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Expression of blood group-related glycoconjugates in the junctional and other oral epithelia of rodents.

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THE ANATOMICAL RECORD 241:310-318 (1995)
Expression of Blood Group-Related Glycoconjugates in the
Junctional and Other Oral Epithelia of Rodents
Dental Branch, University of Texas Houston Health Science Center, Houston, Texas
(I.C.M., G.R.); School of Dentistry, University of Copenhagen, Copenhagen, Denmark
(E.D., L.J.); Department of Oral Anatomy, Fukuoka Dental College, Fukuoka,
Japan (H.T.)
Background: The junctional epithelium (JE) attaches the
gingiva to the non-vital tooth surface and has other unusual properties
which protect the underlying periodontal tissues. The J E differs from other
gingival and oral epithelia in its unusual expression of cytokeratins typical
of both stratifying and of simple epithelia, a phenotypic pattern possibly
related to its specialized functions.
Methods: The patterns of differentiation of rodent gingival and other
epithelia were examined using monoclonal antibodies against various glycoconjugates which are expressed on epithelial cell surfaces and provide
an alternative marker system for regionally-differing patterns of cell maturation.
Results: Markers that are typical of basal cells in other stratifying epithelia were expressed by all cell strata of JE. J E lacked differentiation
markers typical of other stratifying oral epithelia but showed suprabasal
expression of markers typically expressed by simple epithelia and specialized epithelia, such as taste buds.
Conclusions: The phenotype of rodent J E differs from that of other oral
epithelia and the pattern of differentiation assessed by its expression of
glycoconjugates parallels that for other phenotypic markers, such as cytokeratins. Differentiation of rodent J E is similar to that of human JE. The
functional significance of these patterns of expression is not yet clear but
the markers characterizing this unusual epithelium in rodents may be associated with its behavior in periodontal disease and of value to experimental studies of its development. o 1995 Wiley-Liss, Inc.
Key words: Gingiva, Junctional epithelium, Rodents, Mucosa, Differentiation, Blood group antigens
Oral mucosal epithelia show a regional diversity of
structure that is presumably related to regional differences in function (Meyer et al., 1984).A unique feature
of the oral mucosa is its perforation by teeth, and the
patterns of organization of the gingival epithelia are
particularly interesting because of their post-natal development during tooth eruption and their unusual relationship to the tooth. Ultrastructurally, the epithelia
of the human gingival region have been classified as (a)
the junctional epithelium (JE) which extends coronally
from the region of the cemento-enamel junction, (b) the
oral sulcular epithelium (OSE) which is continuous
with the junctional epithelium and extends coronally
from it to the region of the gingival crest, and (c) the
oral gingival epithelium (OGE) which covers the oral
surface of the gingiva from the gingival crest to the
muco-gingival junction (Schroeder and Listgarten,
1977). The function of the gingiva is to provide a seal
between the mineralized tooth surface and the surrounding soft tissues, and histological and ultrastruc0 1995 WILEY-LISS, INC
tural studies indicate that the J E is a highly unusual
epithelium that attaches to the non-vital calcified surface of the tooth and lacks the patterns of differentiation typical of other oral epithelia (Schroeder and
Listgarten, 1977; Marks et al., 1994). The gingiva of
rodents is similar to human gingiva in its pattern of
organization into three distinct epithelial regions (Listgarten, 1975). Rodent J E is also ultrastructurally characterized by its lack of overt patterns of differentiation
(Yamasaki et al., 1979; Shimono et al., 1989; Takata et
al., 1986), the formation of specialized attachment to
the tooth (Hormia et al., 1992; Sawada et al., 1990),
and regeneration after its experimental removal
(Schroeder and Listgarten, 1977; Takata et al., 1986).
Received May 31, 1994; accepted August 8, 1994.
Address reprint requests to Ian C. Mackenzie, Dental Branch, University of Texas Houston Health Science Center, 6516 John Freeman
Avenue, Houston, TX 77030-3402.
Stratified squamous epithelia are continuously renewed by cell proliferation with the molecular markers
that characterize regionally-specific patterns of differentiation being typically expressed when newly formed
cells emigrate from the basal into the suprabasal strata
(Purkis et al., 1990; Dabelsteen et al., 1991). Such expression can be demonstrated by staining with antibodies directed against cell differentiation products, such
as cytokeratins or cell surface carbohydrates, and the
expression of these markers provides a measure both of
the regionally-differing phenotypes of oral epithelia,
and of the stage of differentiation of particular cells
within a n epithelium (Morgan et al., 1987; Purkis et
al., 1990; Dabelsteen et al., 1991). Some differentiation
products are common to the three human gingival epithelia but each epithelial region also expresses some
markers that are absent from the other regions (Morgan, 1987; Steffensen e t al., 1987; Mackenzie et al.,
1989; Mackenzie et al., 1991). The J E is thus not simply a n undifferentiated epithelium (Schroeder and
Listgarten, 1977): evidence for its unusual pattern of
cell maturation is found in the suprabasal expression of
some keratins and cell surface carbohydrates absent
from other gingival epithelia (Mackenzie et al., 1989;
Mackenzie et al., 1991).
