A 23-Year-Old Female Came with Her Male Companion and Was Seen in the Dental School S Emergency

Dental PBL II

A 23-year-old female came with her male companion and was seen in the dental school’s emergency clinic for extreme pain in the oral cavity. You are on rotation in the emergency clinic and are assigned the patient to conduct a work-up of the case. Oral examination presented a number of findings. White lesions were noticed on the lateral regions of the tongue. There were large ulcerations of the palate and gingival mucosa. The patient was also found to have large purple discolorations (possibly due to Kaposi’s sarcoma) in the oral cavity. On the medical history, the patient reports that she has been feeling tired and run down lately. She also reports getting “colds” more frequently, and that they last longer before resolving. The patient was suspected of having contracted the AIDS virus.

1.What is the significance of white lesions on the tongue of this patient?

2.What factors, disease(s) might cause ulcerations of the palate and gingival mucosa?

3.The patient was tested for hemangioma and coagulation defects. What would the rationale for these tests?

4.The patients had lesions that were identified as Kaposi’s sarcoma. What is Kaposi’s sarcoma and is it related to AIDS infection?

5.Please describe the life cycle AIDS virus.

6.What blood tests can be done to confirm AIDS infection in this patient?

7. What drugs are currently prescribed for controlling AIDS infection and what is the mode of their of action?

8.If the patient had AIDS, why would she get “colds” frequently?

9.What course of treatment would you suggest to improve oral health in this patient?

10.How would you handle the oral health of this patient over the long-term?

Reading Material

Faculty Handout

1.White lesions: Like most healthy people, you probably have small amounts of the fungus Candida albicans in your mouth and digestive tract and on your skin. You can't see the fungus and normally won't know it's there — Candida usually doesn't cause problems because normal bacteria (flora) in your body keep its growth in check. But when this balance is disturbed — by medications, stress or illness —Candida can grow out of control, leading to problems such as diaper rash, vaginal yeast infections and a mouth infection called oral thrush. Oral thrush causes creamy white lesions, usually on your tongue or inner cheeks. The lesions can be painful and may bleed slightly when you scrape them or brush your teeth. Sometimes the infection may spread to the roof of your mouth, your gums, tonsils or the back of your throat. Although signs and symptoms often develop suddenly, they may become chronic, persisting over a long period of time.

Oral candidiasis is often the first presenting sign of HIV infection, and it may occur in as many as 90% of patients with HIV. HIV infection should be considered in patients presenting with repeated oral candidiasis and in those who have no other associated risk factors, such as being on steroids or taking oral antibiotics.

The 4 common classifications of candidal infections are as follows: pseudomembranous candidiasis (i.e., thrush), erythematous candidiasis, angular cheilitis, and hyperplastic candidiasis. Pseudomembranous candidiasis is the most common AIDS-related presentation. Removable white plaques on the soft and hard palates, buccal (cheek) mucosa (most commonly), and tongue that leave a reddened area when scraped characterize pseudomembranous candidiasis. The frequency of candidal infection increases as HIV disease progresses. Antifungal treatment is effective, but the effectiveness may decrease over time with repeated infections due to increased resistance. Mouth rinses with chlorhexidine gluconate, Listerine, or hydrogen peroxide in sodium chloride solution may serve as adjunctive therapy.

2.Ulceration of the palate and gingival mucosa: Ulcