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Oral Ulcer
An
Oral Ulcer (from Latin ulcus) is the name for the appearance of an open sore inside the mouth caused by a break in the mucous membrane or
the epithelium on the lips or surrounding the mouth. The types of oral ulcers are diverse, with a multitude of associated causes including: physical
or chemical trauma, infection from microorganisms or viruses, medical conditions or medications, cancerous and sometimes nonspecific processes. Once
formed, the ulcer may be maintained by inflammation and/or secondary infection. Two common oral ulcer types are aphthous ulcers (canker sores) and
cold sores. Cold sores are caused by the herpes simplex virus.
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Causes
There are many processes which can lead to ulceration of the oral tissues. In some cases they are caused by an overreaction by the body's own immune
system. Factors that appear to provoke them include stress, fatigue, illness, injury from accidental biting, hormonal changes, menstruation, sudden
weight loss, food allergies and deficiencies in vitamin B12, iron and folic acid. Oral ulcers are also a common result of ceased cigarette smoking,
affecting about two out of five quitters. Some drugs, such as nicorandil, have also been linked with oral ulcers. Some recreational drugs cause
mouth ulcers.
Trauma
Minor Physical Injuries
Trauma to the mouth is a common cause of oral ulcers. A sharp edge of a tooth, accidental biting (this can be particularly common with sharp canine
teeth), sharp or abrasive food (particularly if left overnight), poorly fitting dentures, dental braces or trauma from a tooth brush may injure the
mucosal lining of the mouth resulting in an ulcer. These ulcers usually heal at a moderate speed if the source of the injury is removed (for example,
if poorly fitting dentures are removed or replaced).
Sugar Injuries
Eating large amounts of sugar can also lead to oral ulcers. These are not a general worry because these subside within a day or two unless large
volumes of sugar continue to be present in a person's diet.
Chemical Injuries
Chemicals such as aspirin or alcohol that are held or that come in contact with the oral mucosa may cause tissues to become necrotic and slough off
creating an ulcerated surface. Sodium lauryl sulfate (SLS), one of the main ingredients in most toothpastes, has been implicated in increased incidence
of oral ulcers.
Infection
Viral, fungal and bacterial processes can lead to oral ulceration.One way to cause oral ulceration by this is to touch your chapped lips without
washing your hands first.
Viral
The most common is Herpes simplex virus which causes recurrent herpetiform ulcerations preceded by usually painful multiple vesicles which burst. Herpes
Zoster (shingles), Varicella Zoster (chicken pox), Coxsackie A virus and its associated subtype presentations, are some of the other viral processes
that can lead to oral ulceration. HIV creates immunodeficiencies which allow opportunistic infections or neoplasms to proliferate.
Bacterial
Bacterial processes leading to ulceration can be caused by Mycobacterium tuberculosis (tuberculosis) and Treponema pallidum (syphilis).
Opportunistic activity by combinations of otherwise normal bacterial fauna, such as aerobic streptococci, Neisseria, Actinomyces, spirochetes, and
Bacteroides species can prolong the ulcerative process.
Fungal
Coccidioides immitis (valley fever), Cryptococcus neoformans (cryptococcosis), Blastomyces dermatitidis ("North American Blastomycosis") are some of
the fungal processes causing oral ulceration.
Protozoans
Entamoeba histolytica, a parasitic protozoan is sometimes known to cause mouth ulcers through formation of cysts.
Immune System
Many researchers view the causes of aphthous ulcers as a common end product of many different disease processes, each of which is mediated by the immune
system.
Aphthous ulcers are thought to form when the body becomes aware of and attacks chemicals which it does not recognize. The presence of the unrecognized
molecules garners a reaction by the lymphocytes, which trigger a reaction that causes the damage of an oral ulcer.
Immunodeficiency
Repeat episodes of mouth ulcers can be indicative of an immunodeficiency, signaling low levels of immunoglobulin in the oral mucous membranes.
Chemotherapy, HIV, and mononucleosis are all causes of immunodeficiency with which oral ulcers become a common manifestation.
