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1. Junctional epithelium
The junctional epithelium (JE) is that epithelium which
lies at, and in health also defines, the base of the gingival
sulcus. The probing depth of the gingival sulcus is mea-
sured by a calibrated periodontal probe. In a healthy-case
scenario, the probe is gently inserted, slides by the sulcu-
lar epithelium (SE), and is stopped by the epithelial at-
tachment (EA). However, the probing depth of the gin-
gival sulcus may be considerably different from the true
histological gingival sulcus depth.
1 Location
The junctional epithelium, a nonkeratinized stratified
squamous epithelium,[1]
lies immediately apical to the
sulcular epithelium, which lines the gingival sulcus from
the base to the free gingival margin, where it interfaces
with the epithelium of the oral cavity.The gingival sul-
cus is bounded by the enamel of the crown of the tooth
and the sulcular epithelium. Immediately apical to the
base of the pocket, and coronal to the most coronal of
the gingival fibers is the junctional epithelium. The JE
attaches to the surface of the tooth by way of the EA with
hemidesmosomes and is, on average, roughly 1 mm in
width in the apico-coronal dimension, constituting about
one half of the biologic width.[2]
The attachment of the
JE to the tooth surface can occur on enamel, cementum,
or dentin. The position of the EA on the tooth surface
is initially on the cervical half of the anatomical crown
when the tooth first becomes functional after tooth erup-
tion.[3][4]
2 Origin
Junctional epithelium is derived from the reduced enamel
epithelium (REE) during tooth development.[5]
Before
the eruption of the tooth and after enamel maturation, the
ameloblasts secrete a basal lamina on the tooth surface
that serves as a part of the primary EA. As the tooth ac-
tively erupts, the coronal part of the fused and surround-
ing epithelium peels back off the crown. The ameloblasts
also develop hemidesmosomes for the primary EA and
become firmly attached to the enamel surface. However,
the cervical part of the fused tissue remains attached to
the neck of the tooth by the primary EA. This fused
tissue, which remains near the cementoenamel junction
(CEJ) after the tooth erupts, serves as the initial JE of
the tooth, creating the first tissue attached to the tooth
surface. This tissue is later replaced by a definitive JE as
the root is formed.[3]
3 Structure
Cells in the junctional epithelium tend to have wide in-
tercellular spaces and fewer desmosomal junctions, to al-
low the transmission of white blood cells (WBCs) from
lamina propria’s blood vessels to the bottom of the gin-
gival sulcus, to help prevent disease. In addition, the JE
is also thinner than the sulcular epithelium, ranging coro-
nally from only 15 to 30 cells thick at the floor of the
gingival sulcus, and then tapering to a final thickness of 3
to 4 cells at its apical part. The superficial, or suprabasal,
cells of the JE serve as part of the EA of the gingiva to
the tooth surface. These superficial, or suprabasal, ep-
ithelial cells of the JE provide the hemidesmosomes and
an internal basal lamina that create the EA, because this
is a cell-to-noncellular type of intercellular junction. The
structure of the EA is similar to that of the junction be-
tween the epithelium and subadjacent connective tissue;
the internal basal lamina consists of a lamina lucida and
lamina densa.[5]
This internal basal lamina of the EA is continuous with
the external basal lamina between the junctional epithe-
lium and the lamina propria at the apical extent of the JE.
The EA is very strong in a healthy state, acting as a type
of seal between the soft gingival tissue and the hard tooth
surface. The deepest layer of the JE, or basal layer, un-
dergoes constant and rapid cell division, or mitosis. This
process allows a constant coronal migration as the cells
die and are shed into the gingival sulcus. The few layers
present in the JE — from its basal layer to the suprabasal,
or superficial, layer — does not show any change in cel-
lular appearance related to maturation, unlike other types
of gingival tissue. Thus, the JE does not mature like ker-
atinized tissue, such as the marginal gingiva or attached
gingiva, which fills its matured superficial cells with ker-
atin.
