The changes in T lymphocyte subsets following periodontal treatment in patients with chronic periodontitis

Objective: The aim of this study was to determine whether there was any change in T‐lymphocyte subsets in patients with chronic periodontitis after applying different periodontal treatment methods. Patients and methods: Twenty‐four patients with chronic periodontitis were included in the study. In every phase of the treatment (pretreatment, initial treatment, curettage and flap operations) the biopsy samples were taken from the gingival tissues at sites of chronic periodontitis. Then CD4⁺ and CD8⁺ lymphocyte and CD4⁺/CD8⁺ ratio values were determined using flow cytometry in the biopsy samples. At the same time, gingival pocket depth, Löe–Silness gingival index, and Silness–Löe plaque index 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 initial treatment, after curettage and after flap operations, we conducted an analysis using a paired t‐test. Results: Flow cytometry findings in the patients with chronic periodontitis showed that CD4⁺ and CD8⁺ lymphocyte values before treatment were under the normal value and the CD4⁺/CD8⁺ ratio was within the normal distribution interval. The CD4⁺/CD8⁺ ratio decreased postcurettage and postflap operation. This decrease was statistically significant (p < 0.001). The CD4⁺ and CD8⁺ lymphocyte values were increased postcurettage and postflap operation. This increase was also statistically significant (p < 0.001). Conclusions: These findings suggest that local immune response was poor in the patients with chronic periodontitis. CD4⁺ and CD8⁺ T‐lymphocytes could play a significant role in chronic periodontitis pathobiology.     

Immature,but Not Mature,Dendritic Cells Are More Often Present in Aggressive Periodontitis Than Chronic Periodontitis: An Immunohistochemical Study

Background: Dendritic cells (DCs) form a key link between innate and adaptive immune responses. The aim of this study is to analyze presence and distribution of immature (im) and mature (m) DCs in gingival tissue samples obtained from patients diagnosed with aggressive periodontitis (AgP), chronic periodontitis (CP), and clinically healthy periodontium (control group). Methods: Gingival tissue samples obtained from patients with: 1) AgP (aged <35 years); 2) CP (aged ≥35 years); and 3) control group (aged >18 years) (n = 10 per group) were collected. Two‐way analysis of variance and posterior Fisher least significant difference test were used to observe differences between the means of cells positively marked for imDC (S100, CD1a, and CD207) and mDC (CD208) immunomarkers. Results: imDCs were more numerous in AgP than CP and control groups, being statistically significant only for S100+ cells. Conversely, mDCs were visualized in higher numbers in CP than AgP and control groups (both P <0.05). Considering frequency of immunostained cells, the number of S100+ cells was greater than CD207+ and CD1a+ cells, followed by a lesser number of CD208+ cells, in all groups. Conclusions: Considering that the ability of DCs to regulate immunity is dependent on DC maturation, results suggest that predominance of imDCs appears to be involved in AgP pathogenesis, probably due to lack of ability to induce immune cell activation. Further studies are necessary to elucidate the role of DC maturation in regulating immune responses in periodontal disease.     

ICAM-1-expressing pocket epithelium, LFA-1-expressing T cells in gingival tissue and gingival crevicular fluid as features characterizing inflammatory cell invasion and exudation in adult periodontitis

