This document provides a detailed overview of the microscopic anatomy of gingival epithelium. It begins by defining the gingiva and classifying gingival epithelium as either keratinized or non-keratinized. The key layers and cellular features of both keratinized and non-keratinized epithelium are then described in depth, including descriptions of the stratum basale, stratum spinosum, stratum granulosum, stratum corneum, and cell-cell attachments such as desmosomes. The functions and characteristics of gingival epithelium are also summarized.

1. MICROSCOPIC ANATOMY OF GINGIVAL EPITHELIUM

2. CONTENTS
• INTRODUCTION
• CLASSIFICATION
• MICROSCOPIC FEATURES
• STRUCTURAL AND METABOLIC CHARACTERISTICS OF
GINGIVAL EPITHELIUM

3. • FORMATION OF DENTOGINGIVAL JUNCTION
• DEFENCE MECHANISM OF GINGIVAL EPITHELIUM
• RENEWAL OF GINGIVAL EPITHELIUM
• REFERENCES

4. INTRODUCTION
GINGIVA DEFINATION
• The part of oral mucosa that covers the alveolar
processes of jaws and surrounds the neck of the
teeth. [CARRANZA 10th edition].
• It is that part of masticatory mucosa covering alveolar
processes and cervical portions of teeth. [LINDHE 5th
edition].

7. CLASSIFICATION

8. MICROSCOPIC FEATURES
Gingiva is composed of :-
• EPITHELIA L LAYER- Consisting of stratified squamous
epithelium, predominantly cellular in nature.
• CONNECTIVE TISSUE LAYER- Known as lamina propria,
less cellular and composed primarily of collagen fibres
and ground substance.

10. TYPES OF KERATINIZATION

11. orthokeratinized parakeratinized nonkeratinized

12. FUNCTIONS AND FEATURES IN GINGIVAL
EPITHELIUM
Mechanical, chemical , water and microbial barrier signaling functions.
Architectural Integrity
Cell to cell attachment , basal lamina, keratin cytoskeleton
Major Keratinocyte

13. Other Cell Types
Langerhans cells, melanocytes, merkel cells
Constant Renewal
Replacement of damage cells
Cell-cell attachment
Desmosomes, Adherens junctions ,Tight junctions

14. GENERAL ASPECTS OF GINGIVAL EPITHELIUM
BIOLOGY
• Epithelial cells play an active role in innate host defense by
responding to bacteria in an interactive manner, which
means that epithelium participates actively in responding to
infection , in signaling further host reactions and in
integrating innate and acquired immune responses.
• Epithelial cells respond to bacteria by:-
• PROLIFERATION- the alteration of cell signaling events .
• DIFFERENTIATION- the alteration of tissue homeostasis.

15. PROLIFERATION-
• Takes place by mitosis in the basal layer and less frequently
in the suprabasal layers ; where a small proportion of cells
remain as a proliferative compartment while a larger number
begin to migrate to the surface.
• Various cytokines that influence epithelial proliferation are
include epidermal growth factor, keratinocyte growth factor,
interleukin-1, and transforming growth factors α and β.

16. DIFFERENTIATION-
• Differentiation involves the process of keratinization, which
consists of progressions of biochemical and morphologic
events that occur in the cell as they migrate from the basal
layer.
• Differentiation ends with the formation of a keratinized
squama, a dead cell filled with densely packed protein
contained within a toughened cell membrane.
• After reaching the surface it is shed or cast off. This
process of shedding of surface epithelial cells is called
desquamation.

17. The main morphologic changes include the following :
(1) the progressive flattening of the cell with an increasing
prevalence of tonofilaments;
(2) the couple of intercellular junctions with the production of
keratohyalin granules; and
(3) the disappearance of nucleus.

18. (4) cells lose the ability to multiply by mitotic division.
(5) cells loose the cytoplasmic organelles responsible for
protein synthesis and energy production.
(6) cells eventually degenerate into a cornified layer due to
the process of intracellular keratinization.
(7) cells are ultimately sloughed away from the epithelial
surface and into the oral cavity as the cell-cell attachment
mechanisms(i.e. desmosomes and gap junctions) finally
disintegrate.

