Influence of subcutaneous administration of recombinant TNF‐α on ligature‐induced periodontitis in rats

Gašperšič, Rok; Štiblar-Martinčič, Draga; Osredkar, Joško; Skalerić, U

doi:10.1034/j.1600-0765.2003.01395.x

Cited by 48 publications

(32 citation statements)

References 26 publications

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“…A number of recent studies suggest that TNF-␣ has a significant role in bone loss during periodontitis. The administration of recombinant human TNF-␣ to rats has been shown to acceler-ate the progression of periodontitis (51), and TNF-␣ receptor knockout mice develop significantly less inflammation and alveolar bone loss (52). In contrast to these results, P. gulae ATCC 51700 induced significantly higher levels of IL-6 than did P. gingivalis (W50 and ATCC 33277).…”

Section: Figcontrasting

confidence: 53%

Porphyromonas gulae Has Virulence and Immunological Characteristics Similar to Those of the Human Periodontal Pathogen Porphyromonas gingivalis

et al. 2016

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Periodontitis is a significant problem in companion animals, and yet little is known about the disease-associated microbiota. A major virulence factor for the human periodontal pathogen Porphyromonas gingivalis is the lysyl-and arginylspecific proteolytic activity of the gingipains. We screened several Porphyromonas species isolated from companion animals-P. asaccharolytica, P. circumdentaria, P. endodontalis, P. levii, P. gulae, P. macacae, P. catoniae, and P. salivosa-for Lys-and Arg-specific proteolytic activity and compared the epithelial and macrophage responses and induction of alveolar bone resorption of the protease active species to that of Porphyromonas gingivalis. Only P. gulae exhibited Lys-and Arg-specific proteolytic activity. The genes encoding the gingipains (RgpA/B and Kgp) were identified in the P. gulae strain ATCC 51700 and all publicly available 12 draft genomes of P. gulae strains. P. gulae ATCC 51700 induced levels of alveolar bone resorption in an animal model of periodontitis similar to those in P. gingivalis W50 and exhibited a higher capacity for autoaggregation and binding to oral epithelial cells with induction of apoptosis. Macrophages (RAW 264.7) were found to phagocytose P. gulae ATCC 51700 and the fimbriated P. gingivalis ATCC 33277 at similar levels. In response to P. gulae ATCC 51700, macrophages secreted higher levels of cytokines than those induced by P. gingivalis ATCC 33277 but lower than those induced by P. gingivalis W50, except for the interleukin-6 response. Our results indicate that P. gulae exhibits virulence characteristics similar to those of the human periodontal pathogen P. gingivalis and therefore may play a key role in the development of periodontitis in companion animals. P eriodontitis is well known to occur in companion animals, particularly in dogs (1). The prevalence and severity of the disease increase with age (1). Chronic periodontitis, as diagnosed by increased periodontal pocket depth and/or gingival recession (1), has been shown to be present in 82% of dogs aged 6 to 8 years and in 96% of dogs aged 12 to 14 years (2). Black-pigmented anaerobic bacteria are commonly isolated from the periodontal pockets of dogs (3-5), with many of the isolates being identified as Porphyromonas species: P. asaccharolytica, P. circumdentaria, P. endodontalis, P. levii, P. gulae, P. macacae, P. catoniae, and P. salivosa. Of these species, Porphyromonas gulae has been found to be the predominant species (6). In humans, chronic periodontitis is an inflammatory disease of the supporting tissues of the teeth, which results in the destruction of the alveolar bone and the supporting tissue (7). It has been estimated to affect up to 25% of the dentate population, with severe forms affecting 5 to 6% and prevalence increasing with age (8, 9). Although the etiology of chronic periodontitis is multifactorial, evidence suggests that the levels of specific Gram-negative, anaerobic, black-pigmented bacteria in the subgingival plaque biofilm play a major role in the pathogenesis of hum...

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Section: Figcontrasting

confidence: 53%

Porphyromonas gulae Has Virulence and Immunological Characteristics Similar to Those of the Human Periodontal Pathogen Porphyromonas gingivalis

et al. 2016

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“…Moreover, these features are dependent upon a bacteria-induced host response, as indicated by decreased loss of attachment and reduced bone resorption in rats treated with chlorhexidine, antibiotics, or prostaglandin inhibitors (Weiner et al, 1979;Kenworthy and Baverel, 1981;Bezerra et al, 2002). Interestingly, bone loss and inflammation are accelerated by the administration of IL-1β or TNF-α (Koide et al, 1995;Gaspersic et al, 2003), which is consistent with results obtained in non-human primates, demonstrating that inhibition of these cytokines reduces alveolar bone loss (Assuma et al, 1998;Delima et al, 2002). By using the rat ligature model, where bone resorption and formation could be separately examined, we tested the hypothesis that type 2 diabetes would aggravate periodontal disease by both increasing bone loss as well as limiting reparative bone formation.…”