Activated T lymphocytes constitute a major component of inflammatory cells in the early periodontal lesion, and also appear in the gingival crevicular fluid. In an attempt to clarify the relationship between the ICAM-1 (CD54) expression of pocket epithelium in gingiva and the infiltrating lymphocyte population, we carried out an analysis of CD11a⁺ (LFA-lα), CD25⁺ (IL-2Rα) and CD4⁺ (Th) cells subjacent to ICAM-1-expressing pocket epithelia and CD11a⁺ CD25⁺CD4⁺ cells in gingival crevicular fluid (GCF). GCF was collected by crevicular washing from 16 patients with periodontitis (P group) and 3 subjects with healthy gingiva (H group). Peripheral blood (PB) was collected at the same time. Mononuclear cells were isolated by Ficoll-paque gradient centrifugation from GCF and PB. Monoclonal antibodies (mAb) to CD11a, CD25, and CD4 were used for three-color flow cytometry. Gingival biopsies were obtained from 7 patients in P group and 3 subjects in H group. Serial cryostat sections (6 μm in thickness) were prepared from each biopsy, on which a double staining was performed. The number of CD11a⁺ CD25⁺ CD4⁺ cells and the fluorescence intensity of FITC conjugated anti-CD 11a were significantly higher in GCF than in PB (p≤0.001 to p≤0.01). CD11a⁺ CD25⁺CD4⁺ cells were not detected in GCF in H group. The pocket epithelia expressed CD54 in P group, but not in H group. The number of CD11a⁺, CD25⁺ and CD4⁺cells infiltrating the connective tissue subjacent to the upper, middle and lower parts of the CD54 positive pocket epithelium (n=16) was 141±26, 38±13, 144±29 (cells/0.04 mm²), respectively, whereas in the CD54 negative pocket epithelium, it was (n=5) 9±2, 3±1, 8±3. In P group, the CD11a⁺CD25⁺CD4⁺cell number in GCF correlated with CD25⁺, CD11a⁺cells in the connective tissue subjacent to the CD54⁺pocket epithelium. These results indicate that expression of ICAM-1 in pocket epithelium is relevant to the migration of CD11a, CD25, CD4 positive cells in connective tissue subjacent to the pocket epithelium into the periodontal pocket. Assessing the relationship of our findings and other adhesion molecules would offer important clues to the understanding of T cell migration in affected gingiva.     

Effect of interleukin-17 on the expression of chemokines in gingival epithelial cells

The role of interleukin (IL)-17 in cellular communication in inflammation has been well described, and a positive correlation between the severity of periodontitis and the level of IL-17 was reported. Although epithelial cells are a major target of IL-17, little is known about the effect of IL-17 on the production of chemokines by human gingival epithelial cells (HGECs). We evaluated the effects of IL-17 on the expression of CXCL8 and CCL2 by HGECs using quantitative real-time PCR and ELISA. In addition, the role of the nuclear factor (NF)-κB signalling pathway in the IL-17-mediated expression of chemokines was assessed using a specific inhibitor. Stimulation with IL-17 up-regulated the expression of CXCL8 mRNA but not of CCL2 mRNA in HGECs, whereas tumour necrosis factor-α (TNF-α) elevated the expression of mRNA for both chemokines. Stimulation with IL-17 up-regulated the secretion of CXCL8 protein, but not the secretion of CCL2 protein. The effect of IL-17 on CXCL8 production was suppressed using an anti-IL-17R Ig, suggesting a role for a specific receptor-ligand interaction. Inhibition of the NF-κB signalling pathway demonstrated that NF-κB activation is required for the CXCL8 expression in HGECs. In conclusion, IL-17 is involved in the regulation of the innate immune response in HGECs by inducing CXCL8 production.     

Expression profile of chemokines and chemokine receptors in epithelial cell layers of oral lichen planus

BACKGROUND: To understand the immunopathological features of oral lichen planus (OLP), we analyzed the expression of chemokines in the epithelial cell layers. Methods: Epithelia from OLP or healthy gingiva were collected by laser microdissection. The chemokine and chemokine receptor expressions in the epithelia were analyzed by DNA microarray. RESULTS: High levels of MIP-3alpha/LARC/CCL20 and its receptor CCR6 were expressed in the lesional epithelia. Furthermore, DC-CK1/CCL18, ELC/CCL19, SDF-1/CXCL12 and CXCR4 expressions were also increased. Immunohistologial analysis showed that high numbers of Langerhans cells (LCs) were present in the epithelia of OLP. Lesional epithelia also expressed high levels of the ligands specific for CXCR3 (e.g. MIG/CXCL9, IP-10/CXCL10 and I-TAC/CXCL11) and CCR5 (e.g. RANTES/CCL5). CONCLUSIONS: Infiltration of LCs is orchestrated by CCR6. Further, LCs residing in the lesional epithelia may be a mature phenotype. Moreover, infiltration of T cells in OLP could be mediated by signaling pathways through CXCR3 and CCR5.     