Although structural studies indicate that there is a
similar pattern of gingival organization in other mammals (Marks et al., 1994), the expression of differentiation markers has not been extensively investigated in
non-human species. Lectin binding studies (Takata e t
al., 1990) indicate that rodent J E lacks the suprabasal
binding of lectins that characterize differentiation in
the other gingival epithelia, but that there are differences in the lectin binding properties of basal and suprabasal J E cells indicative of some type of differentiation process. Rodent J E also appears similar to human
J E in its suprabasal expression of some cytokeratins
typically expressed only in simple epithelia (Mackenzie, 1989a, b).
Cell surface glycoconjugates of the ABH series of antigens, are expressed on oral epithelial cells (Dabelsteen et al,. 1992), and staining with monoclonal antibodies (mAbs) with known specificities for human
carbohydrate epitopes indicates that the pattern of expression of cell surface carbohydrates is consistently
related both to the region of origin and the stage of
differentiation of human epithelia (Mandel et al.,
1992). Rodents are useful for experimental studies of
the development and function of the dento-gingival region (Altman et al., 1987; Hemmerle and Frank, 1991;
Hewage and Heany, 1990; Sashima e t al., 1991) and
phenotypic markers that would permit more detailed
studies of developmental and pathological changes of
the gingival epithelia would be of value. The patterns
of expression of cell surface carbohydrates in rodent
gingiva were therefore examined for comparison with
(a)those for various other rodent epithelia and (b) with
the patterns reported for human gingiva.
were sectioned through the molar region in the frontal
plane to provide a range of oral and other epithelia for
examination. Tissues were fixed in buffered 4% formaldehyde prior to brief decalcification in 1% SSFA,
dehydrated in graded alcohols, passed through xylene,
and wax embedded. Sections were cut a t 6 pm,
mounted on gelatine-subbed slides, and hydrated prior
to staining.
In preliminary work, a wide range of mAbs was
tested for binding to murine tissues. The mAbs used in
this study were selected for their differential staining
of gingival epithelia and are listed in Table 1. These
mAbs have defined specificities for various carbohydrate determinants associated with human Type I1 or
Type I11 chain peripheral cores; information about
their origins and specificities, and about the staining
methods that were used, have been given in detail in
previous publications (Dabelsteen and Clausen, 1992;
Dabelsteen et al., 1991; Mackenzie et al., 1989; Gao et
al., 1989).In brief, mAbs were applied to sections as the
undiluted supernatant and were incubated overnight
at 4°C. After three washes in phosphate buffered saline, pH7.4, sections were incubated with a 1:lOO dilution of polyclonal rabbit antibodies directed against
murine immunoglobulins and conjugated to f luorescein isothiocyanate, alkaline phosphatase, or peroxidase (DAKO). To unmask antigenic determinants
blocked by sialic acid, some sections of each specimen
were incubated in neuraminidase (Sigma, Type 11)
prior to staining. Fluorescent specimens were examined by epi-illumination with appropriate barrier filters. Specimens for histochemical demonstration of
mAb binding were processed to display enzyme activity, as previously described (Mackenzie et al., 1989;
Mackenzie et al., 1991), and examined by transmitted
light. Controls for staining specificity consisted of (a)
omission of the primary antibody (b) staining with irrelevant primary antibodies of similar isotypes, and (c)
comparison of regional binding differences between different antibodies. For each strain or species at least
five different gingival samples were stained with each
primary antibody: most specimens were stained using
both fluorescent and histochemical methods for demonstrating mAb binding.
For each of the mAbs used, the staining methods
provided relatively clear binding patterns with little
non-specific background staining. The strongest binding was typically to the cell surface region of epithelial
cells and, occasionally, to vascular elements within the
connective tissue. Some mAbs showed relatively strong
binding to material on the epithelial surface, possibly
blood or salivary proteins, and most showed binding to
remnants of enamel matrix when present. Essentially
similar staining patterns were observed for both the
Balb/C and the C3H mice and, except where noted, the
following description applies equally to both strains.
