Induction of the immune response to periodontopathic bacteria and its role in the pathogenesis of periodontitis

Ishikawa, Isao; Nakashima, Keisuke; Koseki, Takeyoshi; Nagasawa, Toshiyuki; Watanabe, Hisashi; Arakawa, Shin’ichi; Nitta, Hiroshi; Nishihara, Tatsuji

doi:10.1111/j.1600-0757.1997.tb00193.x

Cited by 100 publications

(87 citation statements)

References 252 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…IgG subclasses and avidity have also been implicated in periodontal disease progression; however, the functional characteristics which may help to define susceptibility to the disease are still to be ascertained (Ishikawa et al ., 1997). Underwood et al .…”

Section: (A) B-cells Inperiodontal Diseasementioning

confidence: 99%

“…the major receptors for P. gingivalis LPS (Shapira et al ., 1994), is down-regulated by IL-4 (Lauener et al ., 1990), and Ishikawa et al . (1997) have suggested that IL-4 may play a major role in the antiinflammatory effects of LPS-stimulated monocytes by downregulating CD14 and cytokine secretion by IL-4.…”

mentioning

confidence: 99%

“…This is based on studies showing that IL-4 inhibits the monocyte secretion of cytokines and PGE 2 (Te Velde et al ., 1990;Corcoran et al ., 1992). Macrophages play a central role in the immune response to bacteria, by acting as APC to initiate responses, producing pro-inflammatory cytokines and other mediators which induce antibacterial responses by effector cells and by the killing of micro-organisms (Ishikawa et al ., 1997). LPS is a component of Gram-negative bacteria, and while several LPS receptors have been identified (Lynn and Golenbock, 1992), binding of CD14 on monocytes, macrophages, and neutrophils mediates cytokine secretion (Wright et al ., 1990;Weinstein et al ., 1993).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Destructive Periodontitis Lesions are Determined by the Nature of the Lymphocytic Response

Gemmell

Yamazaki²,

Seymour³

2002

Critical Reviews in Oral Biology & Medicine

179

152

View full text Add to dashboard Cite

It is now 35 years since Brandtzaeg and Kraus (1965) published their seminal work entitled "Autoimmunity and periodontal disease". Initially, this work led to the concept that destructive periodontitis was a localized hypersensitivity reaction involving immune complex formation within the tissues. In 1970, Ivanyi and Lehner highlighted a possible role for cell-mediated immunity, which stimulated a flurry of activity centered on the role of lymphokines such as osteoclast-activating factor (OAF), macrophage-activating factor (MAF), macrophage migration inhibition factor (MIF), and myriad others. In the late 1970s and early 1980s, attention focused on the role of polymorphonuclear neutrophils, and it was thought that periodontal destruction occurred as a series of acute exacerbations. As well, at this stage doubt was being cast on the concept that there was a neutrophil chemotactic defect in periodontitis patients. Once it was realized that neutrophils were primarily protective and that severe periodontal destruction occurred in the absence of these cells, attention swung back to the role of lymphocytes and in particular the regulatory role of T-cells. By this time in the early 1990s, while the roles of interleukin (IL)-1, prostaglandin (PG) E2, and metalloproteinases as the destructive mediators in periodontal disease were largely understood, the control and regulation of these cytokines remained controversial. With the widespread acceptance of the Th1/Th2 paradigm, the regulatory role of T-cells became the main focus of attention. Two apparently conflicting theories have emerged. One is based on direct observations of human lesions, while the other is based on animal model experiments and the inability to demonstrate IL-4 mRNA in gingival extracts. As part of the "Controversy" series, this review is intended to stimulate debate and hence may appear in some places provocative. In this context, this review will present the case that destructive periodontitis is due to the nature of the lymphocytic infiltrate and is not due to periodic acute exacerbations, nor is it due to the so-called virulence factors of putative periodontal pathogens.

show abstract

Section: (A) B-cells Inperiodontal Diseasementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Destructive Periodontitis Lesions are Determined by the Nature of the Lymphocytic Response

Gemmell

Yamazaki²,

Seymour³

2002

Critical Reviews in Oral Biology & Medicine

179

152

View full text Add to dashboard Cite

show abstract

“…Although there are many studies exploring the role of PD as a chronic infection with implications for several systemic diseases (Ishikawa et al, 1997;Yamazaki et al), there is a lack of studies on chronic pain due to PD. Therefore, studies of this kind are important for managing these chronic disorders, which are very prevalent.…”

Section: Discussionmentioning

confidence: 99%

The Expression of Nitric Oxide in the Gingival Tissue in Subjects with Periodontitis and Chronic Pain

Fabri¹,

Sannomiya²,

Prado

et al. 2014

Int. J. Odontostomat.

View full text Add to dashboard Cite

Periodontal disease (PD) is a chronic infection that may have local and systemic rebound. Although a series of inflammatory mediators are involved in PD, the mechanisms involved in chronic craniofacial pain associated with it require elucidation. The aim of this study was to evaluate the immunoreactivity of substance P (SP), neuronal (nNOS) and inducible (iNOS) nitric oxide synthases in gingival samples of patients with severe PD with and without chronic craniofacial pain. Gingival specimens were obtained during routine periodontal surgery while managing 20 patients with both PD and chronic craniofacial pain (CFP Group) and 18 patients with only PD (PD Group). Following surgical removal, the tissue underwent routine histological techniques and was stained by immunohistochemistry with antibodies against SP, nNOS and iNOS. Using an image analysis system, we assessed the SP, nNOS and iNOS content in total gingival tissue as well as in both epithelial and connective gingival area. We observed high expression of nNOS in gingival tissue obtained from CFP patients (p<0.001), particularly in the epithelium area (p<0.001) comparatively to PD patients. In addition, the iNOS expression was also increased in the CFP group in the connective gingival tissue (p=0.003). There was no difference concerning SP expression between the groups. Our results suggest that nitric oxide, particularly derived from nNOS, modulates not only PD but also chronic craniofacial pain, since patients with this association presented an increase in nNOS and iNOS expression in gingival tissue.

show abstract

“…In CP, there is controversy as to whether cells with a TH1 or TH2 cytokine profile are associated with disease progression, as both TH1 and TH2 cytokines are pro-duced [10]. TH1 cells produce IL-2 and IFN-γ and facilitate cell mediated immune responses and are pro-inflammatory.…”

Section: Introductionmentioning

confidence: 99%

Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease

Hasan¹,

Sadoh²,

Jones³

2014

JIBTVA

View full text Add to dashboard Cite

show abstract

Induction of the immune response to periodontopathic bacteria and its role in the pathogenesis of periodontitis

Cited by 100 publications

References 252 publications

Destructive Periodontitis Lesions are Determined by the Nature of the Lymphocytic Response

Destructive Periodontitis Lesions are Determined by the Nature of the Lymphocytic Response

The Expression of Nitric Oxide in the Gingival Tissue in Subjects with Periodontitis and Chronic Pain

Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease

Contact Info

Product

Resources

About