Tuesday

Potenial New Therapeutics for Periodontal Bone Resorption

In one of the previous posts I had mentioned about the T and B cell mediated bone resorption and how controlling inflammation is important part of the treatment. In one of the recent papers the the potential therapeutic targets to treat bone resorption is very well illustrated. Some of these should be soon used in the dental office in the near future to treat and control periodontal disease induced bone resorption.


















Figure: 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-κB) ligand (RANKL) and RANK juxtacrine interaction. Non-steroidal anti-inflammatory drugs (NSAIDs) and other anti-inflammatory molecules [including p38 mitogen-activated protein kinase (MAPK) inhibitors, c-jun N-terminal kinase (JNK) inhibitors and NF-κB inhibitors] can inhibit the formation of hematoprogenitor cells to pre-osteoclasts. Antibodies to RANKL can also block this interaction. Matrix metalloproteinase (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; TNF-α, tumor necrosis factor-α; TNFsRC, TNF soluble receptor.

Refrence:
Keith L. Kirkwood, Joni A. Cirelli, Jill E. Rogers, William V. Giannobile (2007)
Novel host response therapeutic approaches to treat periodontal diseases
Periodontology 2000 43 (1), 294–315.

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