Altered distribution of type I collagen mRNA in periodontal disease

Larjava, Hannu; Sandberg, M; Vuorio, Eero

doi:10.1111/j.1600-0765.1989.tb02002.x

Cited by 18 publications

(9 citation statements)

References 33 publications

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“…Apart from the endothelial cell the plasma cell was the most heavily stained cell type in all of the sections. Other cell types stained to a lesser extent confirming the observations of previous studies (Takahashi et al 1996, Larjava et al 1989, Abe et al 1994.…”

Section: Discussionsupporting

confidence: 90%

Cell division, synthetic capacity and apoptosis in periodontal lesions analysed by in situ hybridisation and immunohistochemistry

Koulouri¹,

Lappin²,

Radvar³

et al. 1999

J Clinic Periodontology

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In this study, we investigated the synthetic and proliferative activity of infiltrating mononuclear cells in sections of granulation tissue from periodontitis lesions in both adult periodontitis (AP) and early onset periodontitis (EOP) patients. We also investigated the role of apoptosis in the remodelling of the inflamed tissue. We utilised a Ki-67 antigen specific antibody and a histone messenger RNA (mRNA) probe to detect cells undergoing cell division in the sections. Oligonucleotide probes for 28S ribosomal RNA and for the detection of poly A mRNA were utilised to detect cells with synthetic capacity. Apoptosis was determined using terminal transferase labelling of fragmented DNA with Biotin labelled dUTP. Biopsies of granulation tissue were obtained from 9 AP patients, from 10 EOP patients and for comparative purposes, biopsies of gingival tissue from 4 patients with AP. There were no differences regarding the relative proportions of cells with synthetic capacity or in the numbers of dividing cells in the periodontitis tissue sections. However, we observed an increase in the number of dividing cells in the AP granulation tissues compared to the AP gingival sections and that these cells were predominantly fibroblast like in appearance. Apoptotic cells consisted mainly of connective tissue cells; mainly fibroblasts with few if any leukocytes being apoptotic other than polymorphonuclear leukocytes. Only a few cyto-phagocytic macrophages were ever observed in the gingival and granulation tissues. We conclude that the turnover of infiltrating leukocytes in inflamed periodontal tissue is low, that they probably arrive at this site by recruitment from distant lymph nodes, and that neither cell division nor programmed cell death significantly alter the numbers of inflammatory cells. On the other hand, fibroblast apoptosis and cell division occur within the periodontium as these are typical processes in the normal turnover and remodelling of these tissues.

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Section: Discussionsupporting

confidence: 90%

Cell division, synthetic capacity and apoptosis in periodontal lesions analysed by in situ hybridisation and immunohistochemistry

Koulouri¹,

Lappin²,

Radvar³

et al. 1999

J Clinic Periodontology

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“…In addition, IL-10, which is produced primarily by macrophages, was detected among the vast array of cytokines induced by P. gingivalis infection. IL-10 tends to upregulate the M2 macrophage phenotype, which potentially could lead to an increase in arginase production, resulting in collagen accumulation and fibrosis of gingival tissue, which is a common clinical characteristic of chronic periodontitis (101)(102)(103)(104). A significant reduction in the level of P. gingivalis infection was observed in the mice treated with clodronate liposomes relative to the untreated, but infected, animals (Fig.…”

Section: Figurementioning

confidence: 77%

Macrophage Depletion Abates Porphyromonas gingivalis–Induced Alveolar Bone Resorption in Mice

