Another vaping hazard: less-healthy mouths

Author: Serena Gordon, HealthDay Reporter

Your lungs might not be your only concern if you’re trying electronic cigarettes — your mouth may pay the price, too. Vaping alters the natural bacteria found in the mouth, leaving you more vulnerable to oral infections and inflammation, a new study reports.

The researchers said this study is the first to show that vaping can alter the natural balance of beneficial bacteria (microbiome) in the mouth, adding to the list of potential health effects associated with e-cigarette use.

“Cells that are exposed to e-cigarettes are more susceptible to infections,” said the study’s senior author, Deepak Saxena. He’s a professor of basic science and craniofacial biology at NYU College of Dentistry in New York City.

Saxena said that e-cigarettes also lead to increased inflammation, which harms oral health. And once someone develops inflammation, it’s possible to develop white patches in the mouth called leukoplakia that sometimes develop into cancer. However, this study doesn’t have enough long-term evidence to show whether or not these changes could lead to oral cancers in the future, Saxena said.

“Our study is just one piece of this big puzzle on e-cigarettes, and I would advise people to not use them. If you have not started, don’t start. Nicotine is highly addictive,” he said.

A U.S. Centers for Disease Control and Prevention report from November suggested that as many as one out of every five U.S. high school students had vaped in the last month. That’s especially concerning since more than 2,500 Americans have been hospitalized with lung injuries traced back to e-cigarette use. An additive sometimes used when people vape is suspected as a trigger for these injuries. Fifty-four people have died as a result.

People who smoke traditional tobacco cigarettes are known to have a higher risk of gum disease and oral infections. Tobacco causes changes in the mouth’s usual environment that dampen the immune system response and let bad bacteria flourish, the researchers explained.

E-cigarettes have been considered less harmful, but there hasn’t been a lot of research, particularly long-term studies on the new devices.

For the new study, the research team recruited 119 participants, including roughly equal numbers of people who didn’t smoke or vape, people who smoked tobacco cigarettes, and those who had only used e-cigarettes. The researchers performed oral exams and collected saliva samples to test for the bacteria living in the participants’ mouths.

Almost three-quarters of tobacco smokers showed signs of gum disease or infection. Forty-three percent of e-cigarettes users also showed signs of these problems. Only 28% of the nonsmokers had signs of gum disease or infection.

When they tested for bacteria, the researchers found different types of predominant bacteria in the three groups.

“We found there is a shift in the microbiome of e-cigarette users, making it much closer to that of regular cigarette smokers,” Saxena said.

Co-author Xin Li, an associate professor at NYU College of Dentistry, noted that the researchers can’t say if e-cigarettes are more dangerous for oral health than traditional tobacco cigarettes.

“We saw a similar trend to inflammation and periodontitis (a serious gum infection), but I don’t think we can draw any conclusions about whether e-cigarettes are more harmful,” she said.

If you vape and have concerns about these potential changes, Saxena suggested taking greater care with your oral health and perhaps seeing your dentist more frequently. Li said maybe probiotics can help restore the microbiome in the mouth. But both noted these steps haven’t been studied yet.

Li said if you are using e-cigarettes to help with quitting traditional tobacco cigarettes, try to use e-cigarettes for the shortest time you can. Plan on how you’ll cut back. Don’t plan to use e-cigarettes indefinitely, she advised.

Ronald Burakoff is chairman of dental medicine at Long Island Jewish Medical Center and North Shore University Hospital in New York. He said the study’s findings make sense.

“This article describes in detail some of the adverse outcomes associated with [e-cigarette] usage. Firstly, it increases the amount of bacteria in the mouth; secondly, it promotes inflammation of the gums,” Burakoff said. He added that these changes could lead to an increased risk of infection.

Note: The study was published online Feb. 26 in iScience.

2020-02-27T09:26:31-07:00February, 2020|Oral Cancer News|

Management strategies for oral potentially malignant disorders

Author: Joel M. Laudenbach, DMD

Oral potentially malignant disorders (OPMDs) include oral leukoplakia (OL), oral erythroplakia, oral submucous fibrosis, oral lichen planus, proliferative verrucous leukoplakia, and actinic keratosis. Once an OPMD has been clinically diagnosed, execution of management strategy is critical. When formulating the strategy, healthcare providers should consider histopathology, lesion characteristics (ie, surface texture, unifocal, multifocal), lesion location in the mouth (ie, tongue, floor of mouth), patient risk factor assessment, and a detailed medical/cancer history.

In this newly published article, Nadeau and Kerr[1] detail various parameters surrounding evaluation and management of OPMDs. The authors make it clear that OPMDs are challenging, each with their own nuances regarding risk for malignant transformation. For example, when OL is unifocal, nonhomogeneous, nodular, or verrucous, there is a much higher chance of the OL becoming dysplastic (12.63-fold) or demonstrating a focus of carcinoma (8.9-fold) when compared with homogeneous types of OLs.[1]

Provider knowledge of these variables is critical when counseling patients about their diagnosis and management options and when selecting interventions along with follow-up care. Although progression to malignancy is difficult to predict with OPMDs, clinicians can account for multiple risk factors such as smoking/alcohol status, high-risk location in the oral cavity, and size of lesion (>200 mm2) to help formulate a tailored management plan for each patient. Consultation with an oral pathologist to discuss the histologic appearance in the context of specific patient history and lesion characteristics can provide additional perspective and/or recommendations.

Modifiable oral cavity cancer risks related to tobacco and heavy alcohol use should be communicated to patients with OPMDs so that they are able to make changes that may lead to regression/disappearance of certain lesions such as OL. Providers confronted with patients who use tobacco and/or heavy alcohol can integrate recommendations for cessation of tobacco[2] and alcohol[3] because they are both established, independent, causative agents for oral cavity cancer and OPMDs.

Available treatment strategies for OPMDs include surgical removal/ablation, photodynamic therapy, and surveillance. The authors make a clear point with supportive studies that traditional surgical excision of dysplastic OPMDs may decrease malignant transformation (MT) risk, yet it does not fully eliminate that risk and, in some instances, has not changed the MT risk when compared with surveillance alone. Appropriate surgical margin identification for OPMDs is clinically challenging. The authors note that smaller excisional margin sizes (1-2 mm) without marginal histologic assessment are common surgical management goals for OPMDs.[1]

Nadeau and Kerr carefully outline updated considerations for all OPMDs. Healthcare providers involved in screening, diagnosing, referring, and/or managing patients with OPMDs should be well versed in standards of care, including baseline biopsy goals, tobacco/alcohol cessation, currently available interventions, and surveillance care.

Clinicians should also develop a local team of practitioners who are experts in diagnosis and management of OPMDs to help patients obtain the best opportunity for positive outcomes. I encourage readers with interest to retrieve and review the full article by Nadeau and Kerr as a strategy to update your knowledge base and to continue to improve overall morbidity, mortality, and survival rates related to OPMDs.

1. Nadeau C, Kerr AR. Evaluation and management of oral potentially malignant disorders. Dent Clin North Am. 2018;62:1-27.

