Receptor activator NF κB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis

Crotti, Tania; Smith, Malcolm D.; Hirsch, Robert S.; Soukoulis, Steven; Weedon, Helen; Capone, M; Ahern, Michael; Haynes, David R.

doi:10.1034/j.1600-0765.2003.00615.x

Cited by 273 publications

(276 citation statements)

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“…Characteristic features of this disease include soft tissue inflammation in response to gram-negative anaerobic bacteria that collect in the gingival pockets and associated alveolar bone loss [87]. In periodontitis gingival tissues, increased numbers of multinucleated TRAP positive osteoclasts have been detected along with high levels of RANKL and corresponding low levels of its inhibitor osteoprotegerin (OPG) [37].…”

Section: Periodontitismentioning

confidence: 99%

“…In bone loss diseases, including osteoporosis, RA, periodontitis and multiple myeloma, increased numbers of osteoclasts and high levels of Receptor Activator of Nuclear Factor Kappa B ligand (RANKL) have been reported [37][38][39][40][41][42]. Over the past decade, numerous studies have shown that RANKL, produced by cytokine-activated lymphocytes, fibroblasts and plasma cells, drives excessive osteoclastmediated bone resorption in RA, periodontitis and multiple myeloma, respectively [37,38,40,43].…”

Section: Osteoclasts Hdacs and Hdacimentioning

confidence: 99%

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Histone deacetylases (HDAC) in physiological and pathological bone remodelling

Cantley

Zannettino

Bartold

et al. 2017

Bone

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Histone deacetylases (HDACs) 1 play important roles in the epigenetic regulation of gene expression in cells and are emerging therapeutic targets for treating a wide range of diseases. HDAC inhibitors (HDACi) 2 that act on multiple HDAC enzymes have been used clinically to treat a number of solid and hematological malignancies. HDACi are currently being studied also for their efficacy in nonmalignant diseases, including pathologic bone loss, but this has necessitated a better understanding of the roles of individual HDAC enzymes, particularly the eleven zinc-containing isozymes.Selective isozyme-specific inhibitors currently being developed against class I HDAC (1, 2, 3 and 8) and class II HDAC (4, 5, 6, 7, 9 and 10) will be valuable tools for elucidating the roles played by individual HDACs in different physiological and pathological settings. Isozyme-specific HDACi promise to have greater efficacy and reduced side effects, as required for treating chronic disease over extended periods of time. This article reviews the current understanding of roles for individual HDAC isozymes and effects of HDACi on bone cells, (osteoblasts, osteoclasts and osteocytes), in relation to bone remodelling in conditions characterised by pathological bone loss, including periodontitis, rheumatoid arthritis and myeloma bone disease.

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Section: Periodontitismentioning

confidence: 99%

Section: Osteoclasts Hdacs and Hdacimentioning

confidence: 99%

Histone deacetylases (HDAC) in physiological and pathological bone remodelling

Cantley

Zannettino

Bartold

et al. 2017

Bone

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“…RANKL is expressed in synovial tissue from patients with rheumatoid arthritis (27)(28)(29) and has been found to be crucial for osteoclast formation and bone loss in experimentally induced arthritis in mice (30). RANKL is also expressed in gingival tissue from patients with periodontal disease (31,32), and increased RANKL/OPG is associated with bone loss in periodontitis (4,31).…”

mentioning

confidence: 99%

Bradykinin potentiates cytokine‐induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression

Brechter¹,

Lerner²

2007

Arthritis & Rheumatism

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Objective. Bradykinin (BK) stimulates bone resorption in vitro and synergistically potentiates interleukin-1 (IL-1)-induced bone resorption and prostaglandin (PG) formation, suggesting that kinins are important in inflammation-induced bone loss. The present study was undertaken to study 1) the role of the kinin B1 and B2 receptors in the synergistic interaction with IL-1 and tumor necrosis factor ␣ (TNF␣), 2) the molecular mechanisms involved in synergistic enhancement of PG formation, and 3) the effects of kinins on cytokine-induced expression of RANKL, RANK, and osteoprotegerin (OPG) (the latter being crucial molecules in osteoclast differentiation).Methods. Formation of PGs, expression of enzymes involved in arachidonic acid metabolism, and expression of RANKL, RANK, and OPG were assessed in the human osteoblastic cell line MG-63 and in mouse calvarial bones.

