Production of interleukin-8 in vitro by mononuclear cells isolated from human periapical lesions

INTRODUCTION: Interleukin-8 (IL-8) is an important mediator of inflammation. However, little is known about its production in chronic dental periapical lesions and this was the main aim of this work. METHODS: Inflammatory cells were isolated from clinically different periapical lesions and analyzed by morphological criteria. The mononuclear cells were isolated, phenotypically analyzed by immunocytochemistry and cultivated in vitro. IL-8 was measured in culture supernatants of these periapical lesion mononuclear cells (PL-MNC) using a microbeads fluorescence assay. RESULTS: We found a relatively high production of IL-8 in 19 out of 21 periapical lesions included in the study. The level of IL-8 and the proportion of neutrophil granulocytes were significantly higher in the group of symptomatic lesions, compared to the asymptomatic lesions, but there was no statistically significant correlation between these parameters. According to the predominance of CD3(+) T cells and Ig(+)/CD19(+) B cells and plasma cells, lesions were divided into T-type and B-type lesions, respectively. The levels of IL-8 were significantly higher in the culture supernatants of PL-MNC in the T-type lesions and were positively correlated with the proportion of macrophages/dendritic cells (CD11c(+) cells) and CD4(+) T cells. Such a correlation was not shown in B-type lesions. CONCLUSION: These results suggest that PL-MNC are a significant source of IL-8, which is probably an important chemokine for the migration and function of different cell types at the site of chronic inflammation.     

Production of interleukin‐8 in vitro by mononuclear cells isolated from human periapical lesions

Introduction: Interleukin‐8 (IL‐8) is an important mediator of inflammation. However, little is known about its production in chronic dental periapical lesions and this was the main aim of this work. Methods: Inflammatory cells were isolated from clinically different periapical lesions and analyzed by morphological criteria. The mononuclear cells were isolated, phenotypically analyzed by immunocytochemistry and cultivated in vitro. IL‐8 was measured in culture supernatants of these periapical lesion mononuclear cells (PL‐MNC) using a microbeads fluorescence assay. Results: We found a relatively high production of IL‐8 in 19 out of 21 periapical lesions included in the study. The level of IL‐8 and the proportion of neutrophil granulocytes were significantly higher in the group of symptomatic lesions, compared to the asymptomatic lesions, but there was no statistically significant correlation between these parameters. According to the predominance of CD3⁺ T cells and Ig⁺/CD19⁺ B cells and plasma cells, lesions were divided into T‐type and B‐type lesions, respectively. The levels of IL‐8 were significantly higher in the culture supernatants of PL‐MNC in the T‐type lesions and were positively correlated with the proportion of macrophages/dendritic cells (CD11c⁺ cells) and CD4⁺ T cells. Such a correlation was not shown in B‐type lesions. Conclusion: These results suggest that PL‐MNC are a significant source of IL‐8, which is probably an important chemokine for the migration and function of different cell types at the site of chronic inflammation.     

The presence of IL-17+/FOXP3+ double-positive cells in periodontitis

Increasing evidence suggests that distinct inflammatory cytokines convert forkhead box protein P3 (FOXP3(+)) regulatory T-cells (Tregs) into IL-17-producing cells (Th17 cells) in vitro. However, this functional plasticity has not been examined in the pathogenesis of periodontal disease. In this study, we analyzed the IL-17A(+)FOXP3(+) cells present in periodontitis lesions to determine the association between Treg conversion and the pathogenesis of periodontitis. The immunohistochemical analysis of gingival tissues demonstrated that the numbers of Th17 cells (IL-17A(+)FOXP3(-)) and Tregs (IL-17A(-)FOXP3(+)) were greater in periodontitis lesions than in gingivitis lesions. We further identified a small number of IL-17A(+)FOXP3(+) cells in periodontitis lesions but not in gingivitis lesions. The flow cytometry analysis of CD4(+) T-cell lines established from gingival tissues and the peripheral blood of periodontitis patients showed that the proportion of Tregs was reduced and the proportion of IL-17A(+)FOXP3(+) cells among all FOXP3(+) cells was elevated in gingival tissue T-cell lines relative to the proportions in peripheral blood T-cell lines. Our findings indicate that Treg-Th17 conversion may occur in periodontitis lesions. Further studies addressing the role of Treg conversion during inflammatory responses against periodontopathic bacteria are needed.     