2. US Preventive Services Task Force. Final recommendation statement. Tobacco smoking cessation in adults, including pregnant women: behavioral and pharmacotherapy interventions. September 2015. Accessed March 1, 2018.

3. US Preventive Services Task Force. Final recommendation statement. Alcohol misuse: screening and behavioral counseling interventions in primary care. May 2013.
/RecommendationStatementFinal/alcohol-misuse-screening-and-behavioral-counseling-interventions-in-primary-care Accessed March 1, 2018.

Smokeless tobacco, snuff, chew not safe substitutes for cigarettes

Author: staff

As many people are aware, the use of any type of tobacco can lead to major health risks. Many individuals think using smokeless tobacco or chew can be a safe substitute for cigarettes.

A mock model of how dangerous and destructive tobacco products, specifically smokeless tobacco, can be to someone’s health and well-being. Navy photo by Douglas H. Stutz, Naval Hospital Bremerton Public Affairs

Tobacco companies often lead people to believe this; however, this is not true. There is no proof that any smokeless tobacco products help smokers quit smoking.

Smokeless tobacco has four times the amount of nicotine than a cigarette and also contains 30 chemicals known to cause cancers.

A few of these cancers include mouth, tongue, cheek, and gum cancer. Additionally, cancer can be found in the esophagus and pancreas. Along with these health risks there are other problems, including mouth and teeth problems and tooth loss.

Many studies have shown that high rates of leukoplakia in the mouth were found where individuals hold the chew.

Leukoplakia is a white patch in the mouth that could potentially turn into cancer. The white patches, sometimes called sores, within the mouth cannot be scraped off but usually do not cause pain. The longer the use of oral tobacco, the more prone an individual is to develop leukoplakia.

Stopping tobacco use usually allows leukoplakia to heal, however, treatment may be needed if there are signs of early cancer. Along with these issues, there are many others such as bad breath, teeth stains, receding gums, gum disease, cavities and tooth decay.

As well as the health risks one is providing for themselves, children, pets and animals can also suffer health risks from tobacco substances. Children, pets and animals often mistake these substances for candy, gum or something they should put in their mouth.

Ingesting smokeless tobacco can lead to nicotine poisoning and even death. Most children affected by this are under the age of 6 and more than 70 percent are under 1 year of age according to a study in Pediatrics, the journal of the American Academy of Pediatrics.

Smokeless tobacco affects everyone.

2017-11-27T08:15:41-07:00November, 2017|Oral Cancer News|

Mouth cancer survivor: Dental check ups saved my life

Author: Elaine McLaren

“Nobody particularly enjoys visits to the dentist and I’m no exception, but I’ve always looked after my teeth and have never missed a six-month check. So that day back in May 2009, I wasn’t expecting there to be any problems. I hadn’t been in any pain or discomfort, so I was surprised when the dentist voiced his concern.

‘There’s a white patch on the side of your tongue,’ he told me through his mask. ‘It’s probably nothing but you should get it checked out by your GP, just to be on the safe side.’

Examination over, I sat up in the chair as he explained what he thought it could be – a condition called leukoplakia, which was harmless in its mild form and often disappeared without the need for treatment.

So when, a few days later, I was sitting opposite my GP, I was shocked to hear the condition was closely linked to mouth cancer.

My heart sank at the mere mention of the word. Just seven years earlier, I’d lost my dad to lung cancer.

My thoughts immediately turned to my own children, Grace, who was then only eight, and Daniel, five, and whether they’d have to go through the same trauma as I had with Dad.

As quickly as the notion had entered my head, I brushed it aside. I was only 38 then, I didn’t smoke or drink heavily and I ate healthily. Nothing made me a high risk.

But that still didn’t stop my heart pounding as I sat in the hospital waiting to see the consultant a few weeks later. Opening my mouth wide once again, I steeled myself for the worst possible news.

When he told me I had nothing to worry about, I could have cried with relief.

But its habit of developing into something far more sinister meant that wasn’t the end. I was sent for a biopsy to check for irregular cells and continued to see the consultant for check-ups, then discharged 18 months later. I could finally start to relax and believe it was over.

My dentist wasn’t quite so laid-back. As an expert in mouth cancer, he kept a close eye on it, taking photographs every time I saw him to make sure he could track the changes. It became a routine part of my visits and something I barely even thought about, until five years later I started to notice a difference myself.

All of a sudden, the patch started to rub against my teeth, whereas I’d never noticed it before. It started to get red and aggravated and every time I ate spicy foods, an agonising, searing pain would shoot through my tongue.

As luck would have it, I already had an appointment with my dentist booked, so I decided to see him before doing anything else. I was hoping he would tell me it was nothing, but in my heart I knew that wasn’t the case. Sure enough, he took one look at it and recommended I went back to see the GP.

Just weeks later, I was once again sitting in the familiar surroundings of the consultant’s office. I knew from his straight-faced, stilted reaction – so different to the casual reassurance I’d had before – that it was much more serious.

His voice was calm and steady as he told me I would need another biopsy, but I could tell he thought the worst. I had the procedure two days before Christmas 2013 and though I tried to think positively, telling myself that I’d been worried before and it had turned out to be nothing, the truth was I was terrified.

I spent the entire festive season putting on a happy face and trying to make everything as normal as possible for the children when, inside, all I could think about were the impending results. Every waking moment, I worried about the outcome.

When I returned to the consultant early in the new year, I thought I’d prepared myself for what he was about to say. When I eventually heard the words, ‘You have mouth cancer,’ it turns out I wasn’t prepared at all.

Though I’d known deep down that it was coming, it hit me like a bolt out of the blue as if I’d never expected it at all. As the words began to sink in, it came as such a huge shock that he was talking about me.

I’d always assumed it was a disease that only affected older men who smoked heavily. How wrong I’d been. Mercifully, and thanks to the diligence of my dentist, mine had been caught early enough to give me a great chance. I felt incredibly lucky. I was going to beat this.

But just as I was counting my lucky stars, fate dealt me another blow. A routine MRI scan revealed a mass on my right lung. It couldn’t be diagnosed with a biopsy because of its position, so I had no choice but to leave it there until they’d dealt with the cancer in my mouth.

I was determined to get through it and get back to being a mum again.

In January last year, I had a 10-hour operation to remove the cancer in my tongue and have it rebuilt with tissue and a vein from my arm, which was then grafted with skin from my tummy.

As soon as I recovered, in March last year, I was back in theatre again for a four-hour operation to remove the mass on my lung, which did turn out to be cancerous.

Both of the operations were a success and I’m finally getting my life back on track. I know I’ve got the vigilance of my dentist and the fact that I visited him regularly for the fact that it was caught early enough and I can put it all behind me. If it wasn’t for him, I could still be living with a cancer I didn’t even know was there.”

Noninvasive oral cancer test eases patient fears

Author: Donna Domino, Features Editor

A new, noninvasive cytology test for oral cancer, ClearPrep OC, is being offered free to dentists. The test, aimed at “watch and wait” lesions, is less expensive than biopsies and less frightening for patients, according to Resolution Biomedical, the company that is commercializing it.

