Health scan: Cracks may develop in ‘permanent’ dental implants

Most implants develop microscopic cracks and defects over the years.

By
August 9, 2015 02:35
4 minute read.
dentist

Dentist´s instruments. (photo credit: INGIMAGE)

Dental implants – though expensive – are not forever, according to Dr. Keren Shemtov-Yona, who did a master’s thesis on the subject at Haifa’s Technion-Israel Institute of Technology and Rambam Medical Center. Most implants, she found, develop microscopic cracks and defects over the years.

An increasing number of people are getting tooth implants inserted into their jaws to permanently replace their eroded or diseased teeth. The more common they become, however, the higher the number of associated defects and problems. In some cases, replacement with new implants requires a complicated surgical procedure, said Shemtov-Yona, who is working under the guidance of Technion mechanical engineering Prof. Daniel Rittel. In one experiment, they collected hundreds of implanted teeth at four dental clinics around the country that had to be removed due to the receding of the jawbone. The artificial teeth and their anchors looked whole, but 62 percent were found under an electronic scanner to have cracks and other defects.

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Their study, published recently in the Journal of the Mechanical Behavior of Biomedical Materials, aroused much interest among professionals in the field.

“Cracks in implants are rare complications, and each case is different. But there is no doubt that over time, the forces of chewing and closing the mouth can cause mechanical fatigue in the materials, and cracks. Dentists and implant manufacturers must act to improve quality and develop ways to identify minute cracks in time,” she advised.

“The Technion is an ideal place for such research, as it bridges engineering and life sciences. Dental implants can’t exist without dentistry, but without engineering research, they cannot be improved,” she concluded.

EYE COLOR/ALCOHOL DEPENDENCE FOUND A surprising link has been discovered between having blue eyes and a greater risk of becoming alcoholic, according to geneticists at the University of Vermont.

Doctoral student Arvis Sulovari, a doctoral student in cellular, molecular and biological sciences, and microbiology and molecular genetics Prof. Dawei Li published their findings recently in the American Journal of Medical Genetics: Neuropsychiatric Genetics.

They believe that their finding may lead to a better understanding of the causes of psychiatric illnesses.

“This suggests an intriguing possibility – that eye color can be useful in the clinic for alcohol dependence diagnosis,” Sulovari said.

The authors found that primarily European Americans with light-colored eyes – including green, gray and brown in the center – had a higher incidence of alcohol dependency than those with dark brown eyes, with the strongest tendency among blue-eyed individuals. The study outlines the genetic components that determine eye color and shows that they line up along the same chromosome as the genes related to excessive alcohol use. But, Li said, “we still don’t know the reason” and more research is needed, “as there are many genes, and there are many environmental triggers.”

Using a databse of 1,263 samples, the researchers noticed the eye-color connection and retested their analysis three times, arranging and rearranging the groups to compare age, gender and different ethnic or geographic backgrounds. Next, Li wants to delve deeper into the relationship between cultural background and genetic makeup, continuing his quest to find the mechanisms of mental illness. His greatest challenge: “What has fascinated me the most about this work has been investigating the interface between statistics, informatics and biology,” said Sulovari. “It’s an incredible opportunity to study genomics in the context of complex human diseases.”

COLON CANCER: A STEP BACK TO GO FORWARD Recent Weizmann Institute of Science studies are revealing a complex picture of cancer progression in which certain genes that drive tumor growth in the earlier stages get suppressed in later stages. Current research in the lab of molecular cell biology Prof. Avri Ben-Ze’ev suggests that the tumor cells at the invasive front of later-stage human colorectal cancer may take a big step back to go forward.

Colorectal cancer is most deadly when it has metastasized – spread to other organs in the body – mainly to the liver. The Rehovot team had previously discovered that a mutation found in 80 percent of all colorectal cancers leads to enhanced expression of another gene called L1, especially in the cells at the leading edge of metastatic growth. L1 is known to play a role in cell-to-cell adhesion; in the present study, further investigation into L1 expression led the group to yet another gene, called SMOC-2.

The researchers investigated the role of this gene in mouse models of colorectal cancer metastasis to the liver, finding that L1 produced heightened SMOC-2 levels during this stage. When the researchers increased the levels of SMOC-2 in human colorectal cancer cells, their metastasis to the liver was fast and aggressive. Conversely, blocking the gene in colon cancer cells inhibited metastasis, conclusively indicating that the activation of SMOC-2 by L1 plays a crucial role in the spread of this cancer.

SMOC-2 encodes a molecule that is secreted by the cells and then makes it way to the outer part of the cell membrane, where it facilitates movement. The research, said Ben-Ze’ev, provides support for the idea that as cancer develops, it also reverts – that is, some of its cells adopt a less mature, more stem-like state that assists metastasis.

Ben-Ze’ev hopes that further research will point to ways of interfering with the activities of genes like SMOC-2, thus preventing this cancer from metastasizing. In addition, he says, the expression patterns of SMOC-2 could make it an ideal marker for the early detection of human metastatic colorectal cancer.


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