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“…Increased RANKL/OPG ratio accompanies bone resorption involved in a variety of processes such as pathological osteolysis (Grimaud et al, 2003;Tay et al, 2004), periodontitis (Crotti et al, 2003), tooth eruption (Heinrich et al, 2005), and orthodontic tooth movement (Yamaguchi, 2009). The current data adds physiologic mandibular periosteal growth to that list.…”

Section: Discussionmentioning

confidence: 85%

Molecular Variations Related to the Regional Differences in Periosteal Growth at the Mandibular Ramus

Sun

Tee

2010

The Anatomical Record

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Periosteal growth at human mandibular ramus is characterized by bone apposition at the posterior border and resorption at the anterior border. Molecular control of this regional variation is unclear. This study examined the expression of several molecules involved in bone apposition/ resorption at these regions in vivo and in vitro. By using growing pigs as a model, the periosteal growth was assessed at the mandibular ramus by vital staining and histological observations. In parallel, periosteal tissues were harvested and pulverized for RNA and protein extraction. Periosteal cells were also isolated, expanded in osteogenic media, and subjected to a single dose of dynamic tensile strain (0, 5, or 10% magnitude at 0.5 Hz) to examine their responses to mechanical loading. Real-time RT-PCR and Western blot analyses were used to examine mRNA and protein expression from periosteal tissues and cultured cells. Histological observation confirmed an anterior-resorption/posterior-apposition pattern in the pig mandibular ramus. Both in vivo tissue and in vitro cells demonstrated greater mRNA expression of receptor activator of NF-jB ligand (RANKL)/osteoprotegerin (OPG) ratio and bone morphogenetic protein 2 (BMP2) at the anterior region, while OPG expression at the anterior region was lower than the posterior region. In response to the application of a single dose of dynamic tensile strain, cultured periosteal cells appeared to change the expression profile of osteogenic markers but not that of RANKL/OPG and BMP2. These findings suggest that the unique regional variation of periosteal activity at the mandibular ramus is regulated by a differential expression of RANKL/OPG ratio (likely through differential induction of OPG) and BMP2. Anat Rec, 294:79-87, 2011. V V C 2010 Wiley-Liss, Inc.Key words: periosteum; mandibular growth; RANKL/OPG; tissue engineering; cell loadingHuman mandibular growth is mainly through endochondral bone formation at the condyles and intramembranous bone formation at the periosteum (Enlow and Hans, 1996). While condylar growth provides the overall elongation and rotation of the mandible (Bjork and Skieller, 1983), periosteal activity causes extensive surface modeling/remodeling or reshaping of the mandible (Enlow and Hans, 1996). One striking feature of mandibular periosteal activity is at the ramus, where bone resorption takes place at the anterior (rostral) border whereas bone apposition at the posterior (caudal) border (Robinson and Sarnat, 1955;Seiton and Engel, 1969;Hans et al., 1995). At the cell level, osteogenic proliferation is concentrated at the appositional posterior ramal region, whereas osteoclasts are mainly present at the resorptive anterior region (Ochareon and Herring, 2007). However, the molecular mechanisms related to these differential periosteal activities are mostly unknown.

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Receptor activator NF κB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis

Abstract: The change in the levels of these key regulators of osteoclast differentiation may play a major role in the bone loss seen in periodontitis.

Cited by 273 publications

References 42 publications

Histone deacetylases (HDAC) in physiological and pathological bone remodelling

Histone deacetylases (HDAC) in physiological and pathological bone remodelling

Bradykinin potentiates cytokine‐induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression

Molecular Variations Related to the Regional Differences in Periosteal Growth at the Mandibular Ramus

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