The chairside oral cancer test — which can be ordered directly from the company — is designed to be a diagnostic option for assessing lesions when a biopsy is not warranted or the patient fears getting a biopsy, according to Donald Williams, MD, chief medical officer of Resolution Biomedical.

The test involves a cyto-brush sampling method that measures gross changes in the nuclear DNA content of oral epithelial cells, providing information about the precancerous or cancerous state of a lesion, the company explained. The samples are sent to medical testing labs, and the report is sent to the dentist within four to five days, the same time frame as biopsies. Dentists send the samples to the company, which prepares the slides and sends them to labs, which prepare a diagnostic report for the dentists.

“It’s a way to triage patients where something may be suspicious but the patient is balking about getting a biopsy,” Dr. Williams told “It could be leukoplakia lesions or thrush instead of an indication of a neoplasm. It rules out biopsies without an invasive process.”

When dentists refer patients to periodontists to get biopsies of suspicious lesions, many patients don’t follow through on the recommendation because they find it a daunting procedure, Dr. Williams noted.

“Some patients think, ‘I’ve had this for years and it hasn’t killed me, so I don’t want to be biopsied,’ ” he said. “It’s kind of frightening to say you’re going to have a piece of meat cut out of your mouth.”

The most logical application is for worrisome lesions that are likely benign, Dr. Williams said.

Ongoing clinical trial
Resolution Biomedical conducted about five validation studies of the ClearPrep OC test in general practices over six months, Dr. Williams said. It is now being tested with Southern California dentists.

In addition, the test is in the second phase of a trial study with cancer patients in the City of Hope cancer research hospital in Duarte, CA. ClearPrep OC and saliva samples will be taken, and p16 stains will be done on the biopsy specimens. All the modalities then will be combined before a blind match is done. The company plans to do a joint publication based on the results with the University of California, Los Angeles, Dr. Williams said. The test was primarily designed for gynecologic cytology pap tests, but Resolution Biomedical realized it also had potential to detect oral cancer.

The company does not plan on doing an official launch of the product, which has no marketing restrictions since nongynecologic cytology tests are an established medical practice, according to Dr. Williams. As a result, the test does not require U.S. Food and Drug Administration clearance or need to be Clinical Laboratory Improvement Amendments (CLIA)-certified, he said.

While the test is being provided for free to dentists, patients and labs pay $60 to $125 — much less than biopsies, which range from $400 to $500, according to Dr. Williams. It is usually covered by insurance, and dentists can charge a collection fee for the process, including interpreting the final report, according to Dr. Williams. Company revenues will be derived from the testing labs it uses for analysis.

“Biopsies are invasive, expensive, and painful,” said company CEO Mike Friedl. “This is an intermediate way to rule out stuff while you’re still at the dentist rather than going to a specialist.”

The test is especially suitable if the condition is simply a treatable condition, such as a fungal change, and doesn’t require a trip to see a specialist, Friedl noted. Since the human papillomavirus (HPV) is now associated with many oral cancers, the company tests for it if the sample shows any degree of atypism.

Sol Silverman Jr., DDS, a professor of oral medicine in the University of California, San Francisco (UCSF) School of Dentistry and head of one of the oral medicine clinics at UCSF, called the ClearPrep test a good adjunctive diagnostic technique.

“Cytology has been around a long time, and it’s very high-quality,” Dr. Silverman told “Any technique that will accelerate the recognition of dysplasia is important. Early detection is still our best approach to good survival results.”

Decoding the oral leukoplakia/oral cancer link

Author: DrBicuspid Staff

Is there a direct relationship between oral leukoplakia and tobacco and alcohol consumption? Do all oral leukoplakias lead to oral squamous cell carcinoma (OSCC)? Is it possible to detect premalignant oral leukoplakia?

These are some of the questions a recent literature review in Oral Diseases attempted to answer (January 11, 2013).

A team of researchers from Italy, Spain, the U.K., and the U.S. did a literary search of Medline/PubMed, Embase, and Best Evidence from January 1966 to June 2012. Search terms included leukoplakia, oral leukoplakia, preneoplastic oral, precancerous oral, oral precancerous, oral dysplasia, oral mucosal lesion, proliferative verrucous leukoplakia, multifocal leukoplakias, tobacco, and alcohol.

The searches were designed to help the study authors address four key questions:
1.Do tobacco and alcohol cause oral leukoplakias?
2.What percentage of oral leukoplakias evolve into OSCC?
3.Can practitioners distinguish between premalignant and innocent oral leukoplakias?
4.Is proliferative verrucous leukoplakia (PVL) a specific entity or just a form of multifocal leukoplakia?

For the purposes of this study, the term oral leukoplakia was used to recognize “predominantly white plaques of questionable risk, having excluded (other) known diseases or disorders that carry no increased risk of cancer.”

Tobacco, alcohol, and oral leukoplakia
Although oral leukoplakia is generally considered one of the primary clinical precursors of OSCC, “the role of alcohol and smoking in this disorder has never been thoroughly assessed,” the researchers wrote. “Existing evidence suggests that tobacco and alcohol could be associated with at least a subset of [oral leukoplakia].”

It is important to recognize that, during the last few decades, the definition of oral leukoplakia has changed and new variations have emerged, suggesting potential misdiagnoses in older studies, they noted.

While an association between oral leukoplakia, smoking, and alcohol “could be reasonable and plausible,” the researchers wrote, “there is a lack of well-designed studies to examine the precise causal association,” and there are currently no systematic reviews demonstrating such a relationship.

“Current evidence indicates that tobacco consumption appears to be more likely to contribute to epithelial dysplasia than alcohol use,” they concluded.

Oral leukoplakia and OSCC
While the majority of oral leukoplakias are localized and benign, “small subsets of these lesions … acquire progressive dysplastic cellular changes and ultimately develop OSCC,” the researchers wrote (Clinical Cancer Research, June 2001, Vol. 7:6, pp. 1702-1710).

At present, there is no single marker or set of markers that can reliably predict malignant transformation of oral leukoplakia into OSCC, they noted, and the malignant transformation rate for all types of oral leukoplakias varies “enormously” from site to site in the mouth, population to population, and study to study.

However, “it is generally accepted that the detection of epithelial dysplasia is the most important predictor of malignant transformation of oral leukoplakia” (Oral Diseases, March 2007, Vol. 13:2, pp. 126-133), and it has been shown that precancerous lesions are more likely to develop into cancer in the presence of multiple genetic alterations, the researchers found.

While a number of biomolecular targets have been investigated in an attempt to identify markers that can predict the greatest risk of malignant progression, none of these has been “validated as a predictive factor for malignant transformations of oral leukoplakia,” the study authors wrote.

“Further efforts to identify the submicroscopic genetic, molecular, and/or epigenetic alterations are needed to advance this field,” they concluded.

Proliferative verrucous leukoplakia
PVL is generally described as “an uncommon form of progressive multifocal leukoplakia with a high rate of malignant transformation to either OSCC or verrucous carcinoma and a high probability of recurrence.”

