The junctional epithelium is located at a strategically important interface between the gingival sulcus, populated with bacteria, and the periodontal soft and mineralized connective tissues that need protection from becoming exposed to bacteria and their products. Its unique structural and functional adaptation enables the junctional epithelium to control the constant microbiological challenge. The antimicrobial defense mechanisms of the junctional epithelium, however, do not preclude the development of gingival and periodontal lesions. The conversion of the junctional to pocket epithelium, which is regarded as a hallmark in disease initiation, has been the focus of intense research in recent years. Research has shown that the junctional epithelial cells may play a much more active role in the innate defense mechanisms than previously assumed. They synthesize a variety of molecules directly involved in the combat against bacteria and their products. In addition, they express molecules that mediate the migration of polymorphonuclear leukocytes toward the bottom of the gingival sulcus. Periodontopathogens-such as Actinobacillus actinomycetemcomitans or, in particular, Porphyromonas gingivalis-have developed sophisticated methods to perturb the structural and functional integrity of the junctional epithelium. Research has focused on the direct effects of gingipains, cysteine proteinases produced by Porphyromonas gingivalis, on junctional epithelial cells. These virulence factors may specifically degrade components of the cell-to-cell contacts. This review will focus on the unique structural organization of the junctional epithelium, on the nature and functions of the various molecules expressed by its cells, and on how gingipains may attenuate the junctional epithelium's structural and functional integrity.

The Junctional Epithelium: from Health to Disease:

In the context of cellular origins, odontogenic epithelium and oral epithelium are the sources for junctional epithelium during development and during wound healing respectively. In contrast, both odontogenic and non-odontogenic mesenchyme contain the progenitors for gingival fibroblasts in developing tissues while in wounded tissues, gingival fibroblasts are derived from gingival connective tissues and comprise a heterogeneous population of cells with diverse properties and functions. Periodontal ligament, bone and cementum cell populations apparently originate from dental follicle progenitor cells during development, but during wound healing derive from ancestral cells in periodontal ligament and bone. Cellular differentiation in developing periodontium is governed in part by epithelial-mesenchymal interactions that generate specific signals which regulate selective cell populations in time and space. On the other hand, differentiation during wound healing and regeneration is regulated by a vast array of extracellular matrix informational molecules and by cytokines that induce both selective and non-selective responses in the different cell lineages and their precursors. Further, several important signalling systems are irretrievably lost after development is complete. Thus, in the context of cellular origins and differentiation, developing and wounded periodontal tissues exhibit fundamental differences. Future prospects for improved healing and regeneration of periodontal tissues may derive from identification and isolation of informational molecules that are stored in connective tissue matrices. These molecules and elucidation of their functions may open new perspectives in our understanding of the biology of periodontal wound healing and may provide novel approaches to periodontal regeneration.

Cellular origins and differentiation control mechanisms during periodontal development and wound healing

In this study, human gingival fluid from normal subjects was shown to contain a low-molecular-weight factor (molecular weight, 10,000 to 25,000) which augmented murine thymocyte proliferation, enhanced the production of interleukin 2 by T lymphocytes, and augmented the proliferation of fibroblasts. These biochemical and biological properties are characteristic of both macrophage-derived interleukin 1 and epidermal cell-derived thymocyte-activating factor. In addition, we have established that epidermal thymocyte-activating factor or interleukin 1 or both are present to a greater extent in gingival fluid obtained from sites manifesting gingival inflammation. In fact, thymocyte-activating activities were found to be greater in gingival fluid from inflamed than from noninflamed gingival sites from the same subjects. These findings suggest that human gingival fluid contains epidermal thymocyte-activating factor or interleukin 1 or both, which may amplify the inflammatory response in periodontal tissues.

Increased thymocyte-activating factor in human gingival fluid during gingival inflammation.

Quantitative parameters of early human gingival inflammation

Statement of problem The primary function of the periodontal tissues, besides attaching the tooth to the jaw, is gingival protection; that is, to provide a seal against the contaminated environment of the oral cavity. Detailed data regarding protection of the periimplant mucosa in patients with transmucosal implants are lacking. Purpose The purpose of this histological study was to demonstrate the structural and ultrastructural features of the interface between transmucosal titanium implants with oxidized, machined, and acid-etched surfaces and surrounding tissues by combined light and electron microscopy. Material and methods Five patients received 12 experimental titanium, 1-piece mini-implants with an oxidized, acid-etched, or machined surface distal to conventional implants. Following transmucosal healing of 8 weeks and at the abutment connection of the regular implants, the mini-implants were removed with a layer of surrounding hard and soft tissue. The specimens were fixed and processed for light, transmission electron, and scanning electron microscopy. Results For all 3 types of surfaces, substantial structural analogies were demonstrated between gingiva and periimplant mucosa in humans, both shown to provide protection for the underlying soft tissues and alveolar bone. Depending on the implant surface texture, substantial differences were noted in the manner the implants interface with connective tissue. Conclusions The mechanisms of protection in the periimplant mucosa correspond to those in the gingiva surrounding a tooth. The surface texture of implants may affect the orientation of collagen fibers of the connective tissue at the implant surface.

The defense architecture of the human periimplant mucosa: a histological study.

Turnover of the gingival epithelium in marmosets.

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Turnover of the gingival epithelium in marmosets.