Oral pathology sheet # 3 - Amal abu 3awwad

by **Shadi Jarrar** 8/10/2011, 10:17 pm

Oral infections

Viral infections

Herpes Simplex Virus (HSV)

-The herpes virus is a DNA virus that causes ballooning degenerative changes in the cells it infects. It is characterized by latency in nerve tissues; after the primary infection the virus persists in the body as a latent infection. There are two types of HSV; 1 and 2. Type 2 is associated with infections in the genitalia, but it could infect the head and neck region.

- It is a common infection; more than 90% of adults have antibodies for the HSV. In most of the cases it is a subclinical infection so that individuals do not remember being infected.

- The primary infection is transmitted by spreading droplets or contact with the lesion (infected saliva contacting intact mucous membranes or abraded skin), following penetration the virus goes along the peripheral nerves until it reaches the trigeminal ganglia ( if the infection is in the head and neck region ) to become a latent infection. Reactivation may occur, as there are predisposing factors. When reactivation occurs the virus is transported back via the nerve’s axon to the skin or mucous membranes, where the infection manifests as vesicles. 1/3 of the individuals infected by the primary infection develop a recurrent infection.

The primary infection: Primary Herpetic Gingivostomatitis

-It mainly affects young children; younger than 5 years old.

-90% of the cases it is a subclinical infection so that individuals do not remember being infected. Or it could cause a mild pharyngitis, in this case it would be hard to diagnose as HSV infection.

-If it was clinically apparent, it presents as primary herpetic gingivostomatitis; following an incubation period of 5 days during which there are no symptoms apparent, the patient comes complaining of prodromal symptoms; which are:

1-Systemic symptoms such as malaise, fever, loss of appetite and drooling (saliva)

2-Oral symptoms; multiple ulcers on the dorsum of the tongue and the buccal mucosa (these ulcers were vesicles at the beginning of the prodromal phase which rapidly ulcerate, that is why we will see ulcers instead of the vesicles). These 2-3 mm vesicles develop on keratinized or non-keratinized mucosa so ulcers will appear anywhere in the oral cavity but mainly on the dorsum of the tongue. In addition to tender submandibular and cervical lymph nodes and difficulty in swallowing which leads to drooling.

3- Widespread gingivitis (not just on the marginal gingiva) that developed suddenly without any pervious plaque or bad oral hygiene. The gingiva is inflamed, red, and sore and there is bleeding. This is a very characteristic feature.

(Whenever we see these 3 symptoms it should be directly diagnosed as Primary Herpetic gingivostomatitis)

4-Another characteristic feature is the circumoral crusting lesions which develop due to coagulation of blood from the ruptured (ulcerated) vesicles. This feature also helps in diagnosis.

- The infection is transmitted between children in the school or in the house. Parents should keep the infected child and his/her personal things and toys away from their siblings. The child also could transmit the infection extra orally to the skin by their own infected saliva which will manifests as ulcers and inflammations.

-The infection lasts for 1-2 weeks, it is self-limited; will resolve without any management although the virus is susceptible to antiviral agents, but there is no need to use them unless the patient is immunocompromised.

-Viral shedding lasts for 23 days (from the incubation period and lasts after recovery) during which it is contagious. The infected child should not go to school.

-The primary infection in adults manifests as pharyngotonsillitis instead of gingivostomatitis; the patient complains of different symptoms which are related to the pharynx and tonsils such as ulcerations on the tonsils with few systemic symptoms.

Herpetic Whitlow: is an infection involving the nail-bed. It occurs if a child with a primary infection put his/her finger inside their mouth or it could occur to a dentist who treated an infected patient who has a primary, a secondary or an asymptomatic infection without wearing gloves. When the infected saliva contacts the abraded skin of the fingers the virus will penetrate through and reach the peripheral nerves leading to infection in the fingers. This infection manifests as redness, severe pain, ulcers, high fever, vesicles and lymphadenopathy in the axilla. This is very important for us as dentists because such an infection will stop us from work for at least 2 weeks, and this is a recurrent infection.

- Diagnosis:

1- Mainly clinically from the characteristic features.

2- Tissue culture: by scraping the ulcerated tissue and transfer it by a special media to the virology lab, and then we wait 24-48 hours for the signs of the viral infection to appear on the cells. This is usually not needed with the primary infection.

3- Serology: checking antibodies

4- Smears taken from a vesicle and stained to see under the microscope the giant cells (which are originally epithelial cells), they are large due to ballooning degeneration and could be multinucleated or with one nucleus, and surrounded with inflammatory cells.