Interleukin-17 plays a role in exacerbation of inflammation within chronic periapical lesions

Interleukin (IL)-17 plays an important role in inflammation and certain autoimmune diseases. However, its role in the pathogenesis of chronic dental periapical lesions has not been studied. Periapical lesion mononuclear cells (PL-MNC) were isolated from inflammatory cells and phenotypically analyzed by immunocytochemistry. The cells were cultured in vitro and IL-17 and IL-8 were measured in the culture supernatants. Controls were peripheral blood (PB) MNC. The level of IL-17 and the proportion of neutrophils were significantly higher in symptomatic lesions. In addition, the production of IL-17 was higher in culture supernatants of PL-MNC isolated from lesions with a predominance of T cells, and the IL-17 concentration correlated with the proportion of CD3+ and CD4+ cells. There was a positive correlation between the levels of IL-17 and IL-8 in the group of symptomatic lesions. The relationship between these cytokines was additionally confirmed on the basis of augmented production of IL-8 by both PL-MNC and PB-MNC treated with IL-17. Our results suggest that IL-17, by stimulating the production of IL-8, may play a role in exacerbating inflammation within chronic periapical lesions.     

Correlation between phenotypic characteristics of mononuclear cells isolated from human periapical lesions and their in vitro production of Th1 and Th2 cytokines

The development and progression of periapical dental lesions, mediated by the specific immune response, are poorly understood. In these processes, an interplay of different proinflammatory and immunoregulatory cytokines is of crucial importance.

Objectives

To examine the activation of T helper 1 (Th1) and Th2 immune responses in 25 human periapical lesions based on the ex vivo production of interferon-gamma (IFN-γ) and interleukin-4 (IL-4) by mononuclear cells (PL-MNC).

Methods

The levels of IFN-γ and IL-4 in culture supernatants of PL-MNC, determined by ELISA, were correlated with concentrations of these cytokines in cultures of control MNC from peripheral blood (PB-MNC), cellular composition of inflammatory cells and phenotypic characteristics of PL-MNC.

Results

We detected high levels of IFN-γ in all samples, after cell stimulation with phorbol myristate acetate and Ca²⁺ ionophore, that were not statistically different from the levels of IFN-γ in PB-MNC cultures. IL-4 was detected in 76% samples, but its concentrations were much lower than in PB-MNC samples. The levels of IFN-γ were higher in cultures of PL-MNC isolated from periapical lesions with predominance of T cells (T-type lesions) and correlated positively with the proportion of antigen-presenting cells (macrophages and dendritic cells), CD4⁺ T cells and IgG2⁺ B cells/plasma cells. The levels of IL-4 correlated negatively with the proportion of macrophages, but positively with the number of mast cells and IgG4⁺ cells. IL-18R, a stable marker of Th1 cells, was detected on a relatively small proportion of CD3⁺ T cells and its expression correlated with the levels of IFN-γ. However, the expression of ST2L, a stable Th2 cell marker, was not detected. The levels of Th1 and Th2 cytokines did not correlate with clinical characteristics of the lesions, defined by the presence of symptoms.

Conclusion

Cumulatively, our results suggest the predominance of Th1 immune response in periapical lesions.     

