DEFENSE MECHANSIM OF GINGIVA

1. DEFENSE
MECHANISMS Of
GINGIVA

2. Gingiva is constantly subjected to a PLETHORA of mechanical,
chemical and antigenic challenges from bacteria and other foreign
bodies.
Over 300 bacterial species, some of them pathogenic, have been
recognized as commensals of the oral cavity.
Inspite of all adverse environmental conditions, periodontal
tissues remain in a state of health, normally.
This is because of these host defense systems..
INTRODUCTION

3. Defense Mechanisms
The mechanisms by
which health is
preserved in the face
of potential disease.

4. Defense
mechanisms
Nonspecific Specific
Host-
microbial
symbiosis
Adaptive
immunity
Tissue
Resistance
Local
inflammatory
response
Anatomical
factors
Mucous
barrier
Epithelial
barrier
Gingival
crevicular
Saliva
fluid
Eshan V, Apurv J. Defense Mechanisms of Gingiva. Journal of Orofacial Research.2014
April-June;4(2):111-114
CLASSIFICATION

5. Adaptive
immunity
• Slow response
• Activated when innate
fails to protect the host.
• Produces antibodies
• Memory cells
Innate
immunity
• Rapid response
• first line of defense
against infections
• Present since birth.
• Dependent on genetic
makeup

7. Host-Microbial Symbiosis
Close, prolonged association between two or more organisms of different
species, regardless of the benefit to the members.
• Presence commensal habitats essential for host immune
system protects periodontium from pathogenic microbes.
• Bacteria associated with
periodontal health include:
various facultative gram-
positive bacteria
Streptococcus
sanguis
Actinomyces
naeslundii
Streptococcus
mitis
Actinomyces
viscosus.

10. Proposed mechanisms for commensal bacteria
in maintaining health of host tissue
• Commensals promote host tolerance to pathogenic bacteria by:
• Suppressing inflammatory cytokine production.
• Inducing generation of suppressive T- lymphocytes
• Favoring secretion of Th2 cytokine
•
.

11. Certain commensals are capable of inducing release of
antimicrobial peptides from epithelial cells.
F. nucleatum protects oral ep. From P.gingivalis invasion by
inducing release of antimicrobial peptides
• They also prevent over colonization of pathogenic/exogenous
bacteria and compete with them for resources
Zhimin Feng & Aaron Weinberg. Role Of Bacteria In Health And Disease Of Periodontal Tissues Periodontology 2000, Vol. 40,

13. Tissue Resistance
Tissue resistance consists of four barriers:

14. Anatomical Factors:
• Anatomy of gingival tissues is designed for effective mastication
and clearance of food debris.
• Any poor functional tissue relations lead to plaque accumulation.
• Stippling: functional adaptation resistance to mechanical trauma.
• Attached gingiva: contoured to allow for proper deflection of food.

15. Gingival fibers:
• braces marginal gingiva firmly against tooth
surface
• provides rigidity to combat forces of
mastication
• tends to throw out any foreign material into
the sulcus.
• Gingival tissues during function of dentition and
pulse beats.

16. Mucus barrier:
• Mucus barrier is formed by Saliva washing the gingival surface and
Gingival crevicular fluid flowing through junctional epithelium (JE)
into the gingival sulcus.

17. Saliva
• Saliva has been defined as “the fluid secreted by the salivary glands
that begins the digestion of foods”.
• Salivary secretions protective maintain the oral tissues in a
physiologic state.
• Saliva exerts a major influence on
• plaque by mechanically cleansing the exposed
oral surfaces,
• by buffering, the acids produced by bacteria,
• by controlling bacterial activity.

