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CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE |
Department of Periodontology and Fixed Prosthodontics, School of Dental Medicine, University of Berne, Freiburgstrasse 7, CH-3010 Berne, Switzerland;
* corresponding author, dieter.bosshardt{at}zmk.unibe.ch
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ABSTRACT |
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 TOP ABSTRACT (I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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KEY WORDS: junctional epithelium • tooth • implant • periodontal diseases
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(I) INTRODUCTION |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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(II) THE DEVELOPMENT OF THE JUNCTIONAL EPITHELIUM |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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When the tips of the cusps or the incisal edge of the crown breaches the oral mucosa (Ten Cate, 1998), or shortly before the establishment of the first contact between the reduced enamel epithelium and the oral gingival epithelium (Schroeder, 1996), a slow cell transformation process develops. Beginning orally and ending at the cemento-enamel junction 1 to 2 (Schroeder and Listgarten, 1977) or 3 to 4 (Ten Cate, 1998) yrs later, the reduced enamel epithelium gradually converts into junctional epithelium, a multilayer non-keratinizing squamous epithelium (Glavind and Zander, 1970; Listgarten, 1972b; Schroeder and Listgarten, 1977; Schroeder, 1996). During the transformation process, the reduced ameloblasts change their morphology from short columnar to flattened cells that are oriented parallel to the enamel surface. Also, the cells external to the reduced ameloblasts undergo a structural change. However, unlike the reduced and transformed ameloblasts, these external cells regain mitotic activity. These transformed ameloblasts migrate in a coronal direction, are exfoliated at the bottom of the sulcus, and eventually are replaced by the cells external to the reduced/transformed ameloblasts (Schroeder, 1996).
It has been proposed that the junctional epithelium, which was originally derived from the reduced enamel epithelium, may be replaced in time by a junctional epithelium formed by basal cells originating from the oral gingival epithelium (Ten Cate, 1996). This holds true, at least, for de novo formation of the junctional epithelium following gingivectomy (Salonen, 1986; Salonen et al., 1989). However, basal epithelial cells other than those of oral gingival origin may also regenerate a junctional epithelium (Listgarten, 1967, 1972b; Braga and Squier, 1980; Freeman, 1981).
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(III) STRUCTURE OF THE JUNCTIONAL EPITHELIUM |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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). In the interproximal area, the junctional epithelia adjacent to neighboring teeth fuse to form the epithelial lining of the interdental col. The coronal termination of the junctional epithelium is a free surface and is located either at the bottom of the sulcus, at the gingival margin, or at the interdental col area. Under pristine conditions, the epithelial seal extends from the cemento-enamel junction to the gingival margin, averaging about 2 mm in height (Fig. 1) (Gargiulo et al., 1961). ‘Normal’ gingiva, however, expresses sub-clinical signs of slight inflammation (Brecx et al., 1987). Therefore, the coronal termination of the junctional epithelium corresponds usually to the bottom of the gingival sulcus. At its apical and lateral aspects, the junctional epithelium is bordered by soft connective tissue and, at its coronal-most portion, also by the sulcular epithelium. The epithelium-connective tissue interface is smooth, showing an only mild undulation coronally (Figs. 1, 2). Toward the tooth surface, the junctional epithelial cells form and maintain the epithelial attachment (Schroeder and Listgarten, 1977). At its apical termination, the junctional epithelium—at least in porcine teeth—appears at frequent intervals to be in continuity with the network of the epithelial rests of Malassez (Grant and Bernick, 1969; Spouge, 1984).
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, 2). It is a stratified squamous non-keratinizing epithelium that is made up of 2 strata only, i.e., a basal layer (the stratum basale) and a suprabasal layer (the stratum suprabasale). The basal cells face the gingival connective tissue. The basal cells and the adjacent 1 to 2 suprabasal cell layers are cuboidal to slightly spindle-shaped. All remaining cells of the suprabasal layer are flat, oriented parallel to the tooth surface, and closely resemble each other (Fig. 3). The innermost suprabasal cells (facing the tooth surface) are also called DAT cells (= directly attached to the tooth) (Salonen et al., 1989). They form and maintain the ‘internal basal lamina’ that faces the tooth surface.
