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Calcium pyrophosphate deposition disease (CPPD) is a crystal arthropathy associated with diverse and numerous risk factors including age, genetic mutations in the ankylosis homolog gene, previous trauma to the joint, osteoarthritis, hypophosphatasia (an inherited metabolic bone disorder), hyperparathyroidism, hemochromatosis, hypomagnesemia, and monosodium urate gout. Here, a 77-year-old man with a complicated history of inflammatory arthritis presented with an acute episode of debilitating polyarticular arthritis with marked deviation in endocrine markers and electrolytes. While autoimmune, infectious, and reactive arthropathies were considered, arthrocentesis revealed calcium pyrophosphate crystals, leading to diagnosis of acute calcium pyrophosphate disease. This patient's acute symptomatic calcium pyrophosphate disease was thought to be precipitated by metabolic derangements involving calcium and magnesium. hese derangements likely occurred secondary to poor oral intake, malnutrition, and renal wasting syndrome, and were resistant to treatment with electrolyte repletion. [ABSTRACT FROM AUTHOR]

Implantation of biomaterials elicits a foreign body response characterized by fusion of macrophages to form foreign body giant cells and fibrotic encapsulation. Studies of the macrophage polarization involved in this response have suggested that alternative (M2) activation is associated with more favorable outcomes. Here we investigated this process in vivo by implanting mixed cellulose ester filters or polydimethylsiloxane disks in the peritoneal cavity of wild-type (WT) and monocyte chemoattractant protein-1 (MCP-1) knockout mice. We analyzed classical (M1) and alternative (M2) gene expression via quantitative polymerase chain reaction, immunohistochemistry and enzyme-linked immunosorbent assay in both non-adherent cells isolated by lavage and implant-adherent cells. Our results show that macrophages undergo unique activation that displays features of both M1 and M2 polarization including induction of tumor necrosis factor α (TNF), which induces the expression and nuclear translocation of p50 and RelA determined by immunofluorescence and Western blot. Both processes were compromised in fusion-deficient MCP-1 KO macrophages in vitro and in vivo. Furthermore, inclusion of BAY 11-7028, an inhibitor of NFκB activation, reduced nuclear translocation of RelA and fusion in WT macrophages. Our studies suggest that peritoneal implants elicit a unique macrophage polarization phenotype leading to induction of TNF and activation of the NFκB pathway. [ABSTRACT FROM AUTHOR]