20. Composition of Saliva

21. Schematic presentation of the main functions of saliva in
relation to
its constituents

22. Antibacterial
Factors
•Saliva contains numerous inorganic and organic factors that influence
bacteria and their products in the oral environment, aiding in the
defense of the host.
• They are:
• Salivary antibodies
• Enzymes
• Glycoproteins
• Buffer system
• Saliva pH

23. Salivary Antibodies:
• First line of defense in saliva, mucous layer of epithelium & acquired pellicle.
• Salivary Ab:
o Secretory IgA – gland derived
o IgG – Serum/ local plasma cells
o Non- secretory IgA- serum/local plasma cells
o Traces of other Ig like: IgM,D,E

24. FUNCTIONS
: Antibacterial, fungal, viral
Helps in phagocytosis,
Ag presentation,
degranulation,
cytokine production.

25. • Many bacteria coated with IgA,
• bacterial deposits contain both IgA and IgG
• IgA antibodies present in parotid saliva can inhibit the
attachment of oral Streptococcus species to epithelial cells.
• Gibbons and colleagues suggested that antibodies in
secretions may impair the ability of bacteria to attach to
mucosal or dental surfaces.

27. Enzymes:
Derived from the salivary glands, bacteria, leukocytes, oral tissues and
ingested substances;
Major enzyme parotid amylase.
Certain salivary enzymes have been reported in
increased concentrations in periodontal disease:
↑ hyaluronidase and lipase,
↑ β-glucuronidase and chondroitin sulfatase,
↑ aspartate aminotransferase and alkaline
phosphatase,
↑ amino acid decarboxylases, catalase,
peroxidase, and collagenase.

28. • Proteolytic enzymes in the saliva are generated by both the host and
oral bacteria.
• These enzymes have been recognized as contributors to the
initiation and progression of periodontal disease.
• To combat these enzymes, saliva contains:
• Antiproteases cysteine proteases such as cathepsins
• Antileukoproteases elastase.
• Tissue inhibitor of matrix metalloproteinase, activity of
collagen-degrading enzymes.

29. Lysozyme:
• Hydrolytic enzyme
• cleaves the linkage between structural
components of the
glycopeptide muramic acid–containing
region of the cell wall of certain bacteria
in vitro.
• It works on both gram-negative and
gram-positive organisms;
include Veillonella species and
Actinobacillus
actinomycetemcomitans.
•It probably repels certain transient
bacterial invaders of the mouth.

30. Lactoperoxidase–thiocyanate system:
Bactericidal to some strains of Lactobacillus and Streptococcus by
preventing the accumulation of lysine and glutamic acid, which are
essential for bacterial growth.

31. Lactoferrin: Effective against Actinobacillus species.

32. Myeloperoxidase: • similar to salivary peroxidase,
• released by leukocytes
• bactericidal for Actinobacillus,
• inhibits the attachment of Actinomyces
strains to hydroxyapatite.

33. Glycoproteins:
• Bind specifically to many plaque-forming bacteria.
• Facilitate bacterial accumulation on the exposed tooth surface.
• selectively adsorb to the hydroxyapatite to make acquired
pellicle.
• Glycoproteins with blood group reactivity inhibit the sorption of
some bacteria to the tooth surface and to epithelial cells.
• Glycoproteins and a glycolipid, serve as receptors for the
attachment of some viruses and bacteria.

34. Salivary Buffers and Coagulation Factors:
• The maintenance of the pH important function of salivary
buffers.
• The primary effect of these buffers is on dental caries.
• the bicarbonate–carbonic acid system important buffer
system.

35. • Saliva also contains coagulation factors (i.e., factors VIII, IX, and
X; plasma thromboplastin antecedent; and Hageman factor)
that hasten blood coagulation and that protect wounds from
bacterial invasion.
• An active fibrinolytic enzyme may also be present.

36. Saliva buffer system protects oral cavity in 2 ways:
1 many bacteria requires specific pH for their growth, &
altering optimal environment conditions prevents colonization.
2 plaque organisms produce acids which if not rapidly
buffered can cause demineralization of tooth.

37. Salivary pH: • Normally mixed saliva has a pH of 5.6-7.0, average 6.7.
• pH increases with flow due to increased bicarbonate
concentration.
• Low ph favors survival of bacilli, yeasts and streptococci.
• High ph favors proteolytic bacteria.
Ranjith Raj VPRB, Murugan
Thamaraiselvan, Role of Salivary PH
on the Prevalence of Periodontal
Disease: A Cross Sectional Pilot
Study, J Res Med Dent Sci, 2020, 8
(7): 423-427.

