Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 Aug;4(Suppl 2):S256-9.
doi: 10.4103/0975-7406.100244.

Host modulation by therapeutic agents

Affiliations

Host modulation by therapeutic agents

Sugumari Elavarasu et al. J Pharm Bioallied Sci. 2012 Aug.

Abstract

Periodontal disease susceptible group present advanced periodontal breakdown even though they achieve a high standard of oral hygiene. Various destructive enzymes and inflammatory mediators are involved in destruction. These are elevated in case of periodontal destruction. Host modulation aims at bringing these enzymes and mediators to normal level. Doxycycline, nonsteroidal anti-inflammatory drugs (NSAIDs), bisphosphonates, nitrous oxide (NO) synthase inhibitors, recombinant human interleukin-11 (rhIL-11), omega-3 fatty acid, mouse anti-human interleukin-6 receptor antibody (MRA), mitogen-activated protein kinase (MAPK) inhibitors, nuclear factor-kappa B (NF-kb) inhibitors, osteoprotegerin, and tumor necrosis factor antagonist (TNF-α) are some of the therapeutic agents that have host modulation properties.

Keywords: Cytokines; Matrix metalo protienases (MMP); Periodontitis.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1
Figure 1
Potential therapeutic strategies to treat bone resorption: Agents that block the differentiation or activity of osteoclasts are potential therapeutic agents. Osteoprotegerin (OPG) inhibits the differentiation of osteoclasts through its action as a decoy receptor that blocks receptor activator of nuclear factor-kappa B (NF-kB) ligand (RANKL) and RANK juxtacrine interaction. NSAIDs and other anti-inflammatory molecules [including p38 mitogen-activated protein kinase (MAPK) inhibitors, c-jun N-terminal kinase (JNK) inhibitors, and NF-kB inhibitors] can inhibit the formation of hematoprogenitor cells to pre-osteoclasts. Antibodies to RANKL can also block this interaction. MMP inhibitors reduce the protease degradation of the organic matrix, and anti-integrins block the initial osteoclast adhesion to the matrix. IL = interleukin; LPS = lipopolysaccharide; M-CSF = macrophage colony-stimulating factor; sRANKL = soluble RANKL; TNFα = tumor necrosis factor-α; TNFsRc = TNF soluble receptor

References

    1. Page RC, Kornman KS. The pathogenesis of human periodontitis: An introduction. Periodontal. 2000;14:9. 1997. - PubMed
    1. Page RC. Milestones in periodontal research and the remaining critical issues. J Periodontal Res. 1999;34:331. - PubMed
    1. Golub LM, Wolff M, Lee HM, McNamara TF, Ramamurthy NS, Zambon J, et al. Further evidence that tetracyclines inhibit collagenase activity in human crevicular fluid and from other mammalian sources. J Periodontal Res. 1985;20:12–23. - PubMed
    1. Burns FR, Stack MS, Gray RD, Paterson CA. Inhibition of purified collagenase from alkali-burned rabbit corneas. Invest Ophthalmol Vis Sci. 1989;30:1569–75. - PubMed
    1. Golub LM, Ciancio S, Ramamamurthy NS, Leung M, McNamara TF. Low-dose doxycycline therapy: Effect on gingival and crevicular fluid collagenase activity in humans. J Periodontal Res. 1990;25:321–30. - PubMed