Antibody to collagen type I in gingival crevicular fluid

Gingival crevice fluid (GCF) was collected from inflamed sites in 20 patients before and 6 weeks after treatment. Levels of IgG to human collagen Type I were measured in the GCF and autologous serum using an enzyme-linked immunosorbent assay and compared with levels in control sera. IgG antibody to collagen was detected in GCF at significantly (P less than 0.01) higher levels than in control sera, but these levels were not significantly (P greater than 0.05) different from those in autologous sera. The levels of IgG antibody in GCF and autologous sera did not alter significantly (P greater than 0.05) after treatment. IgG antibody to collagen Type I is present in GCF in the diseased and healing state.     

Autoimmunity to collagen in adult periodontal disease: Immunoglobulin classes in sera and tissue

The immunoglobulin class distribution of antibody to human collagen type I has been examined in sera and gingival extracts from patients with adult chronic periodontitis. Tissue extracts were made either by simple washing or ultrasonication. With either method, IgG and IgA antibodies to collagen were present in higher concentration in tissue extracts than in autologous serum when adjustment was made for dilution differences. No significant differences were found for IgM antibodies. Antibodies to human collagen type I are usually "natural antibodies" of the IgM class and, therefore, our findings suggest a class switch to IgG in inflamed gingivae, presumably due to prolonged antigenic stimulation.     

Clinical, microbiological and immunological studies on recurrent periodontal disease

Abstract. The present study was performed to evaluate the clinical, microbiological and immunological aspects in the early stages of recurrent periodontal disease. After clinical monitoring of pockets with recent evidence of disease recurrence, microbiological samples for cultural analysis, serum and gingival crevicular fluid (GCF) samples were taken for IgG antibody analysis from 14 sites, 7 in 6 recurrent periodontitis patients and 7 in 7 periodontally healthy control subjects. IgG responses of serum antibody to 8 gram-negative bacterial strains were compared with those of GCF sampled from the recurrent site. The results clearly demonstrated the predominance of Bacteroides gingivalis in most subgingival plaque samples during the early stages of disease recurrence; the mean proportions of B. gingivalis were significantly different from those of the healthy sites ( p <0.05). 4 out of 6 serum samples showed the elevated antibody responses to B. gingivalis 381: and this was closely correlated to homologous infection by this micro-organism in recurrent sites. Elevated serum antibody responses were also noted to Eikenella corrodens 1073 and Actinobacillus actinomycetemcomitans Y4. However, no relationship with homologous infection was found for A. actinomycetemcomitans. 3 out of 6 GCF samples had greater antibody titers than the serum, suggesting local antibody synthesis by the gingival cells in the recurrent pockets. The present study showed that B. gingivalis might play an important role in the pathogenesis of disease recurrence in its early stages.     

Presence of activated eosinophils, high IgE and sCD23 titers in gingival crevicular fluid of patients with adult periodontitis

Our previous studies showed that the expression of CD23 on polymorphonuclear leukocytes (PMNLs) in gingival crevicular fluid (GCF) from adult periodontitis (AP) patients was higher than in autologous peripheral blood (PB). Percentages of eosinophils in GCF PMNLs ranged between 6 and 14%. The purpose of the present studies was to increase understanding of the potential role of eosinophils and their products, including CD23, in periodontal disease. We analysed the eosinophil fraction in GCF and PB by flow cytometry using monoclonal antibodies to CD23b (BB10), eosinophil cationic protein (ECP) in stored and secretory forms (EG1 and EG2), and CD67 (80H3). Simultaneously, we measured IgE and soluble CD23 titer and GCF and serum by ELISA. Flow cytometric analysis of BB10, EG2 and 80H3 binding showed that GCF eosinophils from AP were activated. A large BB10⁺ EG2⁺ cellular fraction was detected in GCF from AP whereas it was very low in autologous serum (9.30±2.460 vs 0.16±0.10, p>0.001). GCF from gingivitis patients exhibited no flow cytometric evidence for the presence of BB10+ EG2+ cells. BB10+ EG1+ cells, or inactivated eosinophils rated lower in GCF than in PB both in gingivitis and periodontitis patients (0.45±0.63 vs 1.83±0.96 and 0.15±0.30 vs 1.30±0.20, p>0.05. respectively). IgE titer in AP patients reached 1208.1 ±421.2 IU/ml in GCF while only 49.1 ±50.4 in sera. Soluble CD23 in GCF reached 236.1 ±81.3 ng/ml in GCF and 5.6±1.8 ng/ml in sera. GCF of gingivitis patients, however, contained no detectable sCD23. Thus. GCF from AP patients displayed a high rate of activated eosinophils secreting ECP. while GCF of gingivitis patients did not. These results suggest that ECP-secreting activated eosinophils are relevant to the pathology of adult periodontitis.     

