Implant removal is necessary in up to 25% of patients with plate osteosynthesis after proximal humeral fracture. Our new technique of arthroscopic implant removal offers all advantages of minimal invasive surgery. Additionally treatment of concomitant intraarticular lesions is possible. This study outlines the first results after arthroscopic implant removal in comparison with those of open implant removal.

A prospective series of 40 consecutive treated patients had implant removal and arthrolysis after plate osteosynthesis of proximal humeral fracture. Implant removal was carried out due to limitation in range of movement, secondary implant dislocation and implant impingement. 30 patients (median age 63 (30–82) years) had arthroscopic, ten patients (median age 53 (34–76) years) had open implant removal. Median 10 months after implant removal subjective patient satisfaction, Constant Murley Score (CMS) and Simple Shoulder Test were determined.

Arthroscopic implant removal showed comparable first results as open implant removal. There was no significant difference between CMS of both groups. The active shoulder abduction, flexion and external rotation improved significantly after arthroscopic and open implant removal. The simple shoulder test outlined advantages for the arthroscopic technique. After arthroscopic implant removal patients showed higher subjective satisfaction as well as faster pain reduction and mobilization. Analysis of perioperative data showed less blood loss in the group with arthroscopic implant removal. In 85% of patients with arthroscopic implant removal concomitant intraarticular lesions were observed and treated.

The arthroscopic implant removal after plate osteosynthesis of proximal humeral fractures offers all advantages of minimal invasive surgery and comparable first results as the open implant removal. The subjective and objective satisfaction of patients is high. The technique can be applied and established by all arthroscopic trained shoulder surgeons.

Introduction

A review of the literature showed a discrepancy between biomechanical and clinical studies on fracture fixation failure in patients with poor bone quality.

The objective of the present study is to assess the influence of local bone status on complications after surgical treatment of proximal humerus fractures.

Aims: Spinal fractures cause compression of the spinal cord, and nerve cells and nerve fibers are severely damaged. The immediate mechanical injury is subsequently enhanced in a process called secondary damage, and it has been proposed that inflammatory cells such as microglial cells and cytokines such as interleukin (IL)-1 damage nerves and nerve fibers that were initially not affected by spinal cord compression. It was the aim of this study a) to investigate the role of microglial cells and IL-1 in neuronal damage, and b) to investigate whether the anti-inflammatory agent IL-1 receptor antagonist (IL-1ra) that has been successfully used in patients with polyarthritis can protect neurons by inhibiting microglial activation or by antagonising cellular effects of IL-1.

Methods: We investigated the effects of IL-1 and IL-1ra on neurons and microglial cells in organotypic hippocampal slice cultures (OHSC): OHSC derived from rats were excitotoxically lesioned after 6 days in vitro by application of N-methyl-d-aspartate (NMDA) and treated with (IL)-1 (6 ng/ml) or IL-1ra (40, 100, or 500 ng/ml) for up to 10 days. OHSC were then quantitatively analyzed by confocal laser scanning microscopy after fluorescent labeling of neurons and microglial cells.

Results: Treatment of unlesioned OHSC with IL-1 did not induce neuronal damage although the number of microglial cells increased. NMDA-lesioning alone resulted in a massive increase in the number of microglial cells and degenerating neurons. Treatment of NMDA-lesioned OHSC with IL-1 exacerbated neuronal cell death and further enhanced microglial cell numbers. Treatment of NMDA-lesioned cultures with IL-1ra significantly attenuated NMDA-induced neuronal damage and reduced the number of microglial cells, whereas application of IL-1ra in unlesioned OHSC did not induce significant changes in either cell population.

Conclusion: Our findings indicate that a) IL-1 directly affects neurons and acts independently from infiltrating hematogenous cells, b) IL-1 induces microglial activation although it is not neurotoxic per se, c) IL-1 enhances excitotoxic neuronal damage and microglial activation, d) IL-1ra, even when only applied for short periods of time, reduces neuronal cell death and induces a dose-dependent decrease in the number of microglial cells after excitotoxic damage. These findings suggest that IL-1ra has the potential to exert beneficial effects in patients with spinal fractures, and this encourages further in vivo-studies.