阿司匹林对兔颊VX-2鳞状细胞癌炎症微环境中树突细胞的影响

目的探索阿司匹林及炎症对兔颊VX-2鳞状细胞癌上清液中树突细胞（DC）成熟及功能的影响。方法通过瘤粒植入术及机械创伤+高糖饮食的方法,建立兔颊VX-2鳞状细胞癌及其炎症模型,将模型兔分为3组。实验组：制造颊癌及炎症后使用阿司匹林灌胃治疗3 d;对照组：制造颊癌及炎症后以生理盐水灌胃作为对照;空白组：不制造炎症的单纯肿瘤兔组。3 d后收集各组肿瘤标本,制成匀浆,取上清液与正常兔外周血单核细胞共培养以使其向DC分化,采用流式细胞仪检测DC表面分子CD83、CD86、人类白细胞DR抗原（HLA-DR）的表达,混合淋巴细胞反应检测DC刺激T细胞增殖的能力。结果实验组和对照组中CD83、CD86、HLA-DR阳性率均低于空白组（P<0.05）,而实验组和对照组间的差异无统计学意义（P>0.05）;同样,实验组和对照组刺激T细胞增殖的能力弱于空白组（P<0.05）,而两组间刺激T细胞增殖的能力无明显差异（P>0.05）。结论炎症可抑制DC表面分子CD83、CD86、HLA-DR的表达和功能发挥,短期、小剂量服用阿司匹林对兔颊VX-2鳞状细胞癌炎症微环境中DC的表型改善和功能发挥无明显作用。     

Antigen‐presenting cells in human periodontal disease tissues

T cells are present in the inflammatory infiltrates of periodontal disease lesions and require antigen presentation by antigen‐presenting cells (APCs). While it is still not known whether Th1 or Th2 cells predominate in these lesions, it has been reported that different APCs may induce activation of different T‐cell subsets. An immunoperoxidase technique was used to investigate the presence of CD1a+, CMRF‐44+, CMRF‐58+ and CD83+ dendritic cells, CD14+ macrophages or dendritic cell precursors and CD19+ B cells in gingival biopsies from 21 healthy or gingivitis and 25 periodontitis subjects. The samples were divided into three groups according to the size of infiltrate (group 1, small infiltrates; group 2, medium infiltrates; group 3, extensive infiltrates). The presence of numerous CD1a+ Langerhans cells was noted in the epithelium with no differences between the healthy/gingivitis and periodontitis groups. The percentage of CD83+ dendritic cells in the infiltrates was higher than the percentage of CD1a+, CMRF‐44+ or CMRF‐58+ dendritic cells. Endothelial cells positive for CD83 were found predominantly in areas adjacent to infiltrating cells, CD83+ dendritic cells being noted in the region of CD83+ endothelium. The percentage of CD14+ cells in the inflammatory infiltrates was similar to that of CD83+ dendritic cells. B cells were the predominant APC in group 2 and 3 tissues. The percentage of B cells in group 3 periodontitis lesions was increased in comparison with group 1 periodontitis tissues and also in comparison with group 3 healthy/gingivitis sections. Functional studies are required to determine the roles of different APC subpopulations in periodontal disease.     

Antigen-presenting cells in human periodontal disease tissues

T cells are present in the inflammatory infiltrates of periodontal disease lesions and require antigen presentation by antigen-presenting cells (APCs). While it is still not known whether Th1 or Th2 cells predominate in these lesions, it has been reported that different APCs may induce activation of different T-cell subsets. An immunoperoxidase technique was used to investigate the presence of CD1a+, CMRF-44+, CMRF-58+ and CD83+ dendritic cells, CD14+ macrophages or dendritic cell precursors and CD19+ B cells in gingival biopsies from 21 healthy or gingivitis and 25 periodontitis subjects. The samples were divided into three groups according to the size of infiltrate (group 1, small infiltrates; group 2, medium infiltrates; group 3, extensive infiltrates). The presence of numerous CD1a+ Langerhans cells was noted in the epithelium with no differences between the healthy/gingivitis and periodontitis groups. The percentage of CD83+ dendritic cells in the infiltrates was higher than the percentage of CD1a+, CMRF-44+ or CMRF-58+ dendritic cells. Endothelial cells positive for CD83 were found predominantly in areas adjacent to infiltrating cells, CD83+ dendritic cells being noted in the region of CD83+ endothelium. The percentage of CD14+ cells in the inflammatory infiltrates was similar to that of CD83+ dendritic cells. B cells were the predominant APC in group 2 and 3 tissues. The percentage of B cells in group 3 periodontitis lesions was increased in comparison with group 1 periodontitis tissues and also in comparison with group 3 healthy/gingivitis sections. Functional studies are required to determine the roles of different APC subpopulations in periodontal disease.     