Acute‐phase proteins and immunoglobulin G against Porphyromonas gingivalis in peri‐implant crevicular fluid: a comparison with gingival crevicular fluid

This investigation had 2 aims: 1) to determine the levels of acute‐phase proteins and immunoglobulin G (IgG) against Porphyromonas gingivalis in peri‐implant crevicular fluid (PICF) and their association with the clinical condition of the peri‐implant mucosa; and 2) to compare the inflammatory and immunological responses at implants and teeth as reflected by the gingival crevicular fluid (GCF) and PICF levels of acute‐phase proteins and immunoglobulins. Thirty‐one partially edentulous subjects were recruited for this study. PICF was sampled from 1 healthy and 1 inflamed site from each patient; GCF was sampled from an additional 21 healthy and 27 inflamed tooth sites of the same patients. GCF and PICF were collected with paper strips (for 30 s) and analysed using enzyme‐linked immunosorbent assays for α2‐macroglobulin, α1‐antitrypsin, transferrin, lactoferrin and IgG against P. gingivalis . This investigation demonstrated that the absolute amounts of the acute‐phase proteins and IgG against P. gingivalis are higher in GCF and PICF from inflamed than healthy sites. No significant differences were observed between PICF and GCF components at either healthy or inflamed sites, suggesting that inflammatory and immune events are similar in the peri‐implant mucosa and gingiva in humans and that PICF and GCF production is governed by similar mechanisms.     

Expression of interleukin-2 receptor and HLA-DR on lymphocyte subsets of gingival crevicular fluid in patients with periodontitis

Expression of interleukin-2 receptor (IL2R) and HLA-DR on lymphocytes of gingival crevicular fluid (GCF) was examined by two-color flow cytometric analysis. GCF from 15 patients with periodontitis was collected by crevicular washing. Mononuclear cells were isolated by Ficoll-paque gradient centrifugation from inflamed gingival tissue (GT) and peripheral blood (PB) sampled from each of the 15 patients. Lymphocyte subsets were detected by using monoclonal antibodies (mAb) of Leu 12 (CD19), Leu 4 (CD3), Leu 3a (CD4) and Leu 2a (CD8) directed to B cells, T cells, helper/inducer T cells (Th) and suppressor/cytotoxic T cells (Ts), respectively. Anti-IL2R (CD25) and anti-HLA-DR were used as lymphocyte activation markers. IL2R- or HLA-DR-positive fractions in Th, Ts and B cells were calculated. Percentage of IL2R-positive fraction in Th (IL2R+ Th) of GCF (34.0%) was significantly higher than those of GT (18.4%) and PB (13.7%). IL2R-positive fraction in B cells (IL2R+ B) of GCF was the highest among the three groups (23.9% in GCF, 12.5% in GT, 6.3% in PB). Ts did not express IL2R regardless of the origin of the samples. Compared with PB and GT, GCF showed significantly higher HLA-DR expression on Th and Ts in GCF (PB: 8.7% and 27.1%; GT: 27.9% and 50.3%; GCF: 44.7% and 65.3%). These results suggest that lymphocytes in GCF were highly activated and are related to the local host immune response in periodontitis.     

Matrix metalloproteinases (MMP-8 and -9) and neutrophil elastase in gingival crevicular fluid of cyclosporin-treated patients

