Inflammatory Gingival Tissues Research Articles

Combined use of hydrogen-rich water and enzyme-digested edible bird's nest improves PMA/LPS-impaired wound healing in human inflammatory gingival tissue equivalents.

Gingival wound healing plays a critical role in maintaining oral health. However, this process can be delayed by oxidative stress and excessive inflammatory responses. In this study, we established a human inflammatory gingival tissue equivalent (iGTE) to investigate the inhibitory effects of hydrogen-rich water (HW), enzyme-digested edible bird's nest (EBND) and sialic acid (SA) on PMA (an inducer of oxidative free radicals)- and LPS (an inflammatory stimulus)-impaired wound healing. The iGTE was constructed by human gingival fibroblasts (hGFs), keratinocytes and macrophages under three-dimensional conditions. Wounds in the iGTE and hGF/keratinocyte monolayers were created by mechanical injury. Tissues and cells were pretreated with HW, EBND, and SA, and then exposed to the inflammatory and oxidative environment induced by PMA (10ng/mL) and LPS (250ng/mL). The inflammatory cytokines IL-6 and IL-8 were quantitatively analyzed by ELISA. Histopathological image analysis was performed by HE and immunofluorescence staining. In the iGTE, PMA/LPS significantly reduced the epithelial thickness while causing a decrease in K8/18, E-cadherin, laminin and elastin expression and an increase in COX-2 expression along with ulcer-like lesions. In mechanically scratched hGFs and keratinocyte monolayers, PMA/LPS significantly impaired wound healing, and promoted the secretion of IL-6 and IL-8. Pretreatment of HW, EBND, and SA significantly suppressed PMA/LPS-induced wound healing delay and inflammatory responses in cell monolayers, as well as in the iGTE. Remarkably, the combined use of HW and EBND exhibited particularly robust results. Combined use of HW and EBND may be applied for the prevention and treatment of wound healing delay.

The expression levels of chemotaxis-related molecules CXC chemokine receptor 1, interleukin-8, and pro-platelet basic protein in gingival tissues

Background/purposeExcessive host immune response is thought to be an important cause of periodontal tissue damage during periodontitis. The potent chemotaxis produced by locally released chemokines is the key signal to trigger this response. Here, we aimed to investigate the expression of CXC chemokine receptor 1 (CXCR1), and chemokines interleukin-8 (IL-8) and pro-platelet basic protein (PPBP) in human inflammatory gingival tissues compared with healthy tissues. Materials and methodsA total of 54 human gingival tissues, 27 healthy and 27 inflammatory samples, were collected. Fifteen specimens of each group were employed for quantitative reverse transcription polymerase chain reaction to determine the mRNA levels of CXCR1, IL-8, and PPBP. Six samples of each group were used for Western blotting to investigate the protein expression of CXCR1 and for enzyme-linked immunosorbent assay to evaluate the protein levels of IL-8 and PPBP, respectively. ResultsThe mRNA levels of chemokine receptor CXCR1, chemokine IL-8, and PPBP in inflammatory gingival tissues were significantly higher than those in healthy controls (P < 0.05). The protein levels of CXCR1, IL-8, and PPBP in inflammatory gingival tissues were also significantly higher than those in healthy gingival tissues (P < 0.05). ConclusionWhen compared to healthy gingival tissues, the expression of CXCR1, IL-8, and PPBP in inflammatory gingival tissues is higher.

The miR-223-3p Regulates Pyroptosis Through NLRP3-Caspase 1-GSDMD Signal Axis in Periodontitis.

Salivary exosomes contain various components and may play important roles in oral diseases. The purpose of this study was to verify the possible function of miR-223-3p from salivary exosomes in periodontitis. We isolated the salivary exosomes and found that the miR-223-3p content of salivary exosomes from periodontitis was less than the healthy control. Furthermore, we performed dual-luciferase reporter assay and real-time PCR to verify that (NOD)-like receptor (NLR) pyrin domain-containing 3 (NLRP3) was the target of miR-223-3p. When we knocked down the miR-223-3p expression in THP-1-derived macrophages, the expression of NLRP3 and the downstream inflammatory mediators interleukin-1β (IL-1β) and IL-6 were upregulated. By using integrated bioinformatics analysis, we found that pyroptosis and cytokine secretion participated in inflammatory gingival tissues. In addition, NLRP3, and the pyroptosis executioner, gasdermin D (GSDMD) was highly active in inflammatory gingival tissues compared with healthy controls by western blotting and immunohistochemistry. In summary, we speculated that miR-223-3p in salivary exosomes might regulate GSDMD-mediated pyroptosis by targeting NLRP3 in periodontitis. Detection of miR-223-3p expression in salivary exosomes could be used as an important non-invasive method to diagnose and evaluate the severity of periodontitis.

