New research suggests that melanocortin agonism
could represent an innovative way to tame
inflammation, and at the same time, preserve
periodontal bone after infection.
If you hate going to the dentist, here's some good
news. New research published online in The FASEB
Journal, shows that melanocortin agonism may
effectively control the inflammation that often
occurs in gum tissue, which when unchecked,
ultimately accelerates tooth and bone loss. This
research involving mice, opens the door to a new
class of treatments for gum disease.
"Controlling inflammation during gum disease is a
key step to avoid alveolar bone resorption, tooth
loss and, thus, improve the quality of life of
patients," said Mila Madeira, Ph.D., a researcher
involved in the work from the Department of
Microbiology at the Biologic Science Institute at
the Universidad Federal de Minas Gerais in Belo
Horizonte, MG, Brazil.
To make their discovery, Madeira and colleagues used
several groups of mice. The first group was infected
with bacteria related to gum disease and then
treated them with a melanocortin agonist. The second
group had no infection. The third group was
infected, but not treated. The final group was
infected but treated with a placebo. Melanocortin
agonism was associated with reduced alveolar bone
resorption and less inflammation, a critical feature
to be controlled in gum diseases.
"Attenuation of the inflammatory axis of periodontal
pathology cannot be overstated in its importance ,"
said Thoru Pederson, Ph.D., Editor-in-Chief of The
FASEB Journal. "These findings provide an entirely
new approach to this highly prevalent condition."
For more information
The Federation of American Societies for
Experimental Biology
Mila F. M. Madeira, Celso M. Queiroz-Junior,
Trinidad Montero-Melendez, Silvia M. C. Werneck,
Jôice D. Corrêa, Frederico M. Soriani, Gustavo P.
Garlet, Daniele G. Souza, Mauro M. Teixeira,
Tarcilia A. Silva, and Mauro Perretti.
Melanocortin agonism as a viable strategy to control
alveolar bone loss induced by oral infection.
doi:10.1096/fj.201600790R
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