38. Leukocytes:
• Saliva contains all forms of leukocytes,
principal cells are PMNs.
• The number of PMNs varies from person to
person at different times of the day, and it is
increased in the presence of gingivitis.
• PMNs reach the oral cavity by migrating
through the lining of the gingival sulcus.

39. Orogranulocytes: • Living PMNs in saliva
• Their rate of migration into the oral cavity is
termed the orogranulocytic migratory rate.
• Rate of migration correlates with the severity of
gingival inflammation and is therefore a reliable index
for the assessment of gingivitis

41. Role in Periodontal Pathology:
• saliva flow effect plaque initiation
and maturation, calculus
formation,
• periodontal disease and caries.
↓ SALIVA
SECRETION:
↑ inflammatory gingival diseases, dental
caries,
→ rapid tooth destruction (cemental and
cervical caries).

47. Generation of crevicular fluid
Squier & Johnson (1973)
• Intercellular movement of molecules
and ions along intercellular spaces
• Three routes have been described:
• Passage From CT Into The
Sulcus
• Passage From The Sulcus
IntoThe CT
• Passage of Substances through
pathological or experimentally
modified gingival sulcus.

49. Pashley model (1976)
• Based on starling hypothesis
• Predicted that gcf production governed by
interstitial fluids from:-
Capillaries
Tissues
Lymphatic system
• When capillary filtrate exceeds lymphatic uptake
fluid will accumulate as edema or leave the area as
gcf

51. Permeability of junctional & sulcular
epithelium
• Brill and krasse confirmed the permeability by using
fluorescein.
Molecules found in sulcular epithelium :-
Albumin
endotoxin
histamine
Thymidine Horseradish
peroxidase
moleculesupto
1000kd wt.

80. By Oppenheim

89. Clinical Significance
• Amount of GCF is greater when inflammation is present.
• Sometimes proportional to the severity of inflammation.
GCF production is:
 Not Increased by trauma from occlusion
 Increased by : 1. Mastication of coarse foods
2. Toothbrushing
3. Gingival massage
4. Ovulation
5. Hormonal contraceptives
6. Prosthetic appliances
7. Smoking
• Other factors affecting amount of gcf : circadian periodicity &
periodontal therapy

91. Gingival fluid flow and sex
hormones:
Lindhe & Lundgren, 1972 (3 groups of females are studied)
• During mensturation: ↑ in GCF because sex hormones cause ↑
in the gingival vascular permeability.
• Females on birth control pills: significant ↑ GCF
• Females during pregnancy: gingival exudates reached max values
during the last trimester and ↓ to min after delivery.
Loe,1965: During pregnancy
↑ levels of gcf due to
exacerbation of gingivitis.
Muhlemann,1948: menstrual cycle
Sutcliffe,1972: at puberty

92. Circadian periodicity:
↑ in GCF from 6:00AM -10:00PM and ↓ afterward.
• Bisada et al. 1967: Average flow was greater in the evening
and minimal early in the morning.
• SEVIM G ET AL 2014 : No significant difference in vol of gcf
between 8am -6pm
Diabetes: Ringelberg et al 1977 found higher flow of gcf in diabetes
than without diabetes

93. Influence of Mechanical Stimuli
Mechanical stimulation of the marginal gingiva, such as
massage by means of a round instrument, causes a significant
increase in the permeability of the blood vessels located below
the junctional and sulcular epithelium.
Brill in 1959: The amount of gingival fluid was shown to
increase significantly under the influence of chewing.
Mcluaghlin WS et al 1993 Smoking produces an immediate but
transient increase in GCF flow.

94. Periodontal Therapy and Gingival Fluid
• Oral prophylaxis:
Gwinnett et al 1978: GCF flow decreases 1 week after oral
prophylaxis and slowly returned to pretreatment values.
• After surgical procedure:
Suppipat et al 1978: increase in GCF flow during the first 2 weeks during
healing period after surgery, followed by a gradual decrease
Tsuchida & Hara 1981. decrease in GCF flow 4 weeks following root
planing & Curettage
Arnold et al., 1966: One week after gingivectomy there was a
striking increase in GCF flow.