Murine Gingival Epithelia
Specimens were collected from young adult C3H/Fej
or Balb/C mice, and from Sprague-Dawley rats. Gingival tissues were dissected from the jaws en bloc together with the molar teeth and the adjacent alveolar
bone. Some mouse heads were examined whole and
The mAbs against Type I1 chain determinants
showed epithelial binding patterns that varied both regionally and with cell maturation (Table 1).The mAbs
against Lewis antigens X and Y (Le", Ley) both consistently bound to a subpopulation of cells in the J E and,
TABLE 1. Summary of staining data for junctional (JE), oral sulcular (OSE), oral gingival (OGE), palatal (PI,
buccal (B) and simple (S) epithelia and taste buds (TB). Staining is indicated as absent (-) or basally (B),
parabasally (PB) or suprabasally (SB) located in each epithelium. Staining for simple epithelium and taste buds
is recorded only as either present ( + ) or absent (-1. The data shown are for C3H mice. Some small differences
between C3H and Balb/C mice were noted and are discussed in the text. The pattern for the rat was essentially
similar to that for mice but some differences were noted and are discussed in the text.
Type I1 Chain
Type I11 Chain
1B2( + N)
HH8( + N)
in most sections, binding could be clearly localized to
the upper part of the J E in the region where i t abutted
the stratum corneum of the OSE (Fig. lA,B). Usually,
staining for Ley was stronger and more extensive than
that for Le”. In some sections there appeared to be
weak binding to a few suprabasal cells in the deeper
(most apical part) of the OSE and, occasionally, weak
staining of granular cells of the OGE was present (Fig.
1A). Typically, however, there was no staining of either
the OSE or the OGE. Some structures in the sub-gingival connective tissue were occasionally stained (Fig.
lA,B) but i t was difficult to determine whether these
were vascular elements or epithelial rests.
The mAb against N-acetyl-lactosamine (Lac) showed
moderate binding to the area of J E that stained for Le”
and Ley (Fig. 1C). Staining after treatment with
neuraminidase indicated that sialated N-acetyl-lactosamine (Sa-Lac) was present in all epithelial regions.
In the OSE and OGE there was weak staining restricted mainly to cells of the parabasal regions, but
the J E showed weak binding to basal cells and strong
binding to suprabasal cells (Fig. 1D). The antibody
against BGA “B” showed a similar pattern of binding
to the full thickness of the J E and restriction to the
basal and parabasal cells of other epithelia (Fig. 1E).
Staining for Type I1 chain “H” was present at the cell
surfaces of suprabasal cells of the OSE and OGE but
was absent from J E (Fig. 1F).
Epithelial staining for Type I11 chain determinants
similarly differed with anatomical region and degree of
maturation. Weak staining for Tn antigen was occasionally present on the basal and parabasal cells of
OSE and OGE but was usually restricted to the region
of the J E that stained for Le” and Ley (Fig. 1G).
Sialated Tn (Sa-Tn) was present on all suprabasal cells
of the OSE and OGE but was absent from the J E except
for weak staining of the most coronal portion (Fig. 1H).
Staining for unsialated (T) and sialated T-antigen
(Sa-T) was present on basal and parabasal cells of the
OSE and OGE. Staining for both forms was present on
all strata of the J E but was strongest on basal cells.
Staining for Type I1 chain “H” was present on the su-
prabasal cells of OSE and OGE but was absent from the
J E.
Other Murine Epithelia
The buccal and palatal epithelia of C3H mice showed
patterns of glycoconjugate expression that were essentially similar to those of OSE and OGE. No major differences were noted between these epithelia except
that palatal and oral gingival epithelia differed consistently from buccal and oral sulcular epithelia in the
level of transition of staining from “basal” to “suprabasal” markers. The former epithelia, as in the rat (see
below), showed this transition at a higher level in the
epithelium. Balb/C mice differed from C3H mice (Fig.
11) in lacking expression of Type I11 chain “H” in the
buccal epithelium.
The epithelium of the dorsal surface of the tongue
showed binding patterns that varied in relation to the
structure of the filiform papillae: the interpapillary regions and the posterior cell columns of the papillae
showed patterns essentially similar to buccal and palatal epithelia, respectively. However, the suprabasal
cells of the anterior column of the papillae differed
from the other regions in its positive staining for T, Tn,
and Le” (Fig. 2B). In Balb/C, but not C3H mice, this
region also stained for Ley.
The simple epithelia lining the ducts of glands and
the nasal surface of the palate showed markedly different staining patterns from the stratifying epithelia lining the oral cavity. Typically, they showed strong
staining for Lac, Sa-Lac, Le” (Fig. 2A), Ley, T, and Tn
antigens. Weaker staining was seen for Lewis antigens
A and B (Lea, Leb) and B antigen but there was no
staining for Type I1 or I11 chain H, or sialated Tn antigens. The staining of these epithelia was usually
fairly uniform but some mAbs, such as those against
Ley and Lex, stained subpopulations of cells (Fig. 2A).