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), the cisternae of the rough endoplasmic reticulum are abundant, and polyribosomes are numerous. All junctional epithelial cells express a unique set of cytokeratins, including Nos. 5, 13, 14, and 19, and occasionally also weak activity for cytokeratins Nos. 8, 16, and 18 (for review, see Schroeder, 1996).
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), and occasionally by gap junctions (Schroeder, 1969, 1981; Schroeder and Münzel-Pedrazzoli, 1970; Schroeder and Listgarten, 1977; Yamasaki et al., 1979; Saito et al., 1981; Sasaki et al., 1981; Hashimoto et al., 1986). The fluid-filled intercellular spaces may vary in width, but are wider in comparison with the oral gingival or sulcular epithelium (Schroeder and Münzel-Pedrazzoli, 1970). These features account for the junctional epithelium’s remarkable permeability (Figs. 3, 6, 8). A variety of mononuclear leukocytes occupy these interstitial spaces. Neutrophilic granulocytes (= polymorphonuclear leukocytes or simply neutrophils, PMNs) are found in the central region of the junctional epithelium and near the tooth surface (Figs. 3, 6) (Schroeder and Listgarten, 1997). In addition, lymphocytes and macrophages reside in and near the basal cell layer (Schroeder, 1973, 1977). Antigen-presenting cells and Langerhans and other dendritic cells are present as well (Juhl et al., 1988). The junctional epithelium, particularly its basal cell layers, is well-innervated by sensory nerve fibers (Byers and Holland, 1977; Byers et al., 1987; Kondo et al., 1992; Maeda et al., 1994).
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, 2). While a basement membrane, sometimes referred to as ‘the external basal lamina’ (Schroeder, 1996), is interposed between the basal cells of the junctional epithelium and the gingival connective tissue, a basal lamina (also known as the internal basal lamina) forms part of the interfacial matrix between the tooth-facing junctional epithelial cells (also known as DAT cells; see above) and the tooth surface (Fig. 7). At the apical end of the junctional epithelium, the basal lamina is continuous with the basement membrane.
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The basal lamina together with hemidesmosomes (Listgarten, 1966, 1972a; Schroeder, 1969) forms the interface between the tooth surface and the junctional epithelium and is named ‘epithelial attachment’ (Schroeder and Listgarten, 1977). The hemidesmosomes consist of an attachment plaque associated with cytokeratin filaments and the sub-basal dense plate, which is extracellularly located in the lamina lucida (Fig. 7). The lamina densa directly faces the enamel, dentin, or cementum (fibrillar or afibrillar) (Figs. 7, 8). A dental cuticle may be interposed between these tooth matrices (Fig. 9). However, this attachment mechanism has also been demonstrated to exist on a dental calculus layer in a bacteria-free environment (Listgarten and Ellegaard, 1973). The elements of the epithelial attachment are produced and renewed by the adjacent DAT cells (Stallard et al., 1965; Osman and Ruch, 1980) and, hence, are part of the dynamics of the junctional epithelium.
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(IV) DYNAMIC ASPECTS OF THE JUNCTIONAL EPITHELIUM |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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The intercellular spaces of the junctional epithelium provide a pathway for fluid and transmigrating leukocytes. In the absence of clinical signs of inflammation, approximately 30,000 PMNs migrate per minute through the junctional epithelia of all human teeth into the oral cavity (Schiött and Löe, 1970). The tissue fluid transports a variety of molecules through the junctional epithelium to the bottom of the gingival sulcus. These molecules, together with the leukocytes, represent a host defense system against the bacterial challenge. Thus, gingival fluid is an exudate that originates from the sub-epithelial blood vessels of the lamina propria, and its flow rate corresponds to the degree of inflammation.
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(V) EXPRESSION OF VARIOUS MOLECULES AND THEIR FUNCTIONS |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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6ß4 (Hormia et al., 1992, 2001; Thorup et al., 1997; Gurses et al., 1999) and 2ß1, 3ß1, and 6ß1 (Del Castillo et al., 1996) has been documented in the junctional epithelial cells. Of particular interest are those integrins that interact with the matrix constituents of the internal basal lamina and the external basement membrane of the junctional epithelium, since altered expressions of these integrins may adversely influence tissue integrity. Knowledge about structures and molecules involved in the maintenance of cell-cell contacts is particularly important in view of the pathological changes that the junctional epithelium undergoes during its conversion to a pocket lining. The cadherins are responsible for tight contact between cells (Ivanov et al., 2001; Juliano, 2002). E-cadherin, an epithelium-specific CAM, plays a crucial role in maintaining the structural integrity. Immunohistochemical staining for E-cadherin reveals a significant reduction in staining intensity from the oral gingival to the junctional epithelium (Ye et al., 2000). In contrast, in another study, expression of E-cadherin was not detectable at all in the junctional epithelium (Heymann et al., 2001). An analysis of the expression of the carcino-embryonic Ag-related cell adhesion molecule 1 (CEACAM1)—a transmembrane cell-adhesion molecule that is expressed on leukocytes, epithelia, and blood vessel endothelia—revealed a much stronger cell-surface staining in the junctional epithelium as compared with the oral sulcular epithelium (Heymann et al., 2001). Thus, the dynamic cohesion of the junctional epithelial cells may, to a large extent, be mediated by CEACAM1 (Heymann et al., 2001). Since CEACAM1 is also expressed on the surface of PMNs, it likewise may play a role in the guidance of these cells through the junctional epithelium (Heymann et al., 2001). In addition, CEACAM1 participates in the regulation of cell proliferation, stimulation, and co-regulation of activated T-cells (Odin et al., 1988; Kammerer et al., 1998; Singer et al., 2000). Furthermore, it functions as a cell receptor for a variety of different bacteria (Öbrink, 1997; Hauck et al., 1998). As a consequence, bacterial interactions with CEACAM1 may result in altered structural organization of the junctional epithelium (Heymann et al., 2001).
Intercellular adhesion molecule-1 (ICAM-1 or CD54) and lymphocyte function antigen-3 (LFA-3) are additional cell adhesion molecules. Both are members of the immunoglobulin superfamily of recognition molecules. ICAMs are immunoglobulin-like transmembrane glycoproteins that mediate cell-cell interactions in inflammatory reactions. They function as ligands for the ß2 integrin molecules present on leukocytes and participate in the control of leukocyte migration to inflammatory sites. Expression of ICAM-1 and lymphocyte function antigen-3 (LFA-3) has been demonstrated in the junctional epithelial cells (Crawford and Hopp, 1990; Crawford, 1992; Gao and Mackenzie, 1992; Tonetti, 1997; Tonetti et al., 1998). The establishment of a gradient of ICAM-1 expression within the junctional epithelium is thought to be an important mechanism for guiding PMNs toward the bottom of the sulcus, where they could counteract the bacterial challenge (Tonetti, 1997; Tonetti et al., 1998). In this context, the high expression of interleukin-8 (IL-8), a chemotactic cytokine, in the coronal-most cells of the junctional epithelium may be an additional mechanism of routing PMNs toward the bacterial challenge (Tonetti et al., 1994, 1998). Other cytokines—such as interleukin-1 (IL-1), interleukin-1ß (IL-1ß), and tumor necrosis factor- (TNF-)—are strongly expressed in the coronal half of the junctional epithelium (Miyauchi et al., 2001). After exposure to lipopolysaccharide, almost all cells in the junctional epithelium are strongly labeled for these cytokines (Miyauchi et al., 2001). Staining was attributed to both junctional epithelial cells and macrophages. Thus, cytokine production by junctional epithelial cells and macrophages in the coronal half of the junctional epithelium may play a role in the defense against the bacterial challenge in the gingival sulcus. Hence, from a clinical point of view, it has to be realized that the junctional epithelium represents a key mechanism in host-parasite interactions, since it actively participates in the host defense mechanism rather than simply providing an attachment to the tooth surface.
The level of cellular differentiation can be analyzed by the expression of cell-membrane-associated blood-group-specific carbohydrates (Dabelsteen et al., 1982). N-acetyllactosamine—the type 2 chain H precursor of the blood group A-specific carbohydrate, which is usually associated with the lowest level of cell differentiation—is expressed throughout the junctional epithelium (Steffensen et al., 1987). This, in turn, may support the hypothesis that DAT cells may indeed retain their proliferative potential.
The expression of growth factors and corresponding receptors has also been studied in the junctional epithelium. Epidermal growth factor (EGF) is a potent mitogen and is thought to be involved in epithelial growth, differentiation, and wound healing. The EGF signal is transmitted to the cell via the EGF receptor. While EGF receptors are poorly expressed or undetectable in junctional epithelium from the healthy human gingiva, inflamed tissues from patients with chronic periodontitis revealed an intense labeling in proliferating cells (Nordlund et al., 1991). In the ‘normal’ junctional epithelium of rat gingiva, immunohistochemical staining for EGF was observed in the cytoplasm (Tajima et al., 1992).
