Oral Cancer News

HPV ‘Herd Immunity’ Is on the Rise Among Adults

Source: www.webmd.com
Author: Dennis Thompson, HealthDay Reporter

The United States could be approaching a state of herd immunity against human papillomavirus (HPV), a virus linked to several cancers.

Oral HPV infections declined by 37% among unvaccinated 18- to 59-year-old men between 2009 and 2016, according to a Sept. 10 report in the Journal of the American Medical Association.

That included a decline in infections of HPV16, the strain found in more than 9 out of 10 cases of head and neck cancer related to the virus, said senior researcher Dr. Maura Gillison, a professor of medicine at MD Anderson Cancer Center in Houston.

Researchers say men are benefitting from increased HPV vaccination rates among American women, who receive the vaccine to prevent virus-caused cervical cancer.

“In contrast to cervical cancers, we have no means by which to screen for HPV-positive head and neck cancers,” Gillison said. “The vaccine is our best hope for prevention.”

HPV vaccination has been recommended for girls since 2006 and for boys since 2011. The virus has been linked to cancers of the cervix, penis, anus, mouth and throat.

Vaccination rates among boys and girls are steadily rising, according to the U.S. Centers for Disease Control and Prevention.

About half of teens were up to date on the HPV vaccine in 2017, and two-thirds of 13- to 17-year-olds had received the first dose to start the series. On average, the percentage of teens who started the HPV vaccine series rose by 5 percentage points each year between 2013 and 2017, the CDC says.

“At least 75% vaccine coverage of boys and girls would be necessary to eradicate HPV16, the HPV type that is most likely to lead to cancer development,” Gillison said.

But vaccination rates have lagged among males.

To see if males are receiving some protection from greater HVP vaccination among females, Gillison and her colleagues reviewed U.S. federal health survey data gathered between 2009 and 2016.

They found that by 2016, about 15% of women and 6% of men had received the vaccine.

Despite lower vaccination rates among males, oral HPV infections declined from 2.7% to 1.6% in men between 2009 and 2016.

Interestingly, prevention of oral HPV infections and the head and neck cancers they cause is not listed as a reason to get the vaccine, Gillison said. No clinical trials have been undertaken to show that the HPV vaccine could prevent such cancers.

The decrease in HPV infections among the unvaccinated men is consistent with a decline in genital HPV infections among unvaccinated women between 2004 and 2014, the researchers noted.

“This study demonstrates that even with suboptimal uptake of the HPV vaccine, important gains are being made in herd immunity against oral HPV types included in the vaccine,” said Dr. Amesh Adalja, a senior scholar at the Johns Hopkins Center for Health Security in Baltimore. He was not involved with the study.

“Oral HPV infection is a major factor in the development of head and neck cancer, and this vaccine has the potential to be game-changing as more individuals are vaccinated,” Adalja said.

HPV-positive head and neck cancers are the most rapidly rising cancers in the United States among men under age 60, Gillison said.

She called on doctors to use the data from this and other studies to promote HPV vaccination.

“I can guarantee that all of my patients diagnosed with HPV-positive head and neck cancer would exchange two or three shots for three months of toxic cancer therapy in a heartbeat,” she said.

“The HPV vaccine, together with the hepatitis B vaccine, are the two most important advances in the history of cancer prevention, period,” Gillison concluded.

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September, 2019|Oral Cancer News|

Say No to Glow: Reducing the Carcinogenic Effects of ALDH2 Deficiency

Source: blogs.plos.org
Author: Catherine Chang et al.

Turning red after consuming alcohol may seem like a mere social inconvenience. Yet, behind this red complexion lies a far more serious problem. ALDH2 deficiency, more commonly known as Alcohol Flushing Syndrome or Asian Glow, is a genetic condition that interferes with the metabolism of alcohol. As a result, people with ALDH2 deficiency have increased risks of developing esophageal and head and neck cancers . Globally, this deficiency affects 540 million people — 8% of the world population. In East Asia (which includes Japan, China, and Korea), this is a much bigger problem, where 36% of the population is affected [1]. In our home, Taiwan, approximately 47% of the population carries this genetic mutation — the highest percentage in the world [2]!

Normally, ethanol is first converted to acetaldehyde (a toxic intermediate) by the enzyme alcohol dehydrogenase (ADH). A second enzyme, aldehyde dehydrogenase 2 (ALDH2), then converts toxic acetaldehyde into acetate, a compound which can be safely metabolized in the body. For people who carry wild type ALDH2*1, acetaldehyde can be broken down quickly. People with ALDH2 deficiency, however, have a point mutation which leads to the less efficient mutant ALDH2*2 [3], [4]. Enzymatic activity in ALDH2-deficient individuals can be as low as 4% compared to wild type [4], [5], [6], [7]. As a result, acetaldehyde accumulates and induces an inflammatory response that causes the skin to flush after drinking alcohol [8]. Turning red is the most obvious result of ALDH2 deficiency, but symptoms also include headaches, dizziness, hypotension, and heart palpitations [5], [9].

Acetaldehyde accumulates in ALDH2-deficient individuals. Ethanol is first converted to a toxic intermediate, acetaldehyde, by ADH, then converted to acetate by wild type ALDH2*1. The mutant form, ALDH2*2, cannot fully convert acetaldehyde into acetate, and toxic acetaldehyde accumulates as a result.

For people who are ALDH2-deficient and drink, acetaldehyde can accumulate to toxic levels. The International Agency for Research on Cancer classifies acetaldehyde associated with alcohol consumption as a Group 1 carcinogen [10]. Acetaldehyde levels over 50 μM are considered toxic and cause mutations in DNA, and studies show that the strongest effects are seen in the mouth [11], [12]. After consuming roughly 2 to 3 servings of alcohol (0.5-0.6 g alcohol/kg body weight), salivary acetaldehyde levels in ALDH2-deficient individuals reached over 100 μM, compared to normal levels of <20 μM without drinking [13], [14], [15], [16]. Because of the increased salivary acetaldehyde, people with ALDH2 deficiency are 2 to 8 times more likely to develop head and neck cancers (including oral cancer, pharyngeal cancer, laryngeal cancer, etc.), and 2 to 12 times more likely to develop esophageal cancer compared to people with normal ALDH2*1 [17-25].

