Host‐response: understanding the cellular and molecular mechanisms of host‐microbial interactions – Consensus of the Seventh European Workshop on Periodontology

Kinane, Denis F.; Preshaw, Philip M.; Loos, Bruno G.

doi:10.1111/j.1600-051x.2010.01682.x

Cited by 153 publications

(160 citation statements)

References 13 publications

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“…In the context of periodontitis, elevated levels of RANKL and reduced levels of osteoprotegerin (OPG) were detected in the GCF samples of patients with periodontitis and the RANKL/OPG ratio was suggested as a possible biomarker test for detection of bone destruction (Ref. 163). OPG acts as a decoy receptor for RANKL and inhibiting OPG expression enables RANKL to interact with its receptor RANK on other cells.…”

Section: Inflammatory Mediators and Bone Resorptionmentioning

confidence: 99%

Inflammatory mediators in the pathogenesis of periodontitis

Yucel‐Lindberg

Båge

2013

Expert Rev. Mol. Med.

352

334

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Periodontitis is a chronic inflammatory condition of the periodontium involving interactions between bacterial products, numerous cell populations and inflammatory mediators. It is generally accepted that periodontitis is initiated by complex and diverse microbial biofilms which form on the teeth, i.e. dental plaque. Substances released from this biofilm such as lipopolysaccharides, antigens and other virulence factors, gain access to the gingival tissue and initiate an inflammatory and immune response, leading to the activation of host defence cells. As a result of cellular activation, inflammatory mediators, including cytokines, chemokines, arachidonic acid metabolites and proteolytic enzymes collectively contribute to tissue destruction and bone resorption. This review summarises recent studies on the pathogenesis of periodontitis, with the main focus on inflammatory mediators and their role in periodontal disease.

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Section: Inflammatory Mediators and Bone Resorptionmentioning

confidence: 99%

Inflammatory mediators in the pathogenesis of periodontitis

Yucel‐Lindberg

Båge

2013

Expert Rev. Mol. Med.

352

334

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“…Gingivitis is a gingival inflammation without the loss of supporting periodontal tissues, while periodontitis is characterized by impaired attachment and loss of bone (4). Inflammatory biomarkers can provide additional information to disease progression beyond standard clinical and radiographic examinations (5).…”

Section: Introductionmentioning

confidence: 99%

Visfatin levels in gingival crevicular fluid and serum before and after non-surgical treatment for periodontal diseases

et al. 2016

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The purpose of this study was to evaluate visfatin levels at different stages of periodontal disease and in healthy tissues. In addition, the effect of non-surgical periodontal therapy on visfatin levels in gingival crevicular fluid and serum was investigated. Forty-five patients were divided into three groups based on clinical and radiographical findings. Group 1 comprised periodontally healthy individuals (n = 15); group 2 comprised patients with gingivitis (n = 15); and group 3 was composed of patients with generalized chronic periodontitis (n = 15). Gingival crevicular fluid and serum samples were collected before treatment and at 1, 3, and 6 months after treatment. Visfatin levels were measured by enzymelinked immunosorbent assays. Gingival crevicular fluid and serum visfatin levels were higher in patients with chronic periodontitis than those with gingivitis or healthy controls (P < 0.016). In addition, visfatin levels were higher in the gingivitis group than in healthy controls (P < 0.016). Non-surgical periodontal treatment resulted in a significant reduction in gingival crevicular fluid and serum visfatin levels.

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“…About 11% of adults develop clinical periodontitis. The dental plaque is caused by the development of anaerobic bacteria that cause accumulation and activation of neutrophils, which is orchestrated by various mediators and enzymes that destroy the connective tissue [2,3]. Untreated periodontitis ultimately leads to loss of support of the teeth, and atrophy of the alveolar process, causing loss of the teeth.…”

Section: Introductionmentioning

confidence: 99%

Periodontitis and Chronic Obstructive Pulmonary Disease

Spiropoulou¹,

Λάγιου²,

Lykouras³

et al. 2017

Insights Into Various Aspects of Oral Health

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Chronic periodontitis and chronic obstructive pulmonary disease (COPD) are chronic inlammatory diseases in which neutrophilic inlammation plays a major role. There are a few studies showing that these two entities share various predisposing factors and pathogenetic mechanisms; however, a direct connection between them has not yet been achieved. Epidemiology data may also show a connection between the two conditions. Neutrophilic inlammation in periodontitis and COPD is orchestrated by CD8+ lymphocytes and macrophages, leading to the aggregation of neutrophils and causing an imbalance to the proteases and antiproteases equilibrium. Finally, further research is needed to clarify the common pathogenesis of the two diseases to optimize their therapeutic management.

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Host‐response: understanding the cellular and molecular mechanisms of host‐microbial interactions – Consensus of the Seventh European Workshop on Periodontology

Cited by 153 publications

References 13 publications

Inflammatory mediators in the pathogenesis of periodontitis

Inflammatory mediators in the pathogenesis of periodontitis

Visfatin levels in gingival crevicular fluid and serum before and after non-surgical treatment for periodontal diseases

Periodontitis and Chronic Obstructive Pulmonary Disease

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