BACKGROUND: Gingival overgrowth (GO) is one of the most important side effects of cyclosporin A (CsA) medication, but its pathogenesis is not completely understood. The aim of this study was to identify and compare collagenase-2 (MMP-8), gelatinase-B (MMP-9), and neutrophil (PMN)-elastase levels in gingival crevicular fluid (GCF) from 15 renal transplant patients receiving CsA therapy and exhibiting CsA GO, 14 patients with gingivitis, and 10 periodontally healthy subjects. METHODS: Clinical data were obtained on plaque index, papilla bleeding index, and hyperplastic index from each site studied. GCF samples and clinical data were collected from: 2 sites exhibiting CsA GO (CsA GO+) and 2 sites not exhibiting CsA GO (CsA GO-) in each CsA-treated patient; 2 diseased sites in each patient with gingivitis; and 2 healthy sites in each subject with clinically healthy periodontium. CsA GO+ and CsA GO- sites were divided into 2 subgroups as clinically not inflamed (PBI = 0) and inflamed (PBI > or =1). GCF MMP-8, MMP-9, and PMN-elastase levels were analyzed by immunofluorometric assay. RESULTS: GCF MMP-8 and -9 levels and clinical degrees of gingival inflammation in CsA GO+ sites were similar to those in diseased sites. However, GCF elastase levels were significantly lower in CsA GO+ sites compared to those in diseased sites. GCF MMP-8, -9 and PMN-elastase levels were not different between CsA GO- sites and healthy sites. Additionally, GCF MMP-8 and -9 levels in inflamed CsA GO+ sites were higher but not statistically significantly than those in diseased sites. In contrast, GCF PMN-elastase levels in inflamed CsA GO+ sites were significantly lower than the levels in diseased sites. CONCLUSIONS: These results show that CsA therapy does not have a significant effect on GCF MMP-8 and MMP-9 levels, but the gingival inflammation seems to be the main reason for their elevations. However, low GCF PMN-elastase levels can be an important factor in the pathogenesis of CsA-induced gingival overgrowth. CsA therapy does not eliminate the potential use of GCF MMP-8 and -9 as future diagnostic markers of gingival inflammation.     

Hydroxyproline and total protein levels in gingiva and gingival crevicular fluid in periodontally healthy human subjects.

Age is known to be one of the factors which affect the rate of collagen and protein turnover in the connective tissues of the periodontium. The aim of the present study was to determine the levels of hydroxyproline (Hyp) and total protein in both the gingiva and gingival crevicular fluid (GCF) of periodontally healthy human subjects of two different age groups. The subjects of the young group were selected from among patients scheduled for extraction of upper and lower first or second premolars for orthodontic reasons. The second (older) group included individuals whose teeth were to be extracted for endodontic reasons. GCF was obtained before gingival sampling. The tissues surrounding the sockets were harvested immediately after extraction of the indicated teeth. All samples were analyzed biochemically. No significant difference was found in gingival and GCF levels of Hyp (which is unique to collagen) between the groups. Total protein levels in gingiva were significantly higher in the young group than in the older group. GCF total protein levels showed no significant difference between the groups. The higher gingival protein levels in the younger group seem to conform to previous findings.     

Characterization of cellular infiltrate, detection of chemokine receptor CCR5 and interleukin-8 and RANTES chemokines in adult periodontitis

Leukocyte migration is essential for immune surveillance of tissues by focusing immune cells to sites of antigenic challenge. The control of leukocyte migration depends on the combined actions of adhesion molecules and a vast array of chemokines and their receptors. The purpose of the present study was to investigate the involvement of Interleukin-8 (IL-8), RANTES, the associated infiltrating cells and expression of CCR5 chemokine receptors in periodontitis; furthermore, the effect of periodontal therapy on these parameters was evaluated. Patients included in the study had moderate to advanced periodontal disease with at least 5-6 teeth with probing depth > 6 mm, attachment loss > or =3 mm and extensive radiographic bone loss. The inflammatory infiltrate was analyzed by immunohistochemistry in gingival biopsies obtained from subjects at the beginning of the study and 2 months after periodontal treatment. Gingival crevicular fluid (GCF) was collected for 30 seconds using periopaper strips, and chemokines were quantified by ELISA. The cellular components of the inflammatory infiltrate included B (CD19) and T (CD3, CD4+ and CD8+) lymphocytes and monocytes/macrophages (CD11c). CCR5 chemokine receptor expressing cells were exclusively found in periodontitis gingiva. IL-8 and RANTES were detected in the periodontitis group, obtaining a total amount of 212.5 pg and 42.0 pg, respectively. However, IL-8 was also detectable in the GCF of the healthy group (total amount of 44.8 pg). Periodontal therapy reduced the cell number in the infiltrate and the levels of IL-8 and RANTES, suggesting a relationship between these chemokines and periodontal status. We propose that the presence of these chemokines and the expression of chemokine receptors may represent a marker of lymphocyte subsets with the ability to migrate to inflammatory sites.     

Locally produced anti-phosphorylcholine and anti-oxidized low-density lipoprotein antibodies in gingival crevicular fluid from aggressive periodontitis patients

BACKGROUND: Sera from patients with periodontal attachment loss contain higher concentrations of IgG anti-phosphorylcholine (anti-PC) than sera from healthy subjects. Furthermore, a large proportion of plaque bacteria bear PC-containing surface antigens, implicating the oral flora as a source of immunogen for anti-PC. Additionally, anti-PC is cross-reactive with a variety of oral bacterial antigens and human antigens such as oxidized low-density lipoprotein (oxLDL). We hypothesized that, if the oral flora is a source of PC antigens, then we should be able to detect local anti-PC and anti-oxLDL production in gingival crevicular fluid (GCF). METHODS: To test this, we collected 66 GCF samples from 15 patients with aggressive periodontitis and examined both the GCF samples and serum samples for their content of IgG anti-PC, IgG anti-LDL, and IgG anti-oxLDL by enzyme-linked immunosorbent assay. We also determined levels of anti-tetanus toxoid (anti-TT) as a non-oral antigen control. Serum and GCF concentrations of serum albumin (HSA) were also determined for use as a dilution marker. A conservative GCF:serum antibody ratio of greater than 1.5 was considered to be evidence of local antibody production. RESULTS: For the non-oral antigen TT, only one out of 62 samples contained locally produced antibody. Eight out of 64 samples (7 from a single subject) demonstrated local production of anti-LDL. In contrast, 28 out of 66 samples demonstrated local production of anti-PC, and 47 out of 66 samples contained locally produced anti-oxLDL. It was observed that A. actinomycetemcomitans strains containing or devoid of PC could absorb anti-oxLDL from human sera. Although there was a correlation between the ratios of anti-PC and anti-oxLDL (Spearman's rho = 0.35, P = 0.0037), local production of both antibodies was found in only 17 out of 65 samples, indicating that these antibodies are not always reflective of reactivity to the same antigens. CONCLUSION: The local production of anti-PC and anti-oxLDL further implicates the oral flora as a source of antigen that may mediate immune reactions of relevance to cardiovascular and other systemic diseases.     

Localization of interleukin-1 (IL-1) mRNA-expressing macrophages in human inflamed gingiva and lL-1 activity in gingival crevicular fluid

The exact cell type and site(s) involved in interleukin-1 (lL-1) production during gingival inflammation was determined by combining immunohistochemistry and in situ hybridization. IL-1 messenger RNA (mRNA)-expressing cells in human inflamed gingiva were identified as macrophages. The rate of IL-α mRNA expression in these macrophages was the same as IL-1 β mRNA expression. The rate of IL-1 mRNA expression was higher in connective tissue furthest from the pocket epithelium, although more macrophages were present at the connective tissue subjacent to the pocket epithelium. The IL-1 activity in gingival crevicular fluid (GCF) obtained from inflamed gingiva was higher than that from healthy gingiva and decreased after periodontal therapy. The IL-1 activity in GCF was almost completely abolished by the addition of anti-IL-1α antibody but not by anti-IL-1 β antibody, indicating that IL-1α is the predominant form in GCF. However, the IL-1 activity in GCF was unrelated to the number of IL-1 mRNA-exprerssing macrophages in the same gingival site where the GCF was obtained at the same time. The results suggest that macrophages in the connective tissue subjacent to the oral epithelium contribute to the production of IL-1 but those in connective tissue subjacent to the pocket epithelium play a different role in the generation of gingival inflammation.     

龈沟液中存在白细胞介素8降解酶及其自身抗体

目的探究龈沟液中是否存在白细胞介素８（ｉｎｔｅｒｌｅｕｋｉｎ８,ＩＬ８）的抑制因子。方法（１）将１３例成人牙周炎的１４份及８例牙周健康者的９份龈沟液样本各自一分为二,１／２加入丝氨酸蛋白酶抑制剂──苯甲基磺酰氟,另１／２加入等量的磷酸盐缓冲液作为对照。ＥＬＩＳＡ法检测各样本中的ＩＬ８含量。（２）对１５例成人牙周炎的４１份龈沟液样本,用间接ＥＬＩＳＡ法测定龈沟液中的ＩＬ８自身抗体（ＩｇＧ）。结果（１）加入酶抑制剂的龈沟液中ＩＬ８的检出量（３．０１ｍｇ／Ｌ±５．７９ｍｇ／Ｌ）显著高于对照组（０．０５ｍｇ／Ｌ±０．１５ｍｇ／Ｌ）,Ｐ＜０．００１。（２）龈沟液中ＩＬ８自身抗体水平高于阴性对照标准差３倍。龈沟液中加入大肠杆菌超声粉碎液对此检测结果无明显影响。结论龈沟液中存在能降解ＩＬ８的丝氨酸蛋白酶;成人牙周炎的龈沟液中存在ＩＬ８自身抗体     

Neuropeptide Y (NPY) and NPY Y1 receptor in periodontal health and disease

Objectives

Neuropeptide Y (NPY) coordinates inflammation and bone metabolism which are central to the pathogenesis of periodontitis. The present study was designed to determine whether NPY was quantifiable in human gingival crevicular fluid (GCF) and to test the null hypothesis that GCF levels of NPY were the same in periodontal health and disease. A subsidiary aim was to determine the potential functionality of released NPY by detecting the presence of NPY Y1 receptors in gingival tissue.