19. FIG. 1.10 A, Scanning electron micrograph of keratinized gingiva showing the
flattened keratinocytes and their boundaries on the surface of the gingiva
(×1000). B, Scanning electron micrograph of the gingival margin at the edge of
the gingival sulcus showing several keratinocytes about to be exfoliated
(×3000). Source: (From Kaplan GB, Pameijer CH, Ruben MP: J Periodontol
48:446, 1977.

20. KERATINIZED EPITHELIUM

21. STRATUM BASALE
• The basal layer is made up of a single layer of
cuboidal cells.
• The basal cells and the parabasal spinous cells
are referred to as the stratum germinativum but
only the basal cells can divide.
• Basal cells show ribosomes and elements of
rough surfaced endoplasmic reticulum,
indicative of protein synthesizing activity.

22. • The basal cells and the parabasal spinous cells are referred
to as the stratum germinativum but only the basal cells can
divide.

23. FUNCTIONALLY DISTINCT SUBPOPULATIONS :-
1. . One population is serrated and heavily packed with
tonofilaments, which are adaptations for attachment.
The serrated basal cells are a single layer of cuboid or high cuboid
cells that have protoplasmic processes (pedicles) projecting, from
their basal surfaces toward the connective tissue .
2. The other is nonserrated and is composed of slowly cycling stem
cells. The stem cells give rise to slowly dividing cells which serve to
protect the genetic information to the tissue and a large number of
amplifying cells which increase the number of cells for maturation.

24. • Specialized structures called hemi desmosomes, which
abut on the basal lamina, are found on the basal surface.
• They consist of a single attachment plaque, the adjacent
plasma membrane, and an associated extracellular
structure that appears to attach the epithelium to the
connective tissue.
• The lateral borders of adjacent basal cells are closely
apposed and connected by desmosomes .

25. • These are specializations of the cell surface, consisting of
adjacent cell membranes and a pair of denser regions
(attachment plaques) as well as intervening extracellular
structures .
• The basal cells contain tonofilaments, which course
toward, and in some way are attached to the attachment
plaques.

26. • Desmosomes consist of two principal types
of proteins—the transmembranous proteins
and proteins within the cell and related to the
attachment plaque.
• The transmembrane proteins, the
desmogleins and desmocollins, are members
of the cadherin family.
• The desmosomal cadherins are linked to the
keratin cytoskeleton via several cytoplasmic
attachment plaque proteins, including
desmoplakin, plakoglobin (gamma-catenin),
plakophilins, envoplakin and periplakin.

27. • Desmosomal junctions (and hemidesmosomal junctions)
which provide mechanical linkages are frequently seen
amongst oral epithelial cells.
• Gap junctions are low resistance junctions and it allows
electrical and chemical communication; are occasionally
seen. Tight junctions are not observed amongst oral
epithelial cells.

29. STRATUM SPINOSUM
• The spinous cells which make up this layer
are irregularly polyhedral and larger than
the basal cells.
• The spinous (prickle) cells resemble a
cocklebur or sticker that has each spine
ending at a desmosome. of the four layers,
the spinous cells are the most active in
protein synthesis. These cells synthesize
additional proteins that differ from those
made in the basal cells.
.

30. •. On the basis of light microscope, it appears that the cells
are joined by ‘intercellular bridges’ .
•Electron microscopic studies have shown that the
‘intercellular bridges’ are desmosomes and the tonofibrils
are bundles of tonofilaments .
•The tonofilamentsturn or loop adjacent to the attachment
plaques do not cross over into adjacent cells

31. • an agglutinating material joins them to the attachment
plaques.
• The desmosome attachment plaques contain the
polypeptides desmoplakin and plakoglobin.
• The intercellular spaces contain glycoprotein,
glycosaminoglycans, and fibronectin.

32. • The tonofilament network and the desmosomes appear to
make up a tensile supporting system for the epithelium.
• The percentage of cell membrane occupied by
desmosomes is higher in gingiva and palate than in
alveolar mucosa, buccal mucosa, and tongue.
• The spiny appearance of the spinous layer is due to the
shrinkage of cells during tissue preparation causing them
to separate at points where desmosomes do not anchor
them together.

33. STRATUM GRANULOSUM
• This layer contains flatter and wider cells. These cells are
larger than the spinous cells.
• This layer is named for the basophilic keratohyalin
granules (blue staining with hematoxylin and eosin that it
contains.
• This layer still synthesizes protein.
• The nuclei show signs of degeneration and pyknosis.

