The document summarizes the various defense mechanisms of the gingiva. It begins by classifying the defense mechanisms into nonspecific and specific categories. The nonspecific category includes host-microbial symbiosis, tissue resistance via anatomical factors and the mucous barrier, saliva, and the gingival crevicular fluid. It then discusses each of these mechanisms in more detail, focusing on their roles, compositions, and relationships to periodontal health and disease. The document concludes by stating that despite various challenges, the gingiva remains healthy thanks to these innate defense systems.

2. D. Hema
PG-I
DEFENSE MECHANISMS
OF GINGIVA

3. CONTENTS
• Introduction
• Classification
• Host microbial symbiosis
• Tissue resistance
• Anatomical factors
• Mucous barrier
• Saliva
• GCF

4. • Epithelial barrier
• Connective tissue
• Cells involved in defense mechanisms of gingiva
• Role of Nervous system in innate immunity
• Local inflammatory response
• Biological sealing and defense mechanisms in the
transmucosal region around dental implants
• Conclusion
• References

5.  Defense Mechanisms
The mechanisms by which health is preserved in the face of
potential disease.
 The innate immunity system :
Acts as a first line of defense against infections,
Present since birth.
Resistance to infection, which an individual possesses by virtue of
his genetic and constitutional make up.
 The adaptive immune system:
Activated when innate fails to protect the host.
Produces a specific reaction to each infectious agent
Also remembers the infectious agent and can prevent it from
causing disease later.
INTRODUCTION

6. What’s the need for defense mechanisms?

7. Gingiva is constantly subjected to a PLETHORA of mechanical,
chemical and antigenic challenges from bacteria and other foreign
bodies.
During mastication of food the bolus passes over the gingival surface
with force. Gingiva is also exposed to extreme variations in temperature
and pH.
Over 300 bacterial species, some of them pathogenic, have been
recognized as commensals of the oral cavity.
Inspite of all these adverse environmental conditions, periodontal
tissues remain in a state of health, normally. & This is because of these
host defense systems..
The gingiva is able to withstand all of these adverse environmental
conditions, with the help of certain defense mechanisms.

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

9. 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,
Streptococcus mitis, Actinomyces naeslundii and Actinomyces
viscosus.
Host-Microbial Symbiosis

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
• 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 HBD-2,3.
• 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, 2006, 50–76.

11. Tissue Resistance
 Tissue resistance consists of four barriers:

12. 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.

13. • Gingival fibers:
 braces marginal gingiva firmly against tooth surface,
 provides rigidity to combat forces of mastication and
 tends to throw out any foreign material into the sulcus.
 This expulsion is aided by the movement of teeth and
gingival tissues during function of dentition and pulse beats.

14. 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.

15. Saliva
• Saliva has been defined as “the fluid secreted by the salivary glands
that begins the digestion of foods”.
- Contemporary Periodontics, Genco
• 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.

16. Composition of Saliva
Sembulingam K and Sembulingam P (2010). Essentials of medical physiology. 5th ed.

17. Schematic presentation of the main functions of saliva in relation to
its constituents
AV Nieuw Amerongen, ECI Veerman. Saliva-the defender of the oral cavity.
Oral Diseases (2002) 8,12-22

18. 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

19. 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
o Polymeric immunoglobulin receptor (pIgR)
• Functions:
 Antibacterial, fungal, viral
 Helps in phagocytosis, Ag presentation, degranulation,
cytokine production.

20. • 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.

21. 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.

22. • 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  X cysteine proteases such as cathepsins
 Antileukoproteases  X elastase.
 Tissue inhibitor of matrix metalloproteinase, X activity
of collagen-degrading enzymes.

23.  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;
its targets include Veillonella species and Actinobacillus
actinomycetemcomitans.
• It probably repels certain transient bacterial invaders of the
mouth.

24.  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.
 Lactoferrin:
Effective against Actinobacillus species.
 Myeloperoxidase:
• similar to salivary peroxidase,
• released by leukocytes;
• bactericidal for Actinobacillus,
• inhibits the attachment of Actinomyces strains to
hydroxyapatite.

25. 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.

26. 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.
• 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.

27. 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.
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.

28. 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.
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

29. PHILIP D. et al. Influence of saliva on the oral microbiota.
Periodontology 2000, Vol. 70, 2016, 80–92.

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

31. Gingival Crevicular Fluid
• Gingival crevicular fluid (GCF) is an inflammatory exudate
that can be collected at the gingival margin or within the
gingival crevice. (Lamster IB,1997)

32. Studies on gingival crevicular fluid

33. TRANSUDATE OR EXUDATE?
Bickel et al, 1985 concluded that the initial, pre inflammatory fluid
was considered to be a transudate, and, on stimulation and
inflammation, this changed to become an inflammatory exudate.
Brill,1962 and Egelberg,1974 production of GCF was primarily a
result of an inflammatory increase in the permeability of the
vessels underlying junctional and sulcular epithelium.
Alfano,1974 and Pashley,1976:  the initial fluid produced could
simply represent interstitial fluid which appears in the crevice as a
result of an osmotic gradient.