The term was first introduced 35 years ago, but its diagnosis and clinical criteria remain “unresolved,” according to the study authors. It is essentially a clinical diagnosis that requires histological evaluation in order to exclude other conditions and confirm malignant development.

Based upon their literature review, “the distinction between early oral premalignant lesions of both multifocal leukoplakias and PVL is impossible,” the researchers wrote. “The diagnosis and early detection of PVL remain a difficult and challenging task due to the lack of pathologic and diagnostic predictors.”

Consecutive biopsies of the temporal progression of PVL and comparative analysis with conventional multifocal leukoplakias must be carried out to validate the various markers that have been previously suggested, they concluded.

Periodontitis increases risk of oral leukoplakia

Author: Donna Domino, Features Editor

Periodontitis increases the risk of developing oral leukoplakia and mucosal lesions that are predisposed to become oral cancer, according to a study in Oral Oncology (September 2012, Vol. 48:9, pp. 859-863).

The findings provide clues into the complex relationship between systemic and local disease, noted the study authors from the University of Greifswald in Germany.

The development of oral cancer proceeds through discrete molecular changes that are acquired from loss of genomic integrity after continued exposure to environmental risk factors. It is preceded in the majority of cases by clinically evident, potentially malignant oral disorders, the most common of which is leukoplakia, the researchers noted.

Leukoplakia is an asymptomatic lesion in the oral mucosa. Oral cancer — especially oral squamous cell carcinoma — often develops out of these lesions, they added. Studies have shown that as many as 18% of oral premalignant lesions will develop into oral cancer. In addition, periodontal sites are often involved in proliferative types of leukoplakia.

The oral cancer rate attributed to leukoplakia is between six and 29 per 100,000, according to the authors. Smoking and drinking alcohol are the main risk factors for this disease, but acute infections in the oral cavity may contribute to the risk.

Inflammatory markers
The study evaluated 4,310 German residents ages 20 to79 from 1997 to 2001. After five years, 3,300 participants were available for follow-up.

The periodontal assessment included probing depth, clinical attachment loss, plaque, bleeding on probing, and the number of teeth. Among the study population, 123 (2.9%) of the participants had oral leukoplakia, compared with 246 people in the control group who did not have oral lesions.

Patients with oral leukoplakia showed significantly higher measures of periodontal parameters, especially bleeding on probing and gingival attachment loss, the study found. Despite a high variance, the leukoplakia group also exhibited a higher incidence of tooth loss, and there were more diabetics than in the control group (22% versus 13%).

Gingivitis (as characterized by bleeding on probing) is associated with the occurrence of leukoplakia in a dose-dependent manner, the researchers found.

“From the results it may be concluded that there is a continuously increasing risk of leukoplakia with increasing severity of periodontitis or gingivitis,” they wrote. “Increased concentrations of inflammatory markers suggest that tissues irritated by defense processes such as periodontitis are vulnerable to premalignant transformations.”

These study findings echo a 2011 study by researchers in India that showed elevated levels of salivary interleukin-6 — which was used as a marker of malignant progression — among patients with leukoplakia and periodontitis (Clinical Oral Investigations, October 2011, Vol. 15:5, pp. 705-714). Excluding people with periodontitis, the researchers found the leukoplakia cases still had elevated levels of systemic markers of inflammation. Good oral hygiene (brushing at least twice a day) was associated with decreased risk.

One limitation of the German study was that the oral lesions were not biopsied, the researchers noted.

“Our findings give new hints into the complex interrelationship between systemic and local diseases,” they concluded. “Periodontal inflammation may be considered an additional risk acting synergistically with smoking and/or metabolic factors.”

Photodynamic therapy targets oral dysplasia, oral bacteria

Author: Kathy Kincade, Editor in Chief

Imagine being able to treat a suspicious lesion on a patient’s tongue simply by applying a topical agent, waiting a few minutes, then exposing it to light from a handheld laser or light-emitting diode (LED) device.

Imagine being able to treat bacterial and fungal infections in the oral cavity, even periodontal disease, using this same approach.

That is the promise of photodynamic therapy (PDT), a minimally invasive technique that first came into medicine in the early 1900s and has been used to treat a plethora of medical conditions, including skin diseases, localized infections, age-related macular degeneration, and premalignant and malignant disorders.

“PDT in the oral cavity would utilize a photosensitizing compound and a light source to activate the compound,” explained Thomas Mang, PhD, research director in the Laser and Lightwave Research Center at the University at Buffalo School of Dental Medicine. “Traditionally, it has been used in head and neck lesions and oral lesions with a photosensitizer given intravenously. But in applications related to early oral lesions and those involving candida and oral species that may be involved with periodontal disease, we look to apply it topically.”

Distinct advantages
Mang has been investigating PDT disinfection of oral biofilm and previously was involved with the development of PDT for treating cutaneous and other cancers while at Roswell Park Cancer Institute. He sees a bright future for PDT in dentistry, providing more selectivity and flexibility when treating patients with early oral lesions and microbial diseases of the oral cavity.

“With the utilization of a topically applied drug, there is a distinct advantage of using PDT, particularly for bacterial and candida species,” he said. “With bacterial and candida lesions, one of the major advantages of PDT is that it provides the practitioner with a method that is easily applicable in an office setting and that can be used to treat various species in a fairly rapid manner. These species take up the photosensitizing drugs very rapidly — we’ve seen effective doses in one to 15 minutes.”

In addition, many of the candida species and some of the bacterial lesions can become antibiotic-resistant, and PDT has been shown to be effective on antibiotic- and antifungal-resistant species, Mang noted. “So while treating the disease, you can reduce the need for antibiotics or supplement the use of antibiotics in very severe cases,” he said.

With cancerous lesions, PDT offers a localized form of therapy that can be repeated, Mang added.

“We have generally not found any buildup of resistance to PDT, so one could have repeated exposures to benefit the patient and reduce the severity of treatment by taking a more fractionated approach,” he explained. In addition, with early cancerous lesions, PDT generally offers improved functional and cosmetic outcomes versus surgical or radiotherapy approaches, while achieving comparable tumor control, he noted.

Growing body of research
Despite its many advantages, topical PDT for dental applications is still a few years from clinical reality, Mang noted (one exception is Periowave; see sidebar). In the meantime, a growing body of research supports the use of PDT for treating oral diseases and eliminating “bad” bacteria in oral biofilms.

For example, a 2007 study in the Journal of Dental Research (August 2007, Vol. 86:8, pp. 694-707) noted that “applications of PDT in dentistry are growing rapidly: the treatment of oral cancer, bacterial and fungal infection therapies, and the photodynamic diagnosis of the malignant transformation of oral lesions.” In addition, PDT has shown potential in the treatment of oral leukoplakia, oral lichen planus, and head and neck cancer, and photodynamic antimicrobial chemotherapy has been efficacious in treating bacterial, fungal, parasitic, and viral infections, the researchers wrote.

More recently, PDT showed promise in the treatment of early-stage cancer of the mouth and oropharynx, and demonstrated that it has a significant antimicrobial effect in the oral cavity (Lasers in Surgery and Medicine, January 2010, Vol. 42:1, pp. 1-8; July 27, 2012).

