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Periodontics > Pathogenesis Of Priodontal Disease > Flashcards

Pathogenesis Of Priodontal Disease Flashcards

1
Q

What are some host defence mechanisms?

A

Saliva, epithelial barrier

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2
Q

What is the purpose of inflammation?

A

To isolate, neutralise and remove cause and to initiate healing and repair

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3
Q

What is the role of the inflammatory response in periodontal disease?

A

Once the periodontal pathogens produce LPS and other virulence factors this initiates an inflammatory response. If the level of the pathogens is low enough then the inflammatory response will remove the cause and initiate repair (equilibrium).

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4
Q

What happens if the level of periodontal pathogens becomes too large?

A

If the level of periodontal pathogens becomes too large this creates a dysbiotic biofilm which the inflammatory response cannot cope with so it can no longer maintain equilibrium and a state of chronic inflammation is produced which then leads to tissue destruction.

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5
Q

List some of the basic components of the inflammatory response?

A

It is rapid
It is relatively non-specific
It has soluble effectors- complement, kinins
Has cellular components- neutrophils, macrophages
Cytokines are important in its regulation
Degree of bystander damage likely

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6
Q

What are the signs of inflammation?

A 
Heat 
Redness
Swelling 
Loss of function 
Pain (rare in periodontal disease)
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7
Q

What happens in the initial inflammatory response?

A

Dilation of blood vessels
Increased vascular permeability
Fluid exudate- dilutes causative agent, carries plasma proteins

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8
Q

What are the soluble effectors from plasma?

A

Complement system- group of around 20 distinct proteins which have key roles in mediating inflammation
Kinin system- peptides of 9-11 amino acids e.g. bradykinin, an important mediator of vascular permeability, there to ramp up the inflammatory response

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9
Q

Which two pathways is complement initiated by?

A

Classic pathway and the alternate pathway

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10
Q

What does the classic pathway involve?

A

Antigen-antibody reactions

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11
Q

What can the alternate pathway be activated by?

A

LPS

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12
Q

Describe the complement pathway.

A

Complement activated by classic or alternate pathway. Alternative pathway comes in at C3. C3 convertase leads to the breakdown of C3 into 2 component parts C3a and C3b. C3a then combines with C5 to divide C5 into C5a and C5b. This then continues the propagation of the cascading process.

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13
Q

What happens when C5b combines with C6, C7, C8 and C9?

A

This creates cytotoxic peptide leading to bacterial cell death

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14
Q

C3a and C5a

A

C3a leads to activation of C5 which produces C5a and C5b. C3a and C5a have got biological properties they increase vascular permeability, so like bradykinin that’s ramping up the inflammatory response. They are chemotaxic so that will lead to the chemical attraction of neutrophils and macrophages to the area of inflammation.

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15
Q

C3b

A

C3b also biologically active, through a process called opsonisation, where an antigen, which may be difficult to phagocytose, C3b binds to the antigen and makes it easier for a macrophage or a neutrophil to engulf and phagocytose the antigen. The inflammatory cell binds to the C3b attached to the antigen, engulfs the complex and breaks it down and then antigen is destroyed.

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16
Q

What does the cellular exudate include in the inflammatory response?

A

Neutrophils (mostly polymorphonuclear granulocytes (PMNs))

Macrophages

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17
Q

Where are neutrophils produced?

A

Bone marrow

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18
Q

What is the function of neutrophils?

A

Phagocytosis- they contains enzymes (elastin, collagenase and cathepsins), they engulf and degrade foreign agents)
Cytokine release

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19
Q

What are neutrophils?

A

They are white blood cells that exist in the lumen of blood vessels. To have any function in the inflammatory response they need to get out of the blood vessel and into the surrounding tissues.

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20
Q

How do neutrophils move out of blood vessels?

A

Central to this movement is the presence of proteins both on the surface of the neutrophil and also on the surface of the endothelial cells that line the blood vessel. One of the initial responses to the inflammatory response is vasodilation and an increase in the spaces between the endothelial cells that line the blood capillaries. The neutrophils still have to be able to adhere to the endothelial cells to stick to the cell before it can squeeze out between two endothelial cells. On the neutrophil surface there’s the protein LFA-1 (lymphocyte function-associated antigen 1). On the endothelial cell there’s a protein called ICAM-1. LFA-1 on the neutrophil surface binds to ICAM-1 on the endothelial surface, this then causes the neutrophil to be attached to the endothelial cell wall and it can squeeze out between two endothelial cells.

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21
Q

What is LAD-1?

