Disability and satisfaction after Rotator Cuff decompression or repair: a sex and gender analysis

<p>Abstract</p> <p>Background</p> <p>Rotator-cuff pathology is the most common cause of pain and disability in the shoulder. Examining the combined effect of biological and societal factors on disability would potentially identify existing differences between men and women with rotator cuff pathology which would help to provide suggestions for better models of care. Purpose of this study was to determine the overall differences in disability between men and women and to examine the relationship between factors that represent sex (biological factors) and gender (non-biological factors) with disability and satisfaction with surgical outcome 6 months after rotator cuff surgery.</p> <p>Methods</p> <p>Patients with impingement syndrome and/or rotator cuff tear who underwent rotator cuff surgery completed the Western Ontario Rotator Cuff (WORC) index, the American Shoulder & Elbow Surgeons (ASES) assessment form, and the Quick Disabilities of the Arm, Shoulder and Hand (QuickDASH) outcome measures prior to surgery and 6 months post-operatively. They also rated their satisfaction with surgery at their follow-up appointment.</p> <p>Results and Discussion</p> <p>One hundred and seventy patients entered into the study (85 men and 85 women). One hundred and sixty patients (94%) completed the 6-month assessment. Women reported more disability both prior to and after surgery. Disability at 6 months was associated with pain-limited range of motion, participation limitation, age and strength. Satisfaction with surgery was associated with level of reported disability, expectations for improved pain, pain-limited range of motion and strength.</p> <p>Conclusions</p> <p>The results of this study indicate that women with rotator cuff pathology suffer from higher levels of pre- and post-operative disability and sex and gender qualities contribute to these differences. Gender-sensitive approach will help to identify existing differences between men and women which will help to promote more effective and tailored care by health professionals.</p

DNA damage by lipid peroxidation products: implications in cancer, inflammation and autoimmunity

Oxidative stress and lipid peroxidation (LPO) induced by inflammation, excess metal storage and excess caloric intake cause generalized DNA damage, producing genotoxic and mutagenic effects. The consequent deregulation of cell homeostasis is implicated in the pathogenesis of a number of malignancies and degenerative diseases. Reactive aldehydes produced by LPO, such as malondialdehyde, acrolein, crotonaldehyde and 4-hydroxy-2-nonenal, react with DNA bases, generating promutagenic exocyclic DNA adducts, which likely contribute to the mutagenic and carcinogenic effects associated with oxidative stress-induced LPO. However, reactive aldehydes, when added to tumor cells, can exert an anticancerous effect. They act, analogously to other chemotherapeutic drugs, by forming DNA adducts and, in this way, they drive the tumor cells toward apoptosis. The aldehyde-DNA adducts, which can be observed during inflammation, play an important role by inducing epigenetic changes which, in turn, can modulate the inflammatory process. The pathogenic role of the adducts formed by the products of LPO with biological macromolecules in the breaking of immunological tolerance to self antigens and in the development of autoimmunity has been supported by a wealth of evidence. The instrumental role of the adducts of reactive LPO products with self protein antigens in the sensitization of autoreactive cells to the respective unmodified proteins and in the intermolecular spreading of the autoimmune responses to aldehyde-modified and native DNA is well documented. In contrast, further investigation is required in order to establish whether the formation of adducts of LPO products with DNA might incite substantial immune responsivity and might be instrumental for the spreading of the immunological responses from aldehyde-modified DNA to native DNA and similarly modified, unmodified and/or structurally analogous self protein antigens, thus leading to autoimmunity