C3H mice lacked the staining for B antigen seen in a
subpopulation of basally-positioned cells in the simple
epithelia of Balb/C mice. Taste buds showed a pattern
of staining for Type I1 chain determinants that was
more similar to simple and junctional epithelia than to
Fig. 1. (A-H) Sections of the murine gingiva buccal to the first
molar tooth and of the mucogingival region (I) stained with mAbs
against various determinants of the ABO blood group antigen series.
For orientation, the position occupied by the enamel of the tooth
crown prior to decalcification is marked (E) on each figure. (A) Staining for Ley is restricted mainly to the upper part of the J E facing the
OSE. A few suprabasal cells in the deeper part of the OSE often
showed some staining (arrow) and, occasionally, there was weak
staining of stratum granulosum cells in the OGE. Some cell clusters
(*) in the connective tissue, possibly vascular elements, were also
stained, as were remnants of the decalcified enamel matrix. (B) The
pattern of staining for Le” was similar to that for Ley but more restricted to the upper part of the J E and absent from the OGE. (C)
Staining for Lac was similarly restricted to the upper part of the J E .
The plane of the section shown passes obliquely through the J E and
thus shows staining of a wider band of cells. (D)After neuraminidase
treatment, more extensive staining for Lac is seen. There is weak
staining of parabasal cells in OGE and OSE weak basal and strong
suprabasal staining of the JE. (E) Moderately strong staining for
BGA “B’ was seen in the basal and parabasal cells of the OGE with
weaker staining of the OSE. The full thickness of the J E is stained
with the strongest staining seen in the coronal region. (F)Staining for
Type I1 chain “ H is restricted to suprabasal cells in the OGE and
OSE. (GI Staining for Tn is similarly restricted to the upper part of
the J E with a pattern similar to that for Le“ and Ley. (H) Staining for
sialated-Tn shows a similar but more extended pattern of suprabasal
staining of OGE and OSE than for “H” (F).(I) BalbiC differed from
C3H mice in the lack staining of the buccal epithelium for Type I1
Chain “ H . This section, through the region of mucogingival junction
(arrow), shows suprabasal staining of the OGE but no staining of the
buccal epithelium (B).
Fig. 2. Sections of C3H mouse tissues. (A) Simple epithelium lining
of ducts of a sublingual salivary gland shows staining of a subpopulation of cells for Le”. (B) Dorsum of tongue stained for Ley shows
strong staining of the suprabasal cells in the anterior columns of the
filiform papillae. (C) A taste bud at the lateral border of the tongue
stained with hematoxylin and eosin to show its general structure. (D)
Section adjacent to that shown in (C) shows suprabasal staining of the
mucosal epithelium but lack of staining of the taste bud for Type I1
chain “H”. (E & F) Strong staining for Le” and L e y is restricted to the
taste bud.
the other oral epithelia. In particular, they stained
strongly for Le” and Ley (Fig. 2E,F). They did not stain
for Type I11 chain determinants.
staining of basal as well as parabasal cells in the OSE
and OGE (Fig. 3B). As in the mouse, staining for Le”
and Ley was restricted to the junctional epithelium,
and staining for Type I1 and Type I11 chain H was restricted to suprabasal cells of the OSE and OGE and
was absent from the J E (Fig. 3C,D). Staining for Sa-T
was present on the basal and parabasal cells of the OSE
and OGE but, unlike the mouse, suprabasal staining of
the J E was absent and a loop of basal cells, similar to
that seen stained with BGA “B”, passed up onto the
surface of the tooth (Fig. 3E). A further difference between the staining patterns for rat and mouse was seen
in the lack of rat mucosal staining for T antigen.
In the rat, the region of the muco-gingival junction
clearly showed the different levels of transition from
“basal” to “suprabasal” markers in masticatory and
lining mucosae. In the buccal epithelium, staining for
Type I1 and I11 chain “ H was restricted to parabasal
cells, whereas in the OGE i t was seen relatively high in
Rat Epithelia
In the rat, only epithelia of the gingival region were
examined and these generally showed similar staining
patterns to those of the mouse. Being larger, however,
rat gingiva showed regional patterns of staining variation more clearly. In the OSE and OGE, staining for
BGA “B” was restricted to basal and parabasal cells.