Differences in Inflammation and Bone Resorption between Apical Granulomas,Radicular Cysts,and Dentigerous Cysts

IntroductionDental cysts can be of inflammatory (radicular cysts) or noninflammatory (dentigerous cysts) origin. Apical periodontitis is a necrosis of the pulp and infection of the root canal causing the development of apical granulomas or radicular cysts. The immunology of granuloma and cyst formation is important because modern root filling materials are immunologically active and can contribute to the resolution of apical granulomas. In contrast, radicular cysts often require apicectomy. A better understanding of the pathophysiology of inflammation and bone resorption in apical periodontitis could be the basis for developing new root filling materials with superior immunomodulatory properties.MethodsForty-one apical granulomas, 23 radicular cysts, and 23 dentigerous cysts were analyzed in this study. A tissue microarray of the 87 consecutive specimens was created, and human leukocyte antigen–DR isotype (HLA-DR)-, CD83-, receptor activator of nuclear factor kappa B ligand–, macrophage colony-stimulating factor (MCSF)-, galectin-3 (Gal3)-, CD4-, and CD8-positive cells were detected by immunohistochemistry. Tissue microarrays were digitized, and the expression of markers was quantitatively assessed.ResultsHLA-DR, CD83, MCSF, and Gal3 expression was significantly (P < .05) higher in radicular cysts compared with apical granulomas. HLA-DR, CD83, MCSF, receptor activator of nuclear factor kappa B ligand, and Gal3 expression in dentigerous cysts was significantly (P < .05) lower than in both periapical lesions (apical granulomas and radicular cysts). CD4 and CD8 infiltration was not statistically different between apical granulomas and radicular cysts. Dentigerous cysts showed a significantly (P < .05) lower T-cell infiltration than apical periodontitis. The CD4/CD8 ratio was not significantly different between the analyzed groups.ConclusionsThe development of radicular cysts in apical periodontitis is associated with an increased expression of myeloid inflammatory markers and bone resorption parameters. Antigen-presenting cells and myeloid cells might be more relevant for the pathogenesis of apical periodontitis than T cells. Increased inflammation might promote the formation of radicular cysts and more pronounced bone resorption.     

口腔鳞癌中树突状细胞的免疫组化分析

目的　通过分析口腔鳞癌中浸润性树突状细胞的特征性表型,以探讨其在肿瘤微环境中的功能状态。方法　选择未经任何非手术治疗的初发口腔鳞癌患者标本34例作为实验组,30例口腔正常粘膜组织作为对照组。通过免疫组化技术标记组织中树突状细胞(DC)的CD1a,HLA-DR和CD83抗原,观察两种组织中的DC表达3种抗原的状况,结果进行统计学分析。结果　所有病例均未见明显CD83+DC,但均有CD1a+DC,其在口腔鳞癌组织中的浸润程度低于正常口腔粘膜组织,差异有显著性(P<0·05)。在口腔鳞癌组中有27例癌实质内的DC表达HLA- DR抗原,其HLA-DR的阳性表达率为79·41%。结论　口腔鳞癌组织中的DC,其浸润程度下降并存在功能成熟障碍。     

Cytokine expression in periapical granulation tissue as assessed by immunohistochemistry