Targeting TSP-1 decreased periodontitis by attenuating extracellular matrix degradation and alveolar bone destruction

An important factor in periodontitis pathogenesis relates to a network of interactions of various cytokines. Thrombospondin-1 (TSP-1) is upregulated in several inflammatory diseases. We previously found that Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS)-induced TSP-1 production, and that TSP-1 simultaneously and effectively elevated inflammatory cytokines in THP-1 macrophages. This suggests that TSP-1 plays an important role in the pathology of periodontitis. However, the function of TSP-1 on oral cells is largely unknown. This study aimed to elucidate the underlying molecular mechanisms of TSP-1 in human periodontal fibroblasts (hPDLFs). We demonstrated that TSP-1 is highly expressed in the gingival crevicular fluid of patients with chronic periodontitis and in the inflammatory gingival tissues of rats. TSP-1 overexpression or treatment with recombinant human TSP-1(rTSP-1) promoted the expression of MMP-2, MMP-9 and RANKL/OPG in hPDLFs, while anti-TSP-1 inhibited cytokines production from P. gingivalis LPS-treated hPDLFs. Additional experiments showed that SB203580 (a special p38MAPK inhibitor) inhibited MMP-2, MMP-9 and RANKL/OPG expression induced by rTSP-1. Thus, TSP-1 effectively promoted P. gingivalis LPS-induced periodontal tissue (extracellular matrix (ECM) and alveolar bone) destruction by the p38MAPK signalling pathway, indicating that it may be a potential therapeutic target against periodontitis.

Platelets as inflammatory mediators in a murine model of periodontitis.

To investigate the role of platelets during the development of ligature-induced experimental periodontitis in mice. Experimental periodontitis was induced by placement of sterilized 5-0 cotton ligatures around the maxillary and mandibular second molars of C57BL/6 wild-type mice. Flow cytometry was used to analyse platelet activation and platelet-leucocyte aggregate formation, and histologic analysis was used to evaluate inflammation and localization of platelets and leucocytes in periodontal tissues during the development of experimental periodontitis and in experimental periodontitis with and without antiplatelet drug treatment. Experimental periodontitis induced platelet activation and platelet-leucocyte interaction. Platelets and leucocytes gradually infiltrated in inflammatory gingival tissues during the development of experimental periodontitis. The inhibition of platelet activation via drug therapy led to significant inhibition of leucocyte migration and marked reduction in periodontal inflammation. This study revealed that platelets are critical for inflammation and tissue injury in periodontitis and serve as mediators of inflammation in periodontal tissue.

LncRNA MALAT1 regulates inflammatory cytokine production in lipopolysaccharide-stimulated human gingival fibroblasts through sponging miR-20a and activating TLR4 pathway.

It has been reported that long non-coding RNAs (lncRNAs), such as metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), act as key regulators of the development of inflammatory diseases. However, it is unclear whether MALAT1 regulates the function of human gingival fibroblasts (HGFs) in periodontitis. This study is to explore the role of MALAT1 on inflammatory cytokine production of HGFs. Primary HGFs were harvested from human gingiva. MALAT1 was detected in inflammatory and healthy gingival tissues via quantitative real-time PCR (qRT-PCR). Bioinformatics analysis, dual-luciferase reporter assay, and RNA-binding protein immunoprecipitation (RIP) were used to detect the relationship among MALAT1, toll-like receptor 4 (TLR4), and microRNA (miR) -20a. After transfection LPS-treated HGFs with MALAT1 siRNA (si-MALAT1), miR-20a mimic or overexpression MALAT1 plasmid (sno-MALAT1), the levels of MALAT1, miR-20a, TLR4, IL-6 and IL-8 were analyzed by qRT-PCR, enzyme-linked immunosorbent assay, or western blot assay. MALAT1 up-regulated in inflammatory gingival tissues of chronic periodontitis. MiR-20a was bound with MALAT1 and TLR4 3'-UTR in RNA-protein complex with Ago2, respectively. Moreover, MALAT1, TLR4, IL-6, and IL-8 increased while miR-20a decreased after 1μg/mL Porphyromonas gingivalis lipopolysaccharide (LPS) or Escherichia coli LPS stimulation. MiR-20a inhibited the expression of proinflammatory cytokines via binding to TLR4 3'-UTR. In addition, MALAT1 increased TLR4 level and the secretion of inflammatory cytokines. MALAT1 enhances inflammatory cytokine production through sponging miR-20a and releasing TLR4, indicating a regulatory role of MALAT1 in periodontal inflammation.