100. The Epithelial Barrier
• Continuous epithelial sheath consisting of gingival, sulcular and
junctional epithelium.
• Continuity of the epithelium protective barrier to foreign
agents, including bacteria, their toxic products and
antigenic substances.
• The ability of an epithelial surface to resist penetration of
bacterial toxins is related to: .
Thickness of
the
epithelium
Rate of turnover
of the cell
population
Degree of
keratinization

103. Thickness of the epithelium:
• oral mucosa respond to irritation hyperplasia and downgrowth of basal
layers.
• The sulcular epithelium (non-keratinised, thin) easily damaged and
less effective barrier to penetration of the connective tissue by
bacterial products than is the oral mucosa in the other areas.

104. Degree of keratinization
• Protection afforded by the epithelium is dependent
keratinization and its ability to desquamate or shed epithelial cells.
• Desquamation: process wherein dehydrated and flattened cells of
superficial layers are lost and and replaced by cells of underlying layers.
• This limits colonization of bacteria and also removes the already colonized
bacteria from the epithelial surfaces.

105. Rate of turn over of the cell population:
• Constant process of shedding and cell renewal in the oral
epithelium.
• The following have been the reported turn over times time for different
areas in the oral epithelium of experimental animals
Palate, tongue, cheek - 5 - 6 days.
Gingiva
J.E.
- 10 – 12 days
1 – 6 days. (Skougaard et al 1962).
• The high turn over rate of epithelium as well as the connective tissue of
the periodontium, are important aspects of the defense mechanism.

106. Components that contribute to various
aspects of the epithelial barrier
Early responders of
innate immunity
Toughened
mechanically
resistant
surface
Wound healing
Tissue turnover

107. These include cell–cell attachments and the overall integrity of the
tissue as well as the process of differentiation (keratinization) of
the tissue leading to the toughened, mechanically resistant surface.
Desmosomes mediate keratinocyte cell–cell attachment, and
hemidesmosomes mediate keratinocyte–basal lamina attachment.
Langerhans cells (purple dendritic cells) within the epithelium
do not have desmosomal attachments.

108. Constant cell renewal is critical to tissue turnover and
continual differentiation
Cell migration is critical to wound healing and re-
epithelialization.
Constitutively expressed antimicrobial peptides contribute to
the barrier to microbial invasion.

109. Antimicrobial defense of junctional epithelium
1) Rapid turnover- cell exfoliation
2) Funneling of JE towards
sulcus
hinders bacterial colonization
3) Basement membrane forms an
effective barrier against
microbes
4) Release of antimicrobial
substances
5) Release of cytokines from ep.
Cells
6) Cytokines & chemokines
released
attract LC & PMN

110. Gingival Connective Tissue
The gingival turgor: • The resilience and pliability of the attached
gingiva withstand frictional forces and pressures that
result from mastication.
Gingival connective tissue protect the root surface and
alveolar bone from the external oral environment.

111. The fiber apparatus:-
•Controls the positioning of teeth within the dental
arch
Biostability of the gingival tissue.
Protects the cellular defenses located at
the dentogingival interface.
Maintenance of this fibrous complex connective
tissue turnover rate.
Consequently, post inflammatory repair of the
fiber apparatus is completed within 40 to 60 days.

112. Cells of gingiva involved in
defense mechanism
Immune cells
Neutrophils
Monocytes
Macrophages
Lymphocytes
Basophils
Non-immune cells
Keratinocytes
Langerhans cells
Fibroblasts
Eosinophils
Mast cells
Plasma cells

113. Neutrophils
the most predominant inflammatory cells in gingiva.
Adhere to the host substrate,
migrate to the site of infection
recognize the bacteria,
Extend Cytoplasmic processes or pseudopodia
Engulf bacteria & bring about phagocytosis.
integrate the pathogen forming a phagosome
Phagosomes fuse with lysosymes phagolysosome
digestion and destruction of pathogen takes place.

114. • PMNs also undergo degranulation and allow extracellular
killing of pathogens which is considered a principle mode
of reducing bacterial count in the gingival crevice.
• The granules found in PMN consist of primary
(azurophilic) and secondary (specific) granules.
• These can bring about oxygen dependent or independent
killing.