34. • Tonofilaments are more dense in quantity and are often seen
associated with keratohyalin granules .
• Epidermal and oral keratinocytes express additional
differentiation markers, including filaggrin and trichohyalin,
that associate with the keratin cytoskeleton during terminal
differentiation.

35. • Calcium and retinoids influence epithelial differentiation by
altering the transcription of target genes and by regulating
activity of enzymes critical in epithelial differentiation, such
as transglutaminases, proteinases, and protein kinases.
• In the stratum granulosum the cell surfaces become more
regular and more closely applied to adjacent cell surfaces.

37. • At the same time the lamellar granule, a small organelle
(also known as keratinosome, Odland body or membrane-
coating granule) forms in the upper spinous and granular
cell layers.
• The membrane coating granules are glycolipids.
• It has an internal lamellated structure .

38. • Lamellar granules discharge their contents into the
intercellular space forming an intercellular lamellar material,
which contributes to the permeability barrier.
• This barrier forms at the junction of granular and cornified
cell layers.
• The intercellular space of this region has a lamellar
structure similar to that of the lamellar granule and
contains glycolipid.
• At approximately the same time during differentiation, the
inner unit of the cell membrane thickens, forming the
‘cornified cell envelope.’

39. • Influx of calcium and cell death are said to be the causes
for this formation. Thereafter the thickened membrane
contains sulfur-rich proteins stabilized by covalent
crosslinks. It forms a highly resistant structure.
• . All the genes involved in the expression of the proteins of
the cornified envelope are located in the chromosome Iq21
region and are known as epidermal differential complex.

40. • In nonkeratinizing oral epithelium a small organelle
similar to the lamellar granule forms.
• The granules differ in appearance from keratinized and
nonkeratinized epithelium; in being elongated .
• lamellar in keratinized and circular and amorphous in
nonkeratinized epithelium

41. STRATUM CORNEUM
• The stratum corneum is made up of keratinized squamae,
which are larger and flatter than the granular cells.
Thickness of stratum corneum varies at different sites in
the oral cavity and is thicker than most areas of the skin.
• Here all of the nuclei and other organelles such as
ribosomes and mitochondria have disappeared .
• The layer is acidophilic (red staining with hematoxylin and
eosin) and is histologically amorphous. The keratohyalin
granules have disappeared.

43. • The cells of the stratum corneum are densely packed with
filaments in this nonfibrous interfilamentous matrix protein,
filaggrin (named for its function in filament aggregation).
• Crosslinking of tonofilaments by disulfide bonds facilitates
close packing of the filaments and gives mechanical and
chemical resistance to this layer.

44. NON KERATINIZED EPITHELIUM
• A slight increase in cell size occurs in the intermediate cell
layer, as well as an accumulation of glycogen in cells of the
surface layer.
• On rare occasions, keratohyalin granules can be seen at
this level, but they differ from the granules in keratinized
epithelium and appear as regular spherical structures not
associated with tonofilaments.
• Has niether stratum granulosum nor corneum.
.

46. • The cells appear slightly more flattened than in the
preceding layers and contain dispersed
tonofilaments and nuclei, the number of other cell
organelles having diminished.
• The surface layer of nonkeratinized epithelium thus
consists of cells filled with loosely arranged
filaments that are not dehydrated.
• They thus can form a surface that is flexible and
tolerant of compression and distention.

47. • LAYERS-
1) STRATUM BASALE
2) STRATUM SPINOSUM
3) STRATUM INTERMEDIUM
4) STRATUM SUPERFICIALE
• MAJOR COMPONENT – CYTOKERATINS
• CYTOKERATINS – Have been identified by
immunohistochemistry , Gel electrophoresis and immunoblot
techniques.
• It is a multigene family of proteins.

48. • Moll numbers were assigned to the CK proteins which are
products of 2 gene families and which translate into atleast 20k
polypeptides.
• The product of each CK gene family is divided into:-
1) Basic proteins (52-67KD) NUMBERED 1-8
2) Acidic proteins (40-56KD) NUMBERED 9-20
• The keratin proteins are composed of different polypeptide
subunits characterized by their isoelectric points and molecular
weights.

49. • They are numbered in a sequence that is contrary to their
molecular weight.
• Basal cells begin synthesizing lower-molecular-weight keratins [e.g.,
K19 (40KD)], and they express other higher-molecular-weight
keratins as they migrate to the surface.
• K1 keratin polypeptide (68KD) is the main component of the
stratum corneum.