34. The 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 Into
The CT
 Passage of Substances through
pathological or experimentally
modified gingival sulcus.

35. Permeability of junctional & sulcular epithelium
• Brill and krasse confirmed the permeability by using fluorescein.
• Substances that have been shown to penetrate the sulcular
epithelium:
 Albumin
 Endotoxin
 Thymidine
 Histamine
 Phenytoin
 Horseradish peroxidase
Indicate that its
permeable to
molecules upto
1000kd wt.

36. Composition
A. CELLULAR ELEMENTS C. ORGANIC COMPOUNDS
1. EPITHELIAL CELLS 1.CARBOHYDRATES
2. LEUKOCYTES 2.PROTEINS
3. BACTERIA 3.LIPIDS
B. ELECTROLYTE D. METABOLIC END PRODUCTS
1.SODIUM 1.LACTIC ACID 5.CYTOTOXIC SUBSTANCES
2.POTASSIUM 2.ENDOTOXINS 6.HYDROXYPROLINE
3.CALCIUM 3.PG 7.ANTIBACTERIAL FACTORS
4.UREA
E. ENZYMES AND ENZYMES INHIBITORS:
1. ACID PHOSPHATASE
2. ALKALINE PHOSPHATASE
3. PYROPHOSPHATASE
4. β – GLUCURONIDASE
5. LYSOZYME
6. HYALURONIDASE
7. PROTEOLYTIC ENZYMES
8. LACTIC DEHYDROGENASE

37. Source Action Correlation with
disease activity
Epithelial
cells
Junctional &
sulcular
epithelium
Positive correlation
is found
Leucocytes Dentogingiva
l vessels
Phagocytosis
& killing of
microbes
Positive correlation
only in some
instances
Bacteria Oral cavity Poor correlation
between bacterial
count in gingival
fluid and
periodontal
parameters
Cellular elements

38. Electrolytes
Source Action Correlation with
disease activity
Sodium Plasma and
extracellular
fluid
• Genesis of
plaque
• Precipitation of
proteins
• Precipitation of
mucoprotein
along enamel
surface
Na/K significantly
increases in the
presence of
inflammation
Potassium Plasma and
extracellular
fluid
Positive correlation
between potassium
concentration and
the average pocket
depth
Calcium Plasma and
extracellular
fluid
Positive correlation

39. Organic compounds
Source Actions Correlation with disease
activity
Carbohydrates Extracellular
fluid
• Glucose concentration is
increased in inflamed
tissues
• hexosamine & hexuronic
acid
• has no correlation with
variation in gingival
inflammation
Immunoglobul
ins
Plasma
or
locally
synthes
ized
• Control inflammatory reaction
• Elimination of antigen
• Activation of immune cells
• Preparation of microbes and
foreign particles for phagocytosis
• Play a role in immune Response
Positive
correlation
Complement blood

40. Metabolic and bacterial products
Source Actions Correlation with disease
activity
Lactic acid Breakdown
product of
tissue
Positive correlation to both
clinical degree of inflammation
and gcf flow
Hydroxyproline Breakdown
product of
collagen
 presence of inflammation and
one month after surgery.
Returns to baseline postop.
Prostaglandins Various cells Vasodilation
bone resorption
Inhibition of
collagen synthesis
Positively correlated
Urea Breakdown
products of
bacteria
Elevates pH of
supragingival
plaque in presence
of gingivitis and
periodontits
Urea conc. ↓ when gingival
inflammation 

41. Source Actions Correlation with
disease
Endotoxins LPS of cell wall of
Gram-negative
bacteria
Highly toxic to
gingival tissue
Positively
correlated with
the presence
of varying
degree of
periodontal
inflammation
Cytotoxic
substances
like H2S
Bacteria Highly toxic
metabolite
Positively
correlated with
gingival
inflammation
Antibacterial
factors
Saliva Prevents
growth of
bateria

42. Enzyme and enzyme inhibitors
Source Actions Correlation
with disease
activity
Acid
phosphatase
Pmn’s &
desquamating
epithelial cells
• Associated
with
connective
tissue
catabolism.
• Attacks
teichoic acid of
bacterial cell
wall
Negative
correlation with
gcf flow and
bone loss
Alkaline
phosphatase
PMN’s Play a role in
calcification
Positive
correlation with
pocket depth
Pyrophosphat
ase
Plaque
Bacteria
Play a role in
calculus formation
Positive
correlation

