Open capsulorrhaphy with suture anchors for recurrent anterior dislocation of the shoulder.

Forty of 42 consecutive open capsulorrhaphies with suture anchors for treatment of traumatic recurrent anterior dislocation of the shoulder were reviewed after a minimum follow-up of 2 years. Two patients were lost to follow-up. Follow-up was conducted according to the rating systems of Rowe and the Society of American Shoulder and Elbow Surgeons. The surgical outcome was satisfactory in 38 patients (95%). Eighteen of the 22 patients who were involved in competitive overhead or collision sports before surgery returned to their preoperative sports levels. One patient, whose operation was unsuccessful, experienced recurrent dislocation. In one patient a deep infection that occurred as a complication of the surgical technique healed after suture anchor removal. Although a longer follow-up is necessary, this technique appears to have encouraging results as it avoids the risks related to the use of screws and staples.

Oxidative stress by menadione affects cellular copper and iron homeostasis.

Menadione produces DNA strand breaks (DNA sb) in cultured Chinese hamster fibroblasts which are, to a great extent, mediated by OH radical. A reasonable hypothesis is that H2O2, a product of menadione metabolism, reacts with nuclear iron and produces OH radical in situ. Consistent with that, 1,10-phenanthroline (PHEN) prevents menadione-induced DNA sb at low (< 200 microM) concentrations of the chelator. However, at higher PHEN concentrations, the effect is reversed and an enhancement of DNA sb is observed. The PHEN-induced enhancement of DNA sb becomes more evident at high (> 60 microM) menadione concentrations and is strongly prevented by neocuproine (NEO), an efficient copper chelator. However, NEO offers only a slight protection against DNA sb caused by menadione alone. The results are consistent with the following events: (i) the products of menadione metabolism causes copper ion release from some cellular compartment; (ii) in the presence of PHEN, a Cu(PHEN)2 complex is formed; (iii) the Cu(PHEN)2 complex is known to be very clastogenic, inducing DNA damage in a reducing environment. Evidence is also presented that menadione metabolism causes an increase in intracellular chelatable iron: in the presence of a constant 2,2'-dipyridyl concentration, the DNA sb produced by increasing concentrations of menadione become progressively less susceptible to inhibition by the chelator. Therefore the DNA damage originated from menadione metabolism seems to be caused by two conjugated and synergistic events, viz., the production of reactive oxygen species and the release of copper and iron from a cellular storage site into a 'free' form pool, capable of catalyzing DNA damaging reactions.