Thirty-Day Complications of Conventional and Computer-Assisted Total Knee and Total Hip Arthroplasty: Analysis of 103,855 Patients in the American College of Surgeons National Surgical Quality Improvement Program Database.

BACKGROUND: Computer-assisted surgery (CAS) has gained popularity in orthopedics for both total knee arthroplasty (TKA) and total hip arthroplasty (THA) in the past decades. METHODS: The American College of Surgeons National Surgical Quality Improvement Program database was used to identify patients who underwent a primary, unilateral THA and TKA from 2011 to 2013. Multivariate analysis was conducted to compare the postoperative complications in patients whose surgery involved the use of CAS with those by conventional techniques. RESULTS: We identified 103,855 patients who had THA and TKA in the database between 2011 and 2013. There were higher overall adverse events (odds ratio [OR], 1.40; CI, 1.22-1.59), minor events (OR, 1.38; CI, 1.21-1.58), and requirements for blood transfusion (OR, 1.44; CI, 1.25-1.67) in the conventional group when compared with CAS for TKA. However, rate of reoperation was higher in the CAS group for TKA (OR, 1.60; CI, 1.15-2.25). The results also showed higher overall adverse events (OR, 2.61; CI, 2.09-3.26), minor events (OR, 2.82; CI, 2.24-3.42), and requirements for blood transfusion (OR, 3.41; CI, 2.62-4.44) in the conventional group when compared to CAS for THA. Nevertheless, superficial wound infections (OR, 0.46; CI, 0.26-0.81) were shown to be higher in the CAS group undergoing THA. CONCLUSION: The use of CAS in THA and TKA reduced the number of minor adverse events in the first 30 days postoperatively. However, CAS was associated with an increased number of reoperations and superficial infections. The clinical benefits and disadvantages of CAS should be considered when determining the potential benefit-cost ratio of this technology.

Naproxen induces type X collagen expression in human bone-marrow-derived mesenchymal stem cells through the upregulation of 5-lipoxygenase.

Several studies have shown that type X collagen (COL X), a marker of late-stage chondrocyte hypertrophy, is expressed in mesenchymal stem cells (MSCs) from osteoarthritis (OA) patients. We recently found that Naproxen, but not other nonsteroidal anti-inflammatory drugs (NSAIDs) (Ibuprofen, Celebrex, Diclofenac), can induce type X collagen gene (COL10A1) expression in bone-marrow-derived MSCs from healthy and OA donors. In this study we determined the effect of Naproxen on COL X protein expression and investigated the intracellular signaling pathways that mediate Naproxen-induced COL10A1 expression in normal and OA hMSCs. MSCs of OA patients were isolated from aspirates from the intramedullary canal of donors (50-80 years of age) undergoing hip replacement surgery for OA and were treated with or without Naproxen (100 µg/mL). Protein expression and phosphorylation were determined by immunoblotting using specific antibodies (COL X, p38 mitogen-activated protein kinase [p38], phosphorylated-p38, c-Jun N-terminal kinase [JNK], phosphorylated-JNK, extracellular signal-regulated kinase [ERK], and phosphorylated-ERK). Real-time reverse transcription polymerase chain reaction (RT-PCR) was performed to determine the expression of COL10A1 and Runt-related transcription factor 2 gene (Runx2). Our results show that Naproxen significantly stimulated COL X protein expression after 72 h of exposure both in normal and OA hMSCs. The basal phosphorylation of mitogen-activated protein kinases (MAPKs) (ERK, JNK, and p38) in OA hMSCs was significantly higher than in normal. Naproxen significantly increased the MAPK phosphorylation in normal and OA hMSCs. NSAID cellular effects include cyclooxygenase, 5-lipoxygenase, and p38 MAPK signaling pathways. To investigate the involvement of these pathways in the Naproxen-induced COL10A1 expression, we incubated normal and OA hMSCs with Naproxen with and without inhibitors of ERK (U0126), JNK (BI-78D3), p38 (SB203580), and 5-lipoxygenase (MK-886). Our results showed that increased basal COL10A1 expression in OA hMSCs was significantly suppressed in the presence of JNK and p38 inhibitors, whereas Naproxen-induced COL10A1 expression was suppressed by 5-lipoxygenase inhibitor. This study shows that Naproxen induces COL X both at transcriptional and translational levels in normal and OA hMSCs. Elevated basal COL10A1 expression in OA hMSCs is probably through the activation of MAPK pathway and Naproxen-induced COL10A1 expression is through the increased 5-lipoxygenase signaling.