43. Source Actions Correlation with
disease activity
Beta
glucoronidase
PMN’s,
Bacteria,
Macrophages,
fibroblasts,
endothelial
cells
Used as Lysosomal
marker
Positive correlation
with gcf flow and
pocket depth
Lysozyme PMN’s Bactericidal
Lytic effect on
connective tissue
Positively
correlation with
severe periodontal
destruction
Hyaluronidase Serum Widening of intercellular
spaces in junctional
epithelium
Significantly
increases in
presence of
inflammation
Lactic
dehydrogenase
bacteria Catalyzes the conversion
of pyruvate to lactate
No significant
correlation

44. Mammalian proteases
a. Cathepsin-D:
• Lysosomal enzyme seen in WBC
• Attacks various components of epithelium and
connective tissue.
• Positively correlated with periodontal destruction.
b. Elastase:
• Seen in PMN’s
• Active upon elastin, proteoglycans, hemoglobin,
fibrinogen and collagen.
• Widening of epithelial intercellular spaces, partial
destruction of basal membrane and loss of collagen
• Positively correlated with disease
c. Cathepsin-G:
• Serine endopeptidase in PMN’s
• Hydrolyzes Hb., fibrinogen, casein, collagen and
proteoglycans
• Positive correlation

45. d. Plasminogen activator (streptokinase and urokinase):
• Blood
• Fibrinolysis
• Plays a role in inflammation
• Essential for wound healing
• Concentration increases as severity of periodontitis increases
e. Collagenase:
• Specific granules of PMN’s
• Collagenolytic activity
• Higher concentration in chronically inflamed gingiva
f. Bacterial proteases:
• Bacteria
• Tissue damage
• Positive correlation
g. Serum proteinase inhibitor (α2 macroglobulin and α1 antitrypsin):
• Plasma
• Modulates the activity of proteases in the tissue
• Positive correlation

46. Cellular and Humoral activity of GCF
• Analysis of GCF has identified both cellular and humoral activity in
healthy and diseased conditions.
• Cellular immune response:
 Appearance of cytokines in GCF
 IL-1alpha & 1beta increase binding of PMN’s & monocytes
to the endothelial cells stimulate PG E2 production &
release of Lysosomal enzymes.
 IF-gamma inhibits bone resorption activity of IL-1beta.
• Humoral immune response:
 Antibodies produced against bacteria.
 The consensus is that, in a pt. with periodontal disease, a
reduction in Ab response is detrimental & Ab response plays a
protective role.

47. Method of collection of GCF:

48. Evaluation of Amount of Fluid Collected
a. Appreciation by direct viewing and staining
b. By weighing the strip
c. Use of periotron

49. 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 :
 mastication of coarse foods
 Toothbrushing
 Gingival massage
 Ovulation
 Hormonal contraceptives
 Prosthetic appliances
 Smoking
• Other factors affecting amount of gcf : circadian periodicity &
periodontal therapy

50. 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
Muhlemann,1948: menstrual cycle
Sutcliffe,1972: at puberty
↑ levels of gcf due to
exacerbation of gingivitis.
Gingival fluid flow and sex hormones:

51. 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.
• Suppipat et al. 1997: Did not find any systemic differences
between the flow of fluid measured at 9 a.m. & that of the
fluid collected at 3 p.m.
• Sevim Gunday, 2014: Daytime variations did not have
significant impact on GCF volume and the sampling
methodology had no apparent impact on the circadian
periodicity of GCF.

52. Gingival fluid in diabetic patients:
• Hara et al. 1967: found that the exudate from
diabetic pts contained significantly more glucose than
exudate from healthy subjects
• Ficara et al. 1975: similar conc. of glucose in GCF and
serum in healthy and diabetic subjects
• Ringelberg et al in 1977: higher flow rate of gingival
fluid in diabetic patients were reported when
compared to the flow rate of healthy patients.

53. DRUGS IN GINGIVAL FLUID
Drugs that are excreted through the gingival fluid may be used
advantageously in periodontal therapy.
• Bader and Goldhaber: demonstrated that intravenously
administered tetracycline in dogs rapidly emerges within the
sulcus.
• Gordon JM et al (1981) the concentrations of the tetracycline in
gcf was typically 2-10 times blood levels after a single dose of
oral administration.