-No need to take a biopsy from the oral cavity. If it was performed, we would see intraepithelial vesicles; the virus goes through the nerve into the epithelial cells where it replicates causing the death of the cells which will be replaced by a cavity that will be filled with fluids forming the vesicle. So they are superficial vesicles, which is why they quickly rupture and present as ulcers. The infected epithelial cells undergo ballooning degeneration (enlargement of the cells) since the virus is replicating inside them, this is followed by cell lysis and the releasing of new virus particles to infect adjacent epithelial cells.

The secondary infection: Recurrent Herpetic Infection

-1/3 of those who have had the primary infection later will develop recurrent herpetic infection. This is due to reactivation of the virus which remained latent in the sensory ganglion of the trigeminal nerve following the primary infection.

- It is characterized by local symptoms not systemic symptoms; because the patient has already developed immunity against it following the primary infection. It only affects certain areas that the nerve tips supply through which the virus returned from the ganglion, it goes directly to the epithelial cells without reaching the blood. These local symptoms could manifest as:

· Herpes labialis: during the prodromal phase the patient feels slight tingling or burning sensation for few hours. This is followed by the formation of vesicles on the vermillion border that will soon rupture, cluster and then heal without scarring. These vesicles formed at the vermillion border could be unilateral or bilateral. They could appear on the midline near the nose or affect the nostril.

-recurrence rate is variable; some people once a year others every month. It depends on predisposing factors such as stress, trauma ( e.g. dental trauma ), bright sun light, cold/flu, menstrual cycle, immune compromised patients ( those have high recurrence rate), some types of food ( chocolate, nuts ) or it could occur without any predisposing factors. It lasts for a week.

· Intra Oral herpes: it is hard to diagnose unlike the herpes labialis. It appears on the palate especially the greater palatine nerve area, it is unilateral. It is present as multiple vesicles and ulcers. When there are unilateral multiple small irregular ulcers localized to this area, it should be diagnosed as recurrent intra oral herpes. It could also appear on the buccal mucosa, the gingiva and on the tongue. It lasts for one week and does not need any management.

Varicella-Zoster Virus (VZV)

-It is a member of the herpes virus family; latent infection occurs following the primary infection.

The primary infection: Chicken Pox

- Mainly affects children

- Transmitted by inhalation of droplets (sneezing in a closed room without using a tissue).

-Incubation period 2 weeks, followed by non-specific systemic symptoms such as fever and malaise. Then the characteristic rash appears all over the body which starts as [b]macules that enlarge into papules which become vesicles, followed by pus formation which accumulates and become pustules that will rupture, ulcerate, cluster and heal. Ulcers form as an oral manifestation.[/b]

The secondary infection: Herpes Zoster or Shingles

- It is a reactivation of the latent infection in the trigeminal ganglion (if the infection is in the head and neck region)

- It is easily diagnosed because it has characteristic features, which are: development of vesicles unilaterally (same stages as the Chicken Pox; macules, papules, vesicles); do not cross the midline, intra-oral vesicles, ulcers, inflammations, also unilateral (ex. Half of the palate)

- The trigeminal nerve has 3 branches; the ophthalmic, maxillary and the mandibular. It could affect all three divisions or 2 divisions or only one division. Most commonly it affects the ophthalmic division that supplies the area around the eye.

- It is a rare infection compared to herpes labialis (which has a 30% occurrence rate), because it needs strong predisposing factors, such as terminal malignancies or immune deficiencies for it to occur. That is why when this infection occurs we suspect an immune disease or a malignancy so we do extra tests to be sure. Nevertheless, it could develop to healthy people.

-Its prodromal phase is more dangerous than the herpes labialis’ prodromal phase, because it is accompanied by severe pain in the region affected, this pain could be misdiagnosed as toothache; the patient may think he/she has pulpitis and undergo RCT. The pain also continues during the rash phase.

-Complications:

· Scarring

· Post-herpetic neuralgia: after healing, severe pain occurs because of fibrosis that occurred to the trigeminal ganglia

· Ramsay–Hunt Syndrome: presents as a rash at the external ear area and facial paralysis, which means the virus also affected the facial nerve, this will lead to hearing loss, dizziness and compromised taste sensation.

Herpangina:

- It is caused by Coxsackie virus: type A (1-23) & B (1-6), A (1-6, 8, 10, 12, 16, 22), B (1-5)

(it is not a member of the herpes virus family)

-transmitted by inhalation

-affects children as outbreaks; if there was an infected child all the class will get infected

-clinically:

-it is not a very dangerous infection, it resembles the herpes infections. It may cause angina.

-it is self-limiting; lasts for less than one week

-it manifests intra-orally as sore throat, dysphagia (difficulty in swallowing), mild fever and malaise. Small irregular multiple vesicles appear that ulcerate, they are distinguished from the Primary Herpetic Gingivostomatitis by their location; they appear on the posterior part of the oral cavity on the soft palate. No gingivitis.