Now a review in Oral Diseases (September 3, 2012) lends further support to the clinical efficacy of PDT in the management of oral diseases, in this case potentially malignant disorders (PMDs).

“Based on its high efficacy and low side effects, its high patient acceptance/compliance, the simplicity of the procedure, and its minimal pretreatment preparation, topic PDT is believed to have potential to play an important role in the management of PMD, especially for the low-grade dysplasia,” wrote the study authors, from the University of British Columbia and the British Columbia Cancer Research Centre.

More studies needed
However, limitations remain. While some studies have used topical or systemically administered photosensitizers to treat dysplastic lesions in the oral cavity, none of these drugs has regulatory approval for this application, the researchers noted. And while topical ALA (5-aminolevulinic acid) in emulsion form has been the most commonly used form of PDT for treating dysplastic lesions, there is no consensus with regard to protocol.

In order to bring PDT into the clinical arena as a first-line treatment for potentially malignant disorders in the oral cavity, protocols such as illumination scheme, number of treatment cycles, incubation period of the photosensitizer, light source, and fluence rate need to be considered, as well as lesion size, thickness of the surface keratin layer, and the presence and degree of epithelial dysplasia, the researchers emphasized.

In addition to a need for more studies with standardized treatment protocols and randomized clinical trials, several technology advances need to occur as well, they noted.

“In the future, more compact, cheaper light devices such as inexpensive lasers, fiber-optic equipment, and simple dosimetric apparatus could help in bringing down the initial cost of setup,” they wrote. “In addition, use of new targeted photosensitizers, light sources, and drug delivery systems using nanoparticles could significantly contribute in increasing its therapeutic efficacy and specificity.”

Oral cancer and cultural factors in Asia

Authors: Sherry L Priebe, Jolanta Aleksejuniene, Shafik Dharamsi, Christopher Zed

Oral cancer is on the rise worldwide, with over 200,000 cases diagnosed yearly. The predisposing social and cultural habits related to this disease acquired in resource-poor countries in Southeast Asia remain prevalent among its users following migration to other and better resourced countries. As a result, countries that once rarely experienced high levels of oral cancer will likely see an increased incidence of this disease. Therefore, oral health professionals need to be aware of the cultural risk factors and the resulting oral health effects in order to respond effectively to the increasing incidence of oral cancer. The objective of this overview is to inform what is known about populations from resource poor countries in Asia in regards to oral cancer and its related cultural factors.

The social and cultural habits that may predispose people to oral cancer are common in resource-poor countries in Southeast Asia, and remain prevalent among its users following migration to other and better resourced countries. As a result, countries that once rarely experienced high levels of oral cancer will likely see a considerable increase of this disease. It has been suggested that following migration from these countries to North America, the habit has remained prevalent among this ethnic group. (1) Increasing the level of awareness among oral health professionals about oral cancer and its related cultural risk factors, as well as developing better early diagnosis are of key importance in addressing morbidity rates. (2)

Recognizing the need for increased oral health service, oral health prevention and rehabilitative treatment strategies, the faculty of dentistry at the University of British Columbia General Practice Residency program has established a collaborative international rotation in Vietnam. This international experience has been designed to broaden the scope of learning for dental postgraduate students to include an understanding to regional patterns to disease process, treatment modalities and cultural competency. The objective of the present overview is to describe the cultural risk factors associated with oral cancer in immigrant populations from resource-poor Southeast Asian countries with a particular focus on Vietnam.

Facts About Oral Cancer
Oral cancer is a serious public health problem with over 200,000 new cases reported annually worldwide. (3) The overall mortality rate for oral cancer remains high at approximately 50 per cent and even with modern medical services is probably due to the diagnosis only at the advanced stage of this disease. (4) Oral cancer is responsible for more deaths than melanoma, Hodgkin’s disease, or cervical cancer. (5) In most regions of the world, about 40 per cent of head and neck cancers are known to be oral squamous cell carcinoma originating in the oral cavity. (6) In South-Central Asia, 80 per cent of head and neck cancers are found in the oral cavity and oropharynx. (3) Oral squamous cell carcinoma comprises over 90 per cent of the malignancies beginning as inflammatory lesions such as leukoplakia, erythroplasia, and erythroleukoplakia. (7), (8)

In 2002, two-thirds of the new cases and deaths occurring in the world due to oral cancer were observed in resource-poor countries. (9) Annual incidence rates for oral and pharyngeal cancer are estimated at 25 cases per 100,000 in resource-poor countries. (10) In Canada, oral cancer represents approximately 2.6 per cent of all cancers in males and 1.4 per cent in females. (11) In 2008, these cases are estimated as approximately 3,400 new cases and 1,150 deaths. (11) In the United States, the annual incidence rates for oral cancer are estimated at 10 cases per 100,000. (5) Approximately 60 per cent of people diagnosed with oral cancer will survive only up to five years. (5) It is important to emphasize that oral cancer is one of the few cancers whose survival rate has not improved over 30 years. (12) Moreover, in the past three decades there has been a 60 per cent increase in oral cancer in adults under the age of 40. (13) The diagnosis of oral cancer may be delayed because a clinician did not suspect the malignant nature of the lesion due in part to the limitations of visual and manual examination of the oral cavity, head and neck. (13), (14), (15) Studies that previously only involved the southeast Asian traditional cultural and carcinogenic habit of betel quid chewing now reveal a worldwide phenomenon that is increasing at a disturbig rate. (8), (16)

The recognized etiological agents and risk factors for oral cancer include tobacco use, frequent alcohol consumption, s compromised immune system, the use of areca nut, history of cancer, dietary habits and such less well-established factors as infection with certain types of human papilloma viruses. (17-21) Alarmingly, 25 per cent of newly diagnosed cases of oral cancer do not fit the high-risk profile. (22), (23) It has been reported that rapid urbanization leading to an unhealthy lifestyle, such as increased access to and utilization of tobacco in its various forms as well as abuse of alcohol, leads to an increase in the incidence of oral precancer and cancer. (10)

Tobacco use in all its forms is first on the list of risk factors of oral cancer with at least 75 per cent of those diagnosed with oral cancer being tobacco users. (6), (10), (11), (24-27) When tobacco use is combined with frequent alcohol consumption, the risk increases substantially as these tow risk factors act synergistically exacerbating each other’s harmful effects. (6), (10), (25-27)

Oral cancers are more common in parts of the world where areca nut with or without tobacco is chewed. The International Agency for Research on Cancer has classified betel quid without tobacco as a human carcinogen. (6) Consequently, the use of areca nut in any form is not safe for oral health. The commercially manufactured forms of areca nut with additives such as sugar have even more oral health related risks.

