Periodontal and Systemic Responses in Various Mice Models of Experimental Periodontitis: Respective Roles of Inflammation Duration and <i>Porphyromonas gingivalis</i> Infection

Saadi-Thiers, Kenza; Huck, Olivier; Simonis, P; Tilly, Peggy; Fabre, J; Tenenbaum, Henri; Davideau, Jean‐Luc

doi:10.1902/jop.2012.110540

Cited by 53 publications

(82 citation statements)

References 47 publications

(205 reference statements)

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“…Experimental animal models of PD have been largely utilized to reproduce the clinical, radiographic, and histologic features of human disease [7,9,17,21,30,32,34,35,45]. These models allow investigation of cellular and molecular mechanisms as well as mediators involved during the establishment and progression of the PD.…”

Section: Discussionmentioning

confidence: 99%

“…These models allow investigation of cellular and molecular mechanisms as well as mediators involved during the establishment and progression of the PD. Also, they are widely used to investigate the host-bacteria interactions and to test new treatment modalities, providing valuable information on inflammation associated with host-microbial interactions [9,[17][18][19][20][21]46]. However, the variability of mice models found in the literature often complicates a direct comparison among the results and conclusions of different studies.…”

Section: Discussionmentioning

confidence: 99%

“…Various animal models of experimental PD have been used to evaluate the periodontitis pathogenesis, to investigate the host-bacteria interactions, and to test new treatment modalities [8,9,[16][17][18][19][20][21]. Rodents and humans share characteristics of PD such as anatomy, bacterial colonization, and susceptibility to experimentally induced PD.…”

Section: Introductionmentioning

confidence: 99%

“…Rodents and humans share characteristics of PD such as anatomy, bacterial colonization, and susceptibility to experimentally induced PD. Mice are especially important because they provide powerful genetic tools and allow modifications of their genome, enabling the study of specific molecules or cells, to test mechanistic hypotheses in the development and progression of PD [17,18,21]. At the same time, they possess a relatively low cost, are easy to handle, and have a short gestation period, and their inflammatory and immunological process are well known.…”

Section: Introductionmentioning

confidence: 99%

“…The oral gavage model consists in the inoculation of human bacterial strains of a predefined amount of bacterial in a viscous suspension [18]. Oral gavage utilize mainly P. gingivalis [16,17,21,[26][27][28], A. actinomycetemcomitans [6,29], F. nucleatum [9,17,21], as well as a combination of different strains of bacteria [7-9, 15, 30, 31]. The duration of the experiments vary from 10 days [32] to up to 8 weeks [9,21], differing in the levels of gingival epithelial ulceration, in the levels of inflammatory cytokines [17,21], and in the downgrowth of bone loss [9,21,[32][33][34][35].…”

Section: Introductionmentioning

confidence: 99%

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Long-term evaluation of oral gavage with periodontopathogens or ligature induction of experimental periodontal disease in mice

et al. 2015

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The ligature model was an effective approach to induce inflammation and bone loss similar to human periodontitis, but the oral gavage models were not efficient in inducing periodontal inflammation and tissue destruction in the conditions studied. Ligature models can provide a basis for future interventional studies that contribute to the understanding of the disease pathogenesis and the complex host response to microbial challenge.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Long-term evaluation of oral gavage with periodontopathogens or ligature induction of experimental periodontal disease in mice

et al. 2015

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Long-Term Ligature-Induced Periodontitis Exacerbates Development of Bisphosphonate-Related Osteonecrosis of the Jaw in Mice

