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Staphylococcus aureus‐Muoed inflammation and bone destruction in experimental models of septic arthritis
Author(s) -
Josefsson Elisabet,
Tarkowski Andrej
Publication year - 1999
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1999.tb02271.x
Subject(s) - septic arthritis , staphylococcus aureus , arthritis , immunology , immune system , bacterial adhesin , microbiology and biotechnology , superantigen , sepsis , medicine , staphylococcal infections , virulence , antibiotics , inflammation , biology , t cell , bacteria , gene , biochemistry , genetics
Staphylococcus aureus is the most common cause of septic arthritis. This disease often leads to severe joint destruction and high mortality. An experimental model of S. aureus arthritis has been developed to study the course of inflammation and joint destruction, to elucidate the role of bacteria] and host factors for joint pathology and mortality, and to develop therapeutical and preventive devices against septic arthritis and sepsis. Results show that the innate immune system is crucial in defending the host against staphylococcal infection while components of the specific immune system, T and B lymphocytes and their products, are detrimental to the host, mediating joint destruction and increasing mortality rates. Staphytococcal capsule polysaccharides, toxins, cell wall‐attached adhesins and possibly also the chromosomal DNA are virulence determinants in S. aureus arthritis. Several vaccine candidates have recently been described which protects against staphylococcal infections, e.g. staphylococcal surface polysaccharides, enterotoxins devoid of their superantigenic properties and collagen adhesin. There are also new approaches suggested for treatment of ongoing infections, such as the combined use of antibiotics and corticosteroids.