Flow-cytometric analysis of T-lymphocyte subsets after different treatment methods in smokers and non-smokers with chronic periodontitis

Aim : To determine any change in T‐lymphocyte subsets after applying different treatment methods in smokers and non‐smokers with chronic periodontitis. Participants : 50 adults with chronic periodontitis. Method : The subjects were divided into smokers and non‐smokers. Biopsy samples were taken from the gingival pocket wall tissues at sites with chronic periodontitis before treatment, after initial treatment, after curettage and after flap operation and tested for CD4⁺, CD8⁺ lymphocyte and CD4/CD8 ratio values. Gingival pocket depth, gingival index (Gl‐Löe‐Silness) and plaque index (Pl‐Silness‐Löe) scores were also recorded. Analysis aimed at determining the relation between the clinical measurements and the laboratory results. Results : Flow cytometry findings in both groups showed that CD4⁺ and CD8⁺ lymphocyte values before treatment were under the normal value while the CD4⁺/CD8⁺ ratio was within normal distribution interval. The lymphocyte values observed in the smokers were found to be lower than those in the non‐smokers. After treatment the difference between the lymphocyte values in smokers and non‐smokers was found to be statistically significant. However, the difference between the CD4/CD8 rate obtained in smokers and non‐smokers was not found to be statistically significant. Conclusions : The lymphocyte values observed in smokers were found to be lower than those in non‐smokers after applying different treatment methods and the local immune response was poor in the smokers.     

Immunohistochemical analysis of CD45RO+ T cells and vascular endothelial growth factor expression in cyclosporin A-induced rat gingival tissue

Background: The aim of this study is to evaluate CD4⁺, CD8⁺, and CD45RO⁺ T cells, and vascular endothelial growth factor (VEGF) expression in cyclosporin A (CsA)–induced rat overgrown gingival tissue during an 8‐week period. Methods: Sixty male Sprague‐Dawley rats weighing 200 to 250 g were used in this study. Mandibular first molars were ligated with 3–0 silk suture. The rats received daily doses of 0.09% NaCl (control group) or 10 mg/kg body weight of CsA (test group) by intraperitoneal injections. Five rats from the control group and 10 rats from the test group were sacrificed at each experimental period (2, 4, 6, and 8 weeks after the beginning of CsA treatment). The specimens were examined immunohistochemically. Results: CD4⁺, CD8⁺, and CD45RO⁺ T cells, and VEGF expression were more prevalent in the CsA‐treated group than in the control group (P <0.05). VEGF was significantly correlated with CD4⁺ T cells, CD4⁺/CD8⁺ ratio, and CD45RO⁺ cells (P <0.05). Conclusion: Based on our findings, we conclude that VEGF, a major regulator of angiogenesis, and CD4⁺, CD8⁺, and CD45RO⁺ memory T cells play a key role in CsA‐induced gingival overgrowth.     

Age-related changes of CD4+ T cell migration and cytokine expression in germ-free and SPF mice periodontium

ObjectiveIncreasing age is a potential risk factor for periodontal tissue breakdown, which may be affected by commensal flora. The aim of this study evaluated age-related changes in CD4⁺ T cells, C-C chemokine ligand 5 (CCL5), interleukin (IL)-17A, and receptor activator of nuclear factor-kappa B ligand (RANKL) expression using germ-free (GF) and conventionally reared (SPF) mice.DesignGF and SPF mice at 8 (n = 6/group) and 22 weeks old (n = 6/group) were used. Immunohistochemical analyses were performed to determine the effects of aging on protein expression in periodontal tissues. Age-related changes in alveolar bone were quantified using micro-CT analysis.ResultsSPF mice, but not GF mice, showed an age-related increase in alveolar bone loss (P < 0.01). SPF mice at 22 weeks of age increased expression of CD4⁺ T cells, CCL5, IL-17A, and RANKL compared to those at 8 weeks of age in connective tissue and alveolar bone surface (P < 0.01). Furthermore, there was increased CD4⁺ T cells, which were co-expressed with IL-17A and RANKL in SPF mice at 22 weeks of age. On the other hand, the GF mice did not show any significant differences in CD4⁺ T cells, CCL5, IL-17A and RANKL expression between the two age groups.ConclusionsSPF mice induced an age-related increase in CD4⁺ T cells co- expressed with IL-17A and RANKL, with occurring alveolar bone loss. In contrast, GF mice did not show age-related changes in CD4⁺ T cell migration and cytokine expression.     