50. FUNCTIONS-
1) They give mechanical strength to the epithelial sheet.
2) They distribute forces over a wide area.
Other Proteins-Unrelated to keratin are synthesized during the
maturation process.
A) KERATOLININ AND INVOLUCRIN- are precursors of a
chemically resistant structure (the envelope) located below the cell
membrane.
B) FILLAGRIN- has precursors that are packed into the keratohyalin
granules.

51. • Hyperkeratosis of nonkeratinized oral epithelium may be
physiologic but also can be associated with abnormal
cellular changes that eventually lead to cancer of the
squamous epithelium.
• The presence of inflammation in regions such as the
gingiva can reduce the degree of keratinization so that it
appears even parakeratinized or nonkeratinized.

52. CELL–CELLATTACHMENTS

53. • DESMOSOMES- These desmosomes have a typical structure that
consists of two dense attachment plaques into which tonofibrils
insert and an intermediate, electron-dense line in the extracellular
compartment.
• Tonofilaments, which are the morphologic expression of the
cytoskeleton of keratin proteins, radiate in brush-like fashion
from the attachment plaques into the cytoplasm of the cells.
• The space between the cells shows cytoplasmic projections that
resemble microvilli and that extend into the intercellular space
and often interdigitate.

55. • Thus, a desmosome comprises of:-
(1) the outer leaflets (OL) of the cell membranes of two adjoining cells
(2) the thick inner leaflets (IL) of the cell membranes
(3) the attachment plaques (AP), which represent granular and
fibrillar material in the cytoplasm.

56. Ultrastructure
• Symmetric ,consists of 2 apposing dense plagues inside
membranes
• Intercellular Centre- Desmoglea , 30nm
• Thin electron dense midline in center (formed by amino
terminus of desmosomal cadherins)
• Inner dense plaque & outer dense plaque.

57. Biochemical Characterisation
3 Major gene families
Plakins (desmoplakin)
Armadillo proteins (plakoglobins & plakophilins)
Desmosomal cadherins ( desmogleins & desmocollins)
Additional proteins – perp, ninein, kazrin & corneodesmosin

58. Outer dense plaque
• 10-20nm from plasma membrane
• Contains desmosomal cadherins cytoplasmic tails,
plakoglobin,plakophillin,amino terminus of desmoplakin
Inner dense plaque
• 40-50nm from PM
• Carboxy terminus of desmoplakin interacting with KIF

59. DESMOPLAKIN
• Major inner plaque component
• Exists as 1 & 2
• Family includes
BPAG1 , Pectin
plaque proteins of HD envoplakin & periplakin

60. Modular protein
Rod like center
C terminus binds to KF , Amino terminus binds to
plakoglobin
Major link b/w KIF & desmosomal plaque
Also play role in development of epithelium

61. • TONOFILAMENTS( which are morphologic expression of
cytoskeleton of keratin proteins.Radiate in a brush like fashion
from the attachment plagues into the cytoplasm of cells.
• The space between the cells shows cytoplasmic projections
resembling microvilli that extend into the intercellular space and
often interdigitate.

62. TIGHT JUNCTIONS(ZONA OCCLUDENS)-
• Members of adjoining cells are fused.
• Allow ions and small molecules to pass from one cell to another.
• The transmembrane adhesive proteins include
(A) OCCLUDIN
(B) MEMBERS OF CLAUDIN FAMILY
(C) JUNCTIONALADHESION MOLECULE IN SOME TISSUES. THEY
INTERACT HOMOTYPICALLY WITH THE SAME PROTEIN OF THE
ADJACENT CELL.

63. GAP JUNCTION-
• These are plague like regions of the cell membrane where the
intercellular spaces narrows to 2-3nm and transmembrane
proteins of the convexin family form aqueous channels between
the cytoplasm of adjacent cells.
• Six connexin molecules form a connexon , which has a central
channel approaximately 2nm in diameter.
• The connexons in one cell pair with the connexons in the adjacent
cells creating a patent channel.

64. • Gap junction may allow electrical or chemical communication
between the cells and are sometimes called gap junctions.
• Small molecules such as ions and signalling molecules can move
readily from one cell to another.

