immunology of periodontal disease 1

Question 1

what is the immunology of periodontal disaeses?

Answer 1

disease process intiated and sustaine dby factors (substances) produced by the subgingival microbiota
some of these substances can directly injure host cells and tissues
other microbial constituents may activate inflammatory or cellular and humoral immune systems that cause tissue damage.

Question 2

what is the host-parasite rections?

Answer 2

innate (non-specific): inflammatory response

adaptive (specific): immunological responses

Question 3

what is the inflammatory response like ?

Answer 3

polymorphonuclear leukocytes (PMNL’s)

• terminally differentiated of myeloid origin
• 60% of leukocytes and short half-life
• first line of defense
• bridge innate and adaptive immune systems
• effector cells-humoral immunity

Question 4

what is meant by transendothelial migration?

Answer 4

the pro-inflammatory mediators, along with bacteria and their virulence factors, activate endothelial cells to atttract leukocytes into the connective tissues.

Question 5

what are the 7 transendothelial migration phases?

Answer 5

1. Rolling - Leukocytes use Lectin, L-selectin to interact with vascular addressins - along the luminal surface of the endothelium
2. A local insult - release of interleukin 1b, tumor necrosis factor alpha from mast cells which are crucial in initiating PMN recruitment -
3. Signaling endothelium - endothelial cells express P-selectin and E-selectin stimulated by IL-1b, TNF-a, C5a and lipopolysaccharides -
4. Increased rolling
5. Stimulated endothelium releases chemokines
6. Rolling arrest - L-selectin shed which upregulatesthe leukocyte function associated antigen 1 (LFA-1). LFA-1 binds intercellular adjesion molecule 2 (ICAM-2) -
7. CD-31 zipper - platelet-endothelial cell adhesion molecule 1

Question 6

What happens when the PMNL-recruitment and killing happens?

Answer 6

phagocytosis
lysosomes within cytoplasm
- elastase
- lactoferrin increases in severe periodontitis

possess receptors for metabolites of the complement molecule C3
receptors for IgG antibody

Question 7

What happens when the PMNL-recruitment and killing happens?

Answer 7

phagocytosis
lysosomes within cytoplasm
- elastase
- lactoferrin increases in severe periodontitis

possess receptors for metabolites of the complement molecule C3
receptors for IgG antibody

Question 8

what is cyclic neutropenia?

Answer 8

Cyclic neutropenia is a disorder that causes frequent infections and other health problems in affected individuals. People with this condition have recurrent episodes of neutropenia during which there is a shortage (deficiency) of neutrophils.

Additionally, people with this condition often develop open sores (ulcers) in the mouth and colon, inflammation of the throat (pharyngitis) and gums (gingivitis), recurrent fever, or abdominal pain. People with cyclic neutropenia have these health problems only during episodes of neutropenia.

Cyclic neutropenia is a rare condition and is estimated to occur in 1 in 1 million individuals worldwide.

Question 9

what does the mast cell do?

Answer 9

important in immediate inflammation
possess receptors for C3a and C5a and for Fc portion of antibody molecules (IgE, IgG)
feature prominent lysosomes which store inflammatory mediators (histamine, neutrophil chemotactic factor)

Question 10

what do the macrophages do?

Answer 10

monocytes when they leave the blood
present antigent to T cells
macrophage and lymphocytes orchestrate the chronic immune response

Question 11

What are the lymphocytes like?

Answer 11

T lymphocytes
B lymphotes
Natural killer cells (NK)

Question 12

What is the pathogenesis of periodontal disease?

Answer 12

Initial gingivitis, early gingivitis, established gingivitis,

Question 13

what are the stages of inflammation?

Answer 13

inflammatory response –bacterial infection of 2 weeks or less –> acute inflammation
- heat, redness, swelling, pain, loss of function –bacterial infection of long than 2 weeks –> chronic inflammation

Question 14

what are the stages of inflammation?

Answer 14

inflammatory response –bacterial infection of 2 weeks or less –> acute inflammation

• heat, redness, swelling, pain, loss of function –bacterial infection of long than 2 weeks –> chronic inflammation
• no symptoms, no symptoms –persistent onslaught of bacteria–> exaggerated host inflammatory response

Question 15

what are lipid mediated pro-inflammatory pathways?

Answer 15

membrane phospholipids –> arachidonic acid –> prostaglandin, or leukotriene or LIPOXIN (THIS IS PART OF PRO-RESOLUTION)

Question 16

what are the lipid mediated pro-resolution pathways?

Answer 16

membrane phospholipids –> eicosapentaenoic acid – resolvin or protectin

Question 17

what are the lipid mediated pro-resolution pathways?

Answer 17

membrane phospholipids –> eicosapentaenoic acid – resolvin or protectin

Question 18

what are the pathways in acute and chronic inflammation?

Answer 18

healthy tissue –> pathogens invade tissue –> cell damage –> acute inflammation (symtpoms: pain and loss of function. signs: erythema, edema, and heat) –> pathogens killed and removed (then resolution) or pathogens persist –> chronic inflammation (symptoms: no pain and no loss of function. signs: erythema, edema, and heat) –> continued cell damage some evidence of healing

Question 19

what does invasion of endothelial cells by P. gingivalis - 1 do?

Answer 19

this includes expression of cell adhesion molecules (CAMs), toll-like receptors (TLRs), chemokines, and cytokines. These events culminate in monocyte recruitment, elevations in oxidized LDL (ox-LDL), and accelerated atherogenesis

Question 20

what occurs with the immune or adaptive defense systme?

Answer 20

• second line of defense
• regulated by lymphocytes
• in periodontitis lesions, plasma cells represent about 50% of cells
• B cells comprise about 18%
• proportion of B cells is larger than T cells
• T helper cells occur in large numbers than T cytotoxic cells

Question 21

what are the complementary treatment strategies in periodontitis, a comprehensive management approach?

Answer 21

reduction of bacterial burder, risk factor modification, and host modulation therapy

all these overlapped give best chance for clinical improvement

Question 22

what is the host-modulation therapy?

Answer 22

antimicrobials (stop the bacteiral component, the bacterial products)
Periostat and NSAIDS (DONT’S USE THIS) (prostaglandins, cytokines (IL-1, IL-6, TNF) MMPs), this is the host response component
Bisphosphonates (DON’T USE THIS), periostat - block bone resorption (osteoclasts) and connective tissue breakdown (this is host response component), and pocket and CAL, tooth mobility is clinical sequelae

Question 23

what are key steps of the inflammatory process?

Answer 23

pathogens invade tissue (pathogen) –> pathogen release enzymes and toxins (pathogen) –> tissue injury and cell death (host) –> inflammatory response (host) –> increased blood flow (host) –> diapedesis, leukocytes, and plasma proteins enter tissue (host) –> phagocytosis (pathogen) –> killing and removal of pathogens and dead/dying host cells (pathogen) –> some host cells harmed as a side effect (host)

Question 24

what are some concluding remarks about this?

Answer 24

• bacteria play a critical role in the etiology of periodontal diseases
• subgingival bacteria associated with periodontitis show differences
• pathogenesis of periodontitis is modulated by various factos, including local, host, and environmental factors
• periodontitis is characterized by an immunoinflammatory host-mediated destruction of bone and connective tissues