Cause of negative outcomes for implants identified

The health of the surrounding tissue affects the success of a dental implant. Identifying and reducing risk factors is therefore a key step in the implant process. Now a combination of genes has been identified as a possible indicator of greater tissue destruction leading to negative outcomes for implants.

The authors of an article
in the current issue of the Journal of Oral Implantology report on a study of individuals with the combination of interleukin (IL)-1 allele 2 at IL-1A−889 and IL-1B+3954. These people are “genotype positive” and are susceptible to increased periodontal tissue destruction.

Peri-implantitis, or the process of tissue inflammation and destruction around failing implants, is very similar to periodontal disease. The researchers sought to find any association of these genotypes with the severity of peri-implantitis progression and the effect of this combination on treatment outcomes.

This study compared two groups of patients, all of whom had implants. The first group consisted of 25 patients with peri-implantitis, while the second group of 25 patients had healthy tissue. Seventeen patients from the first group and five from the second group were genotype positive.

Patients in the first group, those with peri-implantitis, took part in a treatment and maintenance program. The genotype-positive patients in this group experienced greater periodontal tissue destruction and, increased discharge from tissues. The genotype-negative patients responded better to treatment. Statistically significant differences were noted between the groups.

The combination of these two alleles in patients with inflamed periodontal tissues denotes a risk factor that can lead to further tissue destruction. Patients with the specific genotype can have exaggerated local inflammation. Gene polymorphism may affect the outcomes of treatment for peri-implantitis in genotype-positive people and affect the long-term success of implants.

Full text of the article, “
The Effect of Interleukin-1 Allele 2 Genotype (IL-1a−889 and IL-1b+3954) on the Individual’s Susceptibility to Peri-Implantitis: Case-Control Study,” Journal of Oral Implantology, Vol. 37, No. 3, 2011, is available at http://allenpress.com/publications/journals/orim

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About Journal of Oral Implantology
The Journal of Oral Implantology is the official publication of the American Academy of Implant Dentistry and of the American Academy of Implant Prosthodontics. It is dedicated to providing valuable information to general dentists, oral surgeons, prosthodontists, periodontists, scientists, clinicians, laboratory owners and technicians, manufacturers, and educators. The JOI distinguishes itself as the first and oldest journal in the world devoted exclusively to implant dentistry. For more information about the journal or society, please visit here.

How Cavity-Causing Microbes Invade Heart

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Scientists have discovered the tool that bacteria normally found in our mouths use to invade heart tissue, causing a dangerous and sometimes lethal infection of the heart known as endocarditis. The work raises the possibility of creating a screening tool – perhaps a swab of the cheek, or a spit test – to gauge a dental patient’s vulnerability to the condition.

The identification of the protein that allows Streptococcus mutans to gain a foothold in heart tissue is reported in the June issue of Infection and Immunity by microbiologists at the University of Rochester Medical Center.

S. mutans is a bacterium best known for causing cavities. The bacteria reside in dental plaque – an architecturally sophisticated goo composed of an elaborate molecular matrix created by S. mutans that allows the bacteria to inhabit and thrive in our oral cavity. There, they churn out acid that erodes our teeth.


S. mutans invading a human coronary artery endothelial cell.
Normally, S. mutans confines its mischief to the mouth, but sometimes, particularly after a dental procedure or even after a vigorous bout of flossing, the bacteria enter the bloodstream. There, the immune system usually destroys them, but occasionally – within just a few seconds – they travel to the heart and colonize its tissue, especially heart valves. The bacteria can cause endocarditis – inflammation of heart valves – which can be deadly. Infection by S. mutans is a leading cause of the condition.

“When I first learned that S. mutans sometimes can live in the heart, I asked myself: Why in the world are these bacteria, which normally live in the mouth, in the heart? I was intrigued. And I began investigating how they get there and survive there,” said Jacqueline Abranches, Ph.D., a microbiologist and the corresponding author of the study.

Abranches and her team at the University’s Center for Oral Biology discovered that a collagen-binding protein known as CNM gives S. mutans its ability to invade heart tissue. In laboratory experiments, scientists found that strains with CNM are able to invade heart cells, and strains without CNM are not.

When the team knocked out the gene for CNM in strains where it’s normally present, the bacteria were unable to invade heart tissue. Without CNM, the bacteria simply couldn’t gain a foothold; their ability to adhere was about one-tenth of what it was with CNM.

The team also studied the response of wax worms to the various strains of S. mutans. They found that strains without CNM were rarely lethal to the worms, while strains with the protein were lethal 90 percent of the time. Then, when Abranches’ team knocked out CNM in those strains, they were no longer lethal – those worms thrived.

The work may someday enable doctors to prevent S. mutans from invading heart tissue. Even sooner, though, since some strains of S. mutans have CNM and others do not, the research may enable doctors to gauge a patient’s vulnerability to a heart infection caused by the bacteria.

Abranches has identified five specific strains of S. mutans that carry the CNM protein, out of more than three dozen strains examined. CNM is not found in the most common type of S. mutans found in people, type C, but is present in rarer types of S. mutans, including types E and F.

“It may be that CNM can serve as a biomarker of the most virulent strains of S. mutans,” said Abranches, a research assistant professor in the Department of Microbiology and Immunology. “When patients with cardiac problems go to the dentist, perhaps those patients will be screened to see if they carry the protein. If they do, the dentist might treat them more aggressively with preventive antibiotics, for example.”

