The association between periodontitis and other chronic diseases, such as cardiovascular disease (CVD) and type 2 diabetes mellitus, could be related to systemic inflammation initiated by a local inflammatory challenge. Oliveira et al. have added lack of oral hygiene, and its link with systemic inflammation, to the spectrum of risk factors for CVD.
"These findings suggested that Del-1 could act homeostatically to regulate local inflammation. This concept was demonstrated by studies in animal models of periodontitis (Eskan et al., 2012), a chronic inflammatory disease that leads to inflammatory destruction of tooth-supporting tissues (Pihlstrom et al., 2005) and, in its severe form, adversely affects systemic health, thereby increasing the risk for atherosclerosis and diabetes (Genco and Van Dyke, 2010; Kebschull et al., 2010; Lalla and Papapanou, 2011). Specifically, Del-1- deficient mice were shown to spontaneously develop excessive neutrophil infiltration in the periodontium, leading to severe inflammation and alveolar bone loss (Eskan et al., 2012). "
[Show abstract][Hide abstract] ABSTRACT: New insights into the biological mechanisms involved in modulating periodontal inflammation and alveolar bone loss are paving the way for novel therapeutic strategies for periodontitis. The neutrophil adhesion cascade for transmigration in response to infection or inflammation is a key paradigm in immunity. Developmental endothelial locus-1 (Del-1) is one of several newly identified endogenous inhibitors of the leukocyte adhesion cascade. Del-1 competes with intercellular adhesion molecule-1 (ICAM-1) on endothelial cells for binding to the LFA-1 integrin on neutrophils, thereby regulating neutrophil recruitment and local inflammation. In animal periodontitis models, Del-1 deficiency resulted in severe inflammation and alveolar bone loss, but local treatment with recombinant Del-1 prevented neutrophil infiltration and bone loss. The expression of Del-1 is inhibited by the pro-inflammatory cytokine IL-17. Nucleic-acid-receptor-mediated inflammatory responses may be important in periodontal disease pathogenesis. Bacterial nucleic acids released during inflammation are detected by host microbial DNA sensors, e.g., Toll-like receptor-9 (TLR-9), leading to the activation of pro- and/or anti-inflammatory signaling pathways. DNA from periodontitis-associated bacteria induced pro-inflammatory cytokine production in human macrophage-like cells through the TLR-9 and NF-κB signaling pathways, but had less effect on human osteoblasts. Inhibition of TLR-9 signaling in human macrophages reduced cytokine production in response to P. gingivalis DNA. Differential expression of a polymorphic site in the TLR-9 gene promoter region and increased TLR-9 gene and protein expression were reported in chronic periodontitis. Further research to confirm that periodontal bacterial DNA contributes to destructive inflammation in vivo could provide alternative therapeutic targets to control periodontitis.
Advances in dental research 05/2014; 26(1):23-9. DOI:10.1177/0022034514526240
"This disease is characterized by the progressive destruction of the tooth supporting apparatus and often leads to tooth loss in adults. In addition, chronic infections with periodontal pathogens have been linked to the risk for systemic health conditions such as cardiovascular, diabetic, respiratory, and arthritic diseases (Beck et al., 2008; Genco, 2009; Gomes-Filho et al., 2009; Genco and Van Dyke, 2010; Scher et al., 2012). A group of bacteria known as the “red complex” comprising Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia has been strongly implicated in the initiation and progression of periodontitis (Socransky et al., 1998). "
[Show abstract][Hide abstract] ABSTRACT: Protein modification with complex glycans is increasingly being recognized in many pathogenic and non-pathogenic bacteria, and is now thought to be central to the successful life-style of those species in their respective hosts. This review aims to convey current knowledge on the extent of protein glycosylation in periodontal pathogenic bacteria and its role in the modulation of the host immune responses. The available data show that surface glycans of periodontal bacteria orchestrate dendritic cell cytokine responses to drive T cell immunity in ways that facilitate bacterial persistence in the host and induce periodontal inflammation. In addition, surface glycans may help certain periodontal bacteria protect against serum complement attack or help them escape immune detection through glycomimicry. In this review we will focus mainly on the generalized surface-layer protein glycosylation system of the periodontal pathogen Tannerella forsythia in shaping innate and adaptive host immunity in the context of periodontal disease. In addition, we will also review the current state of knowledge of surface protein glycosylation and its potential for immune modulation in other periodontal pathogens.
Frontiers in Microbiology 10/2013; 4:310. DOI:10.3389/fmicb.2013.00310 · 3.99 Impact Factor
"It is characterized by inflammation and destruction of tooth supporting tissues, in severe cases leading to tooth loss . It is also highly associated with systemic inflammation, resulting in an increased risk for subsequent chronic diseases, such as cardiovascular diseases [3,4], diabetes , metabolic syndrome [6-8], pneumonia [9,10], and rheumatoid arthritis . "
[Show abstract][Hide abstract] ABSTRACT: Periodontitis is a common oral disease that is characterized by infection and inflammation of the tooth supporting tissues. While its incidence is highly associated with outgrowth of the pathogenic microbiome, some patients show signs of predisposition and quickly fall into recurrence after treatment. Recent research using genetic associations of candidates as well as genome-wide analysis highlights that variations in genes related to the inflammatory response are associated with an increased risk of periodontitis. Intriguingly, some of the genes are regulated by epigenetic modifications, supposedly established and reprogrammed in response to environmental stimuli. In addition, the treatment with epigenetic drugs improves treatment of periodontitis in a mouse model. In this review, we highlight some of the recent progress identifying genetic factors associated with periodontitis and point to promising approaches in epigenetic research that may contribute to the understanding of molecular mechanisms involving different responses in individuals and the early detection of predispositions that may guide in future oral treatment and disease prevention.
Parham Parto, Carl J Lavie, Damon Swift, Xuemei Sui
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