Oral cancer in Asia
Oral cancer accounts for up to 40 per cent of all malignancies in Southeast Asia. (28) In Vietnam, 19.80 per cent of all malignant neoplasms are diagnosed as oral cancer. (18) In India, the incidence of oral cancer in women is 3-7 times higher than in resource-rich countries, and smoking and chewing of tobacco betel quid are identified as risk factors. (29) In most regions of India, oral cancer is the most common cancer in men and the third most common canner in women. (30) Information emerging form Taiwan and China indicates that the incidence of oral cancer in men has tripled since the 1980s due to the chewing of betel quid. (10) Tobacco generally is not added to betel quid in these regions.

Oral cancer in Vietnam
Vietnam is a resource-poor country with numerous challenges. Oral health care in Vietnam is aggravated by poverty, lack of health education, and lack of government funding and policies to provide a sufficient number of oral health care workers. (31) The practice of seeing the dentist for a regular dental examination is traditionally not a major priority for many Vietnamese. It is no surprise that oral cancer ranks seventh of all cancers in Vietnam-the ratio of males to females was 1: 1.5 in 1993 compared with a ratio of 1.3:1 in 2001. (18)

Oral malignancies are often not being detected until individuals experience debilitating circumstances to normal oral function. The need for assessment of the imminent oral health problems and their contributing factors in Ho Chi Minh City has been realized. As many as 26 cases in 1000 patients admitted daily to the HCMC Oncology Hospital are diagnosed with advanced oral cancer due to tobacco use and inadequate diet. Consequently, these patients become immuno-compromised with considerably increased secondary risk of oral diseases are oral infections. Moreover, oral cancer is a possible result of cultural, socio-economic and behavioural factors such as limited access to oral health care leading to a diagnosis only at the advanced stages of a disease, inadequate information about oral health and proper nutrition, and the lack of funds and awareness about risk factors such as tobacco use, frequent alcohol use, and the use of betel quid.

In 2000, 4.1 per cent of Vietnamese women chewed areca nut or betel quid. (18) The largest proportions of areca nut chewers are found in the two age groups of 55-64 years (19.70%), and of 65-75 years (8.39%), (18) Precancerous and cancerous lesions found in females comprise 3.51 per cent of 11.49 per cent of oral mucosal lesions in South Vietnam including submucosal fibrosis, pink and white lesions, and oral mucosal lesions of betel quid use. (18) Submucosal fibrosis in betel quid chewers was found to be 124 times higher compared with non betel quid chewers. (18)

Behavioural and Cultural Habits Related to the Risk of Oral Cancer

Tobacco use worldwide
The association between smoking and oral carcinoma has been firmly established from epidomiologic studies, revealing more than twice as many smokers among oral cancer patients as among non smokers. (15) Worldwide, four million people die each year from tobacco related diseases and that number is expected to rise to 8.5 million a year by 2020. (9) Smokers are six times more likely to develop oral cancer than those who do not smoke. (32) Approximately 80 per cent of the world’s smokers live in resource-poor countries such as Vietnam where smoking rates have risen dramatically in the past few decades. (9)

Tobacco use in Vietnam
Worldwide, Vietnam has the highest rate of smoking among males (63.4%). The prevalence of this unhealthy lifestyle is reported to a lesser extent among women (20%). (18) However, smoking rates in Vietnamese women may be underestimated because it is not culturally acceptable for women to smoke. Smoking by youth and women is on the rise.” Vietnamese who are both smokers and drinkers, or who are both smokers and betel quid chewers, have 2-3 times higher risk of contracting oral precancerous and cancerous lesions compared with those who only smoke. (18)

Alcohol use worldwide
Alcohol abuse, defined as more than twenty-one standard drinks in one week, ranks second in risk factors for the development of oral cancer. (34-36) Canadian recommendations are not to exceed more than two standard drinks per day, one standard drink being 13.6 grams of alcohol. Further recommendations are not to exceed more than nine drinks per week for women and not to exceed more than fourteen drinks for men. (34-36) Excessive alcohol consumption is related to oral cancer which is six times more common in drinkers than in non drinkers. (32)

Alcohol’s effect on the mouth may be the key to understanding how it works with tobacco to increase the risk of developing cancer. The dehydrating effect of alcohol on cell walls enhances the ability of tobacco carcinogens to permeate mouth tissues. (37) Another hazardous influence of alcohol is that its excessive consumption leads to nutritional deficiencies which in turn can lower the body’s natural ability to use antioxidants to prevent the formation of cancers. (36), (38) Tobacco use has been proven to increase the risk of oral cancer, consequently people who use both alcohol and tobacco are at an especially high risk of contracting the disease. The combined effects of tobacco and alcohol are illustrated in a study of over 350 individuals who had oral cancer and their mortality rate was 32 per cent in 5 years. (39)

Alcohol use in Vietnam
In December 2006, Vietnamese Deputy Minister of Health Le Ngoc Trong expressed that excessive alcohol consumption had reached alarming proportions with serious consequences for the health and safety of the public. (40) Vietnamese males commonly consume 0.5-1.5 litres of alcohol daily. Apart from individual suffering, alcohol abuse hampers national development and economic growth. According to the Vietnamese Health Strategy and Policy Institute, the cost of dealing with the consequences of excessive consumption of alcohol typically accounts for 2%-8% of national gross domestic product. (40)

Research suggests that Vietnamese youth (15-20 years old) are consuming more alcohol, and at younger ages. Of 480 surveyed youth, 30 per cent had consumed alcohol and approximately 20 per cent of young men, and to a lesser extent young women reported intoxication in a sixmonth period. (41) As oral cancer is being seen in younger populations in both resource-rich and resource-poor countries, more awareness and better communication with the public as well as with oral health and medical professionals about the detrimental effects of alcohol use in younger populations and the associated oral health risk is necessary. (36)

Areca nut and betel quid use worldwide
The areca nut is used as a chewing substance by approximately 600 million people worldwide. (42) Betel quid is a mixture of areca nut (from the areca tree) and slaked lime (calcium hydroxide) wrapped within a betel leaf (from the Piper betel vine) although this mix varies in individuals and communities to include tobacco, various spices, sugar and chemicals. (16) Betel quid is placed in the cheek of the mouth where it is chewed slowly. An estimation of 10%-12% of the world’s population chew areca nut in some form, often mixed in betel quid with or without tobacco. (43) Betel quid chewing is a social and cultural practice for its stimulant effects, and it is thought to diminish hunger and to sweeten the breath. The usage of areca nut is indigenous to India, Sri Lanka, Maldives, Bangladesh, Myanmar, Taiwan and numerous islands in the South Pacific. (43) The habit is popular in parts of Thailand, Indonesia, Malaysia, Cambodia, Vietnam, Philippines, Laos, China and in migrant communities from these countries. (43) The chewing practice of betel quid dates back thousands of years and is deeply entrenched in the culture of the population in several parts of Southeast Asia. (43) Both men and women of all ages in many countries, including children, chew areca nut. (43)