Lam

O'Brien-Simpson

Lenzo

et al. 2014

The Journal of Immunology

115

140

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The role of the macrophage in the immunopathology of periodontitis has not been well defined. In this study, we show that intraoral inoculation of mice with Porphyromonas gingivalis resulted in infection, alveolar bone resorption, and a significant increase in F4/80+ macrophages in gingival and submandibular lymph node tissues. Macrophage depletion using clodronate-liposomes resulted in a significant reduction in F4/80+ macrophage infiltration of gingival and submandibular lymph node tissues and significantly (p < 0.01) less P. gingivalis–induced bone resorption compared with controls in BALB/c and C57BL/6 mice. In both mouse strains, the P. gingivalis–specific IgG Ab subclass and serum cytokine [IL-4, IL-10, IFN-γ, and IL-12 (p70)] responses were significantly (p < 0.01) lower in the macrophage-depleted groups. Macrophage depletion resulted in a significant reduction in the level of P. gingivalis infection, and the level of P. gingivalis infection was significantly correlated with the level of alveolar bone resorption. M1 macrophages (CD86+), rather than M2 macrophages (CD206+), were the dominant macrophage phenotype of the gingival infiltrate in response to P. gingivalis infection. P. gingivalis induced a significant (p < 0.01) increase in NO production and a small increase in urea concentration, as well as a significant increase in the secretion of IL-1β, IL-6, IL-10, IL-12 (p70), eotaxin, G-CSF, GM-CSF, macrophage chemoattractant protein-1, macrophage inflammatory protein-α and -β, and TNF-α in isolated murine macrophages. In conclusion, P. gingivalis infection induced infiltration of functional/inflammatory M1 macrophages into gingival tissue and alveolar bone resorption. Macrophage depletion reduced P. gingivalis infection and alveolar bone resorption by modulating the host immune response.

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“…M2 macrophages have been shown play a role in tissue remodelling by increasing the production of effectors that both synthesize and degrade collagen (59) and are becoming the focus of research in fibrotic diseases (60,61). Fibrotic gingival tissue is commonly observed in chronic periodontitis (25), and gingival fibroblasts have been thought to be largely responsible for collagen remodelling during disease (62). However, an M2 macrophage marker, CD163 (RM3/1), found associated with healthy gingival tissue, also has been found in chronically inflamed periodontal tissue (63,64).…”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis Lipopolysaccharide Weakly Activates M1 and M2 Polarized Mouse Macrophages but Induces Inflammatory Cytokines

et al. 2014

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bPorphyromonas gingivalis is associated with chronic periodontitis, an inflammatory disease of the tooth's supporting tissues. Macrophages are important in chronic inflammatory conditions, infiltrating tissue and becoming polarized to an M1 or M2 phenotype. As responses to stimuli differ between these phenotypes, we investigated the effect of P. gingivalis lipopolysaccharide (LPS) on M1 and M2 macrophages. M1 and M2 polarized macrophages were produced from murine bone marrow macrophages (BMM) primed with gamma interferon (IFN-␥) or interleukin-4 (IL-4), respectively, and incubated with a low or high dose of P. gingivalis LPS or control TLR2 and TLR4 ligands. In M1-M, the high dose of P. gingivalis LPS (10 g/ml) significantly increased the expression of CD40, CD86, inducible nitric oxide synthase, and nitric oxide secretion. The low dose of P. gingivalis LPS (10 ng/ml) did not induce costimulatory or antibacterial molecules but did increase the secretion of IL-1␣, IL-6, IL-12p40, IL-12p70, and tumor necrosis factor alpha (TNF-␣). P. gingivalis LPS marginally increased the expression of CD206 and YM-1, but it did enhance arginase expression by M2-M. Furthermore, the secretion of the chemokines KC, RANTES, eotaxin, and MCP-1 from M1, M2, and nonpolarized M was enhanced by P. gingivalis LPS. TLR2/4 knockout macrophages combined with the TLR activation assays indicated that TLR2 is the main activating receptor for P. gingivalis LPS and whole cells. In conclusion, although P. gingivalis LPS weakly activated M1-M or M2-M compared to control TLR ligands, it induced the secretion of inflammatory cytokines, particularly TNF-␣ from M1-M and IL-10 from M2-M, as well as chemotactic chemokines from polarized macrophages.

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Altered distribution of type I collagen mRNA in periodontal disease

Cited by 18 publications

References 33 publications

Cell division, synthetic capacity and apoptosis in periodontal lesions analysed by in situ hybridisation and immunohistochemistry

Cell division, synthetic capacity and apoptosis in periodontal lesions analysed by in situ hybridisation and immunohistochemistry

Macrophage Depletion Abates Porphyromonas gingivalis–Induced Alveolar Bone Resorption in Mice

Porphyromonas gingivalis Lipopolysaccharide Weakly Activates M1 and M2 Polarized Mouse Macrophages but Induces Inflammatory Cytokines

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