The coronal portion of the J E showed strong staining of
all strata for BGA “B” but in the apical region suprabasal staining was weaker and only a “loop” of basal
cells passing up onto the attachment with the tooth
surface was strongly stained (Fig. 3A). Staining for SaLac was also strongest in the coronal part of the J E
where the full thickness of the epithelium was stained
but staining differed from mouse in that there was
Fig. 3. Sections of rat gingival tissues with the position of the
enamel space marked (E). (A) Staining for BGA “B” is present on the
basal and parabasal cells of the OGE and OSE and there is staining of
the full thickness of JE with particularly strong staining of the coronal region, as in the mouse. (B) Staining for “Lac” after neuraminidase treatment is similar to that for the mouse with weak staining of
basal and parabasal cells in the OGE and OSE and staining of the full
thickness of the J E with strongest staining of the coronal region. (C)
Staining for Type I1 chain “ H shows strong suprabasal staining of the
OGE and OSE and lack of J E staining. (D) A similar pattern of staining is seen for Type I1 chain “H’.
(El Staining for “T” antigen after
neuraminidase treatment is restricted to basal and parabasal cells in
the OGE and OSE. In the JE, staining is restricted to a small loop of
basal cells a t the apical tip which includes cells adjacent to the tooth
Fig. 4. Section of the mucogingival junction of rat. The region of
junction between OGE and buccal (Bt epithelium is marked by arrows. Small but consistent differences in the levels of expression of
basal and differentiation markers are seen between these epithelia.
Both Type I1 chain and Type I11 chain “ H (A,B) are expressed in the
the epithelium (Fig. 4A,B). Reciprocally, staining for
the “basal” markers BGA “B” and Sa-T was more
closely restricted to basal cells in the buccal epithelium
and extended further suprabasally in the OGE (Fig.
OGE at a higher level than in the buccal epithelium where expression
is confined to the parabasal region. Reciprocally, the expression of the
basal markers BGA “ B and Sa-T (C,D) extends well above the basal
region in OGE but is more basally restricted in buccal epithelium.
quite well characterized (Dabelsteen and Clausen,
The ABH series of antigens within the ABO blood
group system are termed “blood group antigens” because of their initial discovery as agents associated
with the agglutination of human red blood cells. SubDISCUSSION
sequently, i t has been shown that such antigens are
The various staining methods employed produced expressed by various other mammalian tissues and
clear patterns of epithelial staining and, for each of that, phylogenetically, their expression on mucous
the mAbs used, demonstrated consistent regional dif- cells, nervous receptors, and epithelia in fact precedes
ferences in the epithelial staining patterns. Lack of their expression on erythrocytes which is found only in
epithelial staining with the irrelevant mAbs used humans (Oriol et al., 1992). Human epithelia show exas controls, and the consistent regional distribution pression of short carbohydrate structures on basal epof staining with mAbs against known human glycocon- ithelial cells and a stepwise elongation is associated
jugates, were indicative of recognition of specific with cell maturation (Dabelsteen et al., 1991). Antiepitopes. Synthesis of cell surface carbohydrates is ge- gens of the ABH series have been previously demonnetically determined by the presence or absence of var- strated on rodent mucosal epithelia but their sequence
ious glycosyl transferases (Clausen et al., 1992) which of expression in relation to differentiation differs from
control the stepwise addition of specific carbohydrate that in human tissues: the longest structures are seen
linkages to the terminal regions of protein or lipid core on basal cells and expression of shorter structures ocstructures (Mandel et al., 1992). Such antigenic carbo- curs during maturation (Reibel e t al., 1994). The mohydrate moieties may be carried on various types of lecular structures recognized in murine tissues by the
protein or lipid cores and the formation of these mole- mAbs used in the present study are not yet well defined
cules depends upon complex patterns of interaction be- and characterization of these rodent antigens will retween substrate availability and the cellular expres- quire further work. However, the staining patterns insion of particular glycosyl transferases (Clausen et al., dicate that they recognize epitopes that are consis1992). For human tissues, the particular core struc- tently expressed by rodent epithelia and thus provide
tures and epitopes recognized by these mAbs have been suitable markers of epithelial differentiation.
In terms of their patterns of epithelial expression in
mice, these antigens appear to provide three general
groups of markers. One group (Sa-Lac, B, T, Sa-T) is
expressed by basal and early differentiating epithelial
cells, by simple epithelia and, variably, by taste buds.
This group of antigens is expressed by all cells of the
JE. A second group (Leb, Sa-Tn, Type 11, and Type I11
chain H) is expressed by differentiating suprabasal
cells of stratifying epithelia and, except for Leb, is not
expressed by simple epithelia and taste buds. This
group is not expressed by JE. A third group (Lac, Lex,
Ley, Lea, Tn) is not expressed by stratifying epithelia
but is expressed by simple epithelia and usually by
taste buds. This group of antigens is expressed suprabasally by differentiating cells in JE.