Design

The periodontitis group consisted of 20 subjects (10 females and 10 males) mean age 41.4 (S.D. 9.6 years). The control group comprised 20 subjects (10 females and 10 males) mean age 37.4 (S.D. 11.7 years). NPY levels in GCF were measured in periodontal health and disease by radioimmunoassay. NPY Y1 receptor expression in gingival tissue was determined by Western blotting of membrane protein extracts from healthy and inflamed gum.

Results

Healthy sites from control subjects had significantly higher levels of NPY than diseased sites from periodontitis subjects. NPY Y1 receptor protein was detected in both healthy and inflamed gingival tissue by Western blotting.

Conclusions

The significantly elevated levels of NPY in GCF from healthy compared with periodontitis sites suggests a tonic role for NPY, the functionality of which is indicated by the presence of NPY Y1 receptors in local gingival tissue.     

Crevicular fluid myeloperoxidase at healthy, gingivitis and periodontitis sites

The volume and myeloperoxidase (MPO) activity of gingival crevicular fluid (GCF) collected with filter paper strips for 30 s from the sulcus of healthy, gingivitis and periodontitis sites of Chinese subjects were measured. MPO/site and MPO/microliter GCF were both greater at gingivitis and periodontitis sites than at healthy sites. Enzyme activity was similar at the 2 categories of diseased sites. Mean GCF volume and MPO activity were calculated for all samples from healthy, gingivitis and periodontitis sites with GI 0, 1, 2 and 0 + 1. GCF volume, MPO/site and MPO/microliter GCF all were greater at GI 2 than GI 0 or 0 + 1. These data indicate that increased GCF MPO previously observed at periodontitis sites is not specific to such sites. Rather increased GCF MPO likely occurs when additional polymorphonuclear leukocytes enter the sulcus as a result of gingival inflammation. A second sample was obtained from 22 sites 4 weeks after the initial collection. These samples were collected for 5 s rather than 30 s. The GCF volume, MPO/site and MPO/microliters GCF were each greater in samples collected for 30 s rather than 5 s. Correlation coefficients showed that the amount of GCF and MPO activity of the fluid collected for 5 s and 30 s was dependent upon the site even though the 5-s and 30-s samples were collected 4 weeks apart.     

Collagenases in gingival crevicular fluid in type 1 diabetes mellitus

BACKGROUND: Studies have demonstrated that high levels of collagenase activity in gingival crevicular fluid (GCF) are associated with degradation of periodontal tissues in progressive periodontitis compared to periodontally healthy tissues. Because the activation of collagenases is an important issue in periodontitis, we have studied the activation of collagenase in gingival crevicular fluid samples of diabetic patients. METHODS: Collagenase activity was studied in human gingival crevicular fluids. Twenty-two poorly controlled diabetic patients (e.g., blood glucose: 11.0+/-0.7 mmol/l; hemoglobin A1c [HbA1c]: 9.6%+/-0.3%) and five well-controlled diabetic patients were compared to six chronic periodontitis subjects and five healthy controls. Collagenase activity against type I collagen was measured using sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis quantitated by laser densitometry. RESULTS: The poorly controlled diabetic patients had more alveolar bone loss than the well-controlled diabetic subjects and controls (P<0.001; t test). The activity of collagenases in GCF in poorly controlled diabetic patients was similar to that seen in chronic periodontitis subjects (P>0.05) but higher than in healthy controls (P<0.01; t test), whereas there was no difference between the well-controlled diabetic subjects and systemically healthy controls (P>0.05; t test). CONCLUSION: Poorly controlled diabetes is strongly related to periodontal tissue destruction, and collagenases in GCF may mediate and reflect this effect.     

