Procedure coding in the American Joint Replacement Registry.

In October 2015, the Centers for Medicare & Medicaid Services transitioned from the 9th version of the International Classification of Diseases (ICD-9) codes for reporting patient diagnosis and medical procedures to the 10th version (ICD-10). The multitude of coding options for total joint arthroplasty in ICD-10-procedural coding (ICD-10-PCS) poses some challenges for the American Joint Replacement Registry (AJRR) in identifying precise procedures being reported. While AJRR participating hospitals are familiar with ICD-10-PCS, this new coding may not have been introduced to most AJRR participating surgeons. To address these issues, AJRR initiated an ICD-10 workgroup to define and map appropriate ICD-10 codes to total joint procedure types. This initiative sought to improve accuracy of AJRR data.

Help, my rating looks bad! Coding comorbidities in arthroplasty.

In medicine today, there is a trend toward increasing transparency. Higher quality and better value are being sought, and one of the methods being used is publicly reported health care outcomes. However, there is a problem that comes from our loss of anonymity. Physicians who are being individually watched have to choose between doing what is best for the patient and doing what would look good when it is publicly reported. Often this might mean choosing not to treat a particularly sick patient who is unlikely to have a good outcome. Adjusting outcomes to account for risk factors should be a way to prevent this effect, but these methods need to be studied more. The current performance measures being released are based on administrative claims data, and to date, much of that information is not properly risk adjusted. To ensure that the increasing transparency reveals an accurate picture, it is critical that the complexity of care provided by surgeons be carefully documented. Therefore, we propose accurate coding of patients' comorbidities during hospitalization for total knee arthroplasty and total hip arthroplasty, and we have included a chart detailing our recommendations of the specific diagnostic codes that are most important.

MicroRNA-27b regulates the expression of matrix metalloproteinase 13 in human osteoarthritis chondrocytes.

OBJECTIVE: Aberrant posttranscriptional regulation of matrix metalloproteinases (MMPs) by microRNA has emerged as an important factor in human diseases. The aim of this study was to determine whether the expression of MMP-13 in human osteoarthritis (OA) chondrocytes is regulated by microRNA. METHODS: Chondrocytes were stimulated with interleukin-1beta (IL-1beta) in vitro. Total RNA was prepared using TRIzol reagent. Polymerase chain reaction (PCR)-based arrays were used to determine the expression profile of 352 human microRNA. Gene expression was quantified using TaqMan assays, and microRNA targets were identified using bioinformatics. Transfection with reporter construct and microRNA mimic was used to verify suppression of target messenger RNA (mRNA). Gene expression of argonaute and Dicer was determined by reverse transcription-PCR, and expression of protein was determined by immunoblotting. The role of activated MAP kinases (MAPKs) and NF-kappaB was evaluated using specific inhibitors. RESULTS: In IL-1beta-stimulated OA chondrocytes, 42 microRNA were down-regulated, 2 microRNA were up-regulated, and the expression of 308 microRNA remained unchanged. In silico analysis identified a sequence in the 3'-untranslated region (3'-UTR) of MMP-13 mRNA complementary to the seed sequence of microRNA-27b (miR-27b). Increased expression of MMP-13 correlated with down-regulation of miR-27b. Overexpression of miR-27b suppressed the activity of a reporter construct containing the 3'-UTR of human MMP-13 mRNA and inhibited the IL-1beta-induced expression of MMP-13 protein in chondrocytes. NF-kappaB and MAPK activation down-regulated the expression of miR-27b. CONCLUSION: Our data demonstrated the expression of miR-27b in both normal and OA chondrocytes. Furthermore, IL-1beta-induced activation of signal transduction pathways associated with the expression of MMP-13 down-regulated the expression of miR-27b. Thus, miR-27b may play a role in regulating the expression of MMP-13 in human chondrocytes.

Green tea polyphenol epigallocatechin-3-gallate inhibits advanced glycation end product-induced expression of tumor necrosis factor-alpha and matrix metalloproteinase-13 in human chondrocytes.

INTRODUCTION: The major risk factor for osteoarthritis (OA) is aging, but the mechanisms underlying this risk are only partly understood. Age-related accumulation of advanced glycation end products (AGEs) can activate chondrocytes and induce the production of proinflammatory cytokines and matrix metalloproteinases (MMPs). In the present study, we examined the effect of epigallocatechin-3-gallate (EGCG) on AGE-modified-BSA (AGE-BSA)-induced activation and production of TNFalpha and MMP-13 in human OA chondrocytes. METHODS: Human chondrocytes were derived from OA cartilage by enzymatic digestion and stimulated with in vitro-generated AGE-BSA. Gene expression of TNFalpha and MMP-13 was measured by quantitative RT-PCR. TNFalpha protein in culture medium was determined using cytokine-specific ELISA. Western immunoblotting was used to analyze the MMP-13 production in the culture medium, phosphorylation of mitogen-activated protein kinases (MAPKs), and the activation of NF-kappaB. DNA binding activity of NF-kappaB p65 was determined using a highly sensitive and specific ELISA. IkappaB kinase (IKK) activity was determined using an in vitro kinase activity assay. MMP-13 activity in the culture medium was assayed by gelatin zymography. RESULTS: EGCG significantly decreased AGE-stimulated gene expression and production of TNFalpha and MMP-13 in human chondrocytes. The inhibitory effect of EGCG on the AGE-BSA-induced expression of TNFalpha and MMP-13 was mediated at least in part via suppression of p38-MAPK and JNK activation. In addition, EGCG inhibited the phosphorylating activity of IKKbeta kinase in an in vitro activity assay and EGCG inhibited the AGE-mediated activation and DNA binding activity of NF-kappaB by suppressing the degradation of its inhibitory protein IkappaBalpha in the cytoplasm. CONCLUSIONS: These novel pharmacological actions of EGCG on AGE-BSA-stimulated human OA chondrocytes provide new suggestions that EGCG or EGCG-derived compounds may inhibit cartilage degradation by suppressing AGE-mediated activation and the catabolic response in human chondrocytes.

Exchange femoral nailing: a new technique for removal of a broken nail.

Exchange femoral nailing is the preferred method for treating femoral nonunions. When the index femoral nail is broken, the difficulty of exchange nailing increases dramatically. In this article, we describe a new technique for removing a broken retrograde nail--advancing it out of the proximal end of the femur.

Atrophic femoral nonunion with bone loss: treatment with monorail transport: a case report.

Nonunions are an uncommon outcome of femoral fractures. Atrophic nonunions with a leg length discrepancy secondary to bone loss are often the most difficult to treat, and the treatment options are limited. We present a case that uses concomitant monolateral external fixation and intramedullary nailing to heal a nonunion and perform a simultaneous 7-cm lengthening procedure in a 33-year-old female.