Section: Introductionmentioning

confidence: 99%

“…To examine separately the impact of diabetes on periodontal bone loss and the formation of new bone following resorption, we carried out studies in a model where a ligature was placed around a molar tooth and the ensuing inflammation, loss of attachment, and bone were measured over a seven-day period (Bezerra et al, 2002;Gaspersic et al, 2003). This model was chosen since it mimics several features of human periodontitis, including the formation of an inflammatory infiltrate, loss of attachment, and loss of alveolar bone.…”

Section: Introductionmentioning

confidence: 99%

Diabetes Enhances Periodontal Bone Loss through Enhanced Resorption and Diminished Bone Formation

et al. 2006

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Using a ligature-induced model in type-2 Zucker diabetic fatty (ZDF) rat and normoglycemic littermates, we investigated whether diabetes primarily affects periodontitis by enhancing bone loss or by limiting osseous repair. Diabetes increased the intensity and duration of the inflammatory infiltrate (P < 0.05). The formation of osteoclasts and percent eroded bone after 7 days of ligature placement was similar, while four days after removal of ligatures, the type 2 diabetic group had significantly higher osteoclast numbers and activity (P < 0.05). The amount of new bone formation following resorption was 2.4-to 2.9-fold higher in normoglycemic vs. diabetic rats (P < 0.05). Diabetes also increased apoptosis and decreased the number of bone-lining cells, osteoblasts, and periodontal ligament fibroblasts (P < 0.05). Thus, diabetes caused a more persistent inflammatory response, greater loss of attachment and more alveolar bone resorption, and impaired new bone formation. The latter may be affected by increased apoptosis of bone-lining and PDL cells.

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“…14,48 In accordance with such hypothesis, systemic administration of TNF-a results in increased severity of ligature-induced PD in rats. 49 A mechanistic explanation for this observation is that TNF-a can interfere with monocytes and dendritic maturation and with the subsequent T-helper polarization, as anti-TNF therapy of chronic inflammatory autoimmune disease models results in impaired development of Th1 and Th17 responses. [50][51][52] Interestingly, AIRmax mice that received pristane injection, but were not submitted to the oral inoculation of periodontopathogens, also developed a significant alveolar bone loss.…”

Section: Experimental Periodontitis and Arthritis Interaction Ap Trommentioning

confidence: 99%

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

Trombone¹,

Claudino²,

Colavite³

et al. 2010

Genes Immun

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Periodontitis (PD) and rheumatoid arthritis (RA) have been found to be clinically associated and to share the chronic nature of the inflammatory reaction associated with bone resorption activity. However, the mechanisms underlying such association are unknown. Therefore, we examined the basis of Actinobacillus actinomycetemcomitans-and Porphyromonas gingivalis-induced PD and pristane-induced arthritis (PIA) interaction in mice. Higher severity PD in the genetically inflammation prone acute inflammatory reactivity maximum (AIRmax) mice strain was associated with higher levels of TNF-a, IL-1b, IL-17, matrix metalloproteinase (MMP)-13, and RANKL, whereas PD/PIA co-induction resulted in even higher levels of IL-1b, IFN-g, IL-17, RANKL, and MMP-13 levels. Conversely, PD/PIA co-induction in AIRmin strain did not alter the course of both pathologies. PIA/PD co-induction resulted in altered expression of T-cell subsets transcription factors expression, with T-bet and RORg levels being upregulated, whereas GATA-3 levels were unaltered. Interestingly, PIA induction resulted in alveolar bone loss, such response being highly dependent on the presence of commensal oral bacteria. No differences were found in PIA severity parameters by PD co-induction. Our results show that the interaction between experimental PD and arthritis in mice involves a shared hyper-inflammatory genotype and functional interferences in innate and adaptive immune responses.

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Influence of subcutaneous administration of recombinant TNF‐α on ligature‐induced periodontitis in rats

Cited by 48 publications

References 26 publications

Porphyromonas gulae Has Virulence and Immunological Characteristics Similar to Those of the Human Periodontal Pathogen Porphyromonas gingivalis

Porphyromonas gulae Has Virulence and Immunological Characteristics Similar to Those of the Human Periodontal Pathogen Porphyromonas gingivalis

Diabetes Enhances Periodontal Bone Loss through Enhanced Resorption and Diminished Bone Formation

Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences

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