65. KERATINOSOMES / ODLAND BODIES
• 0.25µM in length and they consist of a series of
lamellae.
• Present in uppermost cells of stratum spinosum.
• Are modified lysosomes.
• Contains a large amount of acid phosphatase- an
enzyme involved in distribution of organelle
membranes which occur suddenly between the
granulosum and corneum strata.Hence its level is
related to the level of keratinization.

66. NON KERATINOCYTES IN ORAL
EPITHELIUM
• Ultra structural and immunochemical studies is that
they represent a variety of cell types,
1. including pigment-producing cells (melanocytes)
2. Langerhans cells,
3. Merkel cells,
4. and inflammatory cells (e.g., lymphocytes), which
together make up as much as 10% of the cell
population in the oral epithelium.

67. MELANOCYTES
• The color of the oral mucosa is the net result of a
number of factors, one of which is pigmentation. The
pigments that most commonly contribute to the color of
the oral mucosa are melanin and hemoglobin.
• Melanin is produced by specialized pigment cells, called
melanocytes, situated in the basal layer of the oral
epithelium.
• Melanocytes arise embryologically from the neural crest
ectoderm and enter the epithelium at about 11 weeks of
gestation.

69. • In the epithelium they divide and maintain themselves as a
self-reproducing population.
•Melanocytes possess long dendritic (branching) processes
that extend between the keratinocytes, often passing through
several layers of cells.

70. • Melanin is synthesized within the melanocytes as small
structures called melanosomes ,which are transferred into
the cytoplasm of adjacent keratinocytes by the dendritic
processes of melanocytes.
• Groups of melanosomes often can be identified under the
light microscope in sections of heavily pigmented tissue
stained with hematoxylin and eosin.
• These groups are referred to as melanin granules. In lightly
pigmented tissues the presence of melanin can be
demonstrated only by specific histologic and histochemical
stains.

71. •Lightly and darkly pigmented individuals have the same
number of melanocytes in any given region of skin or oral
mucosa; color differences result from the relative activity of
the melanocytes in producing melanin and from the rate at
which melanosomes are broken down in the keratinocytes.
In persons with heavy melanin pigmentation, cells containing
melanin may be seen in the connective tissue.
•These cells are probably macrophages that have taken up
melanosomes produced by melanocytes in the epithelium and
sometimes are termed melanophages.

72. •The regions of the oral mucosa where melanin pigmentation is
seen most commonly clinically are the gingiva , buccal mucosa,
hard palate, and tongue.

73. LANGERHANS CELLS
• Another dendritic cell sometimes seen above the basal
layers of epidermis and oral epithelium is Langerhans
cell.
• Langerhans cell is characterized Melanin pigmentation
of the attached gingiva in a dark-skinned individual.
(Courtesy A. Kauzman.
• ultra structurally by a small rod- or flask-shaped
granule, sometimes called the Birbeck granule (after the
person who first described it under the electron
microscope.

75. • The Langerhans cell usually is demonstrated by specific
immunochemical reactions that stain cell surface antigens.
• Langerhans cells appear in the epithelium at the same time
as, or just before, the melanocytes, and they may be
capable of limited division within the epithelium.

76. • Unlike melanocytes, they move in and out of the
epithelium, and their source is the bone marrow.
• Evidence suggests that Langerhans cells have an
immunologic function, recognizing and processing
antigenic material that enters the epithelium from the
external environment and presenting it to T lymphocytes.
• Langerhans cells probably can migrate from epithelium
to regional lymph nodes

77. MERKEL CELLS
• The Merkel cell is situated in the basal layer of the oral
epithelium and epidermis.
• Unlike the melanocyte and Langerhans cell, the Merkel cell
is not dendritic and does possess keratin tonofilaments
and occasional desmosomes linking it to adjacent cells.

78. •As a result, the Merkel cell does not always resemble the
other clear cells in histologic sections.
•The characteristic feature of Merkel cells is the small
membrane-bound vesicles in the cytoplasm, sometimes
situated adjacent to a nerve fiber associated with the cell

80. •These granules may liberate a transmitter substance across
the synapse-like junction between the Merkel cell and the
nerve fiber and thus trigger an impulse.
•This arrangement is in accord with neurophysiologic
evidence suggesting that Merkel cells are sensory and
respond to touch.