Williams

Ho²,

Lenon³

et al. 2020

Journal of Bone and Mineral Research

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Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is a detrimental intraoral lesion that occurs in patients with long-term or high-dose use of anti-resorptive agents such as bisphosphonates. Tooth extraction is a known risk factor for BRONJ, and such intervention is often performed to eliminate existing pathological inflammatory conditions. Previously, we determined that ligatureinduced periodontitis (LIP) is a risk factor for the development of osteonecrosis in mice, but it remains unclear whether the chronicity of LIP followed by extraction influences osteonecrosis development. In this study, we assess the effect of short-term and long-term LIP (ligature placed for 3 weeks [S-LIP] or 10 weeks [L-LIP], respectively) on osteonecrosis development in mice receiving 250 μg/kg/ week zoledronic acid (ZOL). When compared to S-LIP, L-LIP caused 70% (p ≤ 0.0014) more bone loss without altering microbe composition. In the presence of ZOL, bone loss mediated by LIP was prevented and bone necrosis was induced. When the ligated tooth was extracted, histologic hallmarks of osteonecrosis including empty lacunae and necrotic bone were increased by 88% (p = 0.0374) and 114% (p = 0.0457), respectively, in L-LIP compared to S-LIP. We also observed significant increases in serum platelet factor 4 (PF4) and macrophage inflammatory factor 1 γ (MIP1γ) in mice that received ZOL treatment and had tooth extractions compared to controls, which may be systemic markers of inflammation-associated osteonecrosis development. Additionally, CD3+ T cells were identified as the major immune population in both health and disease, and we observed a 116% (p = 0.0402) increase in CD3+IL23R+ T cells in L-LIP compared to S-LIP lesions following extraction. Taken together, our study reveals that extracting a periodontally compromised tooth increases the formation of necrotic bone compared to extracting a periodontally healthy tooth and that osteonecrosis may be associated with the duration of the preexisting pathological inflammatory conditions.

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Characterization of ligature‐induced experimental periodontitis

Molon

Park

Jin

et al. 2018

Microscopy Res & Technique

134

112

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We sought to better characterize the progression of periodontal tissue breakdown in rats induced by a ligature model of experimental periodontal disease (PD). A total of 60 male Sprague-Dawley rats were evenly divided into an untreated control group and a PD group induced by ligature bilaterally around first and second maxillary molars. Animals were sacrificed at 1, 3, 5, 7, 14, and 21 days after the induction of PD. Alveolar bone loss was evaluated by histomorphometry and microcomputed tomography (μCT). The immune-inflammatory process in the periodontal tissue was assessed using descriptive histologic analysis and quantitative polymerase chain reaction (qPCR). This ligature model resulted in significant alveolar bone loss and increased inflammatory process of the periodontal tissues during the initial periods of evaluation (0-14 days). A significant increase in the gene expression of pro-inflammatory cytokines, interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and proteins involved in osteoclastogenesis, receptor activator of nuclear factor-k B ligand (RANKL) and osteoprotegerin (OPG) was observed in the first week of analysis. In the later periods of evaluation (14-21 days), no significant alterations were noted with regard to inflammatory processes, bone resorption, and expression of cytokine genes. The ligature-induced PD model resulted in progressive alveolar bone resorption with two different phases: Acute (0-14 days), characterized by inflammation and rapid bone resorption, and chronic (14-21 days) with no significant progression of bone loss. Furthermore, the gene expressions of IL-6, IL-1β, TNF-α, RANKL, and OPG were highly increased during the progress of PD in the early periods. Research Highlights• Ligature-induced bone resorption in rats occurred in the initial periods after disease induction • The bone resorption was characterized by two distinct phases: Acute (0-14 days), with pronounced inflammation and alveolar bone loss • Chronic phase (14-21 days): No further disease progression • Several pro-inflammatory cytokines were increased during the progress of periodontitis K E Y W O R D S alveolar bone loss, bone resorption, periodontal disease, periodontitis, rats, X-ray microtomography

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Periodontal and Systemic Responses in Various Mice Models of Experimental Periodontitis: Respective Roles of Inflammation Duration and Porphyromonas gingivalis Infection

Cited by 53 publications

References 47 publications

Long-term evaluation of oral gavage with periodontopathogens or ligature induction of experimental periodontal disease in mice

Long-term evaluation of oral gavage with periodontopathogens or ligature induction of experimental periodontal disease in mice

Long-Term Ligature-Induced Periodontitis Exacerbates Development of Bisphosphonate-Related Osteonecrosis of the Jaw in Mice

Characterization of ligature‐induced experimental periodontitis

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