Our ALDH2*1 probiotic candy significantly reduces acetaldehyde levels in simulated oral conditions. (A) The conversion of acetaldehyde to acetate by ALDH2 uses NAD+ and produces NADH. (B) Experimental setup. The candies were dissolved, the probiotic (Nissle) was lysed to release ALDH2 enzymes, and the supernatant was placed into artificial saliva. NADH concentration was measured by taking absorbance readings at 340 nm. (C) Enzymatic activity of ALDH2*1 and ALDH2*2 from the probiotic candies. A negative control of candy without Nissle was also included (gray). Under these conditions, the ALDH2*1 candies metabolized significantly more acetaldehyde compared to both the ALDH2*2 candies and the negative control. Error bars represent standard error.

To directly address the increased esophageal and head and neck cancer risks, we developed a probiotic (E. coli Nissle 1917) candy carrying recombinant human ALDH2*1 to maintain normal acetaldehyde levels in the mouths of ALDH2-deficient individuals. We tested the candy’s ability to break down acetaldehyde by measuring NADH, a byproduct of acetaldehyde metabolism. In simulated oral conditions, we observed a significant decrease in acetaldehyde levels when we added the contents of our ALDH2*1 candy (compared to the mutant ALDH2*2 or control candy). Through mathematical modeling, we also determined the exact amount of recombinant ALDH2*1 needed in each piece of candy. Our modeling shows that if a consumer eats our candy while drinking, the released ALDH2*1 will be able to combat the high salivary acetaldehyde levels and match the normally low levels found in wild type individuals.

 

Our final product, an ALDH2*1 probiotic candy!

Nearly half of Taiwan’s population is ALDH2 deficient. To combat the increased cancer risks associated with this deficiency, we developed and tested a method to regulate acetaldehyde levels in ALDH2-deficient individuals.

The TAS_Taipei iGEM Team have produced a full research article detailing their project. You can access that article here.

Note:Please note that the team’s full research article has not been peer-reviewed.

Authors: Catherine Chang, Tim Ho, Iris Huang, Justin Wu

References:
1. Brooks PJ, Enoch MA, Goldman D, Li TK, Yokoyama A. (2009). The alcohol flushing response: an unrecognized risk factor for esophageal cancer from alcohol consumption. PLoS Med. 24;6(3):e50.

2. Chang JS, Hsiao JR, Chen CH. (2017). ALDH2 polymorphism and alcohol-related cancers in Asians: a public health perspective. J Biomed Sci. 24(1):19.

3. Larson HN, Weiner H, Hurley TD. (2005). Disruption of the Coenzyme Binding Site and Dimer Interface Revealed in the Crystal Structure of Mitochondrial Aldehyde Dehydrogenase “Asian” Variant. J Biol Chem. 280(34):30550-6.

4. Farrés J, Wang X, Takahashi K, Cunningham SJ, Wang TT, Weiner H. (1994). Effects of changing glutamate 487 to lysine in rat and human liver mitochondrial aldehyde dehydrogenase. A model to study human (Oriental type) class 2 aldehyde dehydrogenase. J Biol Chem. 13;269(19):13854-60.

5. Chen CH, Ferreira JCB, Gross ER, Mochly-Rosen D. (2014). Targeting Aldehyde Dehydrogenase 2: New Therapeutic Opportunities. Physiol Rev. 94(1):1-34.

6. Zhou J, Weiner H. (2000). Basis for half-of-the-site reactivity and the dominance of the K487 oriental subunit over the E487 subunit in heterotetrameric human liver mitochondrial aldehyde dehydrogenase. Biochemistry. 39(39):12019-24.

7. Gross ER, Zambelli VO, Small BA, Ferreira JCB, Chen CH, Mochly-Rosen D. (2015). A personalized medicine approach for Asian Americans with the aldehyde dehydrogenase 2*2 variant. Annu Rev Pharmacol Toxicol. 55:107-27.

8. Ijiri I. (1999). [Biological actions of acetaldehyde]. Nihon Hoigaku Zasshi. 53(3):285-95.

9. Lai CL, Yao CT, Chau GY, Yang LF, Kuo TY, Chiang CP, Yin SJ. (2014) Dominance of the inactive Asian variant over activity and protein contents of mitochondrial aldehyde dehydrogenase 2 in human liver. Alcohol Clin Exp Res. 2014 Jan;38(1):44-50.

10. International Agency for Research on Cancer. (n.d.). List of Classifications, Volumes 1-122. Retrieved from https://monographs.iarc.fr/list-of-classifications-volumes/ .

11. Yamaguchi H, Hosoya M, Shimoyama T, Takahashi S, Zhang JF, Tsutsumi E, Suzuki Y, Suwa Y, Nakayama T. (2012). Catalytic removal of acetaldehyde in saliva by a Gluconobacter strain. J Biosci Bioeng. 114(3):268-74.

12. Kocaelli H, Apaydin A, Aydil B, Ayhan M, Karadeniz A, Ozel S, Yilmaz E, Akgün B, Eren B. (2014) Evaluation of potential salivary acetaldehyde production from ethanol in oral cancer patients and healthy subjects. Hippokratia. 18(3): 269–274.

13. Homann N, Jousimies-Somer H, Jokelainen K, Heine R, Salaspuro M. (1997a). High acetaldehyde levels in saliva after ethanol consumption: methodological aspects and pathogenetic implications. Carcinogenesis. 18(9):1739-43.

14. Yokoyama A, Tsutsumi E, Imazeki H, Suwa Y, Nakamura C, Mizukami T, Yokoyama
(2008). Salivary acetaldehyde concentration according to alcoholic beverage consumed and aldehyde dehydrogenase-2 genotype. Alcohol Clin Exp Res. 32(9):1607-14.

15. Lachenmeier DW, Monakhova YB. (2011). Short-term salivary acetaldehyde increase due to direct exposure to alcoholic beverages as an additional cancer risk factor beyond ethanol metabolism. J Exp Clin Cancer Res. 30 (3).

16. Stornetta A, Guidolin V, Balbo S. (2018). Alcohol-Derived Acetaldehyde Exposure in the Oral Cavity. Cancers (Basel). 10(1). pii: E20.

17. Chao YC, Wang LS, Hsieh TY, Chu CW, Chang FY, Chu HC. (2000). Chinese Alcoholic Patients with Esophageal Cancer are Genetically Different from Alcoholics with Acute Pancreatitis and Liver Cirrhosis. Am J Gastroenterol. 95(10):2958-2964.

