 patients with soft tissue infections. Nine patients were treated with antibiotic chemotherapy alone, and 14 patients were treated with a combination of antibiotic chemotherapy and HBO therapy. The mean bout of treatment was compared between these two groups. RESULTS: The mean bout treated with a combination of antibiotic and HBO was significantly shorter than that with antibiotic alone. CONCLUSION: Our result indicates that HBO therapy combined with antibiotic therapy is able to shorten the bout of treatment for soft tissue infections. Therefore, we recommend HBO therapy combined with antibiotic therapy for soft tissue infections.

Posttraumatic volar tendon subluxation out of the first extensor compartment: a case report.

Symptomatic volar subluxation of the abductor pollicis longus and the extensor pollicis brevis tendons developed in a 29-year-old man after a sprain that occurred with the wrist in flexion and ulnar deviation. The extensor retinaculum, which forms the extensor compartment, was partially avulsed from its insertion on the radius. Palmar abduction and extension of the thumb with the wrist flexed produced subluxation of the tendons over the volar side of the radius ridge where the retinaculum forming the first extensor compartment attached. Nonoperative treatment including steroid injection and splinting was ineffective. Surgery was performed to reconstruct a new tendon restraint with part of the extensor retinaculum.