Cold Sores & Fever Blisters

Preventing the Spread of Herpes Labialis
(Cold Sores/Fever Blisters)

Eric G. Jackson, DDS, MAGD, FICOI, FICD, FADI

In this newsletter article I thought I’d continue the theme of “dental topics that aren’t typically enjoyable to discuss” and focus on Herpes Labialis (aka Cold Sores/Fever Blisters), an extremely common malady that affects nearly 40% of the United States population.[i]  The colloquial term for this condition, “cold sore” comes from the fact that herpes labialis is often triggered by a fever or a bout with the Common Cold or Upper Respiratory Infection.  Although in most people the disease is self-limiting, it is critical to note that the “common cold sore” is not always a trivial disease.  People can transfer the virus from their cold sores to other areas of the body, such as the eye, skin, or fingers.  This is called autoinoculation.  Not only can the virus be spread to other areas of the host, but it can easily be spread to other people.  This is called inoculation.  The virus can quite easily spread to other areas of the host’s body as well as spread to other people.  Preventing the spread of the herpes virus by either autoinoculation or inoculation is incredibly important to overall public health, and will be the primary notion I would like to impart via this article today. 

A Herpes labialis infection occurs when the herpes simplex virus comes into contact with oral mucosal tissue or abraded skin of the mouth.  An outbreak typically causes small blisters or sores on or around the lips or mouth.  These sores typically heal within 2 weeks, but the herpes virus remains dormant in the nerves of the face.  Dormant virus particles can periodically reactivate following periods of mental or physical stress and create sores in the same areas of the original infection.  For most people, cold sore outbreaks typically occur 1-3x per year but some patients report breakouts as often as 12x per year.[ii]   Fortunately, frequency and severity of outbreaks generally decrease for most people over time.  Infection by the type 1 strain of herpes simplex virus (HSV-1) is most common; however, cases of oral infection by the HSV-2 strain are increasing.   Recent findings estimate that HSV-2 has been implicated as causing 10–15% of oral infections.[iii]  Recent studies have established that over 70% of new diagnoses of genital herpes in young people are caused by HSV-1.[iv]  This figure goes against the traditional notion that the HSV-2 traditionally thought to cause genital herpes acted separately than its oral counterpart HSV-1.  We now know that is not always the case and traditionally oral HSV-1 cold sores are causing genital herpes as well as HSV-2.[v]

A cold sore lesion is the result of the virus’s reactivating in the body.  Once HSV-1 has entered the body, it never leaves.  The virus moves from the mouth to remain latent in the central nervous system.  In approximately one-third of people, the virus can “wake up” or reactivate to cause disease.  When reactivation occurs, the virus travels down the nerves to the skin where it may cause blisters (cold sores) around the lips, in the mouth or, in about 10% of cases, on the nose, chin, or cheeks.  Cold sore outbreaks may be influenced by stress, menstruation, sunlight, sunburn, fever, dehydration, or local skin trauma. Surgical procedures such as dental or neural surgery, lip tattooing, or dermabrasion are also common triggers.

In addition to the oral and genital lesions, there are three other maladies caused by the spread of HSV-1 that bear mentioning.  The first, Herpetic Whitlow, is an extremely painful infection that affects the hand and involves one or more fingers.  60% of all Whitlow cases are caused by cold sores, since touching a cold sore can easily transfer the virus to the fingers and hand.  Identified as a specific danger to health care workers, more extreme cases result in disabling pain in the fingers and fingertips, making it a career-endangering infection for dentists and dental care workers.  Herpetic Whitlow can also occur when a child with cold sores or primary HSV-1 infection sucks his fingers.  The second serious malady, Encephalitis, is an acute inflammation of the brain, usually caused by viral infections including HSV-1. Although rare, HSV-1 encephalitis typically affects the young and the elderly.  It occurs most often in infants in their first year.  Advanced symptoms include seizures or convulsions, tremors, and hallucinations, and memory problems.  The third malady, Keratitis, is a viral infection of the eye caused by an infection in the cornea.  The infection can easily be transferred from a cold sore to the eye through touch.  Keratitis is considered the most common cause of non-impact cornea-derived blindness in developed nations, with 1.5 million new cases each year – 40,000 of them resulting in the loss of sight in one or both eyes.[vi]  Stopping the unnecessary spread of herpes labialis is an incredibly important issue, and the best way to accomplish this is by increasing awareness of the topic and early/effective treatment of cold sore lesions.