18. Yang SJ, Wang HY, Li XQ, Du HZ, Zheng CJ, Chen HG, Mu XY, Yang CX. (2007). Genetic Polymorphisms of ADH2 and ALDH2 Associated with Esophageal Cancer Risk in Southwest China. World J Gastroenterol. 13(43):5760-5764.

19. Yokoyama A, Muramatsu T, Omori T, Yokoyama T, Matsushita S, Higuchi S, Maruyama K, Ishii H. (2001). Alcohol and Aldehyde Dehydrogenase Gene Polymorphisms and Oropharyngolaryngeal, Esophageal and Stomach Cancers in Japanese Alcoholics. Carcinogenesis. 22(3): 433-439.

20. Matsuo K, Hamajima N, Shinoda M, Hatooka S, Inoue M, Takezaki T, Tajima K. (2001). Gene-Environment Interaction between an Aldehyde Dehydrogenase-2 (ALDH2) Polymorphism and Alcohol Consumption for the Risk of Esophageal cancer. Carcinogenesis. 22(6): 913-916.

21. Cui R, Kamatani Y, Takahashi A, Usami M, Hosono N, Kawaguchi T, Tsunoda T, Kamatani N, Kubo M, Nakamura Y, Matsuda K. (2009). Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk. Gastroenterology. 2009 Nov;137(5):1768-75.

22. Lee CH, Lee JM, Wu DC, Goan YG, Chou SH, Wu IC, Kao EL, Chan TF, Huang MC, Chen PS, Lee CY, Huang CT, Huang HL, Hu CY, Hung YH, Wu MT. (2007). Carcinogenetic impact of ADH1B and ALDH2 genes on squamous cell carcinoma risk of the esophagus with regard to the consumption of alcohol, tobacco and betel quid. Int J Cancer. 122(6):1347-56.

23. Wu M, Chang SC, Kampman E, Yang J, Wang XS, Gu XP, Han RQ, Liu AM, Wallar G, Zhou JY, Kok FJ, Zhao JK, Zhang ZF. (2013). Single nucleotide polymorphisms of ADH1B, ADH1C and ALDH2 genes and esophageal cancer: a population-based case-control study in China. Int J Cancer. 132(8):1868-77.

24. Huang CC, Hsiao JR, Lee WT, Lee YC, Ou CY, Chang CC, Lu YC, Huang JS, Wong TY, Chen KC, Tsai ST, Fang SY, Wu JL, Wu YH, Hsueh WT, Yen CJ, Wu SY, Chang JY, Lin CL, Wang YH, Weng YL, Yang HC, Chen YS, Chang JS. (2017). Investigating the Association between Alcohol and Risk of Head and Neck Cancer in Taiwan. Sci Rep. 7(1):9701.

25. Hiraki A, Matsuo K, Wakai K, Suzuki T, Hasegawa Y, Tajima K. (2007). Gene–gene and gene–environment interactions between alcohol drinking habit and polymorphisms in alcohol-metabolizing enzyme genes and the risk of head and neck cancer in Japan. Cancer Science. 98: 1087-1091.

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September, 2019|Oral Cancer News|

Light therapy could prevent cancer treatment-related oral mucositis

Source: www.healio.com
Author: Jennifer Southall

Light therapy appeared to be an effective intervention for the prevention of painful oral mucositis associated with cancer treatment, according to results of a systematic review and meta-analysis.

“Many patients [with cancer] can now benefit from this treatment,” Praveen R. Arany, DDS, PhD, assistant professor of oral biology and biomedical engineering at University at Buffalo School of Dental Medicine, said in a press release. “The staggering breadth of clinical application for photobiomodulation therapy, or light therapy, has been both a boon and a bane for the field. Several anecdotal clinical reports have been plagued with questionable rationales and inconsistent outcomes, often relegating this treatment to a pseudoscience.”

Arany and colleagues systematically reviewed published literature in an effort to update the evidence-based clinical practice guidelines on the use of photobiomodulation — including laser and other light therapies — for the prevention and treatment of oral mucositis among patients with cancer. Patients underwent treatment with hematopoietic stem cell transplantation, head and neck radiotherapy, or head and neck radiotherapy plus chemotherapy.

Study findings supported the use of photobiomodulation therapy for the prevention of oral mucositis among certain patients with cancer.

HemOnc Today spoke with Arany about the research and the clinical implications of the findings.

Question: What prompted this research?
Answer: The current forms of cancer treatment are all essential to reduce cancer burden. Unfortunately, complications from these treatments include oral mucositis pain. This not only has a significant impact on quality of life, but also often requires treatment with opioids. The pain and discomfort can be so severe it may even interrupt treatment, which can be lethal. There are no targeted treatments for this condition. We commonly use a mouthwash, which provides relief from symptoms. In contrast to this, there is increasing evidence for the use of light therapy based on precise biological mechanisms.

Q: Can you explain the rationale for this therapy?
A: This treatment has been shown to modulate various biological signaling pathways in cells that results in a positive response, such as alleviation of pain or inflammation. In addition, our lab uncovered a mechanism involving direct activation of a growth factor capable of stimulating wound healing and tissue regeneration. A combination of these responses is responsible for therapeutic benefit in oral mucositis pain.

Q: How did you conduct the study?
A: For the systematic review and meta-analysis, we looked at previously published human clinical studies that focused on how light therapy was used for the prevention of oral mucositis pain. We used the evidence from all studies to establish guidelines, re-analyzing data from each study to develop the final recommendations.

Q: What did you find?
A: There is significant evidence to use photobiomodulation therapy, or light therapy, for the prevention and treatment of oral mucositis pain when patients undergo radiation plus chemotherapy, as well as radiation alone and HSCT. In some instances, photobiomodulation therapy also was used as a preventive measure before and during cancer treatments to reduce the risk for oral mucositis pain.

Q: What will subsequent research entail?
A: The major finding was this treatment is effective. However, most of the studies that we reviewed were performed outside of the United States — including in Brazil, Europe and Asia. It is necessary to conduct studies in the U.S. in a more controlled manner with new devices available. This will be the primary focus of future human clinical research. Preliminary research studies have addressed potential effects of this treatment on tumors and the data are very promising, noting few — if any — deleterious side effects.

