Assessment of complement cleavage in gingival fluid during experimental gingivitis in man

Patters, Mark R.; Niekrash, Christine E.; Lang, Niklaus P.

doi:10.1111/j.1600-051x.1989.tb01609.x

Cited by 59 publications

(74 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: 87%

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: 87%

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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“…Total activation (classic and alternate) may be assessed by C3 conversion and has been studied in GCF by means of an experimental gingivitis model. Patters et al (1985) found higher conversion levels in gingivitis than in normal tissues. In further studies, Patters et al (1989) measured C3c, a cleavage product of C3, in GCF from patients following extensive scaling and root planing treatment.…”

Section: Complementmentioning

confidence: 88%

“…Patters et al (1985) found higher conversion levels in gingivitis than in normal tissues. In further studies, Patters et al (1989) measured C3c, a cleavage product of C3, in GCF from patients following extensive scaling and root planing treatment. The decrease in clinical indices during repair was paralleled by a decrease in conversion ofC3toC3c.…”

Section: Complementmentioning

confidence: 88%

Gingival Crevicular Fluid: Biomarkers of Periodontal Tissue Activity

Embery¹,

Waddington²

1994

Adv Dent Res.

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The lack of precise clinical criteria for assessment of periodontal disease has led to a search for alternative means of determining active disease sites, prognosis of future sites of breakdown, and response to therapy. This review highlights the potential array of biomarkers present in gingival crevicular fluid and which may relate to existing or predicted tissue regions undergoing metabolic change and derived from bacterial or host-cell-derived products. Among the former may be listed endotoxin, amines, butyrate, and a variety of enzymes and their inhibitors, such as trypsin-like proteases and bacterial collagenase. Arising from host cells is a variety of leucocytic hydrolase enzymes, lactoferrin, and lysozyme. These appear to be useful inflammatory markers and may be distinguished from products of connective tissue breakdown which include collagenous and non-collagenous products, including collagen peptides, osteonectin, and fibronectin. The proteoglycans have found particular favor as biomarkers of possible bone-resorptive activity. Attention has also been directed at the immune response, including comment on immunoglobulins, complement, eicosanoids, and cytokines. This review lists available information on the presence of these in gingival sulcus fluid and wherever possible relates their presence to disease activity.

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“…Activation products of the complement components have been detected in the gingival crevicular fluid at the site of gingival inflammation (Patters et al, 1989). C3d, an activation product of C3, is known to be present at high levels in the gingival crevicular fluid of AP patients, but not in serum, suggesting local activation of complement (Schenkein and Genco, 1977).…”

Section: Introductionmentioning

confidence: 99%

Protection of Gingival Epithelium against Complement-mediated Damage by Strong Expression of the Membrane Attack Complex Inhibitor Protectin (CD59)

Rautemaa

Meri

1996

J Dent Res

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Adult periodontitis (AP) is a chronic inflammatory disease of the tooth-supporting apparatus. Activation products of the inflammation-inducing complement system have been detected in the gingival crevicular fluid at the site of gingival inflammation. In the present study, we examined whether evidence for ongoing complement activation in gingival tissues of patients with AP can be obtained. In light of the potential tissue-damaging effects of the complement system, we also examined how the gingival tissue is protected against the cytolytic activity of complement. Surgical and autopsy samples of AP (n = 18) and healthy (n = 11) gingiva were analyzed for the expression or deposition of the complement regulators protectin (CD59) and vitronectin (S-protein) and complement components C3d and C9 by indirect immunofluorescence microscopy with specific antibodies. In healthy gingiva, protection was strongly expressed on the membranes of epithelial cells and on the vascular endothelia of the underlying connective tissue. In AP, protectin was also strongly expressed by endothelial cells, but in the epithelia the expression was granular and weaker than in the healthy gingiva. Coarse granular deposits of complement components were seen in the subepithelial tissues of 61% (C3d), 39% (C9), and 33% (vitronectin) of AP patients, compared with 9% (one case in 11) in healthy controls. In addition, deposits of C3d, C9, and vitronectin were observed on the basement membranes of both pocket and oral epithelium of healthy and AP gingiva but not at sites of protectin expression. The results suggest an increased turnover of the complement system in the gingival tissues of AP patients. The gingival epithelium and connective tissue endothelia are well-protected against damage by the membrane attack complex of complement (MAC). Protection of the underlying connective tissue is insufficient, however, and may allow for deposition of MAC and autologous tissue damage in AP.

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Assessment of complement cleavage in gingival fluid during experimental gingivitis in man

Cited by 59 publications

References 23 publications

Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches

Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches

Gingival Crevicular Fluid: Biomarkers of Periodontal Tissue Activity

Protection of Gingival Epithelium against Complement-mediated Damage by Strong Expression of the Membrane Attack Complex Inhibitor Protectin (CD59)

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