Herpes simplex virus infections

DESCRIPTION:   

Oral infection with herpes simplex virus occurs in three clinical forms. The most common type consists of recurrent small blisters on the lips commonly referred to as fever blisters or secondary herpes labialis. The second type is a generalized oral infection called primary herpetic stomatitis. The third and least common form of oral herpes infection consist of small ulcers usually localized on palatal mucosa.

Herpes labialis is illustration in Figs. 1 and 2. This lesion is well known and unlikely to be  a  diagnostic  problem.  It  tends  to  be  a  recurrent  disease  in  teenagers  and  adults. Elapsed time between recurrences varies from person to person. Recurrences are thought to be triggered by exposure to sunlight, febrile diseases, physical and psychogenic trauma, and other irritants.

Generalized involvement of the oral mucous membrane is called primary herpetic stomatitis and represents the initial exposure to the virus. This is a one time infection, but the patient remains susceptible to recurrent or secondary oral herpes infections (Figs. 3 and 4).

  It  is  more  commonly  seen  in  children,  but  teenagers  and  adults  are  also  affected.

Patients initially have gingivitis with swollen and red gingiva, then small blisters may appear on other mucosal surfaces. The blisters break quickly and are seldom seen by the dentist or physician. After they break, the lesions appear as small ulcers that resemble small aphthous lesions. The primary, generalized infection is accompanied by fever, cervical lymphadenitis, and inability to eat or drink without considerable pain. Patients who suffer recurrent intraoral herpes are few. Recurrent intraoral herpes infections  tend  to  occur  as  vesicles  followed  by  small  ulcers,  mainly  on  the  hard  palate mucosa (Fig. 5) and often follow trauma to the area, such as palatal injections or periodontal therapy.

ETIOLOGY:  

Herpesvirus hominis (herpes simplex virus). Most oral lesions are caused by Type I virus but approximately 10% are thought to be caused by Type II.

TREATMENT:   

Antiviral drugs such as Acyclovir, Famciclovir, Penciclovir, Valacyclovir and over-the-counter Abreva have all shown that they can decrease the time of disease as well as help with pain management. To be beneficial, they must be started at the first sign of disease. Most studies indicate that the drugs decrease the duration of disease by about one day. Acyclovir, Penciclovir and Abreva are available in a topical ointment.

PROGNOSIS:     

Primary  infection  usually  resolves  in  10-14  days.  Once  the  virus  has entered the body, it travels through nerve trunks to the nearest ganglion where it may lie dormant  for  the  remainder  of  the  patient's  life.  Future  recurrences  are  thought  to  be brought about by the "reawakening" of the virus which retraces its steps to cause new lesions in the same general area as the original point of entry. Thus, each recurrence is not a new and different infection from the outside but a recrudescence of the original infection. The ability of the virus to remain latent in deep ganglia makes total eradication almost impossible and will likely frustrate attempts at prevention for the foreseeable future.

Patients with widespread herpetic stomatitis should drink liquids to prevent dehydration. A broad-spectrum antibiotic is commonly given to control secondary bacterial infection, but does not shorten the viral infection. Antiviral drugs may shorten the duration of the disease if they are started early.

Clinicians should be aware that the herpesvirus may cause disseminated infection including encephalitis in which case the prognosis is extremely grave.

DIFFERENTIAL DIAGNOSIS:   

Primary herpetic stomatitis may resemble oral lesions of erythema multiforme, but herpes can be diagnosed by exfoliative cytology.A characteristic multinucleated cell appears in the smear of herpes infections. Culture of the virus is possible if a viral laboratory is available. Lesions of herpangina and hand, foot and mouth disease, both caused by Coxsackievirus, may clinically resemble oral herpes virus infections. Recurrent intraoral herpes may be confused with herpes zoster. Aphthous can be differentiated since it usually does not occur over bone, does not form vesicles and is not accompanied by fever or gingivitis.

