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I'm A Dentist – There Are Telltale Signs Of Deadly Oral Cancer I Can Spot BEFORE I Even Look Inside Your Mouth

WE'RE all taught to be aware of potential signs of cancer - from strange lumps and skin changes to unexplained weight loss and red flags in our poo.

But the early signs of some cancers, like oral cancer, can be harder to spot, with them being subtle in nature or easily mistaken for other conditions.

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Some signs of oral cancer don't necessarily require looking inside the mouth

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Dentist Dr Safa Al-Naher says early detection and awareness of oral cancer is keyCredit: Dr Safa Al-Naher

That's where your dentist comes in.

Dentists are trained to routinely screen for signs of oral cancer during regular check-ups and can often be the first to spot early signs.

Oral cancer, also known as mouth cancer, develops in the oral cavity, which includes the lips, tongue, gums, and the lining of the mouth. 

Last year, the UK saw record mouth cancer cases, with 10,825 diagnosed annually, representing a 133 per cent increase over the last 20 years, according to the Oral Health Foundation's State of Mouth Cancer UK Report 2024. 

In response to this trend, Dr Safa Al-Naher, Founder and Principal Dentist at Serene by Dr Safa in Knightsbridge, London, is highlighting the importance of early detection and awareness.

Dr Safa can see these signs of mouth cancer during a routine check-up:

A lump in your mouth

An ulcer in your mouth that isn't healing

Unexplained bleeding in your mouth

Red, or red and white patches in your mouth

Loose teeth or dentures that no longer fit you properly

But not all signs are evident by looking inside your mouth.

A lump or sore on your lip that doesn't go away after a couple of weeks is a sign, too.

A lump in your neck or enlarged lymph nodes in your neck are also symptoms.

Dentist warns of hidden dangers in your toothbrush - it's grosser than you realize, don't keep it in the bathroom

But Dr Safa says there are two main symptoms that can indicate oral cancer even before you say 'ahh!'.

"These are difficulties with your speech," she said.

"You may sound hoarse or quieter, or you may slur your words.

"And pain in your ear. This can be caused by damage to a nerve near your tongue."

Oral cancer can be deadly, especially if detected late.

But early detection and treatment significantly improve survival rates. 

You can also look out for these signs yourself:

A sore throat that you've had for a long time, and doesn't seem to be getting better

Difficulty or pain when chewing or swallowing

Difficulty moving your jaw

Numbness of your lip or another part of your mouth

Biggest oral problem

One of the biggest risk factors for developing mouth cancer is tobacco use.

In recent years, more smokers have been switching to vaping to ditch the habit with studies showing vaping can be a less harmful alternative.

But Dr Safa revealed some of the most significant oral problems she's seeing are the effects of vapes.

She said: "We're seeing all sorts of weird and wonderful patches in the mouth and on the tongue.

"It is not easy to diagnose why patches are occurring in the mouth. We generally have to rely on taking a medical history and those with patches of this nature usually vape.

"The patches are brown or yellow, and similar to those in people who smoke cigarettes.

"Also, there is often difficulty in mouth healing after extractions with people who vape.

"And they also cause bad breath."

Be cautious of hot drinks

Drinking alcohol is another risk factor for mouth cancer.

But Dr Safa also warns to be wary of hot drinks.

She said: "Drinking hot drinks potentially increases cancer risk if they're very hot and you have a habit of drinking scalding hot drinks.

"If the burn is not allowed to heal, it causes trauma.

"Anything that's not allowed to heal can develop into something a little bit more sinister."

A recent study also found sugary drinks can increase your risk of mouth cancer by five times.

The three most effective ways to prevent mouth cancer

It's also important that you have regular dental check-ups because dentists can often spot the early stages of mouth cancer.

Source: NHS

Bleeding gums aren't always a sign of cancer...

While bleeding gums can be a sign of cancer, particularly leukaemia or gum cancer, they're very often down to gum disease, Dr Safa said.

The good news is, gum disease can be stopped in its tracks.

So what should we do if we notice that our gums are bleeding?

There are five important steps Dr Safa recommends you should take:

1. Brush twice a day for two minutes with a fluoride toothpaste

Effective tooth brushing is the first thing in Dr Safa's top tips list for a reason.

She said: "Brushing our teeth twice a day for two minutes with a fluoride toothpaste is vital for gum health and also helps protect against other tooth decay.

"The best results are achieved if you brush last thing at night and first thing in the morning - ideally before you eat breakfast - using an electric toothbrush."

2. Start using interdental brushes or dental floss

Make this the second step in your daily oral health routine, said Dr Safa.

She explained: "This is because a toothbrush cannot reach between the teeth like interdental brushes or floss can.