115. Keratinocytes:
• Keratinocytes, no longer considered as passive by-standers
• play an active role in the activation of inflammation within
the gingival tissues.
• They synthesize number of cytokines, adhesin molecules,
growth factors and enzymes.

116. produce Interleukin 1, TNF, prostaglandin E2,matrix metalloproteinases
diffuse through JE
enter the gingival connective tissue
initiate the cellular immune reaction.
• Recruitment of neutrophils into the JE is mediated by
promoting
diapedesis
of neutrophils
along the chemical
gradient
Adhesion
molecules
secreted by
keratinocytes
Antigen presenting
cells (Langerhans
cells)

117. Langerhans cells
• Dendritics cells - Modified monocytes
• Reside chiefly in suprabasal layers.
• Act as antigen -presenting cells for lymphocytes.
• Specific elongated g-specific granules called as Birbecks Granules.
• Have marked adenosine triphosphatase activity.
• Only epidermal cells which express receptors for C3 and Fc portion of
IgG.
• Found in oral ep. of normal gingiva.
• Smaller amounts in sulcular ep.
• Absent in healthy junctional ep.

118. Odland Body / Keratinosome / Membrane –
coating granules:
• The upper most cells of the stratum spinosum contain
numerous dense granules, keratinosomes, which are modified
lysosomes.
• They contain a large amount of acid phosphatase,an enzyme involved in
the destruction of organelle membranes, which occurs suddenly between
the granulosum and corneum strata and during the intercellular
cementation of cornified cells.

119. Fibroblasts:
• Principal cell type of connective tissue.
• Provide structural framework, maintains CT integrity.
• Fibroblasts senses pathogens & PAMPs’ inflammatory
mediators regulate inflammatory response
• Express functional TLR’s

120. PRR
• Cells of epithelium and connective tissue express Pattern
Recognition Receptors (PRRs) that bind Pathogen-Associated Molecular
Patterns (PAMPs), found in a broad type of organisms.
• These receptor types
include:
complemen
t receptor-
3,
cluster of
differentiati
on 14
(CD14),
lectins and
scavenger
receptors.
nucleotide-
binding
oligomeriza
tion domain
(NOD)
toll-like
receptors
(TLR)

122. Local inflammatory response
most significant and final barrier to penetration of connective
tissue by bacteria and their toxins.
• This response is stimulated by tissue injury and infection.
• A series of reactions brings about local changes like increased
vascularization leading to increased fluid collection and cellular
exudation that eventually causes accumulation of serum
proteins and phagocytic cells in the affected area.

123. Conclusion
• The oral cavity is well equipped to counterattack any adverse
condition that may harm the gingiva.
• While the innate immunity acts primarily against any foreign
invader, the specific immunity takes a more complex targeted
approach to protect the gingiva.
• Right from its superficial epithelial layer to the innermost
connective tissue, there is a line of defense that acts in harmony
with other oral structures to maintain homeostasis.

124. References
• Newman and Carranza’s clinical periodontology- 13th edition
• Bathla S. Defense Mechanisms of Gingiva. Periodontics Revisited, 1st
edition. New Delhi, India: Jaypee Brothers Medical Publishers. 2011:123-
8.
• Verma E, Jhawar A. Defense mechanisms of gingiva. Journal of Orofacial
Research. 2014:111-4.
• Saxén L, Tenovuo J, Vilja P. Salivary defense mechanisms in juvenile
periodontitis. Acta Odontologica Scandinavica. 1990 Jan 1;48(6):399-407.
• Fujita T, Yoshimoto T, Kajiya M, Ouhara K, Matsuda S, Takemura T,
Akutagawa K, Takeda K, Mizuno N, Kurihara H. Regulation of defensive
function on gingival epithelial cells can prevent periodontal disease.
Japanese dental science review. 2018 May 1;54(2):66-75.
• Mounika B, Jagadish RG, Harinath RS, Rajababu P. Epithelial
antimicrobial peptides in defensive mechanism of gingiva. Indian Journal
of Dental Advancements. 2014 Oct 1;6(4):1686-96.