The interaction between serum amyloid A and Toll-like receptor 2 pathway regulates inflammatory cytokine secretion in human gingival fibroblasts.

Serum amyloid A (SAA) has been identified to trigger inflammation response, and play a crucial role in chronic inflammatory diseases. However, the regulatory mechanism of SAA still remains unclear during the development of periodontitis METHODS: SAA mRNA and protein expression were detected in healthy and inflammatory gingival tissues using real-time polymerase chain reaction (PCR) and immunohistochemistry. Human recombinant SAA (Apo-SAA), Pam3CSK4 (a Toll-like receptor (TLR) 2 ligand), siRNA-SAA, or TLR2 neutralizing antibody was applied to treat human gingival fibroblasts, respectively, or combined. SAA, TLRs, and inflammatory cytokines interleukin (IL)-6 and IL-8 were analyzed by real-time PCR, western blotting, or enzyme-linked immunosorbent assay. SAA expression increased in human inflammatory gingival tissues from patients with periodontitis (P<0.05). Apo-SAA could increase not only the mRNA expression of TLR2 (P<0.05), but also IL-6 and IL-8 mRNA and protein levels (P<0.05) which was suppressed by TLR2 antibody in human gingival fibroblasts. Pam3CSK4 increased SAA, IL-6, and IL-8 levels (P<0.05). However, the expression of SAA, IL-6, and IL-8 decreased after transfection of siRNA-SAA (P<0.05). SAA not only increases in inflammatory gingiva, but also triggers inflammatory cytokine secretion via interacting with TLR2 pathway in human gingival fibroblasts, which indicates that SAA is involved in periodontal inflammation.

Gingival Exudatome Dynamics Implicate Inhibition of the Alternative Complement Pathway in the Protective Action of the C3 Inhibitor Cp40 in Nonhuman Primate Periodontitis.

Periodontitis is a prevalent chronic inflammatory disease associated with dysbiosis. Although complement inhibition has been successfully used to treat periodontitis in animal models, studies globally analyzing inflamed tissue proteins to glean insight into possible mechanisms of action are missing. Using quantitative shotgun proteomics, we aimed to investigate differences in composition of inflammatory gingival tissue exudate ("gingival crevicular fluid"; GCF), before and after local administration of an inhibitor of the central complement component, C3, in nonhuman primates. The C3 inhibitor, Cp40 (also known as AMY-101) was administered locally in the maxillary gingival tissue of cynomolgus monkeys with established periodontitis, either once a week (1×-treatment; n = 5 animals) or three times per week (3×-treatment; n = 10 animals), for 6 weeks followed by another 6 weeks of observation in the absence of treatment. 45 GCF samples were processed for FASP digestion and liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. Data were processed using the ProgenesisQI software. The statistical significance of differences between the groups was determined by RM-ANOVA, and a protein expression change was considered as a true regulation at >2-fold and p < 0.05. The human orthologues were subjected to Gene Ontology analyses using PANTHER. Data are available via ProteomeXchange with identifier PXD009502. 573 proteins with >2 peptides were longitudinally quantified. Both 3× and 1× administration of Cp40 resulted in significant down-regulation of dozens of proteins during the 6-week course of treatment as compared to baseline. Following drug withdrawal at 6 weeks, more than 50% of the down-regulated proteins showed increased levels at week 12. The top scored pathway was "complement activation, alternative pathway", and several proteins involved in this pathway were down-regulated at 6 weeks. We mapped the proteomic fingerprint changes in local tissue exudate of cynomolgus monkey periodontitis in response to C3 inhibition and identified the alternative pathway of complement activation and leukocyte degranulation as main targets, which are thus likely to play significant roles in periodontal disease pathogenesis. Label-free quantitative proteomics strategies utilizing GCF are powerful tools for the identification of treatment targets and providing insights into disease mechanisms.