Until more research is done and a screening or preventive tool is in place, Abranches says the usual advice for good oral health still stands for everyone.

“No matter what types of bacteria a person has in his or her mouth, they should do the same things to maintain good oral health. They should brush and floss their teeth regularly – the smaller the number of S. mutans in your mouth, the healthier you’ll be. Use a fluoride rinse before you go to bed at night. And eat a healthy diet, keeping sugar to a minimum,” added Abranches.

Abranches presented the work at a recent conference on the “oral microbiome” hosted by the University’s Center for Oral Biology. The center is part of the Medical Center’s Eastman Institute for Oral Health, a world leader in research and post-doctoral education in general and pediatric dentistry, orthodontics, periodontics, prosthodontics, and oral surgery.

Additional authors of the study include laboratory technician James Miller; former technician Alaina Martinez; Patricia Simpson-Haidaris, Ph.D., associate professor of Medicine; Robert Burne, Ph.D., of the University of Florida; and Abranches’ husband, Jose Lemos, Ph.D., of the Center for Oral Biology, who is also assistant professor in the Department of Microbiology and Immunology. The work was funded by the American Heart Association.

Vitamin D fights gingivitis and periodontitis

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Laboratory-grown gingival cells treated with vitamin D boosted their production of an endogenous antibiotic, and killed more bacteria than untreated cells, according to a paper in the June 2011 issue of the journal Infection and Immunity. The research suggests that vitamin D can help protect the gums from bacterial infections that lead to gingivitis and periodontitis. Periodontitis affects up to 50 percent of the US population, is a major cause of tooth loss, and can also contribute to heart disease. Most Americans are deficient in vitamin D.

His interest piqued by another laboratory's discovery that vitamin D could stimulate white blood cells to produce natural proteins that have antibiotic activity, Gill Diamond of the UMDNJ -- New Jersey Dental School, Newark, showed that vitamin D could stimulate lung cells to produce LL-37, a natural antibiotic protein, and kill more bacteria. That suggested that , vitamin D might help cystic fibrosis patients. Next, in the new research, he showed that vitamin D has the same effct on gingival cells.

Then, Diamond found that vitamin D also stimulates gingival cells to produce another protein, called TREM-1, which had not been well-studied, but which was thought to be made by white blood cells. He found that it boosts production of pro-inflammatory cytokines.

The new research also showed that vitamin D coordinates expression of a number of genes not previously considered to be part of the vitamin D pathway. Those genes may be involved in additional infection-fighting pathways. A more comprehensive understanding of how vitamin D carries out this regulation at the molecular level -- something Diamond hopes to investigate -- will enable targeted therapies using vitamin D, he says.

Interestingly, Diamond also found that lung and gum cells appear to have the ability to activate inactive forms of vitamin D, says Diamond. "This means that we may even be able to use vitamin D therapy topically, if that proves true."

Vitamin D has become a hot area of research in recent years. In addition to infectious diseases, studies suggest that it has protective effects against autoimmune diseases, and certain cancers.

Diamond says that after he began conducting research on vitamin D, he began taking it as a supplement. Since then, "I have had only one cold in four years, and that one lasted only three days," he says. "Other people I've met who have done the same have seen similar results. We are trying to figure out how it's working, and what other infectious diseases can be mitigated by it."

Healing times for dental implants could be cut

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The technology used to replace lost teeth with titanium dental implants could be improved. By studying the surface structure of dental implants not only at micro level but also at nano level, researchers at the University of Gothenburg; Sweden, have come up with a method that could shorten the healing time for patients.

"Increasing the active surface at nano level and changing the conductivity of the implant allows us to affect the body's own biomechanics and speed up the healing of the implant," says Johanna Löberg at the University of Gothenburg's Department of Chemistry. "This would reduce the discomfort for patients and makes for a better quality of life during the healing process."

Dental implants have been used to replace lost teeth for more than 40 years now. Per-Ingvar Brånemark, who was recently awarded the prestigious European Inventor Award, was the first person to realise that titanium was very body-friendly and could be implanted into bone without being rejected. Titanium is covered with a thin layer of naturally formed oxide and it is this oxide's properties that determine how well an implant fuses with the bone.

It became clear at an early point that a rough surface was better than a smooth one, and the surface of today's implants is often characterised by different levels of roughness, from the thread to the superimposed nanostructures. Anchoring the implant in the bone exerts a mechanical influence on the bone tissue known as biomechanical stimulation, and this facilitates the formation of new bone. As the topography (roughness) of the surface is important for the formation of new bone, it is essential to be able to measure and describe the surface appearance in detail. But roughness is not the only property that affects healing.

Johanna Löberg has come up with a method that describes the implant's topography from micrometre to nanometre scale and allows theoretical estimations of anchoring in the bone by different surface topographies. The method can be used in the development of new dental implants to optimise the properties for increased bone formation and healing. She has also studied the oxide's conductivity, and the results show that a slightly higher conductivity results in a better cell response and earlier deposition of minerals that are important for bone formation.

The results are in line with animal studies and clinical trials of the commercial implant OsseoSpeed (Astra Tech AB), which show a slightly higher conductivity for the oxide and also an exchange between hydroxide and fluoride on the surface of the oxide. Surfaces with a well-defined nanostructure have a larger active area and respond quickly to the deposition of bone-forming minerals.