Emerging and future therapies for the treatment of bone loss associated with chronic inflammation

Haynes, David R.

doi:10.1007/s10787-006-0006-1

Cited by 22 publications

(17 citation statements)

References 37 publications

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“…tissues leading to alveolar bone resorption and tooth loss (Pihlstrom et al, 2005;Chambrone and Chambrone, 2006;Haynes, 2006). Studies reveal that subjects with stress-related depression and exhaustion will have more plaque accumulation, gingival inflammation, and increased levels of IL-6 and cortisol in gingival crevicular fluid compared to normal controls, suggesting that depression might affect immune function, which could lead to impaired periodontal health (Johannsen et al, 2006).…”

mentioning

confidence: 99%

Anti-inflammatory effect of α, β-Amyrin, a pentacyclic triterpene from Protium heptaphyllum in rat model of acute periodontitis

et al. 2007

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This study was aimed to evaluate the anti-inflammatory potential of triterpene alpha, beta-amyrin in rats on acute phase periodontitis. Periodontitis was induced by ligature placement around the maxillary right second molar tooth. Rats (n = 8/group) were pretreated with alpha, beta-amyrin (5 and 10 mg/kg, p. o.), two hours before the induction of periodontal inflammation. Sham-operated and positive controls (lumiracoxib and dexamethasone) were included. Six hours later, plasma levels of TNF-alpha were analysed. Rats were sacrificed at 24 h, and the gingival tissue analysed for myeloperoxidase (MPO) and thiobarbituric acid-reactive substances (TBARS), as measures of neutrophil influx and lipid-peroxidation, respectively alpha, beta-Amyrin as well as dexamethasone significantly inhibited the periodontitis-associated increases of TNF-alpha, and the gingival MPO and TBARS. alpha, beta-Amyrin effect was more prominent at 5 mg/kg. Lumiracoxib manifested varied influence on the studied parameters. These results provide evidence to show that alpha, beta-Amyrin retards acute inflammation in rat model of periodontitis and warrant further study on its efficacy to prevent chronic periodontitis-associated bone loss.

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confidence: 99%

Anti-inflammatory effect of α, β-Amyrin, a pentacyclic triterpene from Protium heptaphyllum in rat model of acute periodontitis

et al. 2007

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“…Alcohol has long been known to be anti-inflammatory and immune-suppressive. Examples include that alcohol reduces the development of destructive rheumatoid arthritis (RA), an autoimmune disease characterized by severe joint inflammation (48, 49). Moderate alcohol intake was also inversely associated with the risk of systemic lupus erythematosus (SLE), another autoimmune disease (50, 51).…”

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confidence: 99%

Non-canonical Glucocorticoid Receptor Transactivation of gilz by Alcohol Suppresses Cell Inflammatory Response

Jennings

Wang

et al. 2017

Front. Immunol.

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Acute alcohol exposure suppresses cell inflammatory response. The underlying mechanism has not been fully defined. Here we report that alcohol was able to activate glucocorticoid receptor (GR) signaling in the absence of glucocorticoids (GCs) and upregulated glucocorticoid-induced leucine zipper (gilz), a prominent GC-responsive gene. Such a non-canonical activation of GR was not blocked by mifepristone, a potent GC competitor. The proximal promoter of gilz, encompassing five GC-responsive elements (GREs), was incorporated and tested in a luciferase reporter system. Deletion and/or mutation of the GREs abrogated the promoter responsiveness to alcohol. Thus, the GR–GRE interaction transduced the alcohol action on gilz. Alcohol induced GR nuclear translocation, which was enhanced by the alcohol dehydrogenase inhibitor fomepizole, suggesting that it was alcohol, not its metabolites, that engendered the effect. Gel mobility shift assay showed that unliganded GR was able to bind GREs and such interaction withstood clinically relevant levels of alcohol. GR knockout via CRISPR/Cas9 gene targeting or GILZ depletion via small RNA interference diminished alcohol suppression of cell inflammatory response to LPS. Thus, a previously unrecognized, non-canonical GR activation of gilz is involved in alcohol modulation of cell immune response.

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“…In RA, bone-active agents, including the biphosphonates, have received significant consideration [126][127][128]. Overall, clinical trials with biphosphonates in RA have been disappointing, but work on animal models with some of the newer biphosphonates continues to be quite promising.…”

Section: Changes In Both Cartilage and Subchondral Bone Are Relevant Tomentioning

confidence: 99%

Inflammation and arthritis: perspectives of the glycobiologist

Brockhausen¹,

Anastassiades²

2008

Expert Review of Clinical Immunology

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This review focuses on the role of glycosylation during the development of joint inflammation and degeneration. Although glycoproteins and glycan-binding proteins have essential functions in bone and cartilage, and in the inflammatory process, their exact roles are still uncertain due to the vast complexity of carbohydrate structures. Glycosylated epitopes have been shown to play a role in the induction of arthritis in animal models. Currently available drugs are aimed at the protection of cartilage and bone structures but new developments in this area should take into account the tight and specific interactions between bone and cartilage. It is anticipated that new agents will help to remodel damaged joints, based on knowledge of cartilage and bone turnover and on the exact role of glycosylated molecules and cell surface receptor glycoproteins in these processes. Highly sensitive imaging techniques and well-characterized In vivo models will accelerate this development.

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Emerging and future therapies for the treatment of bone loss associated with chronic inflammation

Cited by 22 publications

References 37 publications

Anti-inflammatory effect of α, β-Amyrin, a pentacyclic triterpene from Protium heptaphyllum in rat model of acute periodontitis

Anti-inflammatory effect of α, β-Amyrin, a pentacyclic triterpene from Protium heptaphyllum in rat model of acute periodontitis

Non-canonical Glucocorticoid Receptor Transactivation of gilz by Alcohol Suppresses Cell Inflammatory Response

Inflammation and arthritis: perspectives of the glycobiologist

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