The J E pattern of differentiation, assessed by its
staining for carbohydrates, thus clearly differs from
that of the other gingival epithelia and is generally
distinguished by (a) its expression on all cell strata
markers that are typically expressed only on the immature cells of other stratifying epithelia, (b) its lack of
expression of markers that are expressed suprabasally
in other stratifying epithelia and which characterize
“oral” patterns of differentiation, and (c) its expression
of markers typically expressed by simple epithelia but
not by stratifying epithelia. It is interesting that this
pattern for carbohydrate marker molecules parallels
the pattern of expression of cytokeratins in gingival
epithelia. In terms of cytokeratin expression, the phenotype of OGE corresponds to that of masticatory mucosa and that of the OSE to lining mucosa (Morgan et
al., 1991; Mackenzie et al., 1991) whereas, in both humans and rodents, J E shows full-thickness staining for
cytokeratins found in basal cells of other stratifying
epithelia, lack of staining for most cytokeratins expressed suprabasally in other oral epithelia, and staining for cytokeratins usually expressed only in simple
epithelia (Mackenzie et al., 1991; Mackenzie, 1989).
This pattern is similar to that seen for the specialized
epithelial cells in taste buds which were found to share
several differentiation markers with simple epithelia
and have been shown previously to express simple epithelial keratins (Toh et al., 1992).
The arrangement of hard and soft tissues a t the region of junction between the oral mucosa and the teeth
is a n anatomical peculiarity. Elsewhere in the body,
epithelia form a continuous covering of the underlying
tissues which is rapidly restored when continuity is
disrupted, for example, by trauma. During tooth development (Ten Cate, 1989), odontogenic epithelium differentiates into the enamel organ, which defines the
morphology of the tooth crown and secretes enamel,
and then grows apically a s Hertwig’s epithelial root
sheath to define root morphology. At the completion of
development, the root sheath disintegrates into the
rests of Malassez and the enamel organ collapses to
become the reduced enamel epithelium (REE) which
covers the crown of the unerupted tooth. This pattern
of development results in a “free edge” of epithelium at
the region of the cemento-enamel junction of the tooth.
As the tooth erupts, the REE, which forms the primary
epithelial attachment to the tooth, proliferates and
fuses with the oral mucosa. Subsequently, the cells
against the surface of the tooth lose the appearance of
reduced ameloblasts and acquire the typical appear-
ance of JE. It is not entirely clear whether the cells that
initially form the J E are derived from proliferation and
transformation of REE cells, as ultrastructural evidence suggests (Schroeder and Listgarten, 1977), or
from downgrowth of oral epithelial cells (McHugh,
1957). However, whatever its initial cellular derivation, J E is regenerated, apparently from the adjacent
oral mucosal epithelium, after its surgical removal
(Schroeder and Listgarten, 1977).
As yet, little is known about the connective tissue
or other factors that are associated with the formation and reformation of J E . The pattern of cell maturation occurring in other stratified oral epithelia is
associated with the formation of a relatively inert surface barrier but the retention of basal markers through
the full thickness of J E indicates its lack of normal
maturation. As previously pointed out by Squier
(1981),development of a basal lamina against the tooth
surface requires “basal” or immature cell properties
and normal maturation of J E cells would inhibit adherent interactions with the tooth. Cell surface glycoconjugates have been associated with intercellular
adhesion (Clausen et al., 1992) and the development
of strong intercellular bonds, as occurs during the maturation of other stratifying epithelia, would prevent
the type of cell movement necessary for replacement
of the JE. Phagocytic and lysomal activities of J E
cells also play a role in the maintenance of gingival
health (Takata et al., 1986) and it appears that such
functions would similarly be impaired by normal patterns of differentiation. However, the J E is not undifferentiated: it shows a n alternative pathway of differentiation with suprabasal synthesis of macromolecules
characteristic of simple epithelia and taste buds whose
cells are also metabolically active in the mature state.
It may be significant that both taste buds and J E , but
not other oral epithelia (Nagata et al., 1992), have a
high level of innervation. The expression of some glycoconjugates, such as Lex, may facilitate or direct leukocyte traffic through the J E (Dabelsteen and Clausen,
J E properties such as attachment, permeability, and
adhesion may help stabilize the integrity of the dentogingival attachment (Page and Schroeder, 1982; Marks
et al., 1994) but i t is apparent that the epithelial discontinuity produced by tooth eruption is the cause of
vulnerability to inflammation which often progresses,
in both humans and other mammals, to breakdown of
the supporting structures of the teeth (Page and
Schroeder, 1982). Inflammation generates cytokine
networks that typically stimulate proliferation and migration of epithelia (Mauch e t al., 1994) and the process
of periodontal pocket formation is invariably associated with apical migration of the JE. It is unclear what
mechanisms normally prevent downward migration of
the “free edge” of epithelium from the cemento-enamel
junction onto the root of the tooth (Mackenzie,
1989a,b), but some evidence suggests that the J E phenotype is also associated with “passive” or non-migratory properties which may make i t resistant to migratory stimuli derived from the inflammatory response
(Mackenzie, 1987,1989a,b). Further information about
the properties of this epithelium, and its mechanisms
development and regeneration, would therefore be of
value, and the identification of markers characterizing
the J E phenotype in rodents should enable further experimental studies of these questions.