Before we go any further, I think it’s quite important to distinguish between two commonly confused ailments, Cold Sores and Canker Sores, as both occur near the same location, share many of the same triggers (stress, facial trauma, hormonal changes, etc) and can be quite painful.  Being able to distinguish between the two is essential to receiving proper treatment.  This fantastic inforgaphic is from the OraJel website and summarizes both maladies nicely:

Now that we’ve differentiated between the two, let’s refocus on herpes labialis/cold sores.  In order to properly understand viral spread and available treatments, we must briefly discuss the 8 stages of typical Cold Sore/HSV-1 lesions.  Without knowledge of these stages, we won’t be able to properly discuss the timing of common treatment modalities.

Cold Sore symptoms typically progress in a series of eight stages:

1.  Prodromal (~day 0–1):  Symptoms often precede a cold sore lesion and often begin with tingling, itching, and reddening of the skin around the infected site. This stage is quite variable in length and can last from a few days to a few hours preceding the physical manifestation of an infection.  It is the best time to start treatment.
2. Inflammation (~day 1):  The virus begins reproducing and infecting cells at the end of the nerve.  The healthy cells react to the invasion with swelling and redness displayed as symptoms of infection.
3. Pre-sore (~day 2–3):  This stage is defined by the appearance of tiny, hard, inflamed papules and vesicles that may itch and are painfully sensitive to touch.  In time, these fluid-filled blisters form a cluster on the lip (labial) tissue, the area between the lip and skin (vermilion border), and can occur on the nose, chin, and cheeks.
4. Open lesion (~day 4):  This is the most painful and contagious of the stages.   All the tiny vesicles break open and merge to create one big, open, weeping ulcer.   Fluids are slowly discharged from blood vessels and inflamed tissue. This watery discharge is teeming with active viral particles and is highly contagious.   Depending on the severity, one may develop a fever and swollen lymph glands under the jaw.
5. Crusting (~day 5–8):  A honey/golden crust starts to form from the syrupy ooze.  This appears as the healing process begins. The sore is still painful at this stage.  More painful however, is the constant cracking of the scab as one moves or stretches their lips, as in smiling or eating.   Virus-filled fluid will still ooze out of the sore through any cracks.
6. Healing (~day 9–14):  New skin begins to form underneath the scab as the virus begins to retreat into latency.  A series of scabs will form over the sore each one smaller than the last.  During this phase irritation, itching, and some pain are common.
7. Post-scab (~12–14 days):  A reddish area may linger at the site of viral infection as the destroyed cells are regenerated. Virus shedding can still occur during this stage.
8. Latent (~weeks to months incident-free):  The remission period.   After initial infection, the viruses move to sensory nerves where they reside as lifelong latent viruses.  Asymptomatic shedding of contagious virus particles can still occur during this stage.

Prevention & Treatment options

Good preventative methods are to practice good hygiene and steer clear of any visible lesions as they certainly pose the possibly of virus shedding/spreading.  As just mentioned, contagious viral particles can be shed at ANY stage of the lesion, but are most contagious during the “Open Lesion” stage.  Avoiding touching an active outbreak site, washing hands frequently while the outbreak is occurring, not sharing items that come in contact with the mouth, and not coming into contact with others (by avoiding kissing, oral sex, or contact sports) can reduce the likelihood of the infection being spread to others.[ix]  As mentioned, most lesions are self-limiting and will resolve on their own within 2 weeks.  The problem with “non-treatment” option is that it maximizes the lesion lifespan and therefore maximizes the pain and virus shedding/possible spreading.

