PERIODONTOLOGY

2. DefensemechanismofPeriodontium

3. CONTENTS
Introduction.
Classification.
Innate Defense systems.
Adaptive Defense systems.
Conclusion.
References.

4. INTRODUCTION
The Periodontal tissue is constantly subjected
to mechanical and bacterial aggressions.
Defense mechanism factors provide resistance
to these actions.
Clinically the gingival tissue is able to deal with
external challenges without progressing to a
diseased state due to several defensive factors.
Effective defense mechanism is necessary
within the oral cavity to safeguard it from
these attacks.

5. A number of mechanisms operate to protect the body
from attack by foreign bodies and toxins, and
these defense mechanisms can be broadly
classified as follows : - (Jan Linde) Vol.1
Defense Mechanism
NON-
SPECIFIC(INNATE)
INFLAMMATORY
SPECIFIC
(ADAPTIVE)
IMMUNOLOGICAL
1. Bacterial Balance
2. Surface integrity
3. Surface fluid and
enzymes
4. Phagocytosis
5. Inflammatory reaction
1. Cell mediated
Immunity
(T lymphocytes)
2. Humoral
Immunity
(B lymphocytes)

6. 1.Bacterial balance
 The mouth as a whole and various zones in the
mouth , including what has been called the
‘crevicular domain’,can be viewed as ecosystem in
which a balance exists between the different
species of microorganisms and between flora and
the tissues.
 Upset in this balance is most commonly seen after
prolonged use of antibiotics which suppress some
types of bacteria and allow others to flourish to
the detriment of the tissues.

7. 2.Surface integrity
 Surface integrity of skin and mucous membrane
barriers,including the gingiva,is maintained by the continuing
renewal of the epithelium from its base and desquamation of
the surface layers.These two activities balance so that the
thickness of the epithelium remains constant.
 The efficiency of the surface barrier is enhanced by
keratinization and parakeratinization.

8.  ‘’Junctional epithelium ‘’exhibits several unique
structural and functional features that contribute
to preventing pathogenic bacterial flora from
colonizing the subgingival tooth surface.
 J.E is firmly attached to the tooth surface,forming
an epithelial barrier against plaque bacteria.
 It allows access of gingival fluid,
inflammatory cells,and components of the
immunologic host defense
to the gingival margin.

9.  Junctional epithelium exhibits rapid turnover and shedding
rate compared to oral gingival epithelium,which contributes
the host-parasite equilibrium and rapid repair of damaged
tissue,also may explain why gingivitis can be reversible
condition,which is considered a defensive mechanism of this
tissue.

10.  The Junctional epithelium is permeable membrane.
 Molecules injected I.V. can be detected in sulcus.
 Also bacteria in sulcus release
large quantities of metabolites
which diffuse through junctional
epithelium.

11.  Some investigators indicate that the cells of the
junctional epithelium have an ‘endocytic capacity’ to
that of macrophages and neutrophils, and that this
activity might be protective in nature.

12. Junctional epithelium has impressive
antimicrobial systems and is a part of
immune system of defense mechanism.
ANTIMICROBIAL
PEPTIDES

13. It also has sensory function detecting
chemical excreted from bacteria.
BACTERIA

14.  Below the Junctional epithelium is a vascular
network which supplies the epithelium with
nutrients and defense cells.

15.  Therefore,Junctional epithelium in antimicrobial defense has the
role of the epithelial barrier, and the combination of the
epithelial cells themselves can produce effective anti-bacterial
substances, including defensins and liposomal enzymes.
 Epithelial cells can be activated by microbial products chemokines
such as interleukins, cytokines and tumor necrosis factor alpha.
 Cytokines are soluble proteins secreted by cells involved in both
the innate and adaptive host response act by maintenance of
immune and inflammatory responses.
Cytokines - important role in cell mediated immune responses.
 Interleukins are important members of the cytokine group and
are primarily involved in communication between leukocytes and
other cells.

16. 3.Surface fluid and enzymes
GCF
• Tissue fluid that seeps through the crevicular epithelium is
known as gingival crevicular fluid.
• The composition and possible role in oral defense
mechanisms were elucidated by Waerhaug and Brill and
Krasse.
• METHOD OF COLLECTION
 Absorbing paper strips
 Preweighed twisted threads
 Micropippetes
 Crevicular washings

17. COMPOSITION OF GCF
ENZYMES
• Acid phospatase
• Alkaline
phosphatase
• Alpha1-
Antitrypsin
• Arylsulfatase
• Aspartase
aminotransferase
• Chondroitin
sulfatase
• Cystatins
• Cytokines
• Endopeptidases
• Exopepetidases
• Hyaluronidase
• Immunoglobulins
• Lactate
dehydrogenase
• Lactoferrin
• Lactic acid
• Lysozyme etc.
CELLULAR
ELEMENTS
• Bacteria
• Desquamated
epithelial
cells
• Leukocytes
ELECTROLYTES
• Potassium
• Sodium
• Calcium
ORGANIC
COMPOUNDS
• Carbohydrates
• Lipids
• Proteins-
Ig,Complement
components.
METABOLLIC AND
BACTERIAL
PRODUCTS
• Urea
• Endotoxins
• Lactic acid
• Prostaglandins
• Hydroxyproline
• Antibacterial
factors
• Cytotoxic
substances.