Varix (plural: varices)

DESCRIPTION:  Varices appear as red, blue, or deep purple broad-based elevations in  oral mucosa. The size is usually less than 5 mm. The buccal mucosa is a common place to find them, however, they are also found in lip mucosa and ventral and lateral mucosa of the tongue and floor of the mouth. On ventral tongue they are apt to be multiple and the term "caviar tongue" has been commonly used to describe them. They are seen more commonly in the elderly.

ETIOLOGY:  A varix is a distended vein that elevates the overlying mucosa.  The reason  for  venous  distention  is unclear  but  may  be  related  to  weakening  of  the  vessel wall secondary to aging.

TREATMENT:  None usually required. They often thrombose but this is of little clinical consequence.

PROGNOSIS:  Good

DIFFERENTIAL DIAGNOSIS:  Mucocele, hemangioma and angina bullosa hemorragica. 

Snuff lesion (smokeless tobacco lesion)

DESCRIPTION:  The lesion develops on the mucosa where smokeless tobacco is held.  The usual appearance is white, wrinkled or corrugated mucosa. Gingival recession is a  common manifestation with cervical erosion of teeth a less frequent finding. Symptoms are uncommon.

ETIOLOGY:    Prolonged  use  of  smokeless  tobacco  produces such as chewing tobacco or snuff.

TREATMENT:  Biopsy should be done to rule out dysplasia, otherwise no treatment is necessary.

PROGNOSIS:  Verrucous and squamous carcinomas arise in smokeless tobacco lesions more than chance alone can explain. One article noted almost a 50-fold increased risk of cancers of the gingival  and  buccal  mucosa in females who were chronic users. The duration necessary   to   induce   dysplastic   or   malignant   change   is unknown but appears to be at least 20 years.

DIFFERENTIAL  DIAGNOSIS:   The clinical appearance of the  lesion  plus  a  history  of  using  smokeless  tobacco establishes the diagnosis.

Acquired immune deficiency syndrome (AIDS) and its oral manifestations

Description:  Acquired immune deficiency syndrome is characterized by relentless destruction of CD4 T lymphocytes, key cells of the immune system. The eventual collapse of both the cellular and humoral arms of immunity leaves the host vulnerable to  a wide variety of pathogenic organisms including bacteria, viruses, fungi and protozoa.  It is important for health care workers to recognize that it is difficult to transmit the AIDS virus in the health care setting, from patient to worker or the reverse. However, opportunistic infectious diseases that AIDS patients are apt to have including tuberculosis, herpes-virus infections, hepatitis B and hepatitis C are readily transmissible.

Etiology:  The causes of AIDS is an RNA  retrovirus of the lentivirus group. It is designated the human immunodeficiency virus (HIV) and there are several variants:  HIV- 1 is the most common cases of AIDS. The virus attaches to the surface of cells that bear the  CD4  receptor  including  helper  T  lymphocytes,  B  lymphocytes  and  macrophages.

Although they lack a CD4 receptor, microglia, skin fibroblasts, and bowel epithelium become  infected.  The  virus  destroys  the  infected  cells.  With  gradual  depletion  of  the cells of immunity, especially T-helper lymphocytes and macrophages, the host becomes increasingly vulnerable to pathogenic organisms.

Oral Manifestations:

Candidiasis  -  Colonization  and  infection  of  the  oral  mucosa  by  Candida  species  is among the earliest and most common findings in HIV-infected patients. In one study, 88% had oral candidiasis. Lesions range from white to red or red/white combinations.

Fig. 1 illustrates the typical appearance of candidiasis. The lesions may be asymptomatic or there may be mild discomfort. For stubborn infection, fluconazole is recommended.  

