Impact of Depressive Symptomology on Pain and Function during Recovery after Total Joint Arthroplasty.

OBJECTIVES: To determine the effect of preoperative depressive symptoms on patient-reported function and pain following total joint arthroplasty (TJA) after controlling for potential confounding factors; how depressive symptoms changed after TJA; and the impact of postoperative depressive symptoms on recovery. METHODS: A prospective cohort study undertaken in a metropolitan region in Canada enrolled 710 participants; 622 (87%) had complete 6-month data. Participants completed standardized measures preoperatively and at 1, 3, and 6 months postoperatively. The primary outcome was Western Ontario McMaster Osteoarthritis Index (WOMAC) pain and function. Three groups were created: depressive symptoms absent (n = 573, 82%), possible depressive symptoms (n = 58, 8%), and probable depressive symptoms (n = 68, 10%) using the Center for Epidemiologic Scale for Depression score. Risk-adjusted analyses examined the association between WOMAC change and the preoperative Center for Epidemiologic Scale for Depression score. RESULTS: After risk adjustment, preoperative possible and probable depressive symptomology was associated with postoperative WOMAC pain scores that were 7.6 and 11.7 points, respectively, worse and WOMAC function scores that were 8.8 and 14.3 points, respectively, worse than those without preoperative depressive symptoms. Depressive symptoms improved postoperatively; by 6 months post-TJA, only 34 (5%) participants screened as having probable depressive symptoms, whereas only 13(2%) had possible depressive symptoms. Postoperative WOMAC pain and function scores improved, but they were negatively affected by possible and probable depressive symptoms. CONCLUSIONS: Although depressive symptoms improve postoperatively, preoperative depressive symptoms, especially for those with probable depressive symptomology, may negatively affect postoperative pain and functional recovery even after risk adjustment.

Cobalt(II) ß-ketoaminato complexes as novel inhibitors of neuroinflammation.

Neuroinflammation contributes to the pathogenesis of neurological disorders including stroke, head trauma, multiple sclerosis, amyotrophic lateral sclerosis as well as age-associated neurodegenerative disorders including Alzheimer's and Parkinson's diseases. Therefore, anti-inflammatory drugs could be used to slow the progression of these diseases. We studied the anti-neuroinflammatory activity of four novel square planar cobalt(II) compounds bearing tetradentate ß-ketoaminato ligands with variation in the number of CF(3) ligand substituents, as well as their corresponding unmetallated organic ligands. Cobalt (Co) complexes were consistently more active than their corresponding ligands. One of the complexes, L(3)Co at concentrations (1-10 µM) that were not toxic to cells, significantly reduced cytotoxic secretions by human monocytic THP-1 cells, astrocytoma U-373 MG cells, and primary human microglia. This anti-neurotoxic action of L(3)Co was reduced by SP600125 and PD98059, selective inhibitors of c-Jun NH2-terminal kinase (JNK) and extracellular signal regulated kinase (ERK) kinase (MEK)1/2 respectively. L(3)Co had no effect on secretion of monocyte chemotactic protein-1 (MCP-1) by THP-1 cells, but it inhibited the NADPH oxidase-dependent respiratory burst activity of differentiated human HL-60 cells. L(3)Co upregulated heme oxygenase-1 (HOX-1) expression by THP-1 cells, which may be one of the molecular mechanisms responsible for its anti-inflammatory properties. Two of the Co compounds tested showed activity only at high concentrations (50 µM), but L(2)Co was highly toxic to all cell types used. Select Co complexes, such as L(3)Co, may exhibit pharmacological properties beneficial in human diseases involving neuroinflammatory processes. Further studies of the in vivo efficacy, safety and pharmacokinetics of L(3)Co are warranted.