Proteases augment the effects of lipopolysaccharide in rat gingiva

Ekuni, Daisuke; Yamamoto, Tatsuo; Yamanaka, Reiko; Tachibana, K.; Watanabe, Tatsuo

doi:10.1034/j.1600-0765.2003.00694.x

Cited by 35 publications

(46 citation statements)

References 23 publications

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“…13,14 The treated group exhibited apical migration of junctional epithelium characteristic of disease ( Figure 1, A and D). As confirmed by morphology, cryosections from healthy ( Figure 1, B and C) and diseased ( Figure 1, E and F) rats were processed by laser-capture microscopy for the isolation of epithelium.…”

Section: Resultsmentioning

confidence: 99%

“…The number of PMNs was determined per 0.05 mm 2 under a magnification of ϫ400. 13 Means of histological data were calculated for each rat.…”

Section: Morphometric Analysismentioning

confidence: 99%

“…Addition of Streptomyces griseus protease to the LPS treatment further potentiated the LPS-induced effects, yet protease treatment alone had no significant effect. 13 The LPS/protease model also established that the progressive development of disease was associated with apoptosis of adjacent fibroblasts and destruction of collagen fibers relative to both sham-treated and untreated (time 0) controls.…”

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confidence: 99%

“…15 In this study, the established LPS/protease-induced rat chronic wound model [13][14][15] was used to analyze epithelial ROS signaling leading to alveolar bone loss relative to time 0 controls. First, epithelial tissues isolated by lasercapture microdissection were analyzed by expression microarray for transcriptional changes associated with the onset of epithelial disease and alveolar bone loss.…”

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confidence: 99%

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Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

Ekuni

Firth

Nayer

et al. 2009

The American Journal of Pathology

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Reactive oxygen species (ROS) production is an antimicrobial response to pathogenic challenge that may, in the case of persistent infection, have deleterious effects on the tissue of origin. A rat periodontal disease model was used to study ROS-induced chronic epithelial inflammation and bone loss. Lipopolysaccharide (LPS) was applied for 8 weeks into the gingival sulcus, and histological analysis confirmed the onset of chronic disease. Junctional epithelium was collected from healthy and diseased animals using laser-capture microdissection, and expression microarray analysis was performed. Of 19,730 genes changed in disease, 42 were up-regulated >4-fold.

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Section: Resultsmentioning

confidence: 99%

“…The number of PMNs was determined per 0.05 mm 2 under a magnification of ϫ400. 13 Means of histological data were calculated for each rat.…”

Section: Morphometric Analysismentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

Ekuni

Firth

Nayer

et al. 2009

The American Journal of Pathology

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“…The polymorphonuclear leukocytes of the connective tissue subjacent to the junctional epithelium in two standard areas (0.05 mm (depth) Â 0.1 mm each) were counted under a magnification of Â 400. 24 As an indicator of alveolar bone resorption, the distance between the cementoenamel junction and the alveolar bone crest was measured with a microgrid at a magnification of Â 200. 24 The number of TNF-a-positive fibroblasts and total fibroblasts in five standard areas (0.1 mm Â 0.1 mm each) adjacent to the cementum within the periodontal ligament were determined, and the ratios of TNF-a-positive fibroblasts to total fibroblasts were calculated.…”

Section: Analysis Of Periodontal Tissuesmentioning

confidence: 99%

Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n ¼ 24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factora (TNF-a), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic b-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-a were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.

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Periodontal disease and bisphosphonates induce osteonecrosis of the jaws in the rat

Aghaloo

Kang

Sung³

et al. 2011

Journal of Bone and Mineral Research

211

219

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Bisphosphonates (BPs) are medications used commonly to treat primary and metastatic bone cancer, as well as osteoporosis. Although BPs improve bone mineral density, reduce fracture risk, and reduce hypercalcemia of malignancy, some patients develop BP-related osteonecrosis of the jaws (BRONJ). This devastating complication is defined as clinically exposed bone in the maxillofacial region for more than 8 weeks. Despite an increasing number of BRONJ cases since first reported, the disease pathophysiology remains largely unknown. Since published studies suggest a significant role for dental disease in the pathophysiology of BRONJ, we developed a BRONJ animal model where aggressive periodontal disease is induced by ligature placement around the crown of the right maxillary first molar in the presence of vehicle (veh) or zoledronic acid (ZA), a potent BP. Ligature placement induced significant alveolar bone loss, which was attenuated by ZA treatment. Osteonecrosis was observed associated with ligature-induced periodontitis in the ZA-treated group. This was seen as sequestration and extensive periosteal alveolar bone formation on micro–computed tomography (μCT) in the ligated site of BP-treated animals. Histologic examination confirmed these findings, seen as necrotic bone with diffuse loss of osteocytes and empty lacunae, rimming of the necrotic bone by squamous epithelium and inflammation, and exposure to the oral cavity. Importantly, the rat lesions were strikingly similar to those of BRONJ patients. Our data suggest that dental disease and potent BP therapy are sufficient for BRONJ development in the rat.

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Proteases augment the effects of lipopolysaccharide in rat gingiva

Cited by 35 publications

References 23 publications

Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

Effects of periodontitis on aortic insulin resistance in an obese rat model

Periodontal disease and bisphosphonates induce osteonecrosis of the jaws in the rat

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