In communities throughout Southeast Asia, oral cancer including oral squamous cell carcinoma has been predominantly related to traditional areca nut use. (16) In Southeast Asian countries, and specifically in the countries of Taiwan, India and China, a steep rise in oropharyngeal cancers has been observed since the early 1970s. (16) Betel quid chewing worldwide is a known risk factor for oral leukoplakia, oral submucous fibrosis, and oral squamous cell carcinoma. (1), (16), (26), (44), (45) The World Health Organization (WHO) has reported the use of betel quid as a widespread global risk habit that has spread due to increased migration of Asian communities to all continents resulting in an increases in oral cancers around the globe. (16) A review of the approximately 1.5 million cancer deaths in England and Wales from the years 1973-1985 shows that Indian-born men had over two times, and Indian-born woman over five times, greater risks of oral cancer mortality than native English and Welsh individuals. (46) Consequently, public health concern of a worldwide epidemic of oral cancer relates to the use of betel quid and its substitutes by an increasing number of young adolescents. (46)

Areca nut and betel quid use in Vietnam
Evidently, betel quid chewing has cultural and traditional social significance particularly among elderly Vietnamese women. There is a common saying in Vietnamese social circles “the betel begins the conversation”. (47) The traditional wedding gift from a groom to the bride’s mother is an assortment of areca nut, betel leaf, slaked lime, tobacco, and additives such as the bark of the areca nut tree, peel of the areca nut, and the pomello fruit peel, even if betel quid chewing is not practised. Based on a folk tale, the betel leaf and areca nut are important symbols of love and marriage and the phrase “matters of betel and areca” (chuyen trau cau) is synonymous with marriage. (47)

In Vietnam, only the women are known to chew betel quid; although in a recent research study (48) one man was identified as chewing betel quid for thirty-five years. Chewing areca nut is believed by Vietnamese to strengthen the teeth and keep the gums healthy. The teeth become heavily stained from this nut as well as from the practice of “tobacco rubbing” and “tobacco sticking”. Tobacco rubbing and sticking is accomplished by rubbing a small ball of raw dried tobacco over the gingiva on the anterior teeth and buccal mucosa and then sticking the tobacco ball in the cheek vestibule with the areca nut. When chewed, the areca nut creates a red juice that dyes the lips and stains the teeth dark brown. The red dye that leaks on the lips of women is traditionally considered to be attractive to men. Today in Vietnam there is an increasing social stigma as-Priebe, Aleksejuniene, Dharamsi and Zed sociated with this habit among younger women who refer to this habit as being for elderly women only.

Lack of Oral Health Awareness in Resource-poor Countries

Awareness is virtually non-existent in resource-poor countries particularly about oral health risk factors such as sugar consumption, tobacco use, frequent alcohol consumption, betel quid chewing, stress, and inadequate information about health and diet. The trend of the increasing flow of rural to urban migration compounds the problems of the urban poor population including increased oral health treatment needs. This pattern has evolved over the past twenty years, and it is likely to become more the norm than the exception. (49)

The changing socio-economic situation in some countries may have a strong negative association with oral health. (50) For example, a report in the Vietnamese Sunday Morning Post by the Columbia University’s Earth Institute states, “Cheap food, cigarettes and city life are causing millions of early deaths in the developing world … as populations increase in cities. The tobacco scourge, now at epidemic levels in less developed countries, exacts its tolls in many ways …,” (51) The increased incidence of oral cancer is associated with rising affluence which relates to the potential increase in exposure to additional amounts of tobacco and alcohol. (50) As a possible result, rising oral cancer statistics worldwide appear to be a reflection of the currently increasing urbanization and increasing affluence. (50), (51)

Oral health awareness in Vietnam
Medical surgeons and oncologists in southern Vietnam are concerned about oral health education for patients as well as for doctors. The low level of health literacy of oral cancer patients has been related to extreme patient load, lack of time for health care professionals and lack of human resources. People are frightened and confused about their disease perceiving oral cancer as a contagious disease. Therefore, a multidisciplinary approach to oral health care of cancer patients is required. (52), (53) Access to public oral health care education is part of that approach. Many concepts of this education have unclear boundaries between access and demand, between health states and health care and between perceived individual need and social responsibility. (54) Vietnam has a Cancer Prevention Program as well as a National Oral Health Promotion Program, yet there is a lack of patients’ knowledge of their oral disease. The WHO Basic Package of Oral Care (BPOC) is an example of proven effectiveness and is acceptable, feasible and affordable for most disadvantaged communities to improve their oral health care. (55) The three components of BPOC are oral urgent treatment, affordable fluoride toothpaste, and atraumatic restorative treatment (ART). (55)

Worldwide Oral Cancer Education

An awareness of creating a healthy lifestyle and behaviour to prevent oral cancer is dependent on changes in both lifestyle and cultural values. This change can be accomplished through a well planned preventive oral health education based on in-depth understanding of community needs and their specific characteristics, people’s habits and self perceived oral health problems and needs as well as good use of the existing infrastructures.(55) Various non government organizations have contributed to the oral health education of resource-poor countries worldwide. For example, Path Canada is a non profit organization that has greatly advanced the education of the Vietnamese authorities and public in general about the hazardous effects of tobacco use. It is also important to consider that tobacco use and frequent alcohol consumption thrives and competes against basic human needs (56) Through this project, a unique opportunity exists in Vietnam to study the association of intra-household tobacco use expenditures and their impact on child health and poverty (56) Furthermore, the association of betel quid use with the increase of precancerous conditions and oral cancerous lesions highlights the importance of education not only on tobacco cessation and less alcohol consumption but also on betel quid cessation.

It can be concluded that an active preventive educational approach is required to curb the rising increase in oral cancer due to culturally related risk habits especially in Asia and within Asian immigrant populations around the world.

Source: The Canadian Dental Hygienists Association

1. Footnotes and references available here.

Oral epithelial dysplasia: What does it really mean?

Author: Nancy W. Burkhart, RDH, EdD

Patients are sometimes followed for periods of time for what is called dysplasia, leukoplakia, keratotic lesions, and previous frank carcinoma. With any degree of tissue change, the person should be followed closely and an etiology always needs to be determined. Sometimes, removal of a frictional component is suggested; at other times, the lesion may have a more ominous appearance that will alert the clinician that cancer might be high on the differential list. Obviously, in highly suspicious lesions, a biopsy would occur immediately.

Patients will sometimes tell the clinician that they were previously biopsied and the report will note “evidence of dysplasia.” Sometimes a diagnosis is made of dysplasia, but the lesion becomes carcinoma over time, even after the initial removal of the lesion. The reverse may be true as well, where the body responds physically and the tissue regains a state of health.

Figure 1: This image depicts moderate dysplasia, displaying increasing cytologic atypia and alteration of maturation in the lower half of the epithelium. Courtesy of Dr. John Wright, From General and Oral Pathology for the Dental Hygienist. Lippincott Williams & Wilkins, 2008

Why does one individual develop carcinoma while another person may develop a mild epithelial dysplasia? Perhaps the body is able to stop progression or reverse the state of progression. These are questions that researchers continue to evaluate and study.

Frictional keratosis, though, is not in the same category as dysplasia. When the frictional component is removed, the lesion will subside. An example of a common lesion that has a frictional component is cheek chewing or morsicatio buccarum. However, chronic frictional or chemical assault on the tissue over time can also cause dysplastic changes.