Autoimmunity
Autoimmunity is also a cause of oral ulceration. Mucous membrane pemphigoid, an autoimmune reaction to the epithelial basement membrane, causes
desquamation/ulceration of the oral mucosa.
Allergy
Contact with allergens can lead to ulcerations of the mucosa.
Dietary
Vitamin C deficiencies may lead to scurvy which impairs wound healing, which can contribute to ulcer formation. Similarly deficiencies in vitamin
B12, iron, zinc and folic acid have been linked to oral ulceration.
A common cause of ulcers is Celiac disease, in which case consumption of wheat, rye, or barley can result in chronic oral ulcers. If gluten sensitivity
is the cause, prevention means following a gluten-free diet by avoiding most breads, pastas, cakes, pies, cookies, scones, biscuits, beers etc. and
substituting gluten-free varieties where available. Artificial sugars, such as those found in diet cola and sugarless chewing gum, have been reported
as causes of oral ulcers as well.
Cancer
Oral cancers can lead to ulceration as the center of the lesion loses blood supply and necroses. Squamous cell carcinoma is just one of these.
Medical Conditions Associated with Mouth Ulcers
The following medical conditions are associated with mouth ulcers:
- Behçet's disease
- Bullous pemphigoid
- Celiac disease (gluten sensitivity)
- Crohn's disease
- Gingivostomatitis
- Leukoplakia
- oral lichen planus
- Lupus erythematosus
- Neutropenia
- Oral thrush
- Ulcerative colitis
Prevention
The majority of the types of ulceration require treatment of the underlying cause of the oral ulceration for successful prevention;
controlling imbalances in vitamins and minerals related to ulceration, managing or restricting the disease processes has shown to reduce the ulcerative
process. For trauma related cases, avoiding the offending source will prevent ulceration, but since such trauma is usually accidental, this type of
prevention is not usually practical.
Individuals who have a high incidence of opportunistic bacterial infections subsequent to an accidental oral injury (biting etc.) can prevent the injury
from becoming infected by directly bathing the wound with an anti-bacterial mouthwash for one minute every 12 hours for 2 days; it is important to use
a small vessel to contain the solution as most antibacterial mouth washes that remain in the mouth for a full minute will have detrimental effects such
as a prolonged impairment to the sense of taste and the potential loss of otherwise desirable flora. Quantities around 1ml are more than sufficient.
Ideally, the first treatment should occur within 3 hours.
Treatment
Treatments based on antibiotics and steroids are reserved for severe cases, and should be used only under medical supervision.
Some doctors may also prescribe a local anaesthetic, such as lidocaine or benzocaine, for cases of multiple or severe oral ulcers.
Some people benefit from using an over-the-counter topical gel, like Bonjela, which may contain substances such as choline salicylate to help reduce
the pain and inflammation associated with oral ulcers.
Also, putting baking soda directly on the sore and taking l-Lysine has been shown to help with healing and pain.
Holding milk in the mouth over the sore can have a temporary soothing effect upon the sore.
Brushing the teeth and rinsing the mouth with Euthymol toothpaste provides relief for a period of a few hours.
Hydrogen peroxide applied locally reduces infection and often improves healing (recommended by Mayo Clinic for cancer patients who's treatment increase
the occurance of cold sores).
Licorice extract has been used and is now commercially available as "CankerMelts."
In Australia, Vegemite is a common remedy used, directly applied to the ulcer as well as being eaten regularly.
(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Oral_ulcer)
Two Case Reports of Oral Ulcers with Lamotrigine Several Weeks After Oxcarbazepine Withdrawal
Authors: O'Neill A, de Leon J.
University of Kentucky, Mental Health Research Center at Eastern State Hospital and the Department of Psychiatry, University of Kentucky, Lexington, KY 40508, USA.