A

Leukocyte adhesion deficiency, rare genetic disorder where a person lacks CD-18 (the beta component of LFA-1), this causes the function of LFA-1 to be reduced so fewer neutrophils are able to get out of the vasculature. These patients usually have high numbers of recurrent respiratory tract infections, mucosal and infections and aggressive form of periodontitis.

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22
Q

What is cyclic neutropenia?

A

On a regular cyclical basis, neutrophils numbers drop dramatically. Significantly increased risk of bone loss.

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23
Q

Where do macrophages come from?

A

Derived from blood monocytes

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24
Q

What are macrophages lifespan?

A

2-3 months

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25
Q

What are the functions of macrophages?

A

Phagocytosis
Antigen processing and presentation
Cytokine and prostaglandin release

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26
Q

What are the role of cytokines in the inflammatory response?

A

Cell-cell communication
Paracrine (cytokine is produced from a cell and its impact will be on another cell at the same site)/autocrine (cytokine is produced from a cell and it has its affect on that same cell) fashion

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27
Q

What are some kinds of cytokines?

A

Interleukins
Tumour necrosis factor alpha
Prostaglandins

28
Q

What are the complexities of cytokine biochemistry?

A

Several different types of cell produce the same cytokine
Cytokines can induce the release of other cytokines or their receptors
Some cytokines have apparently similar activities
Some cytokines act in synergy with others

29
Q

What are interleukins?

A

Family of cytokines regulating the inflammatory and immune responses- IL-1, IL-6, IL-8

30
Q

What are the sources of IL-1?

A

Macrophages

Epithelial cells, fibroblasts, PMNs

31
Q

What are the effects of IL-1?

A

Activates neutrophils and macrophages
Activates B and T lymphocytes
Induces cytokine release
Induces matrix metalloproteinase release (MMP)
Induces osteoclast activation and bone resorption

32
Q

What are matrix metalloproteinases (MMP)?

A

Family of proteases with zinc ion in active centre

They are capable of degrading full range of ECM molecules

33
Q

What are the secreted forms of MMP?

A

Collagenases, gelatinases, stromelysins

It is secreted as inactive pro-MMP and requires activation in the tissues

34
Q

What are MMPs inhibited by?

A

Tissue Inhibitor of MetalloProteinases (TIMP)

Comes in two forms TIMP-1 and TIMP-2

35
Q

The Metalloproteinase system

A

Cytokine stimulates the release of the Pro-MMP which is then activated by plasmin to create an active enzyme e.g. collagenase, which then breaks down extracellular matrix. The TIMPs act by binding to the collagenase and form a complex with the MMPs which inhibits the enzymatic activity of the MMP and blocks matrix breakdown.

36
Q

What is the role of IL-1 in periodontal disease?

A

IL-1 stimulates osteoclasts precursors to become activated and differentiated into osteoclasts, which will lead to the breakdown of bone. They can also stimulate fibroblasts which stimulates the production of MMPs to produces collagenases which leads to matrix degradation. IL-1’s can lead to the destruction of the two main components of the periodontium- bone and type 1 collagen

37
Q

Activated osteoclast

A

Bone is a mineralised structure and to initiate degradation of bone you need acid, an activated osteoclast releases acid which leads to the demineralisation of bone. The remaining component of bone is mostly collagen, the MMPs being released in the area as well will then lead to the destruction of the non-mineralised component of bone which will lead to bone loss which we see clinically.

38
Q

What produces interleukin-6?

A

Produced by lymphocytes, monocytes and fibroblasts

39
Q

What does IL-6 do?

A

Stimulates plasma cell proliferation

Stimulates osteoclast activation

40
Q

What does IL-8 do?

A

Simulates MMP expression

Chemoattractant for neutrophils

41
Q

What are prostaglandins?

A

Group of long-chained fatty acids derived from arachadonic acid

42
Q

What is the main role of prostaglandins?

A

Pro inflammatory mediators
Induce bone resorption via the RANK ligand signalling pathway
Most important one- PGE2

43
Q

What does RANK stand for?

A

Receptor Activator of Nuclear factor Kappa B

44
Q

How PGE2 activates osteoclast to lead to bone resorption?

A

PGE2 stimulates a stromal cell (e.g. osteoblast) to release or produce RANK ligand on its surface. The RANK ligand will then bind to its receptor called RANK. That receptor is positioned on the surface of an osteoclast precursor. Osteoclast precursors when activated by this RANK binding will combine together with other osteoclast precursors to form one giant multinucleated cell- an osteoclast.

45
Q

What is the inhibitor of RANK ligand?

A

Osteoprotegerin (OPG)

46
Q

How does OPG work?

