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The Two-Way Association of Periodontal Infection with Systemic Disorders: An Overview.

Nagpal R, Yamashiro Y, Izumi Y - Mediators Inflamm. (2015)

Bottom Line: However, despite a significant increase in the prevalence of periodontal infections and systemic diseases in the past few decades, the fundamental biological mechanisms of connection between these ailments are still not fully explicated.Consequently, the mechanisms by which this bidirectional damage occurs are being explored with a concentric vision to develop strategies that could prevent or control the complications of these ailments.This paper attempts to summarize and hypothesize the diverse mechanisms that hint to a certain connection between the two prevalent chronic situations.

View Article: PubMed Central - PubMed

Affiliation: Probiotics Research Laboratory, Graduate School of Medicine, Juntendo University, Tokyo 113-0033, Japan.

ABSTRACT
Oral cavity that harbors diverse bacterial populations could also act as a site of origin for spread of pathogenic microorganisms to different body sites, particularly in immunocompromised hosts, patients, the elderly, or the underprivileged. A number of recent publications have advocated that patients with periodontal diseases are more susceptible to metabolic endotoxemia, inflammation, obesity, type 2 diabetes, and other related systemic complications, concluding that periodontal diseases could be a potential contributing risk factor for a wide array of clinically important systemic diseases. However, despite a significant increase in the prevalence of periodontal infections and systemic diseases in the past few decades, the fundamental biological mechanisms of connection between these ailments are still not fully explicated. Consequently, the mechanisms by which this bidirectional damage occurs are being explored with a concentric vision to develop strategies that could prevent or control the complications of these ailments. This paper attempts to summarize and hypothesize the diverse mechanisms that hint to a certain connection between the two prevalent chronic situations.

No MeSH data available.


Related in: MedlinePlus

A summary of proposed connections between periodontal diseases and metabolic disorders such as obesity, insulin resistance, and type 2 diabetes (LPS: lipopolysaccharide; IL: interleukins; TNF: tumor necrosis factor; PGE2: prostaglandin E2; MCP: monocyte chemoattractant protein; MIP: macrophage inflammatory protein; MMP: matrix metalloproteinase; AGEs: advanced glycation end products; Ig: immunoglobulin).
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Related In: Results  -  Collection


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fig2: A summary of proposed connections between periodontal diseases and metabolic disorders such as obesity, insulin resistance, and type 2 diabetes (LPS: lipopolysaccharide; IL: interleukins; TNF: tumor necrosis factor; PGE2: prostaglandin E2; MCP: monocyte chemoattractant protein; MIP: macrophage inflammatory protein; MMP: matrix metalloproteinase; AGEs: advanced glycation end products; Ig: immunoglobulin).

Mentions: Most of the mechanisms that support the influence of obesity and/or T2DM on periodontium generally share similar characteristics with those implicated in the typical complications of the diabetes [10]. For instance, in T2DM patients, hyperglycemia leads to a higher deposition of advanced glycation end products (AGEs) in tissues where these AGEs bind to the neutrophils and impair their normal functions. Further, these AGEs may also activate several unsought cell-surface receptors (RAGEs) which may alter the macrophages to a destructive phenotype. Both of these situations aggravate an uncontrolled production of proinflammatory cytokines and eventually lead to an increased vascular permeability, collagen fiber breakdown, and destruction of connective tissues and bones through increased lipid peroxidation and raised levels of IgA, IgG, and so forth, thereby making the diabetic patients more prone to periodontitis (Figure 2). Likewise, in patients with periodontal infections, the penetration of pathogen(s) (mainly Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Treponema denticola, and Aggregatibacter actinomycetemcomitans) or their products in lamina propria may lead to endotoxemia and a state of systemic chronic inflammation through the leakage of endotoxins such as lipopolysaccharides (LPS) into the serum. This hyperinflammation may further affect the expression and functioning of important immunoinflammatory molecules such as IL-1β, IL-6, TNF-α, PGE2, IL-8, IL-12, and IL-18, thereby contributing to insulin resistance and an altered lipid and glucose metabolism [11]. Eventually, the functioning of various tissues and cells such as adipocytes, hepatocytes, and endothelial and muscle cells may get impaired, thereby leading to more chronic metabolic states, that is, obesity, T2DM, and so forth in these periodontitis patients (Figure 2).