This work was supported in part by NIH/NIDR
Grants DE05190 and DE10317.
Altman, L.C., C.L. Nelson, B. Povolny, P. Fleckman, B.A. Dale, R.V.
Maier, C. Soderland, and C. Baker 1987 Culture and characterization of rat junctional epithelium. J . Periodont Res., 23:91-99.
Braga, A.M., and C.A. Squier 1980 Ultrastructure of regenerating
junctional epithelium in the monkey. J. Periodontol., 51:386392.
Clausen, H., E.C. Bennett, and E. Dabelsteen 1992 Carbohydrates of
the cell surface: Molecular aspects of glycosyltransferases and
their genes. APMIS Supplement 27,100:9-17.
Dabelsteen, E., and H. Clausen 1992 Carbohydrate Pathology.
APMIS Supplement 27, Vol 100. Munksgaard, Copenhagen.
Dabelsteen, E., U. Mandel, and H. Clausen 1991 Cell surface carbohydrates are markers of differentiation in human oral epithelium. Critical Reviews in Oral Biology and Medicine, 2:493-507.
Gao, Z., I.C. Mackenzie, A.T. Cruchley, D.M. Williams, I. Leigh, and
E.B. Lane 1989 Cytokeratin expression of the odontogenic epithelia in dental follicles and developmental cysts. J. Oral Pathol.,
Gao, Z., and I.C. Mackenzie 1992 Patterns of phenotypic expression of
human junctional, gingival and reduced enamel epithelia in vivo
and in vitro. Epith. Cell Biol., Ir156-167.
Hemmerle, J., and R.M. Frank 1991 Bacterial invasion of periodontal
tissues after experimental immunosuppression in rats. J . Biol.
Buccal., 19t271-282.
Hewaee, S., and T.G. Heaney 1990 Creation of a chimaeric periodonti<m in the rat by isotbpic tooth germ transplantation. Archs
Oral Biol., 35r681-684.
Hormia, M., I. Virtanen, and V. Quaranta 1992 Immunolocalizationof
integrin asp4in mouse junctional epithelium suggest an anchoring function to both the internal and the external basal lamina.
J . Dent. Res., 718:1,503-1,508.
Listgarten, M.A. 1972 Ultrastructure of the dento-gingival junction
after gingivectomy. J. Periodont. Res., 7:151-160.
Listgarten, M.A. 1975 Similarity of epithelial relationships in the
gingiva of rat and man. J. Periodontal., 46:677-680.
Mackenzie, I.C. 1987 Nature and mechanisms of regeneration of the
junctional epithelial phenotype. J . Periodont. Res., 22:243-245.
Mackenzie, I.C. 1990 Formation and sequential changes of the periodontium. In: Contemporary Periodontics. H.M. Goldman, D.W.
Cohen, and R.J. Genco, eds. C.V. Mosby, St. Louis, pp. 55-62.
Mackenzie, I.C. 1989b Factors influencing the stability of the gingival sulcus. In: Periodontology Today. B. Guggenheim, ed. Karger,
Basel, pp. 1-8.
Mackenzie, I.C. 1993 Epithelial-mesenchymal interactions in the development and maintenance of epithelial tissues. In: The Keratinocyte Handbook. B. Lane, I. Leigh, and F. Watt, eds. Cambridge University, pp. 243-258.
Mackenzie, I.C., E. Dabelsteen, and U. Mandel 1989 Expression of
blood group antigen-related carbohydrates by human gingival
epithelia. J . Periodont. Res., 24r289-297.
Mackenzie, I.C., G. Rittman, Z. Gao, I. Leigh, and B. Lane 1991 Patterns of cytokeratin expression in human gingival epithelia. J.
Periodont. Res., 26t468-478.
Mackenzie, I.C., and Z. Gao 1993 Patterns of cytokeratin expression
in the epithelia of inflamed human gingiva and periodontal pockets. J . Periodont. Res., 28.49-59.
Mandel, J., O.W. Petersen, H. Sorensen, P. Vedtofte, S. Hakomori, H.
Clausen, and E. Dabelsteen 1992 Simple mucin-type carbohy~~
drates in oral stratified squamous and salivary gland epithelia.
Carbohydrate Pathology, 97:713-721.