The effect of treatment on IgG, IgA, IgM and alpha-2-macroglobulin in gingival crevicular fluid from patients with chronic adult periodontitis

With a technique for sampling, processing and analysis of gingival crevicular fluid (GCF) that allows multiple constituents to be analysed from a sample collected on a filter paper strip, we have examined IgG, IgA, IgM and alpha-2-macroglobulin (alpha 2M) in GCF from patients with chronic adult periodontitis. Clinical data and GCF were collected before and 3 months after root planing and scaling, and analysed to determine trends for the population. A statistically-significant decrease in the percentage of sites with bleeding on probing, erythema and supragingival plaque was observed 3 months after therapy. The mean amount of each glycoprotein in GCF decreased dramatically at 3 months. In contrast, the mean volume of GCF was virtually identical at the two evaluations. The IgG/IgA and IgG/IgM ratios in GCF were elevated when compared with human serum suggesting the preferential occurrence of IgG in GCF. Correlation of the four glycoproteins with GCF volume and with enzyme markers of the acute inflammatory response in GCF revealed a relationship between arylsulphatase (a lysosomal enzyme), fluid influx, and the passage of larger molecular-weight glycoproteins (alpha 2M, IgM) into the gingival crevice.     

The relationship of serum IgG antibody titers to periodontal pathogens to indicators of the host response in crevicular fluid

Abstract. In this study, the relationship of indicators of the local host response in gingival crevicular fluid (GCF) to the serum antibody titer to periodontal pathogens was examined. 15 patients with chronic adult periodontitis were studied. GCF was collected and analyzed for the total amount of IgG, IgM, the lysosomal enzyme B-glucuronidase (BG) and α-2-macroglobulin (α2M). At the same examination, serum from these patients was collected, and enzyme-linked immunosorbent assays used to determine the serum IgG antibody titer to a panel of 17 periodontal pathogens (Actinobacillus actinomycetemcomitans (3 strains), Bacteroides gingivalis (4), Eikenella corrodens (2), Wolinella recta, Bacteroides intermedius (3), Fusobacterium nucleatum, and 3 Capnocytophaga species). Using Spearman rank order correlation analysis, correlation coefficients were calculated to relate the 4 indicators of host response in GCF to the serum IgG antibody titer to each of the 17 micro-organisms. The mean correlation between total IgG in GCF and the serum IgG antibody liter was positive (r=+0.30), and statistically significant correlations between total IgG in GCF and serum IgG antibody titer were observed for one strain of B. intermedius and C. ochracea. A weaker positive correlation was observed for IgM (r= 0.18). In contrast, the mean correlation between total BG in GCF and the serum antibody titer was negative (r= 0.34). Statistically significant negative correlations were observed for all 3 strains of A. actinomycetemcomitans, one strain of E. corrodens and W. recta. The mean correlation for α2M was r= -0.06. These data suggest that elevated BG activity in GCF, believed to be a marker for lysosomal enzyme released from polymorphonuclear leukocytes in the crevicular environment, may be associated with a reduced serum IgG antibody response to suspected periodontal pathogens. Furthermore, these findings imply that the development of a serum IgG antibody response to suspected periodontal pathogens is consistent with a protective host response.     

Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Background and objective

High mobility group chromosomal protein B1 (HMGB1) and N2 (HMGN2), two members of high mobility group (HMG) family, play important role in inflammation. The purpose of this study was to investigate the expression of HMGB1 and HMGN2 in periodontistis.

Materials and methods

The expression of HMGB1 and HMGN2 mRNA in gingival tissues and gingival crevicular fluid (GCF) in chronic periodontitis (CP), generalised aggressive periodontitis (G-AgP) patients and healthy subjects was detected by real-time PCR. The protein level of HMGB1 and HMGN2 in peri-implant crevicular fluid (PICF), peri-implant crevicular fluid of peri-implantitis (PI-PICF) and normal patients was determined by Western blotting. Furthermore, IL-1β, IL-6, IL-8, TNF-α and HMGB1 levels in GCF, PI-PICF and healthy-PICF samples from different groups were determined by ELISA.

Results

HMGN2 expression was increased in inflamed gingival tissues and GCF from CP and G-ApG groups compared to control group. HMGB1 expression was the highest in the gingival tissues and GCF from CP patients and was accompanied by increased concentrations of IL-1β, IL-6, IL-8 proinflammaory cytokines.

Conclusion

To our knowledge, this is the first study reporting that the expression of HMGB1 and HMGN2 was increased in the gingival tissues and GCF in CP and G-AgP and the PICF in PICF. Our data suggest that HMGB1 may be a potential target for the therapy of periodontitis and PI.