Bacteria responsible for gum disease facilitates rheumatoid arthritis

Sep. 12, 2013 — Does gum disease indicate future joint problems? Although researchers and clinicians have long known about an association between two prevalent chronic inflammatory diseases — periodontal disease and rheumatoid arthritis (RA) — the microbiological mechanisms have remained unclear.In an article published today in PLoS Pathogens, University of Louisville School of Dentistry Oral Health and Systemic Diseases group researcher Jan Potempa, PhD, DSc, and an international team of scientists from the European Union’s Gums and Joints project have uncovered how the bacterium responsible for periodontal disease, Porphyromonas gingivalisworsens RA by leading to earlier onset, faster progression and greater severity of the disease, including increased bone and cartilage destruction.The scientists found that P. gingivalis produces a unique enzyme, peptidylarginine deiminanse (PAD) which then enhances collagen-induced arthritis (CIA), a form of arthritis similar to RA produced in the lab. PAD changes residues of certain proteins into citrulline, and the body recognizes citullinated proteins as intruders, leading to an immune attack. In RA patients, the subsequent result is chronic inflammation responsible for bone and cartilage destruction within the joints.Potempa and his team studied another oral bacterium, Prevotella intermedia for the same affect, but learned it did not produce PAD, and did not affect CIA.”Taken together, our results suggest that bacterial PAD may constitute the mechanistic link between P. gingivalis periodontal infection and rheumatoid arthritis, but this ground-breaking conclusion will need to be verified with further research,” he said.Potempa said he is hopeful these findings will shed new light on the treatment and prevention of RA.Studies indicate that compared to the general population, people with periodontal disease have an increased prevalence of RA and, periodontal disease is at least two times more prevalent in RA patients. Other research has shown that a P. gingivalis infection in the mouth will precede RA, and the bacterium is the likely culprit for onset and continuation of the autoimmune inflammatory responses that occur in the disease.

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New approach to battling tuberculosis

June 18, 2013 — Most humans would like to shed their fatty exteriors, but tuberculosis (TB)-causing bacteria rely on theirs for survival. Scientists at the University of Medicine and Dentistry of New Jersey (UMDNJ)-New Jersey Medical School have now discovered a drug that cripples the TB bug by dissolving its protective fatty coating, a finding that could eventually be used to improve TB treatment in humans. The study has been posted online by Nature Chemical Biology.Share This:TB is caused by infection with the bacterium Mycobacterium tuberculosis (Mtb) and is the second biggest cause of death worldwide, second only to HIV/AIDS. And with drug-resistant strains of Mtb on the rise, there is a critical need for more effective anti-TB agents.”Mtb is a little ball of soap,” says lead author David Alland, MD, a professor of medicine and Director of the Center for Emerging and Re-emerging Pathogens at New Jersey Medical School, describing the meshwork of long fatty acids that make up the bug’s protective cell wall. There are a few anti-TB drugs that disrupt this coat, but so far no single drug has been able to kill the bacteria completely. So his group went in search of new and better drugs by using a simple and rapid approach. They screened for agents that trigger expression of a bacterial gene that gets turned on when cell wall synthesis is compromised.They discovered a class of compound called thiophenes that killed the Mtb in culture without the emergence of drug resistance. And the combination of thiophene and the existing coat-busting drug isoniazid achieved 100% bacterial killing. Thiophenes worked by crippling an enzyme called Pks13 that hitches two long fatty acids together to create the bug’s fatty coat. With additional information on the molecular structure of these drugs bound to Pks13, Alland hopes to discover ways to tweak the compounds to make them even more potent and less toxic.Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is reprinted from materials provided by University of Medicine and Dentistry of New Jersey (UMDNJ), via Newswise. …

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Bacterium that causes gum disease packs a one-two punch to the jaw

June 11, 2013 — The newly discovered bacterium that causes gum disease delivers a one-two punch by also triggering normally protective proteins in the mouth to actually destroy more bone, a University of Michigan study found.Scientists and oral health care providers have known for decades that bacteria are responsible for periodontitis, or gum disease. Until now, however, they hadn’t identified the bacterium.”Identifying the mechanism that is responsible for periodontitis is a major discovery,” said Yizu Jiao, a postdoctoral fellow at the U-M Health System, and lead author of the study appearing in the recent issue of the journal Cell Host and Microbe.Jiao and Noahiro Inohara, research associate professor at the U-M Health System, worked with William Giannobile, professor of dentistry, and Julie Marchesan, formerly of Giannobile’s lab.The study yielded yet another significant finding: the bacterium that causes gum disease, called NI1060, also triggers a normally protective protein in the oral cavity, called Nod1, to turn traitorous and actually trigger bone-destroying cells. Under normal circumstances, Nod1 fights harmful bacterium in the body.”Nod1 is a part of our protective mechanisms against bacterial infection. It helps us to fight infection by recruiting neutrophils, blood cells that act as bacterial killers,” Inohara said. “It also removes harmful bacteria during infection. However, in the case of periodontitis, accumulation of NI1060 stimulates Nod1 to trigger neutrophils and osteoclasts, which are cells that destroy bone in the oral cavity.”Giannobile, who also chairs the Department of Periodontics and Oral Medicine at the U-M School of Dentistry, said understanding what causes gum disease at the molecular level could help develop personalized therapy for dental patients.”The findings from this study underscore the connection between beneficial and harmful bacteria that normally reside in the oral cavity, how a harmful bacterium causes the disease, and how an at-risk patient might respond to such bacteria,” Giannobile said.

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