Marks, S.C. Jr., M.D. McKee, S. ZalZal, and A. Nanci 1994 The epithelial attachment and the dental junctional epithelium: Ultrastructural features in porcine molars. The Anatomical Record,
Mauch, C., T. Oono, B. Eckes, and T. Krieg 1994 Cytokines and
Wound Healing. In: Epidermal Growth Factors and Cytokines.
T.A. Luger and T. Schwarz, eds. Marcel Dekker, Inc., New York,
pp. 325-344.
McHugh, W.D. 1963 Some aspects of the development of gingival
epithelium. Periodontics, 1:239-245.
Meyer, J.,C.A. Squier, S.J. Gerson 1984 The Structure and Function
of Oral Mucosa. Pergamon Press, Oxford.
Morgan, P.R., I.M. Leigh, P.E. Purkis, I.D. Gardner, G.N.P. Van
Muijen, and E.B. Lane 1987 Site variation in keratin expression
in human oral epithelia-an immunocytochemical study of individual keratins. Epithelia, 1:31-43.
Nagata, E., T. Kondo, N. Ayasaka, M. Nakata, and T. Tanaka 1992
Immunohistochemical Study of Nerve fibres with Substance P- or
Calcitonin Gene-Related Peptide-Like Immunoreactivity in the
Junctional Epithelium of Developing Rats. Archs Oral Biol., 37:
Oriol, R., R. Mollicone, P. Coullin, A.M. Dalix, and J.J. Candelier
1992 Genetic regulation of the expression of ABH and Lewis antigens in tissues. APMIS Suppl. 27, vol. 100:28-38.
Page, R.C., and H.E. Schroeder 1982 Periodontitis in Man and Other
Animals. A Comparative Review. S. Karger, Basel.
Purkis, P.E., J.B. Steel, I.C. Mackenzie, W.J.B. Nathrath, I.M. Leigh,
and E.B. Lane 1990 Antibody markers of basal cells in complex
epithelia. J . Cell Sci., 97:39-50.
Reibel, J., E. Dabelsteen, S. Hakomori, W.W. Young, and I.C. Mackenzie 1984 The distribution of blood group antigens in rodent
epithelia. Cell Tissue Res., 237.111-116.
Sawada, T., T. Yamamoto, T. Yanagisawa, S. Takuma, H. Hasegawa,
and K. Watanabe 1990 Electron-immunocytochemistry of laminin and type-IV collagen in the junctional epithelium of rat molar
gingiva. J. Periodont. Res., 25:372-376.
Sashima, M., M. Satoh, and A. Suzuka 1991 Age-related development
of the long-junctional epithelium in the senescence-accelerated
mouse. J . Periodont. Res., 70:1,462-1,466.
Schroeder, H.E., and M.A. Listgarten 1977 Fine structure of the developing epithelial attachment of human teeth. In: Monographs
in Developmental Biology, Vol. 2 A. Wolsky, ed. Karger, Basel.
Shimono, M., T. Inoue, Y. Hamada, Y. Abiko, and S. Hashimoto 1989
A cytochemical study of dense granules in the rat junctional epithelium. J . Periodont. Res., 24:186-191.
Squier, C.A. 1981 Keratinization of the sulcular epithelium-a pointless pursuit? J. Periodontol., 52r426-429.
Steffensen, B., D.E. Lopatin, R.G. Caffesse, and C.T. Hanks 1987
Blood group substances as differentiation markers in human
dento-gingival epithelium. J. Periodont. Res., 22r451-455.
Takata, T., H. Nikai, N. Kjuhin, and H. Okamoto 1986 Ultrastructure
of regenerated junctional epithelium after surgery of the rat molar gingiva. J . Periodontol., 57:776-783.
Takata, T., H. Nikai, M. Miyauchi, H. Ito, J . Kobayashi, and N. Ijuhin
1990 Lectin binding of rat gingival epithelia. J . Periodont. Res.,
Ten Cate, A.R. 1989 Oral Histology. Development, Structure and
Function, Fourth Edition. Mosby, St. Louis.
Thaller, C., and G. Eichele 1988 Characterization of retinoid metabolism in the developing chick limb bud. Development, 103r473483.
Toh, H., G. Rittman, and I.C. Mackenzie 1992 Kertain expression in
taste bud cells of the circumvallate and foliate papillae of adult
mice. Epith. Cell Biol., 2.126-133.
Yamasaki, A,, H. Nikai, K. Niitani, and N. Ijuhin 1979 Ultrastructure of the junctional epithelium of germfree rat gingiva. J .
Periodontol., 50.641-648.
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expressions, epithelium, glycoconjugates, rodents, group, junction, oral, related, blood
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