Q: Is there anything else that you would like to mention?
A: This is a noninvasive and nonpharmacological approach. This is especially important in the context of opioids in cancer care. Clearly, opioids are effective drugs that have an essential role in pain management. Unfortunately, they have a high threshold for abuse. The use of photobiomodulation therapy can reduce this incidence because patients will not be exposed to opioids. Besides mucositis, photobiomodulation therapy also has been noted to reduce hair loss, depression and fatigue — all key concerns for patients undergoing cancer treatment. Hopefully, we soon will see other published reports that will lead to improved cancer care using this simple but potent new technology. – by Jennifer Southall

Reference:
Zadik Y, et al. “Systematic review of photobiomodulation for the management of oral mucositis in cancer patients and clinical practice guidelines” Support Care Cancer. 2019;doi:10.1007/s00520-019-04890-2.

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September, 2019|Oral Cancer News|

Cases of Vaping-Related Lung Illness Surge, Health Officials Say

Source: New York Times
Date: 09/06/19
Author: Matt Ritchel & Denise Grady

Indiana announced a third death linked to the illness on Friday, and Minnesota a fourth. State and federal health officials are working urgently to understand the causes.

Medical experts and federal health officials on Friday warned the public about the dangers of vaping and discouraged using the devices as the number of people with a severe lung illness linked to vaping has more than doubled to 450 possible cases in 33 states. The number of deaths linked to vaping rose to four from two on Friday.

The Indiana Department of Health announced the third death, saying only that the victim was older than 18. Hours later, officials in Minnesota confirmed that a fourth person had died. The patient, who was 65, had a history of lung disease, but state officials said his acute lung injury was linked to “vaping illicit T.H.C. products.”

The Los Angeles County Department of Public Health was investigating a possible fifth death, saying on Friday afternoon that the fatality was “associated with the use of e-cigarettes, also known as vaping.”

“There is clearly an epidemic that begs for an urgent response,” Dr. David C. Christiani of the Harvard T.H. Chan School of Public Health wrote in an editorial published on Friday in The New England Journal of Medicine.

The editorial called on doctors to discourage their patients from using e-cigarettes and for a broader effort to increase public awareness about “the harmful effects of vaping.”

Officials from the Centers for Disease Control and Prevention echoed that call in a briefing.

“While this investigation is ongoing, people should consider not using e-cigarette products,” said Dr. Dana Meaney-Delman, who is leading the C.D.C.’s investigation into the illness.

C.D.C. officials said they believe that some “chemical” is involved as the cause but they have not identified a single responsible “device, product or substance,” Dr. Meaney-Delman said.

Dr. Christiani wrote in The New England Journal editorial that it was not yet clear which substances were causing the damage. E-cigarette fluids alone contain “at least six groups of potentially toxic compounds,” he wrote, but he noted that many of the patients had also vaped substances extracted from marijuana or hemp. The mixed-up stew of chemicals might even create new toxins, Dr. Christiani suggested. The journal also published a study of two clusters of 53 cases in Wisconsin and Illinois.

What looked like scattered cases earlier this summer has become a full-fledged and widespread public health scare, leaving otherwise healthy teenagers and young adults severely ill.

The first case of the mysterious lung illness, in Illinois, came in April, indicating that the syndrome emerged earlier than the mid-June date that federal officials have often cited as the time the afflictions began.

The patients studied in Illinois and Wisconsin were typically “healthy, young, with a median age of 19 years and a majority have been men,” said Dr. Jennifer Layden, chief medical officer and state epidemiologist for the Illinois Department of Public Health. A third were younger than 18.

The journal article about the Illinois and Wisconsin patients said that 98 percent were hospitalized, half required admission to the intensive care unit, and a third had so much trouble breathing that they needed to be placed on ventilators.

Eighty-four percent had vaped a product including T.H.C., the high-inducing chemical in marijuana. Dr. Layden said a majority had also used a “nicotine-based product,” noting that there were “a range of products and devices.”

The journal article about those cases mentions that the heating coils in vaping devices might release metal particles that could be inhaled.

“The focus of our investigation is narrowing but is still faced with complex questions,” said Ileana Arias, the C.D.C.’s acting deputy director for noninfectious diseases. She added, “We are working tirelessly and relentlessly.”

Mitch Zeller, the director of the Center for Tobacco Products at the Food and Drug Administration, said particular concern is developing around products that are jury-rigged by vaping retailers, or tampered with or mixed by consumers themselves. “Think twice,” he said, urging consumers to avoid vaping products purchased on the street or that they have made themselves.

Public health officials have underscored one fundamental point: that the surge in illnesses is a new phenomenon and not merely a recognition of a syndrome that may have been developing for years.

Indiana on Friday confirmed a third death from a severe lung illness linked to vaping shortly before officials in Minnesota confirmed a fourth. Two other people — one in Illinois, the other in Oregon, both of whom were adults — have died from what appears to be the same type of illness, health officials in those states have said.

Patients afflicted with the illness typically have showed up in emergency rooms with shortness of breath after several days of flulike symptoms, including high fever.

In an especially severe case in Utah, a 21-year-old man had such serious lung damage that even a ventilator could not provide enough breathing help. Doctors had to connect him to a machine that pumped oxygen directly into his bloodstream to keep him alive.

Fluid from his lungs contained white blood cells full of fat, not from the substances he had vaped, but more likely a sort of debris from the breakdown of his lung tissue.

“We were flying in the dark with this kid,” said Dr. Sean J. Callahan, a pulmonologist and critical care specialist at the University of Utah, and an author of a letter about six vaping patients in Utah that was published Friday in The New England Journal of Medicine.

“I thought he was going to die,” Dr. Callahan said. “I kept thinking, his parents were there, if this were me and my wife, how crushed we would be for something that is completely avoidable. I worry that these products are really geared toward young people and kids, and we need a call to ban these things. That’s my call to action as a father and a doctor.”

The patient survived, and went home after two weeks in the hospital.

It is too soon to tell whether people with vaping injuries will recover fully, or sustain lasting lung damage, Dr. Callahan said.

He added that doctors need to take better histories of young patients who come in with pneumonialike symptoms to try to find the real cause. Some patients and their families are forthcoming about vaping, but others are not. In one case, he said, medical residents were puzzled by what could have caused the illness. He asked the patient’s mother to leave the room and then, instead of asking if the patient vaped, he simply asked, “What do you vape?” The answer was T.H.C.

The state of New York, where 34 people have become ill, said on Thursday that vaping samples from eight of its cases showed high levels of a compound called vitamin E acetate. Investigators there are focusing on the possibility that the oily substance might be playing a key role in the illness.