OBJECTIVE: To report two cases of mouth ulcers in lamotrigine patients after oxcarbazepine withdrawal. PATIENTS AND METHODS: The first patient was a 35-year-old woman with bipolar disorder II (BD II) started on lamotrigine and tapered off oxcarbazepine while an inpatient. The second patient was a 36-year-old man with BD II. He was discharged on lamotrigine and oxcarbazepine with the recommendation of a slow withdrawal of oxcarbazepine. RESULTS: Many weeks after hospital discharge and after a stable lamotrigine dose had been established, both patients developed painful mouth ulcers that were diagnosed during outpatient visits. The first patient developed ulcers 39 days after oxcarbazepine was stopped and the ulcers resolved 4 days after lamotrigine discontinuation. The second patient was taking 1200 mg/day of oxcarbazepine and after leaving hospital decreased this to 600 mg/day. Twenty-two days after the oxcarbazepine decrease, he developed oral ulcers that resolved with oxcarbazepine and lamotrigine discontinuation. CONCLUSIONS: Lamotrigine is mainly metabolized by glucuronidation, specifically by the uridine 5'-diphosphate glucuronosyltransferases 1A4 (UGT1A4). Carbamazepine is a UGT1A4 inducer. These two cases suggest that oxcarbazepine may also induce lamotrigine metabolism. The discontinuation or dosage decrease of carbamazepine or oxcarbazepine may be associated with a slow increase of lamotrigine levels over several weeks and thus increase risk of lamotrigine toxicity that may manifest as oral ulcers. Hospital psychiatrists need to be aware that discontinuation of inducers may take several weeks to manifest as side effects.
Journal: Bipolar Disord. 2007 May;9(3):310-3
Adapted from PubMed; click here to access full journal article.
Treating Patients with Herpes Simplex Virus Infections: Dental and Dental Hygiene Students' Knowledge, Attitudes, and Professional Behavior
Authors: Kanjirath PP, Peters MC, Inglehart MR.
Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, MI 48109-1078, USA.
Dental and dental hygiene students frequently interact with patients with herpes simplex virus (HSV) infections, often simply referred to as cold sores. The objectives of this study were to assess dental and dental hygiene students' knowledge, attitudes, and professional behavior concerning the treatment of patients with HSV infections and to investigate the relationships among knowledge, attitudes, and professional behavior. Questionnaire data were collected from 337 dental and seventy-three dental hygiene students at regularly scheduled classes. Dental and dental hygiene students did not differ in their overall knowledge concerning HSV infections. Dental hygiene students were more apprehensive about treating patients with these infections, but used more appropriate professional behavior compared to dental students. Dental students' knowledge and appropriateness of professional behavior increased over the course of their education. Overall, it was found that an increase in student knowledge was associated with increased apprehension related to treating these patients. However, the more apprehensive they were, the more they engaged in appropriate professional behavior. Educating future health care providers about the treatment of patients with infectious and communicable diseases can potentially increase the students' apprehension/negative attitudes concerning providing care, while at the same time increasing appropriate professional behavior during their education. Addressing students' apprehensions might be a crucial moderator that will determine whether they will provide the best possible care for these patients in their future professional lives.
Journal: J Dent Educ. 2007 Sep;71(9):1133-44.
Adapted from PubMed; click here to access full journal article.
Treatment of Herpes Simplex Virus Infection: Rationale for Occlusion
Authors: Patel AR, Romanelli P, Roberts B, Kirsner RS.
Department of Dermatology & Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.
Orofacial herpes is a widespread benign malady that is also commonly known as herpes labialis or cold sores. Herpes of this type is generally caused by herpes simplex virus type 1 (HSV-1) and, to a lesser degree, herpes simplex virus type 2 (HSV-2), both of which are DNA viruses. The clinical presentation of herpetic lesions is normally located on mucocutaneous areas of the face and may eventually erode and ulcerate, leaving wounds that are known to be difficult to successfully treat. Focus of treatment has been related to treatment of the viral infection, and limited attention has focused on the resultant wounds. Clinical observation and recent histologic evaluation has demonstrated these wounds to extend through a disrupted cutaneous basement membrane into the dermis, suggesting that HSV is capable of causing partial-thickness wounds. This observation suggests a role for occlusion in the treatment of herpetic-induced partial-thickness wounds because occlusion is well recognized as the treatment of choice for other types of partial-thickness wounds.
