Complement factors in gingival crevice material from healthy and inflamed gingiva in humans

Attstroum, Rolf; Laurel, Anna‐Brita; Lahsson, Ulf; Sjöuholm, Anders

doi:10.1111/j.1600-0765.1975.tb00003.x

Cited by 97 publications

(82 citation statements)

References 23 publications

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“…Moreover, GCF collected from periodontitis patients contains activated complement fragments at higher concentrations than in GCF from healthy individuals [72, 78–81]. Consistent with this, complement components and cleavage products are readily detected in chronically inflamed gingiva, whereas complement is undetectable or present at lower levels in healthy gingival biopsy samples [71, 73, 76, 77, 82–84].…”

Section: Clinical Evidence Linking Complement To Periodontitismentioning

confidence: 86%

Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches

Hajishengallis

Maekawa

Abe

et al. 2015

Advances in Experimental Medicine and Biology

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The complement system is a network of interacting fluid-phase and cell surface-associated molecules that trigger, amplify, and regulate immune and inflammatory signaling pathways. Dysregulation of this finely balanced network can destabilize host-microbe homeostasis and cause inflammatory tissue damage. Evidence from clinical and animal model-based studies suggests that complement is implicated in the pathogenesis of periodontitis, a polymicrobial community-induced chronic inflammatory disease that destroys the tooth-supporting tissues. This review discusses molecular mechanisms of complement involvement in the dysbiotic transformation of the periodontal microbiome and the resulting destructive inflammation, culminating in loss of periodontal bone support. These mechanistic studies have additionally identified potential therapeutic targets. In this regard, interventional studies in preclinical models have provided proof-of-concept for using complement inhibitors for the treatment of human periodontitis.

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Section: Clinical Evidence Linking Complement To Periodontitismentioning

confidence: 86%

Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches

Hajishengallis

Maekawa

Abe

et al. 2015

Advances in Experimental Medicine and Biology

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“…Both immunoglobulin and complement components have been identified in crevicular fluid. [55][56][57] Nisengard and Jarrett 58 reported that subgingival bacteria were coated in vivo with immunoglobulin and complement.…”

Section: Discussionmentioning

confidence: 98%

Opsonophagocytic Effect of Antibody Against Recombinant Conserved 40‐kDa Outer Membrane Protein of Porphyromonas gingivalis

Saito

Hayakawa

Takiguchi

et al. 1999

Journal of Periodontology

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We conclude that antibody against r40-kDa OMP has opsonic activity on human neutrophil function for phagocytosis of P. gingivalis. Subgingival bacteria are coated in vivo with immunoglobulin and complement. When the antibody is specific for crevicular bacteria, immunological interactions can be expected in the crevice. Our observations suggest that the anti-recombinant 40-kDa OMP antibody in concert with the crevicular complement may prevent P. gingivalis colonization r40-kDa OMP may contribute to the development of a local immunotherapy when applied to the crevice of a patient with P. gingivalis-related periodontitis which relates to susceptibility for certain systemic diseases such as diabetes mellitus, cardiovascular disease, and preterm labor.

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“…Microorganisms in gingival sulcus are immersed in GCF, which is a serum-derived tissue exudate. Since complement components are present in GCF at up to 70% of serum concentration (30) and in vivo there is high level of complement activation in gingival fluid of patients with periodontitis (31, 32), successful evasion of complement is paramount for the survival of T. forsythia in the periodontal pockets. One such strategy of defense against complement developed by T. forsythia appears to depend on the production of karilysin, which we now show is not only able to degrade complement factors C4 and C5 but also MBL and ficolin-2 and -3, which are crucial molecules enabling recognition of the majority of pathogens without a need of previous exposure and presence of specific antibodies.…”

Section: Discussionmentioning

confidence: 99%

A Metalloproteinase Karilysin Present in the Majority of Tannerella forsythia Isolates Inhibits All Pathways of the Complement System

Jusko

Potempa

Karim

et al. 2012

The Journal of Immunology

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Tannerella forsythia is a poorly studied pathogen despite being one of the main causes of periodontitis, which is an inflammatory disease of the supporting structures of the teeth. We found that despite being recognized by all complement pathways T. forsythia is resistant to killing by human complement, which is present at up to 70% of serum concentration in gingival crevicular fluid. Incubation of human serum with karilysin, a metalloproteinase of T. forsythia, resulted in a decrease in bactericidal activity of the serum. T. forsythia strains expressing karilysin at higher levels were more resistant than low expressing strain. Furthermore, the low expressing strain was significantly more opsonized with C3b and membrane attack complex from serum compared to the other strains. The high expressing strain was more resistant to killing in human blood. The protective effect of karilysin against serum bactericidal activity was attributable to its ability to inhibit complement at several stages. The classical and lectin complement pathways were inhibited due to the efficient degradation of mannose-binding lectin, ficolin-2, ficolin-3 and C4 by karilysin, while inhibition of the terminal pathway was caused by degradation of C5. Interestingly, karilysin was able to release biologically active C5a peptide in human plasma and induce migration of neutrophils. Importantly, we detected the karilysin gene in over 90% of gingival crevicular fluid samples containing T. forsythia obtained from patients with periodontitis. Taken together, the newly characterized karilysin appears to be an important virulence factor of T. forsythia and might have several important implications for immune evasion.

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Complement factors in gingival crevice material from healthy and inflamed gingiva in humans

Cited by 97 publications

References 23 publications

Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches

Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches

Opsonophagocytic Effect of Antibody Against Recombinant Conserved 40‐kDa Outer Membrane Protein of Porphyromonas gingivalis

A Metalloproteinase Karilysin Present in the Majority of Tannerella forsythia Isolates Inhibits All Pathways of the Complement System

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