Nor does JE mature on a lesser level like nonkeratinized
tissue of the sulcular gingiva and throughout the rest of
the oral cavity, which enlarges its cells as they mature
and migrate superficially. The JE cells do not mature and
form into a granular layer or intermediate layer. Without
a keratinizing superficial layer at the free surface of the
JE, there is no physical barrier to microbial attack. Other
structural and functional characteristics of the JE must
compensate for the absence of this barrier. The JE ful-
1

2. 2 6 REFERENCES
fills this difficult task with its special structural framework
and the collaboration of its epithelial and nonepithelial
cells that provide very potent antimicrobial mechanisms,
such as the white blood cells. However, these defense
mechanisms do not preclude the development of exten-
sive inflammatory lesions in the gingival tissue, and, occa-
sionally, the inflammatory lesion may eventually progress
to the loss of bone and the connective tissue attachment
to the tooth.[6]
The JE cells have many organelles in their cytoplasm,
such as rough endoplasmic reticulum, Golgi complex, and
mitochondria, indicating a high metabolic activity. How-
ever, the JE cells remain immature or undifferentiated
until they die and are shed or lost in the gingival sulcus.
Lysosomes are also found in large numbers in JE epithe-
lial cells; enzymes contained within these lysosomes par-
ticipate in the destruction of bacteria contained in dental
biofilm.[3]
4 Pathology
The increased permeability of the JE that allows emigra-
tion of the PMN type of WBC also allows microorgan-
isms from the dental biofilm (especially noted is P. gingi-
valis, and associated toxins from the exposed tooth sur-
face, to enter this tissue from the deeper lamina propria,
setting up the possibility of infection to occur.[7]
Damage
to the junctional epithelium results in it being irregular in
texture, rather than smooth, at its surface. Most impor-
tantly is the formation of pocket epithelium within the
periodontal pocket, which is a histopathological charac-
teristic of periodontal disease, having the true apical mi-
gration of the EA.[8][9]
In addition, there is the presence
of ulceration with gingival hyperplasia, including the for-
mation of rete ridges and connective tissue papillae at the
one smooth interface of the JE with the lamina propria.
Further, there is increased levels of exfoliation of epithe-
lial cells, WBC migration, and bacterial internalization,
as well as internalization-induced programmed epithelial
cell death.[10]
5 See also
• Oral mucosa
• Periodontal disease
6 References
This article incorporates text in the public domain from the
20th edition of Gray’s Anatomy (1918)
[1] AAP 2010 In-Service Exam, question A-20
[2] Carranza’s Clinical Periodontology, 9th Ed. W.B. Saun-
ders, 2002, page 23.
[3] Illustrated Dental Embryology, Histology, and Anatomy,
Bath-Balogh and Fehrenbach, Elsevier, 2011, page 127
[4] Ten Cate’s Oral Histology, Nanci, Elsevier, 2013, page
351
[5] Masaki Shimono; et al. (2003). “Biological character-
istics of the junctional epithelium”. J Electron Microsc
(Tokyo) 52 (6): 627–639.
[6] Max A. Listgarten, University of Pennsylvania and Tem-
ple University at http://www.dental.pitt.edu/informatics/
periohistology/en/gu0205.htm
[7] Porphyromonas gingivalis invades human pocket epithe-
lium in vitro Sandros,J. et al, Journal of Periodontal Re-
search, Volume 29, Issue 1, pages 62–69, 1994
[8] Bosshardt DD, Lang NP. The junctional epithelium: from
health to disease. J Dent Res. 2005 Jan;84(1):9-20.
[9] Nanci and Bosshardt, Structure of periodontal tissues
in health and disease. Periodontology 2000, Vol. 40,
2006, 11–28 at http://www.nancicalcifiedtissuegroup.
com/documents/Nanci%202006.pdf
[10] Vitkov L, Krautgartner WD, Hannig M. Surface morphol-
ogy of pocket epithelium. Ultrastruct Pathol. 2005 Mar-
Apr;29(2):121-7.

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