81. •The developmental origin of these cells has been a subject
of debate for several decades.
•It was first suggested that they derive either from neural
crest cells or the skin.
•Evidence now confirms that Merkel cells arise from the
differentiation of an epidermal progenitor during embryonic
development

82. INFLAMMATORY CELLS
• When sections of epithelium taken from clinically normal
areas of mucosa are examined microscopically, a number of
inflammatory cells often can be seen in the nucleated cell
layers.
• These cells are transient and do not reproduce themselves
in the epithelium as the other nonkeratinocytes do.
• The most common cell type is the lymphocyte, although the
presence of polymorphonuclear leukocytes and mast cells
is not uncommon.

83. INFLAMMATORY CELLS

84. •Lymphocytes often are associated with Langerhans cells,
which are able to activate T lymphocytes.
•A few inflammatory cells are commonplace in the oral
epithelium and can be regarded as a normal component of
the nonkeratinocyte population.
• Clearly, the association between nonkeratinocytes and
keratinocytes in skin and oral mucosa represents a subtle
and finely balanced interrelationship in which cytokines are
the controlling factors.

85. •Thus keratinocytes produce cytokines that modulate
the function of Langerhans cells. In turn, the Langerhans
cells produce cytokines such as interleukin-1, which can
activate T lymphocytes so that they are capable of
responding to antigenic challenge.

86. ORAL EPITHELIUM
• The oral or outer epithelium covers the crest and outer surface of
the marginal gingiva and the surface of the attached gingiva.
• On average, the oral epithelium is 0.2–0.3 mm in thickness.

87. •It is keratinized or parakeratinized, or it may present various
combinations of these conditions .
•The prevalent surface, however, is parakeratinized.
•The oral epithelium is composed of four layers: stratum basale
(basal layer), stratum spinosum (prickle cell layer), stratum
granulosum (granular layer), and stratum corneum (cornified
layer).

88. SULCULAR EPITHELIUM
• The sulcular epithelium lines the gingival
sulcus.
• It is a thin, nonkeratinized stratified squamous
epithelium without rete pegs, and it extends
from the coronal limit of the junctional
epithelium to the crest of the gingival margin .
• It usually shows many cells with hydropic
degeneration.

89. •As with other nonkeratinized epithelia, the sulcular
epithelium lacks granulosum and corneum strata and K1,
K2, and K10 through K12 cytokeratins, but it contains K4
and K13, the so-called “esophageal-type cytokeratins.”
•It also expresses K19, and it normally does not contain
Merkel cells.

90. • Glucose6-phosphate dehydrogenase expresses a faint
and homogeneous reaction in all strata, unlike the
increasing gradient toward the surface observed in
cornified epithelia.
• Acid phosphatase staining is negative although
lysosomes have been described in exfoliated cells.
• Despite these morphologic and chemical characteristics,
the sulcular epithelium has the potential to keratinize if it
is reflected and exposed to the oral cavity or if the
bacterial flora of the sulcus is totally eliminated.
.

91. • The sulcular epithelium may act as a semipermeable
membrane through which injurious bacterial products
pass into the gingiva and through which tissue fluid from
the gingiva seeps into the sulcus.
• The sulcular epithelium is not heavily infiltrated by
polymorphonuclear neutrophil leukocytes, and it appears
to be less permeable.

92. JUNCTIONAL EPITHELIUM
• The junctional epithelium consists of a collar-like
band of stratified squamous nonkeratinizing
epithelium. It is 3–4 layers thick in early life, but
the number of layers increases with age to 10 or
even 20 layers.
• The junctional epithelium tapers from its coronal
end, which may be 10–29 cells wide to 1–2 cells
wide at its apical termination, which is located at
the cementoenamel junction in healthy tissue.

93. •These cells can be grouped in two strata: the basal layer
that faces the connective tissue and the suprabasal layer
that extends to the tooth surface.
• The length of the junctional epithelium ranges from 0.25 to
1.35 mm.
•The junctional epithelium is formed by the confluence of the
oral epithelium and the reduced enamel epithelium during
tooth eruption.

94. • Cell layers that are not juxtaposed to the tooth exhibit
numerous free ribosomes, prominent membrane-bound
structures (e.g., Golgi complexes), and cytoplasmic
vacuoles that are presumably phagocytic.
• Lysosome-like bodies also are present, but the absence
of keratinosomes (Odland bodies) and histochemically
demonstrable acid phosphatase, which are correlated
with the low degree of differentiation, may reflect a low-
defense power against microbial plaque accumulation in
the gingival sulcus.

