Immunology
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This handout is provided by the CLR.
Development of disease depends on bacterial assault and host response
- Complex set of actions and reactions to the bacteria
Inflammation is protective and destructive
- Stops bacterial assault
- Damage and destroys gingival tissues leading to irreversible
changes
Inflammation
- Vascular and cellular response
- Dilutes, localizes, destroys and removes insult or injury
- Repairs damage and restores normal function
Inflammatory Cells
- Chemotaxis- signaling of cells to an area
 Neutrophils (PMN’s), macrophages, lymphocytes and
plasma cells begin to phagocytize bacteria and remove
damaged tissue
- Flow of gingival crevicular fluid increases (good and bad)
- Migration of PMN’s and crevicular fluid flow peaks at 6-12 days
after the onset of detectable gingivitis
- Cause lysis of cells and induce osteoclastic activity
 Prostaglandins are fatty acids that are synthesized during
gingivitis and periodontitis
- Promote bone destruction and leads to pain
Leukocytes (white cells)
- Defense
- Lymphoid Cells (agranulocytes)
 Lymphocytes and monocytes (give rise to macrophages)
- 3 types of Lymphocytes
 B-Lymphocytes
 T-Lymphocytes
 NK cells
- Main cells of the immune system
- Patrol the body
- Yield antibodies and arrange them on their membrane
- Once a lymphocyte recognizes and antigen, it will
recognize it again in the future
 Self-recognition- differentiates between self
and foreign agents
- B-Lymphocytes
 Derived from liver, spleen and bone marrow
 Receptor site for antigens
 Delivered by macrophages
 Precursors for plasmas cells which secrete
antibodies into the blood steam
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This handout is provided by the CLR.
Stimulate other T-cells so immune system can
grow
- T-Lymphocytes
 Helper T cells
- Assist B- cells in the production of
antibodies
- Stimulate B-cells to differentiate into
plasmas cells which produce antibodies
 Cytotoxic T cells
- Stimulate cytotoxic activity in cells such
as macrophages
- NK Cells
 Produce antibodies
 Stimulate microcidal effects of the immune
response through the production of a variety of
substances
 Effective against viruses and tumor cells
 Macrophages
- Differentiate from monocytes
- Phagocytic cell
- “big eaters”
- Attack antigen and present it to the lymphocyte
- Antigen processed by macrophages » development of
NK cells
- In connective tissues that phagocytize bacteria but
produce enzymes that degrade collagen
B. Granulocytes
 Polymorphonuclear leukocytes (PMN’s)
- Neutrophils
- Major phagocytic cell
- First line of defense
 Once of the first cells recruited to the site of
inflammation
- 70% of circulating leukocytes
 Mast Cells
- Located in the tissue
- Cytoplasm loaded with granules that contain
histamine and heparin
- Key players in the initiation of inflammation
 Basophils
- Rarest leukocyte (less than 1%)
- Small and rich in granules
- Bi or tri lobed nucleus which is hard to see due to
granules
 Eosinophils
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This handout is provided by the CLR.
Attack parasites and phagocyte antigen-antibody
complexes
Effector Molecules
- Antibodies (5 Classes)
 IgG- in blood and extravascular fluids, neutralize toxins and
enhance phagocytosis, 80% of all antibody in serum
 IgM- develops early in immune system, early activation of
complement
 IgE- involved in acute allergic reactions, reaction with
antigen leads to histamine release
 IgD- low levels, important in triggering immune response
 IgA- in saliva, tears and bodily fluids, activates complement
and interferes with bacterial adhesion, in gingival fluid
(different than secretory IgA which does not play a role in
perio disease and does not enter perio pockets)
- Complement
 Made of proteins and glycoproteins
 Account for 10% of proteins in human serum
 Mediate degranulation of mast cells
 Generate chemotactic factors that attract PMN’s,
macrophages and other leukocytes to inflamed areas »
increases phagocytosis of bacteria
 Cascading reaction- once it begins it grows until completion
- Allows for amplification of immune response
 Reaction can lead to tissue destruction due to release of
toxins by bacteria, release of histamine and tissues that
cause collagen destruction and elastin destruction
- Opsonization- process of phagocytosis is more effective if opsonins
are present
 Opsonins are antibodies or complements that bind to the
surface of bacteria
 Coat the bacteria so they are easier identified by PMN’s and
can be “swallowed”
- Cytokines
 Chemical substances that provide communication between
cells
 Produced by stimulated immune cells
 Assist in the development and regulation of activity of the
immune effector cells
 Director in the complex communication system
 Contribute to periodontal bone resorption
- Stimulate an increase in the number of osteoclasts
- Stimulate cells to secrete prostaglandins
Hypersensitivity Reactions
- Overreactions by the immune system
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This handout is provided by the CLR.
Usually protective in nature but may cause periodontal tissue
destruction
- Type 1- Anaphylaxis
 Generalized or localized
 Seen in individuals with food or drug allergies
- Type 2- Cytotoxic
 Results in breakdown of tissues or blood cells
 Not seen in perio or gingivitis
 In other oral diseases such as pemphigus
- Type 3- Arthus
 Occurs when high level of antigen remain without being
eliminated
 Occurs around small blood vessels
 Activates compliment and can cause extensive tissue
damage
- Type 4- Cell-Mediated or Delayed
 Seen in second exposures to an allergic agent
 T-lymphocytes after being sensitized to a specific antigen,
undergo changes which increase the number of
immunocompetent cells sensitive to the agent
Calculus
- Also called tartar
- Supragingival most common on lower anterior lingual surfaces and
maxillary first molar buccal surfaces
 Due to proximity to salivary glands
- Contributes to perio disease but is not the causative agent
 Occurs when plaque is mineralized which occurs within 2448 hours
- Matures in 12 days