Expressions of tissue plasminogen activator (t-PA) (Schmid et al., 1991) and its inhibitor PAI-2 (Lindberg et al., 2001a,b) have been detected in the junctional epithelium. The t-PA is a serine protease that converts plasminogen into plasmin. Plasmin degrades many extracellular matrix proteins and activates matrix metalloproteinases (MMPs). Matrilysin (matrix metalloproteinase-7; MMP-7), a proteolytic enzyme found in many mature epithelial cells, is expressed in suprabasal cells of the human junctional epithelium (Uitto et al., 2002).
The active role the junctional epithelium plays in the innate host defense is also demonstrated by the production of natural antimicrobial peptides and proteins in response to the bacterial challenge (for review, see Dale, 2002). Antimicrobial molecules that may contribute to periodontal health include the - and ß-defensins, the cathelicidin family members (LL-37), and calprotectin. While human ß-defensin 1 (hBD-1) and human ß-defensin 2 (hBD-2) are poorly expressed or undetectable in the junctional epithelium, the -defensins and LL-37 are present in high amounts. Their expressions are attributable to the presence of the PMNs that produce these 2 natural antimicrobials. Thus, the PMNs contribute to the protection of the junctional epithelium by releasing -defensins and LL-37.
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(VI) JUNCTIONAL EPITHELIUM ADJACENT TO ORAL IMPLANTS |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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(VII) REGENERATION OF THE JUNCTIONAL EPITHELIUM |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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Clinical probing results in a mechanical disruption of the junctional epithelial cells from the tooth. Whether and how fast a new epithelial attachment reforms have been the objectives of several studies. In an experimental study in marmosets, following probing, a new and complete attachment indistinguishable from that in controls was established 5 days after complete separation of the junctional epithelium from the tooth surface (Taylor and Campbell, 1972). The re-establishment of the epithelial seal around implants after clinical probing was shown to occur within about the same time period (Etter et al., 2002). In both studies, persistence of tissue trauma and infection as a result of probing were not observed. Based on these 2 studies, probing around teeth and implants does not seem to cause irreversible damage to the soft tissue components.
Oral hygiene practices may be accompanied by undesired trauma to the junctional epithelium as well. Waerhaug (1981) studied healing of the junctional epithelium following the use of dental floss at premolars in 12-year-old humans. Detachment of cells persisted for 24 hrs after flossing ceased. New attachment of junctional epithelial cells started 3 days after flossing ceased. After 2 wks, the cell populations on the experimental and control surfaces were again indistinguishable from each other.
In the above studies, the junctional epithelium was never completely removed from the tooth. However, the application of gingivectomy techniques would completely remove the junctional epithelium. Subsequently, the formation of a new junctional epithelium must occur from basal cells of the oral gingival epithelium (Listgarten, 1967; Innes, 1970; Frank et al., 1972; Listgarten and Ellegaard, 1973; Braga and Squier, 1980). In humans, a new junctional epithelium after gingivectomy may form within 20 days (Listgarten, 1972a,b; Schroeder and Listgarten, 1977).
These studies show that the junctional epithelium is a highly dynamic and adaptive tissue with a fast capacity for self-renewal or de novo formation from basal cells of the oral gingival epithelium.
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(VIII) ROLE OF THE JUNCTIONAL EPITHELIUM IN THE INITIATION OF POCKET FORMATION |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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Several researchers have attributed pocket formation to a loss of cellular continuity in the coronal-most portion of the junctional epithelium (Schluger et al., 1977; Schroeder and Listgarten, 1977). Thus, the initiation of pocket formation may be attributed to the detachment of the DAT cells from the tooth surface or to the development of an intra-epithelial split. Takata and Donath (1988), studying pocket formation in humans, observed degenerative changes in the second or third cell layer of the DAT cells in the coronal-most portion of the junctional epithelium facing the bacterial biofilm. Similar observations were made in a dog model (Hillmann et al., 1990). Several attempts to explain the reason for the cleavage within the junctional epithelium have been made. With increasing degrees of gingival inflammation, both the emigration of PMNs and the rate of gingival crevicular fluid passing through the intercellular spaces of the junctional epithelium increase (Klinkhamer, 1968; Klinkhamer and Zimmerman, 1969; Attström and Egelberg, 1970; Attström, 1970; Kowashi et al., 1980). Moderately distended intercellular spaces are not considered to interfere with the structural and functional integrity of the junctional epithelium (Schroeder and Listgarten, 1997). However, an increased number of mononuclear leukocytes, i.e., T- and B-lymphocytes and monocytes/macrophages, together with PMNs, are considered as factors that contribute to the focal disintegration of the junctional epithelium (Schroeder and Listgarten, 1997). Apart from the view that the host itself is the major source of factors contributing to the disintegration of the junctional epithelium, other possibilities have to be considered as well.