96. • Research has shown that, although numerous migrating
polymorphonuclear neutrophil leukocytes are evident
and present around healthy junctional epithelium, a
considerable increase in polymorphonuclear neutrophil
leukocyte numbers can be expected with the
accumulation of dental plaque and gingival
inflammation.

97. • The different keratin polypeptides of the junctional
epithelium have a particular histochemical pattern.
Junctional epithelium expresses K19, which is absent
from keratinized epithelia, and the stratification specific
cytokeratins K5 and K14.
• Morgan et al reported that reactions to demonstrate K4
or K13 reveal a sudden change between sulcular and
junctional epithelia; the junctional area is the only
stratified nonkeratinized epithelium in the oral cavity
that does not synthesize these specific polypeptides.

98. • Another particular behavior of junctional epithelium is
the lack of expression of K6 and K16, which is usually
linked to highly proliferative epithelia, although the
turnover of the cells is very high.
• Junctional epithelium exhibits lower glycolytic enzyme
activity than outer epithelium, and it also lacks acid
phosphatase activity.

99. • The junctional epithelium is attached to the tooth
surface (epithelia attachment) by means of an internal
basal lamina.
• It is attached to the gingival connective tissue by an
external basal lamina that has the same structure as
other epithelial–connective tissue attachments
elsewhere in the body.

100. • The internal basal lamina consists of a lamina densa
(adjacent to the enamel) and a lamina lucida to which
hemi desmosomes are attached.
• Hemi desmosomes have a decisive role in the firm
attachment of the cells to the internal basal lamina on the
tooth surface.
• Hemi desmosomes may also act as specific sites of
signal transduction and thus may participate in the
regulation of gene expression, cell proliferation, and cell
differentiation.

101. • The junctional epithelium attaches to afibrillar cementum
that is present on the crown (usually restricted to an area
within 1 mm of the cementoenamel junction) and root
cementum in a similar manner.
• Three zones have been described in the junctional
epithelium: apical, middle, and coronal.

102. • The apical zone shows cells with germinative
characteristics, the middle zone is of major
adhesiveness, and the coronal zone is one of greater
permeability.
• Data also have shown that the basal lamina of the
junctional epithelium resembles that of endothelial and
epithelial cells in its laminin content but differs in its
internal basal lamina, which has no type IV collagen.
• These findings indicate that the cells of the junctional
epithelium are involved in the production of laminin and
play a key role in the adhesion mechanism.

103. • The attachment of the junctional epithelium to the tooth is
reinforced by the gingival fibers, which brace the marginal
gingiva against the tooth surface.
• For this reason, the junctional epithelium and the gingival
fibers are considered together as a functional unit referred
to as the dentogingival unit.
• In conclusion, it is usually accepted that the junctional
epithelium exhibits several unique structural and
functional features that contribute to preventing
pathogenic bacterial flora from colonizing the sub gingival
tooth surface.

104. • First, junctional epithelium is firmly attached to the tooth
surface, thereby forming an epithelial barrier against plaque
bacteria.
• Second, it allows access of gingival fluid, inflammatory cells,
and components of the immunologic host defense to the
gingival margin.
• Third, junctional epithelial cells exhibit rapid turnover, which
contributes to the host–parasite equilibrium and the rapid
repair of damaged tissue.

105. DEFENSE MECHANISIM OF GINGIVA
• Gingival and JE cell desquamation and a rapid transit
time.
• Excellent vascularization and comparatively high turnover
rate of connective tissue compartment
• Systemic and local immune responses against the
bacterial products that penetrate JE.
• Mobilization of large number of polymorphonuclear
leukocytes , especially neutrophils. They phagocytose and
kill a variety of microorganisms.
• (PERIODONTICS - GRANT ,LISTGARTEN).

106. RENEWAL OF GINGIVAL EPITHELIUM
• The oral epithelium undergoes continuous renewal. Its
thickness is maintained by a balance between new cell
formation in the basal and spinous layers and the
shedding of old cells at the surface.
• THE MITOTIC RATE-Exhibits a 24-hr periodicity with the
highest and lowest rates occuring in the morning and
evening respectively.
• The mitotic rate is higher in non-keratinized areas.
• Is increased in gingivitis.
• No significant gender differences.