However, some of the more than 100 vaping samples being examined by the federal government did not test positive for vitamin E acetate, so that compound remains only one of many possible causes of the heavy lung inflammation.

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September, 2019|Oral Cancer News|

Minority, low-income individuals less likely to receive oral cancer screening

Source: medicalxpress.com
Author: staff

Despite a recent dental visit, more individuals of a minority race/ethnicity and low socioeconomic status report not receiving an oral cancer screening exam, according to a study published online Aug. 20 in the American Journal of Preventive Medicine.

Avni Gupta, B.D.S., M.P.H., from Brigham and Women’s Hospital in Boston, and colleagues analyzed data from individuals aged 30 years or older who received a dental visit in the previous two years. The likelihood of intraoral and extraoral cancer screening exams was assessed, while adjusting for age, sex, race/ethnicity, education, marital status, poverty income ratio, health insurance, tobacco smoking, and alcohol consumption.

Overall, 37.6 and 31.3 percent of individuals reported receiving an intraoral and extraoral cancer screening exam, respectively. The researchers found that the likelihood of having received intraoral or extraoral cancer screening exams was lower for minority racial/ethnic groups versus white, non-Hispanics; those with less education versus more education; those who were uninsured and Medicaid-insured versus privately insured; and low-income versus high-income participants. The likelihood of being screened did not differ based on smoking status, while the likelihood was increased for alcohol consumers. Less-educated and low-income subgroups were less likely to be screened.

“Efforts to both educate patients about requesting oral cancer screening in dental offices and adequately train dental professionals on culturally sensitive communications might be an effective means to increase oral cancer screening exams among minority high-risk populations,” the authors write

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August, 2019|Oral Cancer News|

Palbociclib plus cetuximab shows antitumor activity among head and neck cancer subset

Source: www.healio.com
Author: Adkins D, et al.

A combination of palbociclib and cetuximab demonstrated substantial antitumor activity among patients with platinum- or cetuximab-resistant HPV-unrelated head and neck squamous cell carcinoma, according to results of a multigroup phase 2 trial published in The Lancet Oncology.

“Currently, effective therapeutic options for patients with cetuximab-resistant HNSCC are few. Traditional chemotherapy has marginal activity, with 6% of patients or fewer achieving a tumor response,” Douglas R. Adkins, MD, professor in the oncology division of the department of medicine at Washington University School of Medicine in St. Louis, and colleagues wrote. “The most effective therapy for these patients might be pembrolizumab [Keytruda, Merck] or nivolumab [Opdivo, Bristol-Myers Squibb], which have resulted in responses in 11% to 16% of patients and median OS of 6.9 months to 8 months. Novel treatment strategies are needed for patients with recurrent or metastatic HNSCC.”

The combination of the cyclin-dependent kinase (CDK) 4/6 inhibitor palbociclib (Ibrance, Pfizer) and epidermal growth factor receptor inhibitor cetuximab (Erbitux, Eli Lilly) appeared safe and tolerable in the phase 1 portion of the multicenter trial, conducted across eight U.S. university sites.

For phase 2, Adkins and colleagues divided 62 patients with HPV-unrelated HNSCC (median age, 66 years; interquartile range [IQR], 58-70; 71% men) into two groups: those who were platinum-resistant (group 1; n = 30) and those who were resistant to cetuximab (group 2; n = 32). Primary tumor sites included the oral cavity (42%) and larynx (29%), and 81% of patients had received one or two prior lines of treatment for metastatic or recurrent disease.

All participants received oral palbociclib (125 mg daily on days 1-21) and IV cetuximab (400 mg/m2 on day 1 of cycle one, followed by 250 mg/m2 once weekly) in 28-day cycles. Objective response, defined as complete and partial responses per RECIST 1.1 criteria, served as the primary endpoint.

Researchers followed patients in group 1 for a median 5.4 months (IQR, 4.4-12.1) and those in group 2 for a median 5.5 months (IQR, 4.3-8.3).

Among 28 evaluable group 1 patients, 11 (39%; 95% CI, 22-59) attained an objective response, including three complete responses. Repeat scans confirmed all but one of the responses. Half of the group 1 patients (n = 14) had stable disease and three (11%) demonstrated progressive disease. Median duration of response was 4 months (IQR, 1.8-5.6), median PFS was 5.4 months (95% CI, 3.4-7) and median OS was 9.5 months (95% CI, 5.3-16.5).

Palbociclib plus cetuximab shows antitumor activity among head and neck cancer subsetAmong 27 evaluable group 2 patients, five (19%; 95% CI, 6-38) achieved an objective response, including one complete response. Four of the responses were later confirmed. Thirteen of the group 2 patients (48%) had stable disease and nine (33%) demonstrated progressive disease. Median duration of response was 6 months (IQR, 2-15.5), median PFS was 3.7 months (95% CI, 2.9-4.3) and median OS was 6.3 months (95% CI, 4.9-10).

In each group, only one patient with a tumor response previously had received immunotherapy.

The most prevalent grade 3 to grade 4 adverse event associated with palbociclib was neutropenia, which occurred in 34% (n = 21) of all patients. The researchers did not document any treatment-related deaths.

The researchers cited various limitations to their study, including its single-group design, and noted that the results will need to be confirmed in a controlled trial with a larger sample size. They acknowledged that immunotherapy might have affected OS outcomes, and that the study design did not permit the evaluation of whether palbocilib’s antitumor activity occurred directly or by reversal of primary cetuximab resistance.

These data suggest a need for further study of palbociclib in patients with recurring or metastatic HNSCC, according to a related editorial by Garth W. Strohbehn, MD, hematology/oncology fellow at University of Chicago, and Everett E. Vokes, MD, professor of medicine and radiation oncology physician-in-chief at University of Chicago Medicine.

“However, we should be circumspect about the prospect of CDK 4/6 inhibitors as standardized, cost-effective therapies in recurrent and metastatic HNSCC,” the authors wrote. “Bringing this class of drugs to head and neck oncology clinics, as either monotherapies or immunotherapy partners, will require appropriately controlled studies linked to biomarker evaluation with both survival and cost-effectiveness endpoints.” – by Jennifer Byrne

Source:
Adkins D, et al. Lancet Oncol. 2019;doi:10.1016/S1470-2045(19)30405-X.
Strohbehn GW and Vokes EE. Lancet Oncol. 2019;doi:10.1016/S1470-2045(19)30484-X.

