Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin E2-mediated RANKL/osteoprotegerin regulation

Kim, M.; Jun, Hye‐Kyoung; Choi, Bong‐Kyu; Heon, Jeong; Yoo, Yun‐Jung

doi:10.1111/j.1600-0765.2010.01298.x

Cited by 13 publications

(7 citation statements)

References 40 publications

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“…Porphyromonas gingivalis has been demonstrated to invade osteoblasts by interacting with integrin α 5 β 1, inducing actin condensation, JNK pathway activation, and osteoblasts apoptosis [24, 25]. Nonetheless, microbial PAMPs promote the expression of the proosteoclastogenic cytokine RANKL in osteoblasts (OBs), thus promoting osteoclastogenesis [26, 27]. All these events, which represent the initial response to the infection, establish a local inflammation proper of the innate immunity.…”

Section: Resident Cells and Innate Immunitymentioning

confidence: 99%

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Benedetto

Gigante

Colucci

et al. 2013

Clinical and Developmental Immunology

250

249

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Periodontal disease (PD), or periodontitis, is defined as a bacterially induced disease of the tooth-supporting (periodontal) tissues. It is characterized by inflammation and bone loss; therefore understanding how they are linked would help to address the most efficacious therapeutic approach. Bacterial infection is the primary etiology but is not sufficient to induce the disease initiation or progression. Indeed, bacteria-derived factors stimulate a local inflammatory reaction and activation of the innate immune system. The innate response involves the recognition of microbial components by host cells, and this event is mediated by toll-like receptors (TLRs) expressed by resident cells and leukocytes. Activation of these cells leads to the release of proinflammatory cytokines and recruitment of phagocytes and lymphocytes. Activation of T and B cells initiates the adaptive immunity with Th1 Th2 Th17 Treg response and antibodies production respectively. In this inflammatory scenario, cytokines involved in bone regulation and maintenance have considerable relevance because tissue destruction is believed to be the consequence of host inflammatory response to the bacterial challenge. In the present review, we summarize host factors including cell populations, cytokines, and mechanisms involved in the destruction of the supporting tissues of the tooth and discuss treatment perspectives based on this knowledge.

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Section: Resident Cells and Innate Immunitymentioning

confidence: 99%

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Benedetto

Gigante

Colucci

et al. 2013

Clinical and Developmental Immunology

250

249

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“…Aggregatibacter actinomycetemcomitans , Treponema denticola and Porphyromonas gingivalis are representative periodontopathogens that possess virulence factors, including lipopolysaccharide, sphingolipid, cytolethal distending toxin, Arg‐gingipain and outer membrane proteins. These virulence factors are involved in osteoclast formation .…”

mentioning

confidence: 99%

Periodontitis mainly increases osteoclast formation via enhancing the differentiation of quiescent osteoclast precursors into osteoclasts

Lee

Kim

Choi

et al. 2014

J of Periodontal Research

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“…Bacterial porins have also been shown to promote calvarial bone resorption in vitro . The Treponema denticola cell‐surface protein, Td92, induces osteoclast formation and inhibits osteoprotegerin synthesis . Another class of protein reported to be a potent stimulator of bone resorption are the molecular chaperones chaperonin 60 and chaperonin 10 .…”

Section: Mechanisms Which Explain Bacterially‐induced Bone Breakdown mentioning

confidence: 99%

Bacterial modulators of bone remodeling in the periodontal pocket

Henderson¹,

Kaiser²

2017

Periodontology 2000

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The signaling network involved in the pathogenesis of periodontal disease is not yet fully understood. This review aims to describe possible mechanisms through which the bacterial modulators may be linked directly or indirectly to the process of alveolar bone loss in periodontitis. From the late 1970s to present, new paradigm shifts have been developed regarding our understanding of pathological bone remodeling in periodontal disease. Upcoming evidence suggests that in periodontal disease the local immune response is exacerbated and involves the existence of signaling pathways that have been shown to modulate bone-cell function leading to alveolar bone loss. Those complex signaling pathways have been observed not only between bacteria but also between bacteria and the gingival surface of the host. More specifically, it has been shown that bacteria, through their secretion molecules, may interact indirectly and directly with immune-type cells of the host, resulting in the production of osteolytic agents that enhance bone resorption. Further research is required to provide a clear understanding of the role of these molecules in the pathogenesis of periodontal disease, and the availability of new technologies, such as next-generation sequencing and metagenomic analysis, may be useful tools in achieving this.

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Td92, an outer membrane protein of Treponema denticola, induces osteoclastogenesis via prostaglandin E2-mediated RANKL/osteoprotegerin regulation

Abstract: These results suggest that Td92 promotes osteoclast formation through the regulation of RANKL and OPG production via a PGE(2) -dependent mechanism.

Cited by 13 publications

References 40 publications

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Periodontitis mainly increases osteoclast formation via enhancing the differentiation of quiescent osteoclast precursors into osteoclasts

Bacterial modulators of bone remodeling in the periodontal pocket

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