Journal: Adv Skin Wound Care. 2007 Jul;20(7):408-12.
Adapted from PubMed; click here to access full journal article.
Replication-Defective Genomic HSV Gene Therapy Vectors: Design, Production and CNS Applications
Authors: Burton EA, Fink DJ, Glorioso JC.
University of Pittsburgh, Department of Neurology, E1246 Bioscience Tower, 200 Lothrop Street, Pittsburgh, PA 15261, USA.
Herpes simplex virus (HSV) is a neurotropic double-stranded DNA virus. In an unmodified form it is a human pathogen, causing recurrent cold sores, keratitis and, rarely, severe encephalitis. Elimination of pathogenic functions results in the generation of a valuable gene transfer vector for neurological applications. Replication-defective genomic HSV-based vectors are highly infectious, and efficiently transduce and express transgenes in a broad range of both dividing and non-dividing cells. Clinically relevant yields of clinical grade vector can be produced by growth in cell lines that complement the viral functions that are deleted in the vectors to eliminate pathogenicity. The viral genome is over 150 kb in length and many of the viral genes may be deleted without compromising viral growth in vitro, and therefore large or multiple transgenes can be accommodated within the vectors. The wild-type virus adopts a lifelong latent state in neurons of sensory ganglia. This property can be exploited in the generation of vectors to allow long-term transgene expression in neurons. In this review, we summarize recent progress in the areas of vector development and vector production, and in developing gene transfer therapeutics to treat malignant glioma.
Journal: Curr Opin Mol Ther. 2005 Aug;7(4):326-36.
Adapted from PubMed; click here to access full journal article.
The Efficacy of Valacyclovir in Preventing Recurrent Herpes Simplex Virus Infections Associated with Dental Procedures
Authors: Miller CS, Cunningham LL, Lindroth JE, Avdiushko SA.
Department of Oral Health Practice, University of Kentucky College of Dentistry and College of Medicine, Lexington 40536-0297, USA. cmiller@uky.edu
BACKGROUND: Oral herpes simplex virus, or HSV, infections recur after trauma and stress. The prevalence of these infections after dental procedures is not known. Also, it is unclear whether antiviral agents are effective in preventing dental procedure-induced HSV recurrences. This study determined the efficacy and safety of oral valacyclovir in suppressing dentally related cold sore outbreak and HSV shedding. METHODS: The authors enrolled 125 otherwise healthy HSV-seropositive adults who reported having recurrent herpes labialis (more than one episode per year and at least one episode in the previous year) in a randomized, double-blind, placebo-controlled study and gave them valacyclovir prophylactically (2 grams taken twice on the day of dental treatment and 1 g taken twice the next day) or a matching placebo. To detect the presence of the virus, the authors used clinical examinations, viral cultures and real-time polymerase chain reaction analysis of saliva. RESULTS: During the one-week observation period after treatment, there were more clinical lesions (20.6 percent versus 11.3 percent), more HSV-1-positive culture specimens (7.9 percent versus 1.6 percent) and more HSV-1-positive saliva specimens (7.9 percent versus 4.0 percent) in placebo than in valacyclovir-treated patients, respectively. The percentage of patients who developed recurrences and shed HSV-1 in saliva 72 hours after dental procedures was significantly smaller in the valacyclovir group than in the placebo group (11.3 percent versus 27 percent; P = .026). The mean time to pain cessation was significantly less in the valacyclovir group (3.2 days) than in the placebo group (6.2 days) (P = .006). CONCLUSION: HSV recrudescence after routine dental treatment is suppressed by valacyclovir prophylaxis. CLINICAL IMPLICATIONS: HSV recrudescence is common after routine dental treatment. Clinicians should consider antiviral therapy for patients at risk of experiencing a recurrence, as well as to minimize transmission of the disease.
Journal: J Am Dent Assoc. 2004 Sep;135(9):1311-8.
Adapted from PubMed; click here to access full journal article.
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