A

It gets in the way on RANK ligand-RANK binding, it will bind to the RANK ligand and prevents the RANK ligand binding to the RANK on the osteoclast precursor and an activated osteoclast won’t form. If there’s more OPG than RANK in this tissue then we will get no activation of osteoclasts and no bone resorption but if there are more RANK than OPG then we will get activation of osteoclasts and bone resorption.

47
Q

What is the treatment of osteoporosis and metastatic cancer?

A

Denuomab- monoclonal antibody to RANKL. Does the same thing as OPG and inhibits the activation of osteoclasts and less resorption of bone.

48
Q

What are some of the factors of the adaptive immune response?

A 
Has memory 
Is highly specific 
Has soluble effectors- antibody 
Has cellular components- T and B lymphocytes, plasma cells, macrophages 
Cytokines important for regulation 
Bystander damage less likely
49
Q

What are the two types of adaptive immune response?

A

Humoral immunity and cell-mediated immunity

50
Q

What is humoral immunity?

A

Protection against extracelllar infectious agents and production of antibodies by B-cells under influence of activated T-helper cells

51
Q

What is cell-mediated response?

A

Protection against intracellular infectious agents, mainly through the release of toxic agents by cytotoxic T-cells, stimulated by IFN gamma, produced by activated T-helper cells

52
Q

How is the humoral response initiated?

A

Bacterial antigen -> macrophage -> local lymph node -> presented to B-lymphocyte -> plasma cell -> secretes antibody -> gingival tissues via circulation -> interacts with specific antigen

53
Q

What is the role of T helper cells?

A

Required for maturation of B cells and activation of phagocytes

54
Q

What is the role of T suppressor cells?

A

Inhibit immune response

55
Q

What is the role of T killer cells?

A

Cytotoxic

56
Q

What antibacterial effects does saliva have?

A

Washing effects- wash away the bacteria
Contains sIgA which inhibits the attachment of bacteria
Killing bacteria by peroxidase system
Killing bacteria by lysozyme, lactoferrin, histatins

57
Q

What can cause xerostomia?

A

Drug-induced- antihypertensives, antidepressants
Head and neck radiation
Salivary disease
Mouthbreathing

58
Q

What is the role of the epithelial barrier in the host defence mechanisms?

A

Barrier against invading microbes
Release of pro-inflammatory cytokines
Produces antimicrobial peptides e.g. defensins
Bacterial proteases e.g. gingipains from P gingivalis break down barrier function

59
Q

Junctional epithelium

A

JE cells exhibit a high turnover, contributing to host-parastite equilibrium and rapid repair
JE is relatively permeable- increasing risk of bacteria/products entering tissues
Permeability ensures GCF, cells, defence proteins gain access to sulcus
Extremely high turnover rate

60
Q

What is the role of epithelial cells in the inflammatory response?

A

LPS will bind to TLRs (toll-like receptors) and cause the epithelial cells to produce IL-8 and this will attract neutrophils into the area to phagocytose the bacterial product. The epithelial cells are involved in activating the immune response.

61
Q

What did the Loe et al study (1965) demonstrate?

A

The cause and effect relationship between accumulation of microbial plaque and the development of experimental gingivitis
When plaque was allowed to accumulate, gingivitis developed between 7-21 days. When plaque control was initiated, the gingivitis was reversed to clinically healthy gingiva within 1 week.

62
Q

Healthy gingiva

A

Few PMNs migrating through JE

Clinically normal

63
Q

Early lesion- 4-7 days

A

If you stop brushing your teeth more plaque is going to form
Increased PMN migration
Macrophage and lymphocytic infiltrate
Localised collagen degradation
Localised fibroblast fibroblast degeneration
Clinically normal- no signs of redness or swelling

64
Q

Established lesion (gingivitis) 14-21 days

A

PMNs walling off plaque
Increased lymphocytic infiltrate (macrophages, plasma cells)
60-70% collagen destruction
Lateral proliferation of JE with micro-ulceration
Gingival redness and swelling- false pocket formation
Base of the gingiva is still at the CEJ, alveolar bone still in its original position

65
Q

Histology of Periodontitis

A 
Apical migration of JE
Loss of periodontal ligament attachment 
Loss of alveolar bone 
Rete pegs 
Micro-ulceration of JE- break in the JE
True pocket formation 
Tissues are filled with immune cells- macrophages, neutrophils
66
Q

What does the burst hypotheses show?

A

The attachment loss of periodontal disease takes place over a long period of time and instead of constant attachment loss there are periods of active loss and periods of no loss over time.

Periodontics (6 decks)

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