54. • Stephen et al (1980) measured the conc. of ampicillin,
cephalexin, tetracycline, erythromycin, clindamycin and
rifampicin in serum, saliva and GCF after a single dose
administration. Except on one occasion, individual GCF
antibiotic conc. were equal to or considerably greater than
those found in saliva.
• Eiserbeng et al 1991: Metronidazole is another antibiotic
that has been detected in human GCF.
• Pin-Chuang Lai et al 2011:Azithromycin concentrations in
GCF were higher and more sustained than those in serum.

55. 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 epithelia.
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.

56. 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: inc 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.

57. 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.
 Degree of keratinization
 Rate of turnover of the cell population

58. 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.

59. 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.

60. 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 - 10 – 12 days
J.E. - 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.

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

62. 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 desmosome lattachments.
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.

63. 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

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

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

66. • 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.
Neutrophils

67. • 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.

68. 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.
• They also produce Interleukin 1, TNF, prostaglandin E2,
matrix metalloproteinases, that diffuse through JE, enter
the gingival connective tissue and initiate the cellular
immune reaction.
• Recruitment of neutrophils into the JE is mediated by
antigen presenting cells (Langerhans cells), and adhesion
molecules secreted by keratinocytes, promoting diapedesis
of neutrophils along the chemical gradient.

69. • Dendritics cells - Modified monocytes belonging to RES.
• 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.
Langerhans cells

70. 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.

71. Fibroblasts:
• Principal cell type of connective tissue.
• Provide structural framework maintains CT integrity.
• Many studies shown that,
fibroblasts senses pathogens & PAMPs’
inflammatory mediators
regulate inflammatory response
• Express functional TLR’s

72. 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:
 toll-like receptors (TLR),
 nucleotide-binding oligomerization domain (NOD)
proteins,
 cluster of differentiation 14 (CD14),
 complement receptor-3,
 lectins and scavenger receptors.

74. Role of nervous system in defense
mechanisms
• The periodontal tissues are innervated by the sensory fibers
of the maxillary and mandibular divisions of the trigeminal
nerve.
• Luthman et al., 1988: Fibers innervating the periodontal
tissues in humans are immunoreactive to a number of
neuropeptides, including SP, CGRP, VIP, and NPY.
• Bartold et al., 1994: SP has been localized by
immunohistochemistry in normal human gingival tissues
perivascularly and within the rete pegs.
• Kvinnsland et al., 2000: Neuroendocrine cells within the
epithelial cell rests of Malassez have been shown to express
SP, CGRP, and VIP.

75. ROLE OF NEUROPEPTIDES IN DEFENSE MECHANISMS

76. 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.
Local inflammatory response

77. Biological sealing and defense mechanisms in
the transmucosal region around dental implants
Takayoshi Yamaza and Mizuho A. Kido. Biological Sealing and Defense Mechanisms in
Peri-Implant Mucosa of Dental Implants. Implant Dentistry – The Most Promising
Discipline of Dentistry.

78. Interface of the transmucosal region of the peri-implant mucosa
PIE:
• Nonkeratinized Stratified sq. ep.
• Permeable in nature
• Allows inward & outward flow of PICF.
• Innermost PIE cells extend short
cytoplasmic processes to the titanium
surface, probably forming a loose
attachment (Ikeda et al., 2000)
• Intracellular endosome/lysosome
systems
• Has rich sensory innervation, along
with release of neuropeptides
• PMN’s penetrate PIE, to prevent peri-
implant inflammation/ disease by
their phagocytotic capacity

79. • 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.
Conclusion

80. REFERENCES
• Eshan Verma, Apurv Jhawar. Defense Mechanisms of
Gingiva. Journal of Orofacial Research, April-June
2014;4(2):111-114
• Defense mechanism of gingiva. Newman Takei, Klokkevold
Carranza. Carranza’s Clinical Periodontology. 12th ed.
• Pathogenesis of periodontitis. Jan Lindhe, Niklaus P.Lang,
Thorlid Karring. Clinical Periodontology and Implant
Dentistry. 5th ed.
• Sembulingam K and Sembulingam P (2010). Essentials of
medical physiology. 5th ed.

81. • Zhimin Feng & Aaron Weinberg. Role Of Bacteria In Health
And Disease Of Periodontal Tissues Periodontology 2000,
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Periodontology 2000, Vol. 31, 2003, 9–11
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biology of the gingiva. Periodontol 2000. 2000 Oct;24:28-55.
• Takayoshi Yamaza and Mizuho A. Kido. Biological Sealing and
Defense Mechanisms in Peri-Implant Mucosa of Dental
Implants. Implant Dentistry – The Most Promising Discipline
of Dentistry.

82. • Beverly Dale. Periodontal epithelium: a newly recognized
role in health and disease. Periodontology 2000, 2002 ,Vol.
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