The body has the miraculous ability to repair damage caused by our environment and lifestyle factors. We are discovering, for example, the role that our food plays in reducing cancer risks and even altering our susceptibility toward genetic factors. Our mental, physical, and spiritual make-up will play a very strong role in individual disease states, as well as during recovery. Researchers are now discovering that the very food we place in our bodies has great healing powers and may prevent many known diseases while promoting total health. Along the same lines, exposure to environmental agents has been documented as having profound effects on our bodies as well.

The factors that allow an oral pathologist to diagnose a tissue specimen as dysplastic (see Figure 1) are the following (Wright J, 2008):

An increase in cellular nuclear/cytoplasmic ratio
Rounded rete ridges often described as “saw-tooth” in appearance
Noticeable maturation
Evident mitosis with atypical findings, as well as mitosis in upper layers of the epithelium
Visible changes in pleomorphism in the cell size as well as the shape of individual cells
Dark, staining cells are visible –nuclear hyperchromatism
Nucleoli are enlarged and appear darkly stained
Cellular adhesion is lost
Abnormal keratinization patterns arise

All of the features will vary with individual tissue specimens, and the degree to which the dysplasia is classified may vary with pathologists viewing the same tissue specimen. Generally, three classifications occur – mild dysplasia, moderate dysplasia, and severe dysplasia.

If the tissue is not treated surgically or ablated with laser surgery, carcinoma in situ or frank squamous cell carcinoma will likely result. Any contributing lifestyle such as alcohol or tobacco use may lead to the progression of dysplasia and should be discontinued. As progression continues, invasion of the transformed cells to the tissue below the basement membrane will occur and the designation of invasive carcinoma is evident.

The importance of the oral exam, including both the extraoral and intraoral, cannot be emphasized enough. Despite the newest techniques with lights, rinses, and various tests, the gold standard in any unexplained finding, when an etiology cannot be found, is to biopsy for microscopic confirmation. Some lesions cannot be seen – especially those in the most posterior regions and the tonsils/tonsillar crypts – and palpation along with careful visual screening is a key factor.

The dilemma occurs when a suspicious area has no known cause and the decision rests on whether to biopsy at that time, follow the area, or use one of the available adjunct devices for more information. All adjuncts that can be used are just that – adjuncts. Nothing takes the place of a thorough intraoral and extraoral exam when performed correctly. With all of the information available, the clinician must decide along with the patient what the optimal choice must be at that time. The choices would be to proceed with a referral, perform a biopsy, or monitor the lesion.

A recent editorial written by Dr. Mark Lingen, editor-in-chief, of Oral Surgery, Oral Medicine, Oral Pathlogy, Oral Radiology, and Endodontology, emphasized the need for dental education in head and neck screening for squamous cell carcinoma. With an annual incidence worldwide of more than 500,000 cases, it is the sixth most common malignancy. Dr. Lingen praised the efforts of the American Academy of Oral Medicine and the Academy of Oral and Maxillofacial Pathology for their continued focus on educating dental students in performing the head and neck exam. He applauded the efforts put forth by the American Dental Association’s Commission on Dental Accreditation to require that dental students be proficient in the oral cancer exam during school and as a proficiency exam by graduation. He also asked some good questions about how these efforts will be carried out and how the students will be assessed long-term.

The editorial speaks to the question of how will schools ensure that their own faculties are proficient as well in the dental exam in order to teach the students. Dr. Lingen cites several research studies in the past few years that suggest the graduating dental students and practitioners do not feel comfortable with the dental exam in detecting head and neck cancer and that they feel inadequately prepared. He also emphasizes the need for continuation of pathology and dental exam skills during all the years that a dental student spends in school.

Over the years, I have corresponded with thousands of patients who have contacted me through The International Oral Lichen Planus Support Group (founded in 1997). I have heard more times than I want to mention that “the dental office really never checks my lichen planus and they just tell me to learn to live with it – it is only lichen planus.”

We hear so many times from patients who have long-term oral lesions – lichen planus, ulcerative disease states, and even long-term undiagnosed lesions – and somewhere along the way the tissue became dysplasia or ultimately oral cancer. Any lesion needs to have a diagnosis, and long-standing disease states need to be carefully monitored at frequent intervals. Long-term inflammation anywhere in the body is detrimental. Even previous dysplasia and cancer should be followed carefully because of potential recurrence. The concept of “field carcinogenesis” means that other malignancy may occur from new foci and cell transformation related to the previous lesion.

We have heard from family members who tell us that the person who corresponded with us has died, but they are contacting us to say thank you for trying to help even though it was too late.

Often, it is the person who is undergoing surgery with radiation treatment who emails me to update me on their progress.

Emotional support is time-consuming but greatly needed and freely given. Busy offices are usually pressed for time, but answering questions, following up with patients, and offering your concern is part of a healing process. It is truly sad that so much emphasis is placed on cosmetic procedures, yet there is so little time for a good oral exam in the office. I think that hygienists need to make the oral exam a prime focus in their practices for every patient and at every visit.

If you do not feel confident in your own abilities with the oral exam, search for a CE course in your region to update your skills. No one is so knowledgeable that they cannot use a little more updating and education to make themselves a better healthcare provider.

Life is an ongoing educational process, no matter what aspect we are addressing. Education by its very nature is never wasted time.

As an educator, I feel strongly that continuing education is needed for key areas such as oral pathology and oral medicine – not only in dental schools but in offices as well. We are primary healthcare providers who can tell so much about a person by just performing a good intraoral and extraoral exam. With an aging population, an increase in oral cancer for those under 40 years of age, and even children developing oral disease states not usually found in the past, we need to concentrate on what is truly important. Update your skills and start sharing your expertise in helping others!

Keep listening to your patients and always ask good questions!

1. Nancy W. Burkhart, BSDH, EdD, is an adjunct associate professor in the department of periodontics, Baylor College of Dentistry and the Texas A & M Health Science Center, Dallas. Dr. Burkhart is founder and co-host of the International Oral Lichen Planus Support Group ( and co-author of General and Oral Pathology for the Dental Hygienist. Her website for seminars is

1.Cannick GF, Horowitz AM, Drury TF, Reed SG, Day TA. Assessing oral cancer awareness among dental students in South Carolina. J Am Dent Assoc 2005;136:373-8.

2. Kahn M. Adjunctive Oral Premalignant Screening Devices-Clinical Protocol #12. From: DeLong L, Burkhart NW. General and Oral Pathology for the Dental Hygienist. Lippincott, Williams & Wilkins. Baltimore, 2008.

3. Lingen M. Assuring dental student head and neck cancer screening competency. Editorial in Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2011;111:3,267-68.

4. Pannone G, Santoro A, Papagerakis S, Lo Muzio L, De Rosa G, Bufo P. The role of human papillomavirus in the pathogenesis of head and neck squamous cell carcinoma: an overview. Infect Agent Cancer2011;Mar 29:6:4.

5. Siegel M, Murrah V, Aloise D. Head, Neck and Oral Cancer Examination. MedEdPORTAL; 2009. Available from:

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