There are numerous available treatments for cold sores including oral antiviral mediation, complementary medicine, laser therapy, and topical medication.  The final two are my preferred methods but that‘s not to discount the others.  Oral antivirals (Zovirax/Acylovir, Valtrex/Valacyclovir, Famvir/Famciclovir, etc.) are systemic prescription drugs that, in my opinion, are more effective at suppressing outbreaks in individuals who experience frequent outbreaks than addressing individual lesions as they appear.  Like all treatment modalities, they are most effective when applied in the prodromal phase (~0-1 days) from onset.  Not everyone has a filled, non-expired prescription ready to go at a moments notice and therefore they miss the effective prodromal window thereby reducing effectiveness of the medication.  For generations, complementary medical techniques have been utilized to combat cold sores with some of the most notable being Vitamin-C, Lysine, Lemon Balm, and Zinc Oxide topical cream.   Like the prescription antivirals, these complementary techniques are most effective when applied during the prodromal phase and express a significant reduction in effectiveness once the lesion surfaces/becomes visible.  Let’s discuss my two favorite treatment methods now.

Laser treatment of Cold Sores

In our office we often use our laser to treat cold sores in the prodromal phase.  Personally, it is my favorite method of treating the prodromal HSV-1 lesion.  There are numerous benefits to this method of treatment:

• Often completely prevents eruption of the lesion if treated during prodromal phase & if the lesion does erupt is remarkably less pronounced in both intensity and duration
• Symptomatic relief is immediate and often profound
• Completely non-invasive = there is no cutting of any kind with the laser
• Treatment typically takes only a few minutes, does not require anesthetic, and is painless
• It is high tech, yet affordable and sometimes covered by dental insurance

So how does the laser treatment work?  Essentially, the laser creates a source of both heat and tissue bio-stimulation which bolsters the nearby tissue/bodily defense mechanisms thereby making the body more efficient at suppressing the virus.  According to Dr. Phil Harrington, an employee of K-Laser USA, “When we look at the basic mechanism of how it works, we are enhancing the microcirculation.  We are getting more red blood cells flowing to the area.  But it’s not just the arterial blood supply to the area; we are enhancing the venous and the lymphatic return from the area.  We’re also increasing oxygenation of those tissues.  We are stimulating the hemoglobin molecule to dump off oxygen at the treatment site, so we are increasing the oxygenation of those tissues.”[x]  Laser treatment, like all herpes labialis treatment, does not completely eradicate the virus as it resides in localized nerve fibers for a lifetime.  It is however, a fantastic method of preventing an outbreak, and thereby preventing a lesion that can spread to other parts of a patient’s body or other people. 

Preventing the spread of the herpes virus via autoinoculation and inoculation of others is an incredibly important public health goal.  Through increased subject knowledge and early/effective treatment, I am hopeful that we can curb this pandemic condition and improve overall public health.  As always, if you have any additional questions or would like to speak further about this topic, please do not hesitate to contact me.

Sincerely,

Eric G. Jackson, DDS, MAGD, FICOI, FICD, FADI

Email: [email protected]

Twitter: @EjacksonDDS

 Snoeck R, De Clercq E. Treatment of herpes simplex virus infections. Infect Med 1999;16(4):249–65.

• http://en.wikipedia.org/wiki/Herpes_labialis
• http://en.wikipedia.org/wiki/Herpes_labialis
• Roberts C, Pfister J, Spear S. Increasing proportion of herpes simplex virus type-1 as a cause of genital herpes 3 infections in college students. Sex Transm Dis 2003; 30(10):797–800.
• http://www.thehelpernewsletter.org/index.php?option=com_content&view=article&id=121:genital-hsv-1-and-young-adults-the-changing-face-of-genital-herpes&catid=166:herpes-research&Itemid=228
• http://www.viroxyn.com/dentists/medical-benefits
• http://www.orajel.com/en/Resource-Center/Mouth-and-Canker-Sore-Pain-Relief/Canker-sore-vs-Cold-sore
• http://en.wikipedia.org/wiki/Herpes_labialis
• http://en.wikipedia.org/wiki/Herpes_labialis
• http://www.prweb.com/releases/2014/01/prweb11457237.htm
•  McCarthy, J, Browning W, Teerlink C, Veit G, Treatment of Herpes Labialis: Comparison of Two OTC Drugs and Untreated Controls, McCarthy, J, Browning W, Teerlink C, Veit G, Treatment of Herpes Labialis: Comparison of Two OTC Drugs and Untreated Controls, Journal of Esthetic and Restorative Dentistry, 2012, 24(2) p103-109.2012, 24(2) p103-109.