18. CLINICAL SIGNIFICANCE
 GCF is an inflammatory exudate.
 The amount of GCF is greater when inflammation is present.
• Circadian periodicity: There is a gradual increase in GCF amount
from 6AM to 10PM and a decrease afterward.
• Sex hormones:Female sex hormones,Pregnancy,ovulation
• and hormonal contraceptives increase gingival fluid production.
• Mechanical Stimulation: Chewing and vigorous gingival brushing
stimulate the flow of GCF.
• Smoking: Immediate transient but marked increase in GCF flow.
• Periodontal therapy: There is increase in GCF production during
the healing period after periodontal surgery.

19. • DRUGS IN GCF
Drugs that are excreted through the GCF may be used
advantageously in periodontal therapy(Bader and Goldhaber)
• Tetrayclines
• Metronidazole
LEUKOCYTES IN THE DENTOGINGIVAL AREA.
 The main port of entry of leukocytes into oral cavity is the
gingival sulcus.
 Leukocytes found are predominantly PMNs.
 The majority of these cells are viable and have phagocytic
and killing capacity.
 Therefore, leukocytes constitute a major protective
mechanism against the extension of plaque ito the gingival
sulcus.

20. SALIVA
 Salivary secretions are protective in nature because they
maintain the oral tissues in a physiologic state.
 Saliva exerts a major influence on plaque by mechanically
cleansing the exposed oral surfaces,by buffering acids
produced by bacteria,and by controlling bacterial activity.
COMPOSITION OF SALIVA
Electrolytes
 Sodium
 Calcium
 Potassium
 Magnesium

21. ORGANIC CONSTITUENTS OF SALIVA
 Proteins
 Mucin
 Amylase
 Cystatins
 Peroxidases
 Carbonic anhydrases
 Histatins and Statherins
 Proline rich proteins and glycoproteins.

22. ANTIBACTERIAL FACTORS IN SALIVA
Immunoglobulin proteins
• Secretory IgA
• IgG
• IgM
Non-immunoglobulin proteins
• Lysozyme
• Lactoferrin
• Proline rich proteins
• Histidine rich proteins
• Salivary peroxidase system
Agglutinins
• Mucins
• Fibronectin
• Alpha2- Macroglobulins

23. ROLE OF GCF COMPONENTS IN DEFENSE
MECHANISMGCF COMPONENT DEFENSE MECHANISM
Leucocytes Phagocytosis and killing of microorganisms
Immunoglobulins
IgG more prevalent
Control of inflammatory action
preparation of microbes and
foreign bodies for phagocytosis
Salivary
antibacterial
factors
Prevents growth of bacteria
Acid phosphatase Attacks techoic acid ,one of the components of the bacterial
cell wall
Lysozyme Bactericidal properties
Streptokinase Plays a role in inflammation.

24. ROLE OF SALIVARY COMPONENTS IN
DEFENSE MECHANISM
COMPONENTS MODE OF ACTION
Lysozyme Lysis of bacterial cell wall.
Lactoferrin Binds to iron leading to inhibition of bacterial cell growth.
Lactoperoxidase Catalyses hypothiocynate ion which disrupts bacterial
proteins.
Secretary IgA Interfere with bacterial attachment to the host tissues by
agglutinating specific bacteria.
Salivary
glycoproteins
Can act as special bacterial agglutinins.
Bicarbonates Can buffer organic acids produced during sugar
fermentation.

25. 4.PHAGOCYTOSIS
Certain cells in the blood stream and in the tissues
are capable of engulfing and digesting foreign
material.
The two most important phagocytic cells are the
 Polymorphonuclear leucocyte
 Macrophage

26. Polymorphonuclear leucocyte
 Provide the first cellular host mechanism to control
periodontopathic bacteria.
 Produced in the bone marrow ,they are the most
important blood cell for protecting the body
against acute invasion by bacteria.
 As they possess an amoeba like ability to change
shape and move rapidly they can pass through the
tissue.

27. • The direction in which they move is determined by
chemical substances,mainly derived from bacteria
or the complement cascade.
• These attract PMNs to the site of damage where
foreign particles are engulfed and digested.
• While their role is primarily defensive, PMNs can
also produce proteolytic enzymes which can destroy
the surrounding tissue.

30. Macrophages
 The macrophage is an indiscriminate scavenger of
foreign material.
 It starts life as a monocyte which moves into the
tissues and matures to become the extremely
efficient phagocyte,the macrophage, which is
capable of digesting large foreign particles.
 If a bacterial disease lasts more than a few days
the number of monocytes in the tissues increase
until there may be as many monocytes as PMNs.