The aims of this study were to investigate the expression of pro-inflammatory, anti-inflammatory and immune-related cytokines present in periapical lesions. We investigated the expression of cytokines: namely interleukins IL-2, IL-4, IL-6, IL-10 and interferon-gamma (IFN-gamma) in formalin-fixed, paraffin-embedded sections of periapical granulation tissue. The study samples were biopsies from 24 patients with periapical lesions: 12 with periapical granulomas and 12 patients with radicular cysts. Immunohistochemistry was also performed on tonsillar tissue which served as a control. We utilised a set of specific monoclonal antibodies and polyclonal monospecific antibodies to detect cells that expressed the different cytokines within the tissues. We also considered the nature of the periapical immune response by investigation of the T-helper 1 (Th-1) and T-helper 2 (Th-2) lymphocyte subsets using their cytokine profile, i.e., Th-1: IL-2 and IFN-gamma and Th-2: IL-4, IL-5 and IL-6. Only a few cells were weakly positive for the IL-2 protein in each of the tissue sections. Cells that expressed IL-4 or IL-6 were far more numerous than cells that expressed either IL-2 or IFN-gamma. Thus, we demonstrated a greater number of Th-2 cells in periapical lesions. This relative ratio of the T-cell subsets underlines the importance of the anti-inflammatory mechanisms taking place in the diseased tissue manifested by the wide array of IL-10-expressing cells: B cells, T suppressor cells (CD8 (+)) and tissue macrophages. The numbers of inflammatory cells expressing the anti-inflammatory molecules far outnumbered the cells that expressed pro-inflammatory cytokines. Thus, the downregulation of the inflammatory response and the predominant Th-2 or humoral immune response in periapical periodontitis may be important features that dictate the outcome of the disease process in the periapical lesion.     

Cytotoxicity of direct current with antibacterial agents against host cells in vitro

The purpose of this study was to investigate the cytotoxicity of iontophoresis treatment using direct current (DC) with or without antibacterial agents. The following antibacterial agents were used: diamine silver fluoride (AgF); sodium fluoride (NaF); and iodine zinc iodide (JJZ). The cytotoxic activity of DC with or without antibacterial agents against human polymorphonuclear cells (PMNs) was evaluated by the 3-[4, 5- dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay. It was noted that DC (2 mA) killed PMNs in a time-dependent manner and the cytotoxicity was enhanced when DC was combined with antibacterial agents. The toxic effect of antibacterial agents was in the order: AgF>JJZ>NaF. The death of PMNs by DC was evaluated by flow cytometry using annexin V-FITC/propidium iodide staining. DC appeared to induce necrosis rather than apoptosis of PMNs. These results suggest that iontophoresis treatment using DC and antibacterial agents may induce necrotic cytotoxicity in host cells around periapical lesions.     

Flow-cytometric analysis of T-lymphocyte subsets after different treatment methods in patients with pericoronitis.

PURPOSE: The aim of this study was to determine whether there was any change in T-lymphocyte subsets in patients with periocoronitis after the application of different treatment methods. PATIENTS AND METHODS: Twenty-six patients with acute pericoronitis were included in the study. In every phase of the treatment (pretreatment, postcurettage, and postextraction), the biopsy samples were taken from the gingival tissues at sites of pericoronitis. Then, CD4(+) and CD8(+) lymphocyte and CD4(+)/CD8(+) ratio values were determined using flow cytometry in the biopsy samples. At the same time, gingival index (L?e-Silness) and plaque index (Silness-L?e) scores were recorded to assess the periodontal status in patients. To determine the correlation between the clinical measurements and the laboratory results obtained before the treatment, after curettage, and after extraction, we conducted an analysis using a paired t-test. RESULTS: The normal values in peripheral blood of CD4(+) and CD8(+) lymphocytes are 25% to 29% and 19% to 48%, respectively. However, the CD4(+) and CD8(+) lymphocyte values in the patients with acute pericoronitis were found to be 22.12% +/- 6.15% and 7.69% +/- 4.12%, respectively. These values are lower than the normal values. The CD4(+) lymphocyte value increased to 31.06% +/- 7.09% postcurettage and to 32.24% +/- 3.11% postextraction. The CD8(+) lymphocyte value increased to 16.21% +/- 5.27% postcurettage and to 18.25% +/- 3.13% postextraction. The CD4/CD8 ratio increased postcurettage and postextraction. This increase was statistically significant (P <.001). Postcurettage, there was decrease in clinical indexes, which was statistically significant (P <.001). A significant correlation between CD4(+) lymphocyte and ginigival index values and also between CD8(+) lymphocyte and plaque index values was determined postcurettage (P <.05). CONCLUSION: CD4(+) and CD8(+) T-lymphocytes could play a significant role in pericoronitis pathobiology.     

