Host-Bacterial Interactions In Periodontal Disease Flashcards
What is the main difference between gingivitis and periodontal disease?
Gingivitis is inflammation localised to gingival tissues and periodontitis is inflammation of gingival tissues and supporting periodontal structures (chronic inflammation).
What are the main characteristics of normal gingival appearance?
-pink gingiva, scalloped edges, stippled appearance and no swelling.
What microbes are associated with periodontal disease?
P. gingivalis, T. denticola, T. forsythia.
Name some normal flora within the oral cavity.
C. gingivalis, S. Oralis, A. actino.
What is the difference between colonisation and infection?
Colonisation does NOT involve disease- bacteria is present but is not invading tissues or is pathogenic.
What is a pathogen called when it starts off as commensal and changes to pathogenic?
Opportunistic pathogen.
What does it mean if P.gingivalis is asaccharolytic?
it does not use carbohydrates as energy.
Name virulence factors of P.Gingivalis.
- Asaccharolytic- doesn’t use carbohydrates for energy.
- Gingipains- family of proteinases secreted by P.gingivalis that degrade host proteins and activate MMPs.
- Inflammophillic- inflammatory environment favours expression of virulence.
- Atypical LPS-TLR4 receptor.
What can modify host-bacterial interactions?
Environment and genetic risk factors. For example- smoking, medical conditions and drugs.
What are toll like receptors?
They are a class of proteins that play a key role in the innate immune response. They are on macrophages and dendritic cells and they recognise antigens on bacterial surface.
What are MMPs?
They are a group of enzymes that cause the degradation of the ECM proteins.
Name some immune defences in the oral cavity.
Saliva- lysozyme, peroxidase, lactoferrin, histamines, cystitis etc.
Oral mucosa- AMPs, cytokines and chemokines.
GCF- cytokines, chemokines, IgG and AMPs.
What is a symbiotic biofilm?
It works and benefits us.
What happens to the biofilm in the oral cavity during gingivitis?
Increased TLR stimulation which increases the production of pro-inflammatory mediators and triggers the acute immune response. This causes swelling, redness and vasodilation.
What disease causes the neutrophils not being able to enter the oral cavity as they are trapped in the blood?
Leukocyte adhesion deficiency.
How do neutrophils cause neutrophil destruction?
Excessive infiltration is associated with chronic inflammation. This is because neutrophils contain enzymes which contribute to attachment loss (connective tissue destruction).
Describe the adaptive immune response in relation to periodontal disease.
T and B cells are present early. Rich in CD4 T cells, B cells and dendritic cells as the lesion progresses. The biofilm extends deeper in the pocket as the immune system is unable to regulate. IgG fails to regulate the immune response. This is either PROTECTIVE (so no systemic infection is caused) or it is DESTRUCTIVE (alveolar bone loss due to inflammation).
Describe the cellular and molecular events linking bacterial induced inflammation with pathologic tissue destruction.
- Bacterial products bind TLR on the epithelium which stimulates the secretion of cytokines, chemokines and AMPs.
- Vasodilation and recruitment of leukocytes.
- Bacterial products activate neutrophils and further release of other pro inflammatory mediators. Amplification loop of neutrophil infiltration.
- Activated lymphocytes express RANKL. RANKL/OPG balance disrupted.
- RANKL binds RANK on osteoclast precursors (monocytes). Activates osteoclastogenesis leading to alveolar bone resorption.
- Pro-inflammatory cytokines (IL-1, IL-6, IL-17, TNFa) contribute to bone resorption by inhibiting bone formation.
- Elevated and dysregulated MMP activation contributes to connective tissue destruction.
What determines the progression and severity of periodontal disease?
The interaction between bacteria and host immune system that determines the progression and severity of the disease.
