The effect of antibiotics on the destruction of cartilage in experimental infectious arthritis.

Smith, R. Lane; Schurman, David J.; Kajiyama, Glen; Mell, Matthew W.; Gilkerson, Ellen

doi:10.2106/00004623-198769070-00015

Cited by 129 publications

(66 citation statements)

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“…Collective data confirmed that up to 50% of glycosaminoglycans and 37% of collagen could be lost in spite of joint irrigation and early administration of antibiotics [20,21,24,25]. Adjunctive treatment with nonsteroidal anti-inflammatory drugs or inhibitors of reactive oxygen species have been used in animal models but could only partially lessen the post-infectious complications [20,23,24].…”

Section: Discussionmentioning

confidence: 91%

“…In joints with pyogenic infection, prolonged destruction of cartilage may occur in spite of prompt and effective antibiotic therapy [20,21,25]. Although secreted bacterial toxins and the host inflammatory response account for early processes of cartilage destruction [3,7,8,25,30,31], the precise mechanisms causing hypocellularity and early degenerative change after septic arthritis remain unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Although secreted bacterial toxins and the host inflammatory response account for early processes of cartilage destruction [3,7,8,25,30,31], the precise mechanisms causing hypocellularity and early degenerative change after septic arthritis remain unclear. Mechanisms of reduced cellularity include cell necrosis and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Signal transduction pathways and apoptosis in bacteria infected chondrocytes

Lee

Yen

Ueng

et al. 2001

Journal Orthopaedic Research

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The mechanism underlying chronic destructive arthropathy after pyogenic arthritis is not clear. This study evaluated the role of apoptosis in Staphylococcus aureus infected human articular chondrocytes and investigated the signal transduction pathways activated by bacterial infection. Chondrocytes cultured in monolayer were challenged with bacteria for 6 h and were analyzed after incubation for 2, 18, and 24 h. Chondrocytes showed morphologic and biochemical evidences of apoptosis after infection and the following incubation period. Although treatment with extensive washing and vancomycin could ameliorate the amount of apoptosis from 31% to 15% at 2 h, from 48% to 23% at 18 h, and from 58% to 33% at 24 h, the infected samples with treatment still had higher amount of apoptosis than the un-infected controls (ANOVA P < 0.001). Accompanying with the increasing amount of apoptosis, the caspase activity was upregulated in bacteria infected samples and remained high in samples with treatment (ANOVA P < 0.05).Signal transduction pathways activated by bacterial infection were assessed by co-transfection technique. After infection, the c-Jun N-terminal kinase, extracellular signal-regulated kinase, and cyclic AMP-dependent protein kinase activities were elevated by 7.6-, 7.3-, and 3.2-fold, respectively, compared to the uninfected controls. The data support the hypothesis that human chondrocytes will undergo apoptosis after infection by a single organism. Apoptosis and activated intracellular kinase activities may be related to the pathogenesis of post-infectious destructive arthropathy.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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Signal transduction pathways and apoptosis in bacteria infected chondrocytes

Lee

Yen

Ueng

et al. 2001

Journal Orthopaedic Research

View full text Add to dashboard Cite

show abstract

“…Smith [108] showed that cartilage destruction starts to occur as early as 8 h after infection. Early administration of antibiotics helps to slow down the process, but even if intravenous antibiotic therapy is started within the first 24 h of infection, significant glycosaminoglycan destruction and collagen disruption occurs.…”

Section: Aetiology and Pathogenesismentioning

confidence: 99%

“…This is only to be expected as the drugs reduce the body's ability to resist infection. -Long duration of symptoms and long delay in treatment [83,108]. If the degree of damage to the joint by bacterial and other enzymes is related to the length of time these enzymes are in action, then delay in treatment is likely to be detrimental to the outcome.…”

Section: Prognosismentioning

confidence: 99%