"It's important to get into these areas which a toothbrush cannot reach, otherwise pockets of plaque may build up, potentially causing problems for our gums.

"When we first start using interdental brushes or floss it is not uncommon for our gums to bleed. 

"If this happens, it is important to persist and keep going. 

"After a week or two the bleeding should stop.

"I am often asked how many teeth I should floss between - and I reply, only the teeth you want to keep!"

3. Use a mouthwash

Using a mouthwash is beneficial for oral health as it helps to clear our mouth of debris, said Dr Safa.

She added: "It also helps prevent plaque build-up on our gums, in-between our teeth, and on the surface of our teeth in between brushing.

"It can also help to freshen our breath by killing bacteria.

"It's important when considering a mouthwash to chooseone containing fluoride to help give the mouth extra protection throughout the day."

4. Visit the dentist and/or dental hygienist

If you have bleeding gums it's a good idea to contact your dentist or dental hygienist, especially if you haven't seen yours for over a year, said Dr Safa.

She explained: "We may want to see you more frequently, for example every three to six months, if there are signs of gum disease.

"We can give our advice on cleaning techniques and remove any tartar build-up which may develop faster or in larger quantities if you are not quite removing plaque efficiently at home.

"If you are pregnant, you may be more prone to bleeding gums which is why your dental treatment is free during your pregnancy and it may prevent your baby being born early or underweight."

5. Look at your diet and lifestyle

Smoking increases the risk of gum disease so it's a good idea for both your oral health and overall health to quit.

This is because smoking causes a lack of oxygen in the bloodstream,so the infected gums don't get the chance to heal, said Dr Safa.

She added: "It's also a good idea to keep your alcohol consumption in check as it can also affect the health of the mouth.

"Adopting a healthy lifestyle is also important in order for our mouth to function properly.

"A diet rich in fresh fruit and vegetables can help us to prevent gum disease.

"Watch out though as processed foods with 'no added sugar' don't mean that they are sugar-free, it just indicates that no extra sugar has been added, but does not include the presence of naturally-occurring sugars.

"You may want to avoid dried fruit, for example, as not only are they very high in natural sugars, but they cling to the teeth like glue!"

Elevated Salivary Microvesicles Linked To Oral Ulcers And Cancer

A recent study has revealed that elevated levels of salivary microvesicles (MVs) could serve as a potential biomarker for non-healing oral ulcers and oral cancer. Microvesicles, small membrane-bound particles secreted by cells, have long been present in the saliva of healthy individuals but have also been linked to malignant tumours. However, the precise role of MVs in diseases like oral cancer has remained unclear. 

The study, which involved 73 patients with non-healing oral ulcers and diagnosed oral cancer, as well as 62 healthy volunteers with oral ulcers, aimed to investigate the proportion of apoptotic MVs in saliva. Samples were analysed using advanced techniques such as dynamic light scattering, transmission electron microscopy, and flow cytometry. Results indicated that saliva from patients with non-healing oral ulcers and oral cancer showed a significantly higher number of apoptotic MVs compared to the healthy group (p < 0.001). These vesicles were typically round or slightly elongated, with diameters ranging from 100 to 1,000 nm. 

The findings also revealed a strong correlation between the number of salivary apoptotic MVs and the severity of the oral ulcers in patients (p<0.001). Notably, none of the oral cancer patients had a history of smoking or alcohol consumption, ruling out these factors as contributing causes. 

This study suggests that salivary apoptotic MVs could be a promising diagnostic tool for identifying oral cancer and assessing the severity of related oral ulcers. 

Helena Bradbury, EMJ 

Reference 

Zhao J et al. Salivary apoptotic microvesicles as biomarkers for prognostic non-healing oral ulcers and oral cancer: a cross-sectional study. Scientific Reports. 2025;15:9297.  

Mapping The Shift From Healthy Stem Cells To Oral Cancer

Last year, more than 70,000 people in the United States were diagnosed with head and neck cancers, and its rates have steadily risen worldwide. These cancers arise from squamous epithelial cells lining these areas, with tobacco and alcohol as the primary culprits. However, for about 30 percent of patients, human papillomavirus (HPV) is to blame.

While researchers have studied HPV-positive cancer cells in advanced stages, the mechanisms driving the earliest events in the transformation of healthy cells into malignant ones remain unclear. This motivated molecular biologist Jorge Silvio Gutkind at the University of California, San Diego to capture the elusive but crucial factors that cause healthy stem cells to infiltrate tissue as they transition to cancer cells.

While certain HPV proteins are known to promote cancer, they don't act alone. Gutkind and his colleagues previously found that alterations in the Hippo pathway, which regulates tissue growth and organ size, also contributed to head and neck squamous cell carcinomas.1

Jorge Silvio Gutkind studies growth-promoting signal transduction pathways in cancer to better understand cancer progression.