Kaposi's  sarcoma  -  AIDS  patients  are  vulnerable  to  a  variety  of  oral  malignancies including Kaposi's sarcoma, malignant lymphoma and squamous carcinoma. Kaposi's sarcoma is the most common. In one study, 20% of AIDS patients had Kaposi's sarcoma and of these, the tumor was in the oral cavity in 1 of every 5 patients; the palate is the most common site. In the early stage, the tumor appears as a red to purple bruise (Fig. 2). The tumor grows and eventually appears as a hemorrhagic mass (Fig. 3). The cell of origin  is  endothelium;  thus  Kaposi's  sarcoma  is  a  variety  of  angiosarcoma.  They  are locally invasive, cause pain and bleeding and interfere with normal function. Low-dose radiation  therapy  and  intralesional  or  systemic  chemotherapy  are  the  treatments  of choice. Herpes virus type VIII is thought to play a role in the pathogenesis of this tumor.

Hairy leukoplakia  -  This  variety  of  leukoplakia  was  first  recognized  in  HIV-infected patients but has been encountered in other immune deficiency states such as organ transplant patients who are intentionally immune suppressed. The lateral tongue is the most common location (Fig. 4). Lesions are of rough texture, adherent and asymptomatic. The diagnosis of hairy leukoplakia can be suspected on routine biopsy specimens, but confirmation requires demonstration of the presence of the causative virus, the Epstein-Barr herpesvirus. This is ordinarily achieved by DNA in situ hybridization. A word of caution: hairy leukoplakia may be confused with candidiasis. A patient who presents with a white lesion should be treated with antifungal therapy first. If it fails to heal, it most likely is hairy leukoplakia.

Gingival and periodontal lesions  - HIV-infected patients are vulnerable to necrotizing gingivitis and periodontitis (Fig. 5). The organisms recovered from these lesions are the same as those in non-HIV-positive patients. Lesions are treated by dental prophylaxis, debridement, and metronidazole. Good oral hygiene and daily rinses with chlorhexidine are beneficial.

Others - HIV patients also develop major aphthous-like lesions that respond to tetracycline and topical steroid therapy.

Thalidomide has been used successfully in their management. The human papillomavirus has also been found in both condylomas and focal epithelial hyperplasia. Cytomegalovirus infections and several fungal infections such as histoplasmosis  and  coccidiodomycosis  are  also  common.  Lastly,  xerostomia  secondary  to  salivary  gland  destructions  has  been reported. 

Leukoedema

Leukoedema was first described in 1953 by Sandstead and Lowe. 

DESCRIPTION:   Leukoedema id characterized by a widespread whitening of the inner lining of the cheek oe other mouth tissues, due to an increase in the amount of fluid being retained by the skin’s cells. Leukoedema is persistant, and is most common in indivuals with dark skin. The cause of this condition is unknown.

Leukoedema is much like another abnormal condition, leukoplakia, in that both give the inner mouth tissues a white appearance. A simple test t overify the condition is to streatch the skin over the fingers; is the normal pink colour returns, it is leukoema. It is important that we distinguish leukoedema from leukoplakia, as leukoplakia can be pre-cancerous condition and should be biopsied for accurate diagnosis.

Leukoedema appears as a filmy, opaque, and white to slate gray discoloration of mucosa, chiefly buccal mucosa. Redundancy of the mucosa may impart a folded or wrinkled appearance to the relaxed mucous membrane. It partially disappears when the mucosa is stretched. It is stated to be seen in 90% of Blacks and 10-90% in Whites. This variation may be due to the difficulty in observation of leukoedema in  non-pigmented mucosa. Leukoedema is accentuated in smokers.

ETIOLOGY:   Leukoedema  is  a  variation  of  normal  that  should   not   be   confused   with   something   ominous.  Intracellular edema of the superficial epithelial cells coupled with retention of superficial parakeratin is thought to  account for the white appearance. Microscopic examination  reveals  superficial  squamous  cells  have  a  clear, seemingly  empty  cytoplasm  but  it  has  not  been  shown that there is an increase in intracellular water. Thus, the  term edema is questionable.

TREATMENT:  None required.

PROGNOSIS:  Good

DIFFERENTIAL DIAGNOSIS:  White sponge nevus, hereditary benign intraepithelial dyskeratosis, and dyskeratosis  congenital. All are extremely rare. 

Leukoedema