Inhibitory Effects of Incadronate on the Progression of Rat Experimental Periodontitis by <i>Porphyromonas gingivalis</i> Infection

Tani‐Ishii, Nobuyuki; Minamida, Genshi; Saitoh, Daisuke; Chieda, Keiko; Omuro, Hiromasa; Sugaya, Akira; Hamada, Naoki; Takahashi, Yusuke; Kiyohara, Shiro; Kashima, Isamu; Teranaka, Toshio; Umemoto, Takuya

doi:10.1902/jop.2003.74.5.603

Cited by 23 publications

(27 citation statements)

References 23 publications

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“…Alencar et al 11 analyzed the preventive and healing effects of subcutaneous disodium chlodronate in rats with experimental periodontitis and found that high doses inhibit bone loss. Another study on experimental periodontitis by Porphyromonas gingivalis infection in rats showed that oral administration of incadronate prevents bone loss and the migration of polymorphonuclear neutrophil leukocytes (PMNs) 27 …”

Section: Discussionmentioning

confidence: 99%

Effect of Topical Administration of Monosodium Olpadronate on Experimental Periodontitis in Rats

Goya

Paez

Mandalunis

2006

Journal of Periodontology

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Section: Discussionmentioning

confidence: 99%

Effect of Topical Administration of Monosodium Olpadronate on Experimental Periodontitis in Rats

Goya

Paez

Mandalunis

2006

Journal of Periodontology

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“…2,34 Most pharmacological attempts to control bone loss have focused on inhibiting bone resorption. [3][4][5][6] The induction of a formative reaction to restore destroyed bone, appeared beyond reach. RG1503 treatment introduces a new paradigm, as it targets both aspects of bone balance.…”

Section: Rg1503 Treatment Rebuilds Lost Alveolar Bonementioning

confidence: 99%

“…The most generalized form of destruction, horizontal bone loss, cannot be reversed by current therapies. Strategies based on chemical disease control can stabilize disease progress [3][4][5][6] but are unable to rebuild the lost tissues. Comprehensive treatment for periodontitis should include the control of gingival inflammation that fuels bone loss, inhibition of osteoclastic resorption, and stimulation of bone formation.…”

Section: Introductionmentioning

confidence: 99%

Periodontitis destructions are restored by synthetic glycosaminoglycan mimetic

Lallam-Laroye

Escartin

Zlowodzki

et al. 2006

J Biomedical Materials Res

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Periodontitis are bacterium-driven inflammatory diseases that destroy tooth-supporting tissues whose complete restoration is not currently possible. RGTA, a new class of agents, have this capacity in an animal model. Periodontitis was induced in hamsters and, starting 8 weeks later, injected RG1503, a glycosaminoglycan synthesized from a 40 kDa dextran behaving like a heparan sulfate mimetic (1.5 mg kg(-1) w(-1)) or saline for 8 weeks. The three periodontium compartments were evaluated by immunohistochemistry and morphometry. The gingival extracellular matrix disorganized by inflammation was restoring under treatment. The collagen network was repaired and resumed its previous organization. Fibrillin-1 expression was restored so that the elastic network rebuilt at a distance from the pocket and began to reconstruct near the pocket. Apoptotic cell numbers were decreased in the pocket epithelium, and more so in the infiltrated connective tissue. The continuity and the thickness of the basement membrane were restored and testified normalization of epithelium connective tissue interaction. The amount of alveolar bone increased around the first molar, and the interradicular bone was rebuilt. The root cementum was thickened and the number of proliferating cells in the periodontal ligament was increased close to the cementum. RG1503 treatment induces potent anabolic reactions in the extracellular matrices of the different tissues of the periodontium and recruitment of progenitors. In particular, the cell proliferation close to the root surface suggests the reformation of a functional attachment apparatus. These results demonstrate that RG1503 reverses the degenerative changes induced by inflammation and favors the conditions of a regenerative process. Thus, RGTA, a known matrix component mimetic and protector, may be considered as a new therapeutic tool to regenerate the tissues destroyed by periodontitis.

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“…Clinical studies demonstrated a reduction of radiological and/or clinical signs of PD, including alveolar bone loss, gingival index and bleeding [8], [9], [10], [11], [12]. These beneficial effect of bisphosphonates on mandibular bone loss have also been demonstrated in animal models of PD such as the rice rat [13], [14], and/or as induced by elastic rings [15], [16], tooth ligature [7], [17], and bacterial inoculations [18], [19].…”

Section: Introductionmentioning

confidence: 99%

Zoledronate Effects on Systemic and Jaw Osteopenias in Ovariectomized Periostin-Deficient Mice

et al. 2013

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Osteoporosis and periodontal disease (PD) are frequently associated in the elderly, both concurring to the loss of jaw alveolar bone and finally of teeth. Bisphosphonates improve alveolar bone loss but have also been associated with osteonecrosis of the jaw (ONJ), particularly using oncological doses of zoledronate. The effects and therapeutic margin of zoledronate on jaw bone therefore remain uncertain. We reappraised the efficacy and safety of Zoledronate (Zol) in ovariectomized (OVX) periostin (Postn)-deficient mice, a unique genetic model of systemic and jaw osteopenia. Compared to vehicle, Zol 1M (100 µg/kg/month) and Zol 1W (100 µg/kg/week) for 3 months both significantly improved femur BMD, trabecular bone volume on tissue volume (BV/TV) and cortical bone volume in both OVX Postn+/+ and Postn−/− (all p<0.01). Zol 1M and Zol 1W also improved jaw alveolar and basal BV/TV, although the highest dose (Zol 1W) was less efficient, particularly in Postn−/−. Zol decreased osteoclast number and bone formation indices, i.e. MAR, MPm/BPm and BFR, independently in Postn−/− and Postn+/+, both in the long bones and in deep jaw alveolar bone, without differences between Zol doses. Zol 1M and Zol 1W did not reactivate inflammation nor increase fibrous tissue in the bone marrow of the jaw, whereas the distance between the root and the enamel of the incisor (DRI) remained high in Postn−/− vs Postn+/+ confirming latent inflammation and lack of crestal alveolar bone. Zol 1W and Zol 1M decreased osteocyte numbers in Postn−/− and Postn+/+ mandible, and Zol 1W increased the number of empty lacunae in Postn−/−, however no areas of necrotic bone were observed. These results demonstrate that zoledronate improves jaw osteopenia and suggest that in Postn−/− mice, zoledronate is not sufficient to induce bone necrosis.

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Inhibitory Effects of Incadronate on the Progression of Rat Experimental Periodontitis by Porphyromonas gingivalis Infection

Abstract: These results showed that incadronate inhibits bone resorption and PMN migration in P. gingivalis-induced periodontitis.

Cited by 23 publications

References 23 publications

Effect of Topical Administration of Monosodium Olpadronate on Experimental Periodontitis in Rats

Effect of Topical Administration of Monosodium Olpadronate on Experimental Periodontitis in Rats

Periodontitis destructions are restored by synthetic glycosaminoglycan mimetic

Zoledronate Effects on Systemic and Jaw Osteopenias in Ovariectomized Periostin-Deficient Mice

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