Disclosures: Adkins reports research funding from Pfizer as part of the work presented in the study; personal fees for advisory/consultant roles from Celgene, Cue Biopharma, Eli Lilly, Loxo Oncology, Merck and Pfizer; and research funding from AstraZeneca, Atara, Blueprint Medicine, Bristol-Myers Squibb, Celgene, CellCeutix, Celldex, Eli Lilly, Enzychem, Exelixis, Gliknik, Kura, Matrix Biomed, Medimmune Innate, Novartis, Pfizer and Polaris outside the submitted work. Please see the study for all other authors’ relevant financial disclosures. Vokes reports consultant/advisory roles with AbbVie, Amgen, AstraZeneca, Bristol-Myers, Celgene, EMD Serono, Genentech, Merck, Novartis and Regeneron. Strohbehn reports no relevant financial disclosures.

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August, 2019|Oral Cancer News|

Israeli researchers find new way to eliminate drug-resistant cancerous tumors

Source: www.xinhuanet.com
Author: Wu Qin

Israeli researchers have found a way to deal with cancerous tumors that have developed drug resistance, Israel’s Ben-Gurion University (BGU) reported on Tuesday. The study was conducted by researchers from BGU and the Soroka Medical Center – both located in the southern city of Beer Sheva – and published in the journal JCI Insight.

The researchers were able to suppress a drug-resistant protein found on the wall of head and neck cancer cells, resulting in shrinkage and even disappearance of the tumors.

Head and neck cancer is considered deadly, with low survival rates, while the efficacy of existing treatments is inadequate.

One of the new treatments currently being given to patients is a drug called BYL719, which inhibits a signal transmission pathway in the cells. This pathway, called phosphoinositide 3-kinases (PI3K), is increased in head and neck cancer patients and leads to the rapid progression of the disease.

The first clinical study using the drug indicated an improvement in patients’ condition; however, many of the cancer cells developed drug resistance.

Previous research has shown that resistance to the treatment is caused by the rise of the AXL protein, which is located on the cancer cell’s wall and causes the growth and survival of the cancer cells.

The new study found that suppressing AXL expression through genetic engineering or drug inhibition restored the cancer cells’ susceptibility to the drug and significantly stopped the disease, to the extent of tumor shrinkage and disappearance.

This suppression was also effective in mice with tumors taken from head and neck patients who underwent surgeries at Soroka Medical Center.

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August, 2019|Oral Cancer News|

cole Gibbs on the dental visit that led to a cancer diagnosis and how it reaffirmed her love for tennis

Source: ESPN
Date: August 1st, 2019
Author: Nicole Gibbs, as told to D’Arcy Maine

 

Nicole Gibbs is a 26-year-old professional tennis player, currently ranked No. 137 in the world and playing for the Orange County Breakers of World TeamTennis. The former NCAA singles and doubles champion was diagnosed with cancer in the spring after a routine dentist appointment. She shared her story with us amid her comeback to the court.

Shortly before Caroline Wozniacki’s bachelorette party festivities in April, I received a promotional email for a free teeth-whitening from my new dentist. “Oh, sweet!” I remember thinking. Naturally, I wanted to look good for the weekend (knowing how much of it was going to end up on Instagram and all), and for at least two years I was slacking on getting a regular cleaning.

So I went. And it changed everything.

It was my first time seeing this dentist, and he instantly noticed a small growth on the roof of my mouth. I mentioned this to my primary doctor at least five years ago; she told me it was nothing to worry about, a common bone growth that didn’t seem to be growing rapidly or doing anything of concern. My dentist at the time felt the same. It was about a centimeter in diameter and not causing me any pain or discomfort. However, my new dentist felt differently — the growth set off major alarm bells for him, and he encouraged me to get it biopsied. He felt certain it was not a bone growth.

I went to an oral surgeon the very next day. He thought it would be benign, based on its history, how long it had been in my mouth and how slowly it was growing. But the biopsied sample was sent to a pathology lab for an official diagnosis. I then, happy to at least not have that hanging over my head, went to the Bahamas to celebrate Wozniacki.

Shortly after getting back home, about a week after the initial dentist appointment, I got the call with the results.

It was cancer.

As soon as the doctor said the word, I glazed over. I didn’t hear much else, but I am pretty sure I cracked an awkward joke. It wasn’t until I called my fiancé, Jack Brody, that it really hit me. I started to fall apart and panic. It felt like my biggest fear come true. Since a very young age, I had been terrified about getting cancer. I almost started to question myself, like, had I manifested this with my anxiety about it? Did I bring this upon myself somehow by being so concerned about it?

Then my thoughts went to the tennis court. Would I ever be able to play again?

I made the mistake of going to WebMD and doing a Google search for oral cancer because I didn’t have any more specifics at that point, and the first thing that popped up was “17 percent five-year survival rate.” I thought, “Oh cool, I’m going to die.” It was terrifying, but I thankfully discovered soon after I had mucoepidermoid carcinoma, which is more of a subset and much less scary. I didn’t let myself play internet doctor after that and told Jack he was the only one allowed to Google anything from that point forward.

Everyone was hopeful we could treat the cancer with surgery alone, but radiation was also a possibility if the surgeons weren’t able to remove it all. While that is worrisome enough on its own, someone mentioned to me I could potentially lose all my teeth as a consequence of radiation. Leading up to the procedure, I kept thinking, “Please just be a surgery, please just be a surgery.” I didn’t want my teeth to fall out.

I had the surgery on May 17. The typical recovery period is four to six weeks, but my surgeon believed that, as a professional athlete, I could be on the low end of the timetable. My goal was to be back in time for Wimbledon qualifying, which started on June 24, and that felt possible.

However, there were a number of complications that made us throw that dream right out of the window, starting with the procedure being significantly more invasive than they initially planned. Too much of the tumor was taken out during the biopsy, and as a result, they didn’t have a clear idea of where it was. They needed to cut in further and wider to ensure they got it all out.

Not only that, but the prosthetic — really just a glorified retainer — I needed to wear on the roof of my mouth to protect it after the surgery didn’t fit properly. So they had to screw it in. Do you know what happens when you have a screwed-in retainer that doesn’t get to be taken out and cleaned? It causes an infection. So instead of the two days I had expected to stay in the hospital, I was there for seven long, agonizing days.