Detection of fascin and CCR-7 positive mature dendritic cells in oral lichen planus

Background: Dendritic cells (DC) play a crucial role in the pathogenesis of oral lichen planus (OLP) with respect to antigens presented to T cells. We performed immunohistochemical analysis to elucidate the process of activation of DC in OLP. Methods: Thirty biopsy specimens were obtained from the patients with OLP. The expressions of CD1a, Langerin, S‐100, fascin, chemokine receptor‐7 (CCR‐7), D2‐40, cyclooxygenase‐2 (COX‐2), and microsomal prostaglandin E synthase‐1 (mPGES‐1) in DC from OLP and disease free control were investigated using specific antibodies. The distribution and number (1 mm²) of DC were assessed in the intra‐epithelium and the submucosa specimens. Correlation between the number of DC and epithelium thickness was also determined. Result: Immature DC (Langerin⁺, CD1a⁺, and S‐100⁺) were identified in the epithelia from OLP patients and control, though the numbers of Langerin⁺ and CD1a⁺ positive cells were decreased in the OLP samples as compared to the control. Mature DC (fascin⁺) were identified in the submucosa specimens, not found in the epithelium from OLP or control. Double immunostaining revealed DC positive for fascin and CCR‐7 in the submucosa, which had migrated into D2‐40⁺ lymph vessels. Furthermore, keratinocytes expressed both Prostaglandin E₂ (PGE₂) converting enzymes, COX‐2, and mPGES‐1, indicating PGE₂ synthesis in the epithelial layer of the OLP specimens. Conclusion: Our results indicate that DC change from immature to mature in the epithelium and are then drawn out to the submucosa. We demonstrate that mature DC localized in the submucosa, it consequently migrates into lymph vessels. This maturation process of DC is an important immunopathological feature of OLP.     

High Levels of CXC Ligand 12/Stromal Cell–derived Factor 1 in Apical Lesions of Endodontic Origin Associated with Mast Cell Infiltration

Introduction

CXC ligand 12/stromal-derived factor-1 (CXCL12/SDF-1) is a pleiotropic chemokine that regulates the influx of a wide range of leukocytes. The aim of this study was to characterize CXCL12/SDF-1 in apical lesions (ALs) of endodontic origin, with special emphasis in associated immune cell populations.

Methods

In this case-control study, 29 individuals with chronic apical periodontitis and 21 healthy volunteers were enrolled. ALs and healthy periodontal ligament samples were obtained for tissue homogenization, immune Western blotting, and enzyme-linked immunosorbent assay to determine CXCL12/SDF-1 forms and levels. Anatomopathologic diagnosis, immunostaining for CXCL12/SDF-1, CD117-CXCL12/SDF-1, and toluidine blue were also performed to identify tissue and cell localization. Finally, a set of tissue samples were digested and analyzed by flow cytometry to identify CXCL12/SDF-1 in different immune cell populations. Data were analyzed with Stata v11 and WinDi 2.9 software, and significance was considered if P < .05.

Results

CXCL12/SDF-1 was predominantly identified as monomers; levels of CXCL12/SDF-1 were significantly higher in ALs compared with controls, and it was primarily localized to inflammatory infiltrates. Expression of CXCL12/SDF-1 was colocalized to mast cells in tissue sections. Furthermore, CD117⁺ mast cells were the second most frequent infiltrating cells and the main CXCL12/SDF-1 expressing cells, followed by CD4⁺ lymphocytes, monocytes/macrophages, neutrophils, and dendritic cells.

Conclusions

ALs of endodontic origin demonstrated higher levels of CXCL12/SDF-1 compared with controls. CXCL12/SDF-1 was identified in immune cell populations, whereas mast cells represented the major CXCL12/SDF-1 expressing cells, suggesting that this chemokine might play a central role in apical tissue destruction, most probably inducing persistent recruitment of immune cells, particularly of mast cells.     

Hypertension favors the inflammatory process in rats with experimentally induced periodontitis