Regulatory T Cells in Mouse Periapical Lesions

IntroductionT-regulatory (Treg, CD4+ FOXP3+) cells constitute a unique subpopulation of CD4+ T cells that inhibit T-cell responses and prevent disease development/exacerbation in models of autoimmunity. In the present study, we tested the hypothesis that Treg cells are induced in periapical lesions by dental pulp infection.MethodsIn situ hybridization (ISH) was used to localize FOXP3+ cells on day 21 after pulp exposure of the first molar teeth and infection with bacteria from the oral environment. FOXP3/GFP knock-in transgenic mice were used to quantify FOXP3+ Treg cells that infiltrate into periapical lesions by flow cytometry on days 7, 14, and 21 after infection. Periodontal ligament from uninfected teeth served as a negative control.ResultsISH showed strong signals that showed the presence of FOXP3+ cells mainly at the periphery of periapical lesions. In contrast, no positive cells were present in the periodontal ligament of uninfected controls. Flow cytometry showed an increase in the number of FOXP3+ Treg beginning between day 7 and day 14 (0.69% of the infiltrate) after infection and increased to day 21 (0.94%) (p < 0.05 and p < 0.001, respectively, vs uninfected controls). Treg were also increased in number in draining cervical lymph nodes after pulpal infection.ConclusionsThese results show that Treg cells are induced to infiltrate into periapical lesions by pulpal infection and suggest that they increase in a time-dependent manner.     

Quantitative analysis of the immunocompetent cells in periapical granuloma: correlation with the histological characteristics of the lesions

Granuloma formation includes an immune response in oral tissues to various microorganisms and their products. The immunocompetent cells of both series (T and B) are present in the periapical lesions. In order to further analyze the relative contribution and pathophysiological significance of the T cell subsets in granuloma formation, we undertook the quantitative analysis of the CD3-positive, CD4-positive, CD8-positive and Ig-positive cells in these lesions by using indirect immunofluorescence. Evidence is provided showing predominance of T cells in diffuse and B cells in focal mononuclear infiltrates. CD8-positive cells were more frequent in diffuse infiltrates and in particular in granulomas with distinct epithelium while CD4-positive cells were more numerous in focal infiltrates. It appears that the presence and ratios of different subsets of immunocompetent cells reflects the pathogenesis of granuloma and transformation to cyst.     

Antigen-presenting-cell function of interferon γ-treated human gingival fibroblasts

The present study was carried out to examine the antigen-presenting cell (APC) functions of human gingival fibroblasts (HGF) elicited with IFNy. Stimulation of HGF with IFNy clearly induced HLA-DR expression and enhanced expression of intercellular adhesion molecule-1 (ICAM-1) on HGF. Despite the phenotypical resemblance of IFNγ-treated HGF to so-called APC, HLA-DR positive HGF were unable to induce proliferation of allo-reactive peripheral blood T cells (PBT) isolated from different donors. The failure of IFNγ-treated HGF to stimulate unprimed allo-reactive PBT was not due to the lack of production of IL-1 or the immunosuppressive effect of PGE₂ from HGF. On the other hand, the fact that detectable expression of CD80, ligand for CD28, was not found on IFNy-treated HGF may at least in part explain the ineffective function of HGF as APC. Interestingly, IFNγ-treated HGF induced proliferation of primed allo-reactive CD4⁺ T cells in a HLA-DR dependent manner, suggesting that IFNγ-treated HGF may have the ability to stimulate pre-activated T cells. We then confirmed that high levels of IFNγ mRNA were detectable in inflamed gingival tissue. Although it cannot be concluded from this study that HGF are incapable of effectively presenting antigenic peptides to autologous T cells bearing appropriate T cell receptors, present results suggest that HGF may be affected by locally-secreted IFNy and that the IFNγ-stimulated HGF may play a role in regulating immune responsiveness in inflammatory periodontal lesions.     