During my extended stay, I also got some unexpected news: Turns out I didn’t have mucoepidermoid carcinoma, but instead microcystic adnexal carcinoma. Don’t worry if you’ve never heard of it. My doctors told me they had only ever seen 12 recorded cases of it.

That’s right — 12. I was lucky No. 13.

While that didn’t change the treatment much, it did mean the cancer had a greater risk of being elsewhere in the body. It has the potential to travel aggressively along nerve pathways. When I asked what exactly that meant, my doctor said, “In layman’s terms, that means it can jump tissue.” How frightening is that? Thankfully, I already had a full-body PET (positron emission tomography) scan, and there were no signs of cancer anywhere else. But still, it was alarming. (I still haven’t quite determined if the rarity and odds of this type of cancer mean I should now engage in every risk-taking activity or become a bubble kid and never go outside, but I’ll let you know when I figure that out.)

We thought I would be on a feeding tube for two days, as I couldn’t ingest food orally, and then I would graduate to soft foods once I got home. However, one of the stitches in my mouth blew open (another fun setback!), and every time I would try to eat or drink, it would come out of my nose. Sure, it’s sort of a great party trick, but not really what I was going for. In the end, I had to go home with the feeding tube — and use it for 3½ weeks in total.

It was tough. I definitely gained a new appreciation for how brutal medical trauma can be. I found it really dehumanizing. It’s so challenging to have a tube hanging out of you and looking visibly ill. You can’t hide from it. And then losing the ability to socialize around food, which is so much of our lives. I didn’t want to go out to dinner while I had a feeding tube and couldn’t eat anything.

I made sure to get out of the house, just to get some sunshine, at least once a day. I took long walks and tried to find small things to do, to give me a little purpose. But it brought me to my breaking point on several occasions. I remember looking at Jack and saying, “I really can’t do this anymore.” But I quickly realized that I didn’t have a choice. I knew I just had to tough it out.

The worst moments were when I was getting off the pain medication after 2½ weeks of strong dosages. I don’t know the mechanics of it, but I ended up feeling very depressed once I stopped taking it for about 48 hours. It was right around the time I started to go back to the gym to slowly train. On the first morning off the medication, I said to my trainer, Daniel Ciccolini, “I just can’t do this today.” I don’t think I had said a word other than that or smiled at all, and I was just in the worst mood. I was incapable physically of much of anything, but he was so patient. He took me through all of these easy core and mobility exercises. Whatever we could accomplish that day, we did, even though it was such a brutal day.

Because I was able to accomplish something that day, anything really, it gave me hope. If I hadn’t had that, it would have been devastating.

And every day after that, I felt a little bit better and made a little bit more progress. I did more with my trainer and my incredible support system. I could feel myself gaining in physical strength, and I was like, “OK, I’m getting somewhere!”

I returned to competitive tennis in early July at a tournament in Hawaii. I went in with no expectations whatsoever. I still can’t even drink too much water during changeovers without it going out my nose. (The doctors are hoping the hole in my mouth will fully close up on its own in the next few months, but otherwise, I will need another surgery.) I surfed every day in Hawaii and even had a glass of wine with dinner some nights — things I would have never done while competing. I shocked even myself and ended up making it to the final.

I ended up losing in the championship match to Usue Maitane Arconada, but when I thought about where I had been less than two months before, I certainly felt like a winner.

Before this experience, I was constantly wondering, “Is tennis something that I really love? Would I miss it in my life if it was gone?” And I’m blessed in so many ways to have been forced into that answer. I wasn’t ready for tennis to be taken away from me.

It may sound weird, but I’m thankful that this happened for a number of reasons, one of which is because it reconfirmed my love of sports and tennis. It reminded me that I’m not done. It’s given me such a fresh perspective, and I’m grateful for that.

I’ve been playing for the Orange County Breakers for the World TeamTennis season. It’s been a little bit of a whirlwind — I went from playing in the final in Honolulu on Sunday to playing in our opener the very next day in Orlando — but it’s been great, and I’m making up for lost time in terms of getting match experience this summer. My teammates have been so sweet. Every time I say, “Guys, I’m so sorry, I’ve been playing terribly,” they’re like, “Remember where you were five weeks ago?” The support has been so incredible.

I’m still finalizing my upcoming schedule, but I’ll be playing in several tournaments over the next few weeks before going to New York for US Open qualifying in the middle of August. My newfound semi-relaxed attitude worked in Hawaii, so I’m going to try and maintain that going forward. I was so disciplined before. I would never have surfed during a tournament; I would have been concerned about getting hurt or being too tired. But ultimately, that’s just no way to live. And I would never tell my best friend to live their life that way, in fear of bad things happening or being so worried about results. Ironically, I think it’s going to free me up to play much better tennis. And if it does, it does. If it doesn’t, then I’m at least having fun and enjoying my life.

At the end of the day, I feel so lucky. Yes, I’m lucky because the cancer could have been so much worse, but really, I’m lucky because I think I needed this experience in my life. I am genuinely thankful that it happened.

I know that sounds nuts, but early on when we were getting the diagnosis, Jack said, “I think if this isn’t the worst thing that ever happens to us, it’ll be the best thing that ever happens to us.” And so far, that’s been really, really true.

I want to hold on to all of these lessons and remember that tennis is not everything. It’s a lot of fun, and it should be. But it’s put my life into a new sense of balance I didn’t have, and I think I’m going to be a much happier person for the rest of my life as a result if I can keep this perspective. You have to enjoy the time you have because you’re not guaranteed to always be here. I knew that in theory, but to actually feel like my life might be taken away, it was such a powerful reminder to enjoy every day and every moment.

Cancer was initially my nightmare, but it weirdly turned into a dream-come-true diagnosis because it made me confront so many things in my life. It was debilitating and scary at times, but look at me — I’m back up on my feet so soon after and appreciating every second. It’s a win in my book.

 

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August, 2019|Oral Cancer News|

Which HPV vaccination schedule is best: 1, 2 or 3 doses?

Source: www.precisionvaccinations.com
Author: Don Ward Hackett

A new cervical cancer prevention study of women first offered Human Papillomavirus (HPV) vaccine found that 1-dose of quadrivalent HPV vaccine was as effective as 3-doses at preventing histologically confirmed, high–grade cervical lesions.

This Australian study’s finding published online on July 15, 2019, supports the hypothesis that the 1-dose HPV vaccination schedule may be a viable strategy when working towards the global elimination of cervical cancer.

