Impact of Drug Use on Oral Health

People with increased drug use or substance use disorders were found to have tooth decay and periodontal disease when compared to the general population, these patients were less likely to receive dental care, finds a new review published in the scientific journal Addiction.


Around 3 million new users are found to have substance use disorders every year, with the increased drug use, it may even affect oral health. Drug use affects oral health through direct physiological routes such as dry mouth, an increased urge for snacking, clenching and grinding of teeth, and chemical erosion from applying cocaine to teeth and gums. The lifestyle that often accompanies problematic drug use also affects oral health through high sugar diets, malnutrition, poor oral hygiene, and lack of regular professional dental care. Dental care can be further compromised by tolerance to painkillers and anaesthetics.


Oral health has significant consequences on quality of life and general health. In addition to functional and self-esteem issues that accompany bad teeth, the chronic inflammation and bacteraemia (bacteria in the blood) characteristic of poor oral health increases the incidence of coronary heart disease, stroke, diabetes and respiratory disease.


There are simple steps that both dentists and doctors can take to improve this population’s oral health. Dentists should screen their patients for substance use, notice any advanced dental or periodontal disease inconsistent with patient age and consider referral to medical doctors for management. In patients with suspected substance use disorders, dentists should be aware of issues concerning treatment and consent when the patient is intoxicated and be alert to the possibility of resistance to painkillers.


Doctors and clinicians who care for people with substance use disorders should screen for oral diseases and arrange for dental care as needed, consider using sugar-free preparations when prescribing methadone, and warn patients of the oral health risks associated with dry mouth and cravings for sweet foods.


These findings mirror those of increased dental decay and periodontal disease in people with severe mental illness, eating disorders and people with alcohol use disorders, compared with the general population.


The review combined the results of 28 studies from around the world, which collectively provided data on 4,086 dental patients with substance use disorder and 28,031 controls.




Source: Eurekalert



Tissue Regeneration from Mouse Teeth!

Researchers hope to one day use stem cells to heal burns, patch damaged heart tissue, even grow kidneys and other transplantable organs from scratch. This dream edges closer to reality every year, but one of the enduring puzzles for stem cell researchers is how these remarkable cells know when it’s time for them to expand in numbers and transform into mature, adult cells in order to renew injured or aging tissue.

The answer to this crucial decision-making process may lie in a most remarkable organ: the front tooth of the mouse.

Constantly growing incisors are the defining feature of all rodents, which rely on these sharp, chisel-like gnashers for burrowing and self-defense as well as gnawing food. Inside the jaw, a mouse’s incisors look more like a walrus’s tusks or the teeth of a saber-toothed tiger, with only the sharpened tips showing through the gums at the front of the mouth.

As the front of the tooth gets ground down, a pool of stem cells deep inside the jaw, at the very inner part of the tooth, is constantly building up the back of each incisor and pushing the growing tooth forward — a bit like the lead of a mechanical pencil.

“As we grow older our teeth start to wear out, and in nature, once you don’t have your teeth anymore, you die. As a result, mice and many other animals — from elephants to some primates — can grow their teeth continuously,” said UC San Francisco’s Ophir Klein, MD, PhD, a professor of orofacial sciences in UCSF’s School of Dentistry and of pediatrics in the School of Medicine. “Our lab’s objective is to learn the rules that let mouse incisors grow continuously to help us one day grow teeth in the lab, but also to help us identify general principles that could enable us to understand the processes of tissue renewal much more broadly.”

In a new study, published online April 27, 2017, in Cell Stem Cell, Jimmy Hu, PhD, a postdoctoral researcher in the Klein laboratory, has discovered that signals from the surrounding tissue are responsible for triggering these dental stem cells to leave their normal state of dormancy, hop on the conveyor belt of the growing tooth, and begin the process of transforming into mature tooth tissue.

“We usually think of stem cells responding to chemical signals to start proliferating and differentiating, but here there’s an exciting interaction between the physical environment and the cells that can prompt them to meet the demands of the growing tooth,” Hu said.

In their study, Hu and colleagues discovered that integrins, proteins that sit in cell membranes and link the internal skeleton of cells to the larger protein scaffolding of the surrounding tissue, trigger a newly described signaling cascade within the stem cells that causes them to begin rapidly multiplying — a process called “proliferation.”