Enhanced expression of activation-associated molecules on macrophages of heterogeneous populations in expanding periapical lesions in rat molars

Exudative macrophages are the most prevalent inflammatory cells during the entire pathogenetic process in experimentally induced rat periapical lesions. To clarify the significance of macrophages in the pathogenesis of periapical lesions, the way in which the phenotype of ED1 (a general marker for mononuclear phagocytes)-positive cells is modulated in actively expanding lesions was investigated, by immunoperoxidase staining with a panel of antibodies that recognize several activation-associated molecules on macrophages. Periapical lesions were induced experimentally by exposing the pulp in the lower first molars of Wistar rats. Active lesion expansion with morphological diversification of ED1-positive cells occurred between 14 and 28 days after the injury. Double immunoperoxidase staining revealed that ED1-positive cells coexpressing class II molecules of the major histocompatibility complex (MHC) molecules, inducible nitric oxide synthase (iNOS) and/or CD11a increased during the period of active lesion expansion. Increases of endothelial cells expressing intracellular adhesion molecule-1 and CD25 (interleukin-2 receptor)-expressing lymphocytes were also seen during the same period. Moreover, there existed two particular subpopulations of ED1 + cells in the established lesion at 28 days: (1) ED1++/class II MHC - /iNOS+ cells, located around the periapical abscess, and (2) ED1+/class II MHC+/ iNOS- cells with slender or dendritic morphology, distributed predominantly in the outer portion of the lesion where T lymphocytes were abundant. The first cell type could be a macrophage with potent phagocytic and antimicrobial actions, and the second might possess sufficient antigen-presenting capacity to cause the activation of T lymphocytes. It was concluded that macrophages, when activated, may participate in triggering lesion expansion. Functionally distinct subpopulations of macrophages may occupy different sites within the lesion where they can most effectively exert their specific functions.     

Inflammatory lesions in the gingiva following resective/non-resective periodontal therapy

BACKGROUND: Findings from previous experiments have revealed that inflammatory cell infiltrates may remain in the gingiva following clinically successful non-surgical periodontal therapy. PURPOSE: To investigate the presence of inflammatory lesions in the gingiva following a periodontal treatment procedure that included either soft-tissue resection [gingivectomy (GV)] or non-resective open-flap debridement (OFD). MATERIAL AND METHODS: Fifteen patients with advanced generalized chronic periodontitis were recruited. Following oral hygiene instruction and supragingival debridement, one tooth site in each quadrant (non-molar, probing pocket depth>5 mm, bleeding on probing(+) and >50% bone loss) was selected and a soft-tissue biopsy was obtained and prepared for immunohistochemical analysis. Using a split-mouth design, two quadrants were randomly selected for periodontal therapy including GV, while the two remaining quadrants were exposed to non-resective OFD procedure. Six months after completion of surgical treatment, a new set of biopsies was obtained from GV and OFD sites. RESULTS: The inflammatory lesions residing in the gingival biopsies obtained prior to surgical therapy were 1.33-1.41 mm(2) large and contained similar proportions of CD19(+)- (B-cells, 15%), CD3(+)- (T-cells, 7%) and elastase(+)- (polymorphonuclear cells, 2%) cells in the two treatment groups. The corresponding lesions identified in the soft-tissue specimens obtained after 6 months of healing were twice as large at OFD as at GV sites (0.19 versus 0.08 mm(2), p=0.002). The densities of CD19(+)- and elastase(+)-cells in these lesions were significantly greater at OFD than at GV sites. CONCLUSION: The findings of the present study indicate that surgical therapy including soft-tissue resection results in regenerated gingival units that contain smaller lesions with lower densities of immunocompetent cells when compared with the lesions remaining in sites treated by non-resective means.