Bonato CF, do‐Amaral CCF, Belini L, Salzedas LMP, Oliveira SHP. Hypertension favors the inflammatory process in rats with experimentally induced periodontitis. J Periodont Res 2012; 47: 783–792. © 2012 John Wiley & Sons A/S Background and Objective: Cardiovascular diseases are significantly correlated with chronic periodontitis. The aim of this study was to evaluate bone‐loss level, neutrophil migration, CXCL2/CINC‐2α, CXCL5/LIX, CCL20/MIP‐3α and tumor necrosis factor‐α (TNF‐α) production, inducible nitric oxide synthase (iNOS) expression and C‐reactive protein (CRP) release in spontaneously hypertensive rats (SHRs) and normotensive (WTK) rats after experimental induction of periodontal disease. Material and Methods: Periodontitis was induced by placement of silk yarn ligatures around the first molar counterparts. The levels of CRP, CCL20/MIP‐3α and CXCL5/LIX were evaluated in the peripheral blood, and bone‐loss level, neutrophil recruitment, the production of myeloperoxidase, CXCL2, CXCL5, CCL20 and TNF‐α, and the expression of iNOS were evaluated in the gingival tissue. Histological sections were taken to evaluate and measure bone resorption and neutrophil recruitment in the furcation region. Results: Rats with periodontitis had alveolar bone resorption. SHRs with periodontitis showed marked bone loss and increased neutrophil infiltration in comparison with WTK rats. SHRs with periodontitis showed increased levels of TNF‐α and CXCL2, and a slight tendency for increased levels of CXCL5, in the gingival tissue but no increase in the level of CCL20. In SHRs, even without periodontitis, the levels of TNF‐α, CXCL2, CXCL5 and CCL20 showed a slight tendency to increase. In the WTK rats, TNF‐α, CXCL2 and CXCL5 levels were increased with periodontitis, but the level of CCL20 was not. iNOS was expressed in the gingival tissue of WTK rats and SHRs with periodontitis; however, SHRs appeared to express a higher level of iNOS than did WKT rats. The CRP level was elevated in both types of rats with periodontitis; however, the CRP level was higher in SHRs with periodontitis than in WTK rats with periodontitis. Conclusion: In SHRs, the hypertensive condition per se seems to favor the inflammatory processes that become potentiated with periodontitis, when compared with WKT rats.     

Aggressive and Chronic Periodontitis Correlate With Distinct Cellular Sources of Key Immunoregulatory Cytokines

Background: Chronic periodontitis (CP) and aggressive periodontitis (AP) are inflammatory diseases and the main cause of dental loss in adults. We aimed to investigate the expression of adhesion molecules and the source of proinflammatory and anti‐inflammatory cytokines in circulating mononuclear cells from patients with CP and AP. Methods: Peripheral blood mononuclear cells from healthy controls and CP or AP patients were collected. The expression of the cell adhesion molecules CD11a and CD11b, and the cellular sources of interleukin (IL)‐4, IL‐10, IL‐12, interferon‐γ, and tumor necrosis factor‐α by distinct subpopulations of circulating leukocytes were determined using flow cytometry. Results: The expression of CD11a, but not CD11b, was significantly higher within the CD4⁺ and CD8⁺ T cells in CP and AP than in healthy controls. The frequencies of tumor necrosis factor‐α–expressing CD4⁺ T cells and CD14⁺ cells were higher in AP and CP, compared to healthy controls, respectively. Moreover, the frequency of IL‐10 expressing CD14⁺ cells was higher in CP, but not AP, compared to healthy controls CD4⁺ T cells committed to IL‐4 production was higher in CP than in healthy controls. Conclusion: These results suggest the participation of CD11a in the pathogenesis of periodontal lesions and show distinct cellular sources of immunoregulatory cytokines in AP versus CP.     

Evaluation of interleukin-10 producing CD19+ B cells in human gingival tissue

ObjectiveThis study aimed to evaluate IL-10 producing CD19⁺ B cells and to examine the correlation between these cells and the expression levels of IL-1β, TNF-α, RANKL, and IL-10 cytokines in the gingival tissues of individuals with and without chronic periodontitis.DesignData were obtained from 20 patients with chronic periodontitis and 10 healthy controls. The gingival samples were analyzed by immunofluorescence, while real-time PCR and enzyme-linked immunosorbent assays were performed to determine cytokine levels.ResultsThe number of IL-10 producing CD19⁺ B cells and the expression levels of IL-10 were significantly higher in the inflamed gingival tissues than in the healthy tissues. A positive correlation between the expression levels of IL-10 and the number of IL-10 producing CD19⁺ B cells were observed. IL-1β, TNF-α, and RANKL expression levels were significantly elevated in diseased gingivae compared to healthy tissues, and there was a positive correlation between the expression levels of these pro-inflammatory cytokines and the number of IL-10 producing CD19⁺ B cells.ConclusionWhile IL-10 producing CD19⁺ B cells are present in the gingival tissues of patients with periodontal disease and of those with a healthy periodontium, the diseased gingival tissues had a much greater number of these cells than the healthy. The mRNA and protein levels of IL-10, IL-1β, and RANKL, as well as mRNA levels of TNF-α, were positively correlated with the number of IL-10 producing CD19⁺ B cells, which highlights the importance of these factors in the development and progression of periodontitis.     