Kyles Dykes/University of California San Diego Health Sciences

A disruption in the Hippo pathway resulted in the activation of yes-associated protein (YAP), a transcription factor involved in stem cell maintenance and growth. Because of this, the researchers were interested in YAP's role as a cancer driver. Their new study, published in Nature Communications, revealed that unrestrained YAP expression, in combination with HPV oncoproteins, triggered a rapid cascade of genetic and cellular changes that reprogrammed normal stem cells into cancerous ones.2 These findings illuminate the earliest steps of cancer initiation and highlight potential targets for detecting and preventing HPV-positive cancers.

Gutkind and his team focused on HPV-positive oral cancer, which involves the loss of function of two key tumor suppressor genes, tumor protein 53 and cyclin-dependent kinase inhibitor 2A. The researchers can model this either by editing the genes themselves or inhibiting their expression with HPV E6 and E7 oncoproteins. These two oncoproteins help drive HPV-associated cancers by activating the Hippo pathway to promote cell proliferation. Although YAP is a known effector downstream of Hippo, Gutkind aimed to characterize its direct effects alongside E6-E7 expression on cancer initiation.

The researchers used a genetic mouse model that conditionally expressed either constitutively active YAP (Y), E6-E7 (E), or a combination of YAP and E6-E7 transgenes (EY). Feeding the mice doxycycline-infused chow activated these genes, allowing the researchers to observe their combined effects on tumor development.

Gutkind was surprised by how quickly the tumors formed. "Within no more than two weeks, we [saw] the cancer," he remarked. EY mice developed thickened tongues with deeply invasive macroscopic lesions, while those with only E or Y genes had fewer and smaller lesions. Control mice lacking these genetic alterations developed no lesions.

"Their comparison of the activation of E6 and E7 to the hyperactivation of YAP is an interesting one that I haven't seen done directly in that way," said Elizabeth White, a molecular biologist at Tufts University who was not involved in the study.

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To pinpoint the genes linked to tumor initiation, the team performed bulk RNA sequencing (RNAseq) on mouse tongues 15 days after gene induction. E mice expressed 60 unique genes; Y mice exhibited 167 differentially expressed genes compared to control mice. However, EY mice expressed more than 2,000 unique genes, which were related to cell proliferation, epithelial cell development and identity, and inflammatory responses.

Compared to normal cells, EY cells also exhibited increased epigenetic reprogramming, resulting in increased chromatin accessibility of numerous genes, which promoted proliferation, invasion, and inflammation. Notably, the team saw an association with the mammalian target of rapamycin (mTOR) signaling pathway, commonly activated in cancer.

Then, Gutkind aimed to track the progression of oral stem cell fate over time, focusing on cellular diversity to better understand the subtle changes that drive the transition from healthy stem cells to a cancerous state. To examine this cellular heterogeneity in more detail, the researchers used single-cell RNAseq. "At the single-cell level, we can [see] every individual cell and see what decisions they make," Gutkind remarked. The team analyzed live cells from the control mice and all three types of transgenic mice and identified eight distinct cell clusters: five corresponding to normal renewing epithelial stem cells and three associated with the transgene-expressing groups (E, Y, and EY). Among these, EY cells formed a cluster resembling tumor-initiating (TI) cells. These formerly normal stem cells began proliferating and acquiring invasive properties—a hallmark of cancer.

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Next, the researchers used transcriptomics and microscopy to explore the processes by which these cells initiated tissue invasion. To their surprise, they found that TI cells recruited myeloid immune cells to the tumor microenvironment.

The team assessed TI gene expression and found increased markers specific to recruiting granulocytes. These granulocyes can produce collagenase, an enzyme that breaks down collagen in tissue. Tissue imaging confirmed this, showing fewer collagen fibrils in EY tissue compared to normal tissue. Flow cytometry provided further evidence showing an increase in infiltrating immune cells. The researchers believe these immune cells and TI cells work together to degrade collagen, clearing a path for tumor invasion. Gutkind also remarked that co-opting immune cells may be an early strategy for cancer cells to evade immune detection.

"We can also identify, by also focusing on the immune cells and other cells, all of the interplay [and communication] between the cells to initiate the cancer," added Gutkind. "That was very exciting."

Overall, the researchers demonstrated that YAP activation affected cell programs in oral epithelial progenitor cells, which drove cells towards more aberrant proliferation and led to the recruitment of myeloid cells to aid tissue infiltration.

For Gutkind, the next step is to apply the same technology to understand the progression in HPV-negative oral cancers and develop YAP inhibitors. White agreed and noted that, "There's great evidence that [YAP is] a very powerful cancer driver, so there's a great opportunity for therapeutic intervention in that sense."

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