107. • Opinions differ as to whether it increases or decreases
with age.
• ORDER:-
BUCCAL MUCOSA> HARD PALATE>SULCULAR
EPITHELIUM>JE>OUTER SURFACE OF MARGINAL
GINGIVA>ATTACHED GINGIVA
• TURNOVER TIMES:-
PALATE,TONGUE,CHEEK-5 TO 6 DAYS.
GINGIVA-10 TO 12 DAYS(WITH SAME OR MORE TIME
REDUCED WITH AGE).
JE-1 TO 6 DAYS.

108. FACTORS AFFECTING EPITHELIAL TURNOVER:-
• SYSTEMIC HORMONES – Oestrogen stimulates it.
Corticosteroids inhibit it.
• GROWTH FACTORS:-
Epidermal growth factor(EGF),Transforming growth factor A
(TGF-A) – Stimulate it.
TGF – B – Inhibits it.
Mechanical stimulation ,mild irritation and inflammation
increase it.
Hypoglycemia and nutriotional deficiencies decrease the
mitotic rate.(Manson,Eley 4th edition).

109. • The term cuticle describes a thin, acellular structure with a
homogenous matrix, sometimes enclosed within clearly
demarcated linear borders.
• LISTGARTEN has classified cuticular structures into:-
1. ACQUIRED/POST-ERUPTIVE /SECONDARY COATINGS –
Include those of exogenous origin such as saliva, bacteria,
calculus and surface stains.
o Also produced by adsorption of dietary, microbial and
hematogenous materials to tooth surface and possibly to
calculus. (RAMJFORD 1ST EDITION)

110. 2. DEVELOPMENTAL/PRE- ERUPTIVE /PRIMARY COATINGS- Are those
formed as part of tooth development.
INCLUDE:-
A) REDUCED ENAMEL EPITHELIUM-
After enamel formation is complete, the ameloblastic epithelium is reduced to
1 or 2 layers of cells that remain attached to the enamel surface by
hemidesmoses and a basal lamina. This reconsist of postsecretory
ameloblasts and cells from the stratum intermedium of the enamel organ.

111. (B)CORONAL CEMENTUM- In some animals, the REE disappears entirely
and very rapidly.
Thereby placing the enamel surface in contact with the connective
tissue.
• Connective tissue cells then deposit a layer of cementum known as
coronal cementum on the enamel.
• In humans ,thin patches of afibrilar cementum may be seen
sometimes in the cervical half of the crown.

112. C)DENTAL CUTICLE – Seen on electron microscopy.
• Consists of a layer of homogenous organic material of variable
thickness (Approximately 0.25µm) overlying the enamel surface.
• It is not always present.
• In some case near the CEJ , It is deposited over a layer of
afibrillar cementum which in turn overlies enamel.
• It may be present between the JE and the tooth.
• Ultra structural histochemical studies have shown it to be
proteinaceous in nature, and it may be an accumulation of tissue
fluid components.

113. LISTGARTEN has described two types of cuticular
deposits:-
1)TYPE A CUTICLE - Found on both erupted and
unerupted teeth.
• Has a granular matrix with appositional lines.
• Usually restricted to the cervical area around the CEJ.
• 1-5µM thick.
• Mineralized.
• Thought to be a form of afibrillar ,acellular cementum.

114. 2)TYPE B CUTICLE- Found only in erupted teeth.
• Located between the enamel (or TYPE A CUTICLE) And
internal basal lamina of JE.
• Has no appositional lines.
• Does not mineralize.
• Formed by precipitation of tissue fluid proteins on the
enamel and/or cementum surface.
(ORAL CELLS & TISSUS – P.R.GARANT)

115. REFERENCES
• CLINICAL PERIODONTOLOGY - CARRANZA (9TH,10TH
EDITIONS)
• CLINICAL PERIODONTOLOGY & IMPLANTOLOGY - JAN
LINDHE (4TH ,5TH EDITIONS)
• ORAL HISTOLOGY – TENCATE (7TH EDITION)
• ORAL HISTOLOGY – ORBAN’S (12TH EDITION)

116. •CLINICAL PRIODONTOLOGY – MANSON & ELEY (4TH
EDITION)
•CLINICAL PERIODONTOLOGY – GENCO , GOLDMAN,
COHEN (1990)
•PERIODONTICS – GRANT,STERN,LISTGARTEN(6TH
EDITION)