infection vs. Inflammation
Know your Periodontal pathogen load, know your risk for periodontal disease
- Bacterial infection as the etiology for periodontal disease has been established using both experimental gingivitis studies and animal models.
- Three bacteria species were defined as periodontal pathogens at the 1996 World Workshop in Periodontics.
- Porphyromonas gingivalis is a gram negative obligated anaerobe that forms a “red complex” with Treponema denticola and Tannerella forsythia that is associated with advanced periodontal lesions.
- Actinobacillus actinomycetemcomitans (Aggregatibacter actinomycetemcomitans) is a gram-negative facultative anaerobic bacillus that is associated with localized aggressive periodontitis and bone resorption.
- Tannerella forsythia is a gram-negative fastidious anaerobic rod, which displays a synergistic relationship with P. gingivalis for growth and virulence.
- Subgingival microbiome analysis suggests that periodontal disease is the consequence of an oral microbiome shift from a symbiotic to dysbiotic relationship to the host.
- Total bacterial loads are 3-log higher in periodontitis than in health.
- The percentage of health-associated bacterial species is decreased from 60% in health to 10% in periodontitis.
- The percentage of periodontitis-associated bacterial species is increased from 5% in health to 50% in periodontitis.
- The microbiome shift in periodontitis involves allsubgingival sites
PERIODONTAL DISEASE AND inflammation
Healthy gingiva and normal inflammatory response
- Low level inflammation in a healthy periodontium is beneficial to the host. Inflammation is the host’s first line of defense against foreign intruders, mediated by the innate immune response system. Tissue residential immune cells, such as macrophages, identify and eliminate foreign substances through phagocytosis. They secrete cytokines to recruit additional immune cells to the site of intrusion. Finally, the innate immune system also activates adaptive immune responses through antigen-presentation.
Resolution of Inflammatory response
- Complete resolution of an acute inflammatory response is necessary for the return of local homeostasis, avoiding chronic inflammation and overall host health. This is an active and highly regulated process involving specialized pro-resolving lipid mediators, including lipoxins, resolvins, protectins, and maresins. They are potent agonists that control the magnitude and duration of inflammation.
- Lipoxins are bioactive eicosanoids derived from arachidonic acid. They attenuate neutrophil respiratory burst and transendothelial migration. Application of lipoxins in experimental periodontitis in animal models lead to bone regeneration.
- Resolvins are derived from Omega-3 fatty acids, such as eicosapentaenoic acid and docosahexaenoic acid. They stop neutrophil trans endothelial migration. Application of resolvins in experimental periodontitis in animal models leads to bone regeneration.
- Protectins are produced from Omega-3 fatty acids, such as docosahexaenoic acid.
Chronic inflammatory response and tissue damage
- When inflammation persists, acute inflammation leads to chronic inflammation as additional immune cells are recruited to the site, as well as the continued production of inflammatory cytokines.
- Bone loss occurs when both bacterial products and inflammatory cytokines disrupt the balance between osteoblast and osteoclast activities.
- Inflammatory cytokines promote the release of matriculates metalloproteinases, which leads to the destruction of periodontal tissues.
Link between periodontal disease and systemic disease
- Periodontal inflammation can be both an indicator and a modifier of systemic inflammation.
- Systemic chronic inflammation has been linked to diseases such as diabetes, cardiovascular disease, rheumatoid arthritis, Alzheimer’s disease, osteoporosis, and cancer.
Modifiers for Periodontal Disease
Although bacterial infection is essential for the initiation of periodontal disease, both environmental exposures and host genetics influence the body’s immune response to bacterial infection, as well as the onset and outcome of periodontal disease.
- Poor oral hygiene
- Genetic abnormalities in