The Two-Way Association of Periodontal Infection with Systemic Disorders: An Overview.

Nagpal R, Yamashiro Y, Izumi Y - Mediators Inflamm. (2015)

A summary of proposed connections between periodontal diseases and metabolic disorders such as obesity, insulin resistance, and type 2 diabetes (LPS: lipopolysaccharide; IL: interleukins; TNF: tumor necrosis factor; PGE2: prostaglandin E2; MCP: monocyte chemoattractant protein; MIP: macrophage inflammatory protein; MMP: matrix metalloproteinase; AGEs: advanced glycation end products; Ig: immunoglobulin).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4539125&req=5

fig2: A summary of proposed connections between periodontal diseases and metabolic disorders such as obesity, insulin resistance, and type 2 diabetes (LPS: lipopolysaccharide; IL: interleukins; TNF: tumor necrosis factor; PGE2: prostaglandin E2; MCP: monocyte chemoattractant protein; MIP: macrophage inflammatory protein; MMP: matrix metalloproteinase; AGEs: advanced glycation end products; Ig: immunoglobulin).
Mentions: Most of the mechanisms that support the influence of obesity and/or T2DM on periodontium generally share similar characteristics with those implicated in the typical complications of the diabetes [10]. For instance, in T2DM patients, hyperglycemia leads to a higher deposition of advanced glycation end products (AGEs) in tissues where these AGEs bind to the neutrophils and impair their normal functions. Further, these AGEs may also activate several unsought cell-surface receptors (RAGEs) which may alter the macrophages to a destructive phenotype. Both of these situations aggravate an uncontrolled production of proinflammatory cytokines and eventually lead to an increased vascular permeability, collagen fiber breakdown, and destruction of connective tissues and bones through increased lipid peroxidation and raised levels of IgA, IgG, and so forth, thereby making the diabetic patients more prone to periodontitis (Figure 2). Likewise, in patients with periodontal infections, the penetration of pathogen(s) (mainly Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Treponema denticola, and Aggregatibacter actinomycetemcomitans) or their products in lamina propria may lead to endotoxemia and a state of systemic chronic inflammation through the leakage of endotoxins such as lipopolysaccharides (LPS) into the serum. This hyperinflammation may further affect the expression and functioning of important immunoinflammatory molecules such as IL-1β, IL-6, TNF-α, PGE2, IL-8, IL-12, and IL-18, thereby contributing to insulin resistance and an altered lipid and glucose metabolism [11]. Eventually, the functioning of various tissues and cells such as adipocytes, hepatocytes, and endothelial and muscle cells may get impaired, thereby leading to more chronic metabolic states, that is, obesity, T2DM, and so forth in these periodontitis patients (Figure 2).

Bottom Line: However, despite a significant increase in the prevalence of periodontal infections and systemic diseases in the past few decades, the fundamental biological mechanisms of connection between these ailments are still not fully explicated.Consequently, the mechanisms by which this bidirectional damage occurs are being explored with a concentric vision to develop strategies that could prevent or control the complications of these ailments.This paper attempts to summarize and hypothesize the diverse mechanisms that hint to a certain connection between the two prevalent chronic situations.

View Article: PubMed Central - PubMed

Affiliation: Probiotics Research Laboratory, Graduate School of Medicine, Juntendo University, Tokyo 113-0033, Japan.

ABSTRACT
Oral cavity that harbors diverse bacterial populations could also act as a site of origin for spread of pathogenic microorganisms to different body sites, particularly in immunocompromised hosts, patients, the elderly, or the underprivileged. A number of recent publications have advocated that patients with periodontal diseases are more susceptible to metabolic endotoxemia, inflammation, obesity, type 2 diabetes, and other related systemic complications, concluding that periodontal diseases could be a potential contributing risk factor for a wide array of clinically important systemic diseases. However, despite a significant increase in the prevalence of periodontal infections and systemic diseases in the past few decades, the fundamental biological mechanisms of connection between these ailments are still not fully explicated. Consequently, the mechanisms by which this bidirectional damage occurs are being explored with a concentric vision to develop strategies that could prevent or control the complications of these ailments. This paper attempts to summarize and hypothesize the diverse mechanisms that hint to a certain connection between the two prevalent chronic situations.

No MeSH data available.


Related in: MedlinePlus