High Mobility Group Box 1 Protein Level as a Novel Biomarker for the Development of Peri-Implant Disease

Peri-implant disease is a chronic inflammation of the soft and hard tissues around a dental implant, resulting from bacterial infection. Recent evidence indicates that some pro-inflammatory cytokines and chemokines released by immunocytes are substantially responsible for the progress and consequence of inflammation. High mobility group box 1 (HMGB1) is released into the extracellular matrix and acts as a key pro-inflammatory factor during injury, necrosis and inflammation. A higher concentration of HMGB1 has been found in gingival crevicular fluid from inflammatory gingival tissue than from healthy sites. HMGB1 mRNA and protein are overexpressed in murine periodontal ligament fibroblasts stimulated with lipopolysaccharide (LPS) and IL-1β. Thus, this study sought to assess HMGB1 expression in peri-implant crevicular fluid (PICF) at each stage of peri-implant disease and to investigate the correlation between HMGB1 and peri-implant disease progress. The results demonstrated that the HMGB1 expression level in PICF is indicative of the progress of peri-implant disease and hence may be a useful diagnostic and prognostic biomarker for peri-implant tissue.

Assessment of IL-6, IL-8 and TNF-α levels in the gingival tissue of patients with periodontitis

In periodontal diseases, inflammatory mediators, including interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α), may promote the degeneration of inflamed periodontal tissues. In previous studies, levels of these three cytokines were demonstrated to be elevated in inflammatory gingival tissues and gingival crevicular fluid. The aim of the present study was to quantify IL-6, IL-8 and TNF-α levels in the human gingival tissues of patients with periodontitis and to assess the correlation of these three cytokines with each other. In this study, human gingival tissues from 19 patients with periodontitis (male, n=14; female, n=5) were collected. The tissues were homogenized, centrifuged and the protein in the supernatant was quantified. Enzyme-linked immunosorbent assay (ELISA) was used in the measurement of the IL-6, IL-8 and TNF-α levels, and the mean levels were observed to be 8.41±0.25, 34.01±1.09 and 20.70±0.31 pg/ml, respectively. The mean levels of IL-8 were higher than those of the other two cytokines. In each sample, the level of TNF-α expression was consistently high, with little difference between the results, which contrasted with the fluctuations in IL-6 and IL-8 levels. The expression of the two ILs (IL-6 and IL-8) showed a positive correlation (r=0.932, P=0.01), whereas TNF-α levels were not correlated with IL-6 or IL-8 levels. These results suggest that IL-6, IL-8 and TNF-α may be relevant in the pathophysiology of periodontitis, and the measurement of these cytokines may be beneficial in the identification of patients with periodontitis.

Inflammatory environment induces gingival tissue‐specific mesenchymal stem cells to differentiate towards a pro‐fibrotic phenotype

Human gingival tissues are prone to hyperplasia under inflammatory stimuli. We have identified gingival tissue-specific mesenchymal stem cells (GMSCs) and found their functional change being correlated with drug-induced gingival hyperplasia. However, whether these cells exhibit characteristics of pro-fibrotic phenotype under inflammatory condition remains unknown. GMSCs isolated from human normal gingival tissues (N-GMSC) and inflammatory gingival tissues (I-GMSC) were cultured in vitro, representative cytokines were added to simulate the in vivo inflammatory environment. Under the influence of the inflammatory cytokines, GMSCs exhibited higher rate of proliferation than those under normal condition, while their potential for osteogenic and adipogenic differentiation was suppressed. The expression of matrix metalloproteinases (MMP)-1, MMP-2, IL-1, IL-6, TNF-α and type 1 collagen was significantly higher in I-GMSCs than in N-GMSCs. Furthermore, compared with dental pulp stem cells, GMSCs showed different pattern of gene expression and extracellular matrix formation in inflammatory environment. Inflammatory microenvironment induces GMSCs to differentiate towards a pro-fibrotic phenotype, which could underlie the hyperplastic appearance of inflammatory gingiva.

