Host Microbial Interactions to Prolonged Dental Biofilm

Question 1

What is the critical pathway model (Salvi et al. 1997)?

Answer 1

look at the slides

Question 2

What are the clinical differences between healthy periodontal tissues, gingivitis and periodontitis?

Answer 2

Healthy: Intact alveolar bone, probing pocket not more than 3mm, no bleeding

Gingivitis: Swelling of the free gingiva, increased probing pocket, bleeding on probing, no destruction of periodontal tissues

Periodontitis: irreversible, bleeding on probing, pocket depth greater than 3mm, resorption of alveolar bone

Question 3

What are the mechanisms for tissue damage during peridontitis?

Answer 3

Migration of the JE in health is prevented by the healthy underlying connective tissue

In periodontitis, the JE migrates apically into the space of destroyed gingival connective tissue and periodontal ligament fibres

Question 4

How does the PDL break down in periodontitis?

Answer 4

-Breakdown of collagen fibres inserting between the alveolar bone and the cementum

-Damaged fibroblasts-reduction in fibres and ground substance due to inflammatory infiltrate

-Build up of host factors and bacterial factors in connective tissue

-Necrotic cementum

Question 5

Once the PDL fibres is destroyed, what happens?

Answer 5

Cementum cannot gain nutrients from the PDL blood vessels like it usually does, so it becomes necrotic.

Question 6

How does alveolar bone damage occur in periodontitis?

Answer 6

-Bacterial products (LPS) stimulate the release of cytokines, leukotrienes, prostaglandins.

-Which activate osteoclasts

-Neutrophils, macrophages, fibroblasts, endothelial cells, osteoblasts all secrete inflammatory mediators

-Some bacterial products cause direct damage

-Osteoclasts lead to the direct absorption of alveolar bone