It’s not clear yet exactly what external signals are responsible for triggering the stem cells to proliferate, the authors say, but they propose that the cells could be detecting that they have moved into a region where the back of the tooth needs to actively produce more cells based on changes in local tissue stiffness or the physical forces pulling and pushing on the cells.

“Our data clearly show that as stem cells move into their designated proliferating space, they ramp up integrin production. These integrins allow the cells to interact with extracellular molecules and become triggered to expand in numbers before eventually producing a large pool of mature dental cells,” Hu said.

Of additional interest to the researchers is the fact that both integrins and YAP — one of the molecules involved in the newly discovered integrin-triggered signaling cascade — have previously been implicated in the growth of certain types of tumors, which are thought to share some features of stem cell biology. This finding adds evidence to a growing sense among cancer researchers that interactions between cancer cells and the surrounding tissue may be a key step in triggering tumor growth.

“Integrins and YAP had been implicated in cancer before, but our work connects the two in an organ as opposed to in a Petri dish,” Klein said. “Wouldn’t it be nice if the same insights that let us learn to grow new tissues in the lab also lead to improved therapies to prevent the growth of tumors in patients?”

Story Source: Materials provided by University of California – San Francisco. Original written by Nicholas Weiler. Note: Content may be edited for style and length.

First-ever study shows e-cigarettes cause damage to gum tissue

A University of Rochester Medical Center study suggests that electronic cigarettes are as equally damaging to gums and teeth as conventional cigarettes.

The study, published in Oncotarget, was led by Irfan Rahman, Ph.D. professor of Environmental Medicine at the UR School of Medicine and Dentistry, and is the first scientific study to address e-cigarettes and their detrimental effect on oral health on cellular and molecular levels.

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First-ever study shows e-cigarettes cause damage to gum tissue

A University of Rochester Medical Center study suggests that electronic cigarettes are as equally damaging to gums and teeth as conventional cigarettes.

The study, published in Oncotarget, was led by Irfan Rahman, Ph.D. professor of Environmental Medicine at the UR School of Medicine and Dentistry, and is the first scientific study to address e-cigarettes and their detrimental effect on oral health on cellular and molecular levels.

Electronic cigarettes continue to grow in popularity among younger adults and current and former smokers because they are often perceived as a healthier alternative to conventional cigarettes. Previously, scientists thought that the chemicals found in cigarette smoke were the culprits behind adverse health effects, but a growing body of scientific data, including this study, suggests otherwise.

“We showed that when the vapors from an e-cigarette are burned, it causes cells to release inflammatory proteins, which in turn aggravate stress within cells, resulting in damage that could lead to various oral diseases,” explained Rahman, who last year published a study about the damaging effects of e-cigarette vapors and flavorings on lung cells and an earlier study on the pollution effects. “How much and how often someone is smoking e-cigarettes will determine the extent of damage to the gums and oral cavity.”

The study, which exposed 3-D human, non-smoker gum tissue to the vapors of e-cigarettes, also found that the flavoring chemicals play a role in damaging cells in the mouth.

“We learned that the flavorings-some more than others — made the damage to the cells even worse,” added Fawad Javed, a post-doctoral resident at Eastman Institute for Oral Health, part of the UR Medical Center, who contributed to the study. “It’s important to remember that e-cigarettes contain nicotine, which is known to contribute to gum disease.”

Most e-cigarettes contain a battery, a heating device, and a cartridge to hold liquid, which typically contains nicotine, flavorings, and other chemicals. The battery-powered device heats the liquid in the cartridge into an aerosol that the user inhales.

“More research, including long term and comparative studies, are needed to better understand the health effects of e-cigarettes,” added Rahman, who would like to see manufacturers disclose all the materials and chemicals used, so consumers can become more educated about potential dangers.



Source: Isaac K. Sundar, Fawad Javed, Georgios E. Romanos, Irfan Rahman. E-cigarettes and flavorings induce inflammatory and pro-senescence responses in oral epithelial cells and periodontal fibroblasts. Oncotarget, 2016; DOI: 10.18632/oncotarget.12857