-it also manifests extra-orally affecting the palms of the hands and soles of the feet as multiple ulcers

-If the patient has vesicles/ulcers intra orally and on the hands and feet it is called: Hand, foot, and mouth disease. It is caused by Coxsackie virus (A 16, 9). It causes outbreaks between children. It has systemic symptoms (fever, malaise). It usually starts on the hand and feet, then appear in the oral cavity.

Infectious Mononucleosis:

-it is caused by Epstein-Barr virus (EBV), it is a member of the herpes virus family

-it causes generalized lymphadenopathy, it may lead to hepatosplenomegaly that is why it is called glandular fever

-clinically: with children it is subclinical, but with adults it is called the kissing disease

-incubation period: more than one month, followed by malaise, fever , anorexia, fatigue, sore throat and generalized lymphadenopathy

-oral features appear especially in the posterior region: petechiae (which are multiple small bleeding pinpoint spots at the junction between the soft and the hard palate), creamy tonsillar exudates on the tonsils and pericoronitis which is associated with a partially erupted third molar (so it could be a viral infection).

-Note: the EBV also causes Hairy Leukoplakia, Burkitt’s lymphoma, Nasopharyngeal Carcinoma and non-Hodgkin Lymphoma

Measles

-it is caused by paramoxyvirus

-it manifests as a skin rash with or without pneumonia and may spread and cause encephalitis, fever, cough, and headache

-it may have oral features which are Koplik’s spots; they are multiple (reaches up to one hundred) small whitish papules on the buccal mucosa surrounded by a reddish background. It is hard to distinguish between them.

-children who have measles, malaria and certain types of bacterial infections that affect the gingiva develop Gangrenous Stomatitis (also known as Cancrum Oris or Noma ) which is severe necrosis in the oral and peri-oral region causing damage to the tissues. Measles in this case helped the spreading of the bacteria beyond the gingiva.

Cytomegalovirus

- In immunocompetent individuals it manifests as a mild disease, but in immunocompromised patients it causes severe fatal infections.

- It is transmitted in early childhood by secretions from infected patients; blood, intimate contact or organ transplant.

- Severe fatal infections such as encephalitis, inflammation all over the body.

-Oral manifestations in AIDS patients present as non-specific ulcerations

Bacterial Infections

Necrotizing Ulcerative Gingivitis

- Also known as Trench-mouth because it first appeared in individuals that spent so much time in trenches, these people suffered from poor oral hygiene, stress, malnutrition and fatigue.

- It affects children and young adult males

- It is characterized by:

1- A sudden onset of ulcers on the interdental papillae; they are called crater-like ulcers, which then migrate to the adjacent marginal gingiva. These ulcers are covered by a greyish-whitish membrane.

2- Soreness, burning sensation, spontaneous bleeding in the gingiva, halithosis (bad breath), metallic taste and hyper salivation. And it may manifest as fever and malaise at its late stages.

-Histologically: there is no surface epithelium. The slough (the whitish membrane) consist of fibrin, necrotic cells, bacteria and RBCs. The lamina propria underneath it shows marked acute inflammatory cell infiltrate (if it was chronic there will be a chronic inflammatory cell infiltrate). When the slough is stained with Gram stain, anaerobic spirochetes & fusibacterium can be seen, these bacteria in addition to other types are considered the main cause of the necrotizing ulcerative gingivitis. Under the microscope these bacteria appear invading the tissues (the gingiva). They are endogenous bacteria (already present in the oral cavity not from an external origin, like the normal oral flora, but because of the predisposing factors, it caused the disease), so it is not contagious.

- Predisposing factors include poor oral hygiene, smoking, fatigue, stress and trauma, or it could be associated with other diseases that cause decrease in the immunity, such as malaria, malnutrition which will lead to the development of Cancrum Oris causing necrosis.

Actinomycosis

- It is caused by actinomyces species, which are inflammatory bacteria. They used to consider it a type of fungus. The types that cause the disease are Actinomyces israelii, viscosus and naeslundii. These bacteria are already present in the oral cavity; they cause disease in individuals who had an injury, surgery, extraction, periapical infection or pericoronitis.

-It manifest as soft tissue swellings, red in color, especially at the submandibular region. At first they have a firm texture (hard swellings), which eventually soften and are accompanied by the formation of pus that discharges through multiple sinuses followed by scarring. So it is diagnosed by an area that is red, swollen and with multiple sinuses.

- Lymphadenopathy is absent.

- Histologically: it is also easily distinguished; granulation tissue and inflammation is present. There are ‘sulphur granules’ inside the pus, which are a collection of the filamentous bacteria, 1 mm in diameter that could leave the sinuses, so it could be distinguished clinically ( yellowish particles coming out of the sinus )

Done!

3/10/2011

Lecture # 3

Amal Abu-Awwad