CCL3 and CXCL12 production in vitro by dental pulp fibroblasts from permanent and deciduous teeth stimulated by Porphyromonas gingivalis LPS

Objective:

The aim of this study was to compare the production of the chemokines CCL3 and CXCL12 by cultured dental pulp fibroblasts from permanent (PDPF) and deciduous (DDPF) teeth under stimulation by Porphyromonas gingivalis LPS (PgLPS).

Material and Methods:

Primary culture of fibroblasts from permanent (n=3) and deciduous (n=2) teeth were established using an explant technique. After the fourth passage, fibroblasts were stimulated by increasing concentrations of PgLPS (0 - 10 µg/mL) at 1, 6 and 24 h. The cells were tested for viability through MTT assay, and production of the chemokines CCL3 and CXCL12 was determined through ELISA. Comparisons among samples were performed using One-way ANOVA for MTT assay and Two-way ANOVA for ELISA results.

Results:

Cell viability was not affected by the antigen after 24 h of stimulation. PgLPS induced the production of CCL3 by dental pulp fibroblasts at similar levels for both permanent and deciduous pulp fibroblasts. Production of CXCL12, however, was significantly higher for PDPF than DDPF at 1 and 6 h. PgLPS, in turn, downregulated the production of CXCL12 by PDPF but not by DDPF.

Conclusion:

These data suggest that dental pulp fibroblasts from permanent and deciduous teeth may present a differential behavior under PgLPS stimulation.     

Reduced expression of lipopolysaccharide‐induced CXC chemokine in Porphyromonas gingivalis‐induced experimental periodontitis in matrix metalloproteinase‐8 null mice

Hernández M, Gamonal J, Salo T, Tervahartiala T, Hukkanen M, Tjäderhane L, Sorsa T. Reduced expression of LIX/CXCL5 in Porphyromonas gingivalis‐induced experimental periodontitis in matrix metalloproteinase‐8 null mice. J Periodont Res 2011; 46: 58–66. © 2010 John Wiley & Sons A/S Background and Objective: Matrix metalloproteinase‐8 (MMP‐8) is a central mediator in chronic periodontitis. Recently developed MMP‐8‐deficient mice show an impaired polymorphonuclear neutrophil response and more severe alveolar bone loss in Porphyromonas gingivalis‐induced experimental periodontitis. The main mediators involved in neutrophil and monocyte/macrophage recruitment and in bone loss include lipopolysaccharide‐induced CXC chemokine (LIX/CXCL5), stromal‐derived factor‐1/CXC chemokine ligand 12 (SDF1/CXCL12) and RANKL. Therefore, the aim of this study was to characterize the expression of LIX/CXCL5, SDF1/CXCL12 and RANKL in Porphyromonas gingivalis‐induced experimental periodontitis in MMP‐8^?/^? (knockout) and wild‐type mice. Material and methods:  MMP‐8 null and WT P. gingivalis‐infected and uninfected mice were included. Histopathological changes were assessed and LIX/CXCL5, SDF1/CXCL12 and RANKL were immunodetected and quantified. Results: Typical histopathological features of chronic periodontitis were seen in P. gingivalis‐infected groups. LIX/CXCL5 expression was restricted to the gingival papilla in all four groups. Significantly lower expression of LIX/CXCL5 was seen in the knockout group compared with the wild‐type infected group (p < 0.05). SDF1/CXCL12 and RANKL expression was mainly localized to the alveolar crest, including inflammatory leukocytes, vascular endothelium, osteoblasts and osteoclasts. Significant increases of SDF1/CXCL12 and RANKL were seen in both knockout and wild‐type P. gingivalis‐infected groups compared with uninfected groups (p < 0.05). Conclusion: RANKL and SDF1/CXCL12 are up‐regulated in P. gingivalis‐induced periodontitis and they appear to be associated with the pathogenesis of the disease. MMP‐8 is associated with a reduced expression of LIX/CXCL5 in the P. gingivalis‐induced experimental periodontitis model.