3. Periodontal Immunology

Question 1

What does immunology regulate (2)

Answer 1

Oral microbial colonisation

Failure to regulate, microbial colonisation leads to pathology

Question 2

Features of early colonisers

Answer 2

Typically commensal species that modify the environment and lead to bacterial interactions

Question 3

Features of late colonisers

Answer 3

Typically gram-negative anaerobes

Question 4

Definition of gingivitis (2)

Answer 4

Physiological response to dental plaque that aims to restore the oral biofilm to homeostasis
Amplification of the immune processes already active in healthy tissues

Question 5

Hallmark of periodontitis

Answer 5

Pathologic bone loss

Question 6

Aetiology of periodontal disease

Answer 6

Dental plaque biofilm

Question 7

Immune response is responsible for (2)

Answer 7

Balance between host and biofilm

Host-biofilm interactions determine severity and duration of disease

Question 8

Definition of periodontal health

Answer 8

Dynamic balanced states in which immune responses actively regulate microbial colonisation to maintain tissue integrity

Question 9

Immune response in health (3)

Answer 9

PRRs recognise PAMPs
This leads to the release of pro-inflammatory mediators (cytokines, chemokines)
This causes vasodilation, increased blood flow and immune cell migration

Question 10

Features of complement (2)

Answer 10

Opsonise bacteria

Serum-derived (found in GCF)

Question 11

Role of neutrophils

Answer 11

Traverse through the gingival epithelium following a gradient of IL-8/CXCL8

Question 12

Activation (via PRRs) leads to (2)

Answer 12

Release of pro-inflammatory mediators

Enhanced phagocytic capacity

Question 13

Immune response in gingivitis (6)

Answer 13

Increased PRR stimulation
Increased production of pro-inflammatory mediators
This triggers inflammation (redness, bleeding, swelling, increased vasodilation, cell migration)
Neutrophils remain predominant cell type in initial lesion
Monocytes are recruited, activated and differentiate into macrophages
Lymphocytes are recruited to fine-tune the immune response

Question 14

Immune response in periodontitis (6)

Answer 14

Oral biofilm extends further into pocket
Adaptive immune responses start to predominate
Aggregates become rich in dendritic cells, CD4 T cells, B cells and plasma cells
Amplification of pro-inflammatory cells and mediators
Evolution of pathogenic biofilm
Connective tissue destruction and alveolar bone resorption

Question 15

Role of MMPs

Answer 15

Enzymes involved in degradation of the extracellular matrix during tissue remodelling

Question 16

Features of bone metabolism (10)

Answer 16

Osteoclastogenesis and osteoblastogenesis are balanced in health. This balance can be disrupted by persistent inflammation
The processes are regulated by RANK/RANKL/OPG
RANKL (receptor activator of nuclear KB ligand) is a cytokine (TNF family)
RANKL is membrane-bound (osteoblasts) or secreted (activated T and B lymphocytes)
RANKL binds to RANK to stimulate osteoclast differentiation (bone resorption)
RANKL binds RANK on osteoclast precursor
Osteoblasts express mRANKL
sRANKL couples inflammation with bone metabolism
OPG is a soluble decoy receptor for RANKL
High RANKL/OPG favours osteoclastogenesis and bone loss

Question 17

General risk factors of periodontitis (6)

Answer 17

Smoking
Diabetes
Stress
Drugs
Systemic disease
Nutrition

Question 18

Risk determinants include (3)

Answer 18

Genetics
Socioeconomic status
Genfer

Question 19

Current treatment for periodontitis (4)

Answer 19

Non-surgical biofilm removal
Systemic antibiotics
Periostat
Immune-modulatory drugs (NSAIDs, resolving, monoclonal antibodies, denosumab)

Question 20

Features of chronic periodontal inflammation (2)

Answer 20

Disrupts normal bone metabolism

Leads to alveolar bone resorption