The junctional epithelium is an ‘open system’ that allows cells and substances to emigrate from the gingival connective tissue into the sulcus, thereby clearing and counteracting the continuous bacterial challenge. In contrast, the bacteria and their products also have the opportunity to enter the junctional epithelium. It has already been hypothesized that pocket formation is the result of subgingival spreading of bacteria under impaired defense conditions (Schroeder and Attström, 1980). Particular attention has been paid to elucidating the mechanisms by which Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis (P. gingivalis), 2 pathogens implicated as major etiological agents in aggressive and chronic periodontitis, adhere to, invade, and replicate in epithelial cells (Lamont et al., 1992, 1995; Sandros et al., 1994; Madianos et al., 1996; Meyer et al., 1997; Njoroge et al., 1997; Deshpande et al., 1998; Huard-Delcourt et al., 1998; Lamont and Jenkinson, 1998; Fives-Taylor et al., 1999; Forng et al., 2000; Quirynen et al., 2001). Among the virulence factors produced by P. gingivalis, the cysteine proteinases, referred to as gingipains, have been the focus of research over the last few years (Potempa et al., 2000; Curtis et al., 2001; Imamura, 2003). Recently, a new effect of gingipains has emerged. It has been shown that gingipains specifically degrade components of the epithelial cell-to-cell junctional complexes (Wang et al., 1999; Katz et al., 2000, 2002; Chen et al., 2001; Hintermann et al., 2002). Epithelial cells challenged by P. gingivalis exhibit proteolysis of focal contact components, adherens junction proteins, and adhesion signaling molecules (Hintermann et al., 2002). Furthermore, epithelial cells exposed to P. gingivalis, or to proteinases derived from it, showed reduced adhesion to extracellular matrices, changes in morphology, impaired motility, and apoptosis. The recent observation that gingipains may also disturb the ICAM-1-dependent adhesion of PMNs to oral epithelial cells, an immune evasion mechanism by P. gingivalis, points to the importance of these molecules for the disintegration of the junctional epithelium (Tada et al., 2003). Thus, bacterial products penetrating the junctional epithelium at the bottom of the sulcus may directly perturb the structural and functional integrity of the junctional epithelium. The proteolytic disruption of the epithelial integrity may not only be a significant factor in the initiation of pocket formation, but may also pave the way for bacterial invasion into the sub-epithelial connective tissue in advanced stages of the lesion. The same mechanisms of destruction of cell-to-cell contacts may further perturb the structural and functional integrity of the connective tissue. In this regard, degradation of cell adhesion molecules on fibroblasts and cell death were shown to be induced by the arginine-specific cysteine proteinase (Arg-gingipain) in vitro (Baba et al., 2001). Whether periodontopathogens use the same strategy in vivo is an important question that remains to be solved.
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(IX) CONCLUDING REMARKS |
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TOPABSTRACT(I) INTRODUCTION(II) THE DEVELOPMENT OF...(III) STRUCTURE OF THE...(IV) DYNAMIC ASPECTS OF...(V) EXPRESSION OF VARIOUS...(VI) JUNCTIONAL EPITHELIUM...(VII) REGENERATION OF THE...(VIII) ROLE OF THE...(IX) CONCLUDING REMARKSREFERENCES |
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ACKNOWLEDGMENTS |
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is courtesy of Dr. H.E. Schroeder, and Fig. 2 is courtesy of Dr. A. Nanci. This work was supported by the Clinical Research Foundation (CRF) for the Promotion of Oral Health, University of Berne, Switzerland. Received May 12, 2004; Accepted October 10, 2004
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