Serum antibodies to <i>Bacteroides ginglvalis</i> in periodontitis: A longitudinal study

Mouton, Christian; Desclauriers, M.; Allard, H.; Bouchard, Martin

doi:10.1111/j.1600-0765.1987.tb01611.x

Cited by 47 publications

(43 citation statements)

References 18 publications

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“…This further confirms that systemic exposure of the host to the pathogen and corresponding host responses accompany oral infections (29,35,42,45,46). Our results therefore are in line with the concept that chronic periodontitis should be considered a risk factor for the progression of cardiovascular disease.…”

supporting

confidence: 79%

Local and Systemic Responses in Matrix Metalloproteinase 8-Deficient Mice duringPorphyromonas gingivalis-Induced Periodontitis

et al. 2009

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Periodontitis is a bacterium-induced chronic inflammation that destroys tissues that attach teeth to jaw bone. Pathologically excessive matrix metalloproteinase 8 (MMP-8) is among the key players in periodontal destruction by initiating type I collagen degradation. We studied MMP-8 in Porphyromonas gingivalis-induced periodontitis by using MMP-8-deficient (MMP8 ؊/؊ ) and wild-type (WT) mice. Alveolar bone loss, inflammatory mediator expression, serum immunoglobulin, and lipoprotein responses were investigated to clarify the role of MMP-8 in periodontitis and systemic inflammatory responses. P. gingivalis infection induced accelerated site-specific alveolar bone loss in both MMP8؊/؊ and WT mice relative to uninfected mice. The most extensive bone degradation took place in the P. gingivalis-infected MMP8 ؊/؊ group. Surprisingly, MMP-8 significantly attenuated (P < 0.05) P. gingivalis-induced site-specific alveolar bone loss. Increased alveolar bone loss in P. gingivalis-infected MMP8 ؊/؊ and WT mice was associated with increase in gingival neutrophil elastase production. Serum lipoprotein analysis demonstrated changes in the distribution of high-density lipoprotein (HDL) and very-low-density lipoprotein (VLDL) particles; unlike the WT mice, the MMP8 ؊/؊ mice underwent a shift toward a smaller HDL/VLDL particle sizes. P. gingivalis infection increased the HDL/VLDL particle size in the MMP8 ؊/؊ mice, which is an indicator of lipoprotein responses during systemic inflammation. Serum total lipopolysaccharide activity and the immunoglobulin G-class antibody level in response to P. gingivalis were significantly elevated in both infected mice groups. Thus, MMP-8 appears to act in a protective manner inhibiting the development of bacterium-induced periodontal tissue destruction, possibly through the processing anti-inflammatory cytokines and chemokines. Bacterium-induced periodontitis, especially in MMP8 ؊/؊ mice, is associated with systemic inflammatory and lipoprotein changes that are likely involved in early atherosclerosis.

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confidence: 79%

Local and Systemic Responses in Matrix Metalloproteinase 8-Deficient Mice duringPorphyromonas gingivalis-Induced Periodontitis

et al. 2009

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“…The role of dental plaque bacteria in the etiology of periodontitis is widely accepted (40). It is also well-established that periodontitis, as a chronic infection, is accompanied by systemic host responses, such as elevation of levels of antibody against periodontal pathogens in serum (8,16,25). In the absence of clinical data, serology has commonly been used in epidemiological studies to reveal various present or past bacterial and viral infections (9,10,33), but only rarely as regards periodontal infections (30).…”

Section: Discussionmentioning

confidence: 99%

Multiserotype Enzyme-Linked Immunosorbent Assay as a Diagnostic Aid for Periodontitis in Large-Scale Studies

et al. 2002

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Periodontitis is a common chronic oral infection caused by gram-negative bacteria, including Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Periodontitis evokes inflammatory host response locally in the periodontium but also systemically. The systemic humoral antibody response against oral pathogens can conveniently be measured by an immunoassay. The aim of the study was to measure serum immunoglobulin G class antibodies against A. actinomycetemcomitans and P. gingivalis by an enzyme-linked immunosorbent assay (ELISA) in which mixtures of several serotypes of the pathogens were used as antigens to avoid biasing of the results in favor of a particular strain. For A. actinomycetemcomitans the antigen consisted of six strains representing serotypes a, b, c, d, and e and one nonserotypeable strain. In the P. gingivalis ELISA, antigens representing serotypes a, b, and c were used. Serum samples from 90 subjects, including 35 samples from patients with diagnosed periodontitis, 10 samples from periodontally healthy controls, and 45 samples from randomly selected apparently healthy volunteers (referred to as "healthy subjects"), were tested. For both pathogens the antibody levels (means ؎ standard deviations) of the patients-expressed as area under the dilution curve-were significantly higher than those for healthy controls or healthy subjects, with values for A. actinomycetemcomitans and P. gingivalis, respectively, as follows: patients, 22.

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“…Many studies have reported that antibody titers to P. gingivalis remained unchanged or decreased after periodontal therapy (1, 3) or, in one instance, there was an initial increase in titer, followed by a net reduction of 50% by the end of 1 year posttreatment (24). Titers to LPS have been reported to decrease posttherapy (36).…”

Section: Vol 72 2004 Humoral Response To Gingipains In Vivo 1379mentioning

confidence: 99%

Humoral Responses to Porphyromonas gingivalis Gingipain Adhesin Domains in Subjects with Chronic Periodontitis

Nguyen¹,

DeCarlo

Paramaesvaran³

et al. 2004

Infect Immun

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The gingipains have been implicated in the pathogenicity of Porphyromonas gingivalis, a major etiologic agent of chronic periodontitis. Mature gingipains often present as a membrane-bound glycosylated proteinaseadhesin complex comprising multiple adhesin domains (HA1 to -4) and a catalytic domain. Using recombinant adhesin domains, we were able to show that patients with chronic periodontitis produce significantly more immunoglobulin G reactive with gingipain domains than a corresponding group with healthy periodontium. Titers were predominantly directed toward the carbohydrate epitopes shared between the gingipains and the lipopolysaccharide of P. gingivalis with little recognition of the peptide backbone of the catalytic domains. Distribution of titers to peptide epitopes of the adhesin domains was as follows: HA4 Ϸ HA1 > HA3 Ͼ Ͼ HA2. No correlation was observed between markers of disease severity and titers to individual adhesins within the disease group. Posttreatment titers showed no change or a decrease in titers for the majority of patients except for titers to the HA2 domain which showed marked increases in a few responding patients. Since the HA2 domain is important in hemoglobin binding and acquisition of essential porphyrin, boosting titers of antibodies to this domain may have the potential to control the growth of this organism.

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Serum antibodies to Bacteroides ginglvalis in periodontitis: A longitudinal study

Cited by 47 publications

References 18 publications

Local and Systemic Responses in Matrix Metalloproteinase 8-Deficient Mice duringPorphyromonas gingivalis-Induced Periodontitis

Local and Systemic Responses in Matrix Metalloproteinase 8-Deficient Mice duringPorphyromonas gingivalis-Induced Periodontitis

Multiserotype Enzyme-Linked Immunosorbent Assay as a Diagnostic Aid for Periodontitis in Large-Scale Studies

Humoral Responses to Porphyromonas gingivalis Gingipain Adhesin Domains in Subjects with Chronic Periodontitis

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