35. • Unlike PMNs, monocytes are capable of several
divisions within the tissues which progressively
increase the number of macrophages.
• While PMNs are the main line of defense in acute
infection the monocytes are more important in
long-term chronic infection.
• The macrophages also take up antigens from the
circulating fluid for processing and presentation to
the lymphocytes.

36.  Phagocytosis is aided by a battery of nine related
proteins known as ‘complement’.
 The complement cascade is initiated by the
combination of immunoglobulin and the C1
component.
 The final product of the cascade is an esterase
which damages cell membranes and leads to
bacteriolysis.

37. Complement Pathway :
The functions of complement are:
• Chemotaxis cellular activation:Complements
products released in this reaction attracts
phagocytes to the site of infection.e.g.C3a and C5a
• Opsonization:once they arrive at the site of
infection the complement coat the bacterial surface
and allow the phagocytes to recognize the bacteria
and there by facilitating the bacterial
phagocytosis.e.g.C3b
• Cytolysis:Damage to the plasma membranes of the
cells can lead to lysis of the cell,e.g.C5-C9

39. 5.THE INFLAMMATORY REACTION
Inflammation may be defined as the reation of
living tissues to the injury in essence,it is a
defense mechanism in itself.This reaction is a
beneficial one.

40. 5.THE INFLAMMATORY REACTION
Tissue Injury and infection stimulates
inflammatory reaction.
Changes in the local microcirculation
Hyperaemia, increased vascular
permeability
Formation of a fluid and cellular exudate
In this way serum proteins and phagocytic
cells accumulate around the irritant.

41. ADAPTIVE IMMUNE SYSTEM
The unique surveillence and attack system
developed has three following main
characteristics:
1. It can distinguish between itself and the
enemy,i.e. between ‘self’ and ‘non-self’ so that it
does not attack parts of itself.

42. 2.The defenses contain elements specific against
any given antigen.This is possible because each
antigen contains specific amino acid sequences
or ‘flags’ which the immune system uses to
recognize ‘non- self’.
3.The system has memory .
The first contact with the antigen produces a
primary response in which the uneducated
lymphocytes proliferate and mature,and the
antigen is memorized so that the further
contact provokes a ready secondary response.

43.  Adaptive immune system is brought about by
actions of an array of cells which take up , process
,present and react to foreign proteins known as
antigens.
 APCs such as macrophages roam the body ingesting
the antigen they find and fragmenting it into
antigenic peptides.
 Within the cell these species of peptide are joined
to the major histocompatibility complex(MHC)
molecules and displayed on the surface of the cell.

44.  The T-Lymphocytes are activated by the process
and divide to produce memory and effector cells.
 B lymphocytes which also have specific receptor
molecules on their surface respond to these signals.
 When activated they differentiate into plasma
cells that secrete specific antibodies.
 By binding to antigen the antibodies can neutralize
them or precipitate their destruction by activating
the complement cascade or enabling phagocytic
cells to destroy them.

49. CONCLUSION

50.  The defense mechanisms of GCF,leukocytes,saliva
and the epithelial barrier of the gingival sulcus are
generally effective in controlling the deleterious
effects of the heavy concentration of bacteria
found in dental plaque.
 If this balance between host and parasite is
slightly changed,the result can be progressive
periodontal breakdown.
 Small clinical alterations,such as an over-contoured
restoration or an open subgingival margin,can allow
the bacteria to gain a small advantage over the
host defenses,resulting in increased gingival
inflammation and eventual loss of attachment.

51. • In summary, the closed role of the epithelial
attachment, combined with rapid epithelial cell
renewal and repair, saliva rinse,gingival crevicular
fluid washing,complement of immune function, and
granulocyte cells and monocyte / macrophage
phagocytosis and bactericidal effect, etc.,
constitute a multiple defense mechanisms of the
periodontal tissues.
• This defense mechanism against bacterial invasion
and destruction play a vital role to resist the plaque
to the gingival sulcus extension and protection
periodontal tissue.

52. REFERENCES:
 Host defense processes, Clinical periodontology and
Implant dentistry(5th Edition) Jan Lindhe Vol 1.
 Carranza’s Clinical Periodontology Tenth edition.
 Outline of periodontics,J.D.Manson,B.M.Eley.
 Essentials Of Periodontology,Sahitya Reddy S.
 Basic defense mechanisms in periodontal
diseaseMed Oral Patol Oral Cir Bucal. 2009 Dec
1;14 (12):e680-5.
 Polymicrobial Diseases ,Janet M. Guthmiller and
Karen F. Novak.
 Journal of Dental Research,The Junctional
Epithelium: from Health to Disease,D.D. Bosshardt
and N.P. Lang, J dent res, 2005 84: 9