These researchers said ‘If one dose could prevent precancerous cervical lesions, then global cervical cancer prevention would be greatly facilitated.’

This is an important goal since about 90 percent of cervical cancer cases are caused by HPV. This study included 250,648 women in Australia with 19.5 percent unvaccinated, 69.8 percent had received 3-doses, 7.3 percent 2-doses, and 3.4 percent just 1-dose of the HPV vaccine.

This study’s limitations include some degree of under–linkage and inaccurate data linkage because Australia does not have a unique national identifier, which impacts the classifications of vaccinated women as unvaccinated.

Additionally, these researchers said ‘we believe that these data support decision-makers to consider how a 1-dose HPV vaccination schedule, or a planned schedule with a 3–5 year interval between doses, could reduce vaccine demand globally, which currently exceeds vaccine supply.’

But the Gardasil 9 vaccine manufacturer appears to be resolving this supply/demand imbalance. During July 2019, Merck said it is spending $1.68 billion, opening 2 new Gardasil production plants, and adding 525 related jobs.

To clarify the Gardasil 9 vaccine dosing schedule, the Centers for Disease Control and Prevention (CDC) publish the following information:

Who should still receive a 3-dose schedule?
The CDC continues to recommend a 3-dose schedule for persons starting the HPV vaccination series on or after the 15th birthday, and for persons with certain immunocompromising conditions. The 2nd vaccine dose should be given 1–2 months after the 1st dose, and the 3rd dose, should be given 6 months after the first dose.

Who should receive just 2-doses?
Two doses of the HPV vaccine are recommended for all boys and girls at ages 11-12; the vaccine can be given as early as age 9. If you wait until they’re older, they may need three doses instead of two.

In the USA, HPV vaccines have been licensed for use among women since 2006 and among men since 2010.

HPV infections are so common that nearly all men and women will get at least one type of HPV at some point in their lives. Nearly 80 million Americans are currently infected with some type of HPV, says the CDC. About 14 million Americans, including teens, become infected each year. HPV is spread through intimate skin-to-skin contact. You can get HPV by having vaginal, anal, or oral sex with someone who has the virus.

Cervical cancer is the only type of HPV cancer with a recommended screening test. The other types of HPV cancer may not be detected until they cause health problems. HPV vaccination helps prevent these cancers by preventing infections that cause these cancers, says the CDC. HPV vaccines, like any medicine, can cause side effects, which you are encouraged to report to the CDC or a healthcare provider.

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August, 2019|Oral Cancer News|

How clean is your toothbrush?

Source: versionweekly.com
Author: rajathe

Dental care has become increasingly difficult in this fast-paced era and due to the scarcity of time. Therefore, following minute steps or procedures could be highly effective to evade colossal dental problems and save time in the long run. And an effective measure towards this, is to sanitize your toothbrush. The mouth contains bacteria and so does the bathroom. So, it is impossible for the toothbrush to stay sanitized with just a water wash after cleansing the teeth.

Toothbrush sanitizing ¡s not synonymous to sterilizing. Sanitation helps in getting rid of almost 99.9 percent of bacteria whereas sterilization kills living organisms. Brushing our teeth is quite vital ¡n our day-to-day life in order to keep and maintain personal oral hygiene and for the removal of plaque. And for this, certain appropriate measures need to be taken.

As a result of a recent research, scientists have found that toothbrushes engulf microorganisms that can result in an oral, dental or infection of some kind. We are acquainted with the fact that an oral cavity is an umbrella to hundreds of different types of microorganisms, which in a way gets transferred to the toothbrush. There is also a probability that the microorganisms in the environment make room for itself on the toothbrush on its own. Also, toothbrushes may even have bacteria on them right out of the box since they are not required to be sold in a sterile package.

Toothbrush Hygiene
Our schedules are so busy that we have time for nothing and that leads to the negligence of petty issues like washing toothbrush properly, which in turn contributes to dental problems. The majority of us simply clean or scrub the head of the toothbrush only once after we complete the brushing process. It would be more hygienic if the toothbrush could be rinsed in lukewarm water to get rid of food debris and leftover toothpaste in the bristles.

Clinically there is no evidence that if a toothbrush is soaked in antibacterial mouthwash ¡t would deliver positive results but it won’t disrupt the toothbrush in any way either.

The proper procedures for sanitizing the toothbrush is as follows:

  • Keep the toothbrush immersed in the mouthwash and warm water mix
  • Take the brush out of the solution after 15 minutes
  • Don’t keep it immersed for too long, or it will destroy the bristles
  • Don’t reuse the mixed solution as it defeats the cleansing or sanitizing process

Gum disease (periodontal) and health complications share a strong alliance and result in hazardous diseases such as stroke, heart disease, etc. It also affects pregnant women in terms of low birth weight and pre-term babies. Research shows that 90 per cent of diseases and health hazards are likely to have oral manifestations like swollen mouth ulcers, gums, excessive gum problems, and dry mouth. Other diseases include diabetes, leukaemia, pancreatic cancer, oral cancer, kidney disease and heart disease.

A dentist may be a saviour if a proper diagnosis can be conducted from the roots in its infant stages. Routine visits to a dentist can also help in keeping one’s smile attractive. This would also enable dentists to foretell a lot more about one’s health which includes whether or not one may develop a disease like diabetes in the near future.

Research has proven that our mouth acts like a mirror that reflects the condition of the body. On the contrary, poor oral health, heralds a plethora of health problems. And, good oral health keeps diseases from occurring.

Recommendations
According to dentists, the growth and abundance of bacteria on toothbrushes requires dark, warm and humid conditions. Veiling a toothbrush in a dosed area can invite problems. One should always keep the toothbrush dry, airy and in a holder that does not come in contact with the bristles or other toothbrushes. The toothbrush should be replaced every three to four months. Also, keep in mind that the sharing of toothbrushes contribute to the problem on a massive scale.

Precautions
If anyone in the family gets infected because of a contagious agent, following some preventive measures can help. Replacing toothbrushes every three to four months, purchasing expendable toothbrushes and using an antibacterial mouthwash for rinsing and soaking is beneficial. Also, you need to know that a UV sanitizer will not result in a maximum removal of germs. Another flaw in the usage of UV sanitizer is that the ultraviolet light may destroy the bristles.

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August, 2019|Oral Cancer News|