The expressions of C-reactive protein and macrophage colony-stimulating factor in gingival tissue of human chronic periodontitis with hypertension

Purpose: The purpose of this study was to quantify and compare the expressions of CRP and M-CSF in the gingival tis- sues of the patients with chronic periodontitis associated to hypertension. Methods: Gingival tissue samples were obtained during periodontal surgery or tooth extraction. Clinically healthy gingival tissue samples from systemically healthy 12 patients were categorized as group 1 (n=12). Inflammatory gingival tissue sam- ples from patients with chronic periodontitis were categorized as group 2 (n=12). Inflammatory gingival tissue samples from patients with chronic periodontitis associated with hypertension were categorized as group 3 (n=12). Tissue samples were prepared and analyzed by Western blotting. The quantification of CRP and M-CSF were performed using a densitometer and statistically analyzed by one-way ANOVA followed by Tukey test. Results: There were significant differences between group 1 and group 2 and between group 1 and group 3 in both CRP and M-CSF. The differences between group 2 and group 3 were not statistically significant in both proteins. However, the expression levels of CRP and M-CSF in hypertensive inflammatory gingiva showed increased tendency compared to non-hypertensive inflammatory gingiva. Conclusions: It is suggested that CRP and M-CSF might be used as inflammatory and bone resorption markers in perio- dontal diseased tissue. It is assumed that hypertension may be associated with the progression of periodontal inflammation and alveolar bone resorption. (J Korean Acad Periodontol 2009;39:391-398)

Do Langerhans cells behave similarly in elderly and younger patients with chronic periodontitis?

Objective The purpose of this study was to compare the number, the distribution and the expression of markers of maturation of Langerhans cells (LC) in elderly and younger patients with chronic periodontitis in order to evidence the effect of aging on LC in inflammatory gingival tissue. Methods Gingival tissue specimens presenting chronic periodontitis from 8 elderly patients aged >75 (group E) and from 8 younger patients aged 50–60 (considered as controls, group C) were used for immunohistochemistry with monoclonal antibodies against CD45RB (leucocytes), CD1a (LC), markers of LC maturation (DC-LAMP, CD83) and number of immunolabelled cell subsets was evaluated using image analysis. Results The difference in the number of CD45RB+ leucocytes in the upper connective tissue between groups was not significant. In group E, the number of CD1a+ LC was significantly decreased ( P < 0.002) in the epithelium and significantly increased ( P < 0.0004) in the upper connective tissue. Furthermore, in group E, intraepithelial CD1a+ LC are more often observed in the upper epithelium and their dendritic processes were shorter and less numerous. Concerning the expression of markers of maturation, the numbers of intraepithelial DC-LAMP+ cells and CD83+ cells were significantly increased ( P < 0.0007 and P < 0.02, respectively) in group E. Conclusion During chronic periodontitis in elderly patients, the decrease in the number of intraepithelial LC and the alteration of dendritic processes could be balanced by a cellular distribution often observed in the upper epithelium associated with changes in cell maturation in response to bacterial elements.

Induction of calprotectin release by Porphyromonas gingivalis lipopolysaccharide in human neutrophils.

Calprotectin, a major cytosolic protein of leukocytes, is detected in neutrophils, monocytes/macrophages, and epithelial cells. This protein is known to be a marker for several inflammatory diseases and is detected in inflammatory gingival tissue with periodontal disease. Recently, we found that the calprotectin level in gingival crevicular fluid from periodontitis patients was significantly higher than that of healthy subjects. However, the regulation of calprotectin in periodontal disease is unclear. In the present study, we investigated the effect of lipopolysaccharides of periodontopathic bacteria on calprotectin release from human neutrophils. Neutrophils from healthy donors were treated with lipopolysaccharides from Porphyromonas gingivalis (P-LPS), Actinobacillus actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, and Escherichia coli. Calprotectin of neutrophil was identified by immunoblotting and calprotectin amount was determined by ELISA. Two subunits (10 and 14 kDa) of calprotectin were observed in the cell and medium fractions from neutrophils. P-LPS increased calprotectin release from seven to 16 times the control level after 30 min and its effect appeared in a dose-dependent manner (10-1000 ng/ml). Lipopolysaccharides from A. actinomycetemcomitans, P. intermedia, F. nucleatum, and E. coli also induced calprotectin release from neutrophils. These results suggest that lipopolysaccharides from periodontopathic bacteria induce calprotectin release from human neutrophils.

DNA microarray analysis of human gingival fibroblasts from healthy and inflammatory gingival tissues

In the inflammatory gingival tissues of patients with periodontitis, cytokines such as interleukin (IL)-1α, IL-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α have been detected. Gingival fibroblasts are the major constituents of gingival tissue. We recently demonstrated that lipopolysaccharide (LPS) from periodontopathic bacteria induces inflammatory reactions in various tissues via CD14 and/or Toll-like receptors (TLRs) in gingival tissues [Biochem. Biophys. Res. Commun. 273 (2000) 1161]. To confirm this, we examined the expression of IL-1α, IL-1β, IL-6, IL-8, TNF-α, CD14, TLR2, and TLR4 in human gingival fibroblasts (HGFs) obtained from patients with healthy or inflammatory gingiva using DNA microarray analysis. We also studied the expression levels of these proteins by flow cytometric analysis (FACS). The expression levels of all eight genes in the HGFs of the Inflammatory group were significantly higher than those in the Healthy group on DNA microarray analysis. FACS revealed that the expression levels of all eight proteins on the HGFs of the Inflammatory group were higher than those on the Healthy group. Our data indicated that these eight proteins in HGFs are involved in inflammatory conditions in the gingiva, including periodontal disease. Our results suggested that these eight proteins, in turn, act directly or indirectly on the immune response by activating host cells involved in inflammatory processes.

A correlation study of inflammatory cell mobilization in response to subgingival microbial colonization.

This study evaluated site-by-site the relations between subgingival microbial colonization and gingival tissue reactions. Experimental, deep periodontal defects were established at buccal surfaces of mandibular and maxillary canine teeth in 5 beagle dogs. The root surfaces were instrumented by a flame-shaped, fine-grained, rotating diamond point, or by a sharp curet. Following a 10-day postsurgical healing period, the dogs were fed a plaque-inducing diet for 70 days. The animals were then sacrificed and tissue blocks of the experimental sites including teeth and periodontal tissues were secured. The buccal gingiva was removed and processed for histomorphometric analysis while the teeth were prepared for scanning electron microscopic evaluation of the extent of subgingival microbial colonization. The results revealed that inflammatory cell density in the junctional epithelium and in the connective tissue were positively correlated to subgingival microbial colonization (P < 0.01). Furthermore, the degree of significance decreased with increasing distance from the plaque. The present study demonstrates that a close relation may exist between the extent of subgingival microbial colonization and inflammatory gingival tissue reactions.

Lectin binding to chronic inflammatory gingival tissue: possible adhesion mechanisms based on lectin-carbohydrate interactions.

In this study, we analyzed the expression of different leukocyte surface antigens, of the adhesion molecules ELAM-1 and GMP-140 and binding of various lectins and neoglycoproteins in inflamed gingival tissue. Cell suspensions from collagenase-digested gingiva were analyzed by flow cytometry in a FACScan. The expression of ELAM-1, GMP-140, carbohydrate structures and lectins in gingival specimens was also studied by immunohistochemistry. Gingival tissue of patients with active periodontal disease contained between 5% and 50% CD45+ mononuclear cells, consisting mainly of CD19+ cells (B lymphocytes). CD62, resembling GMP-140, and ELAM-1 were strongly expressed on endothelial cells of these patients. Control subjects usually contained almost no CD45+ cells in their gingiva and no CD62+ or ELAM-1-positive endothelial cells could be found in 5 of 6 control persons. Analysis of the glycosylation pattern revealed staining of infiltrating cells by peanut agglutinin (PNA; specificity for galactose), whereas soy bean agglutinin (SBA; specificity for N-acetyl-galactosamine) bound to epithelial cells. An endogenous lactosyl-specific lectin could be detected on endothelial cells by binding of lactosyl-BSA. Ulex europeus I agglutinin (UEA-1, specific for fucose) showed selective staining of endothelial and epithelial cells. Expression of a fucose-binding lectin, demonstrated by binding of fucosylated BSA, could be found on infiltrating cells. The adhesion molecules ELAM-1 and GMP-140 seem to be involved in cell adhesion during chronic inflammation of the gingiva. Interaction of other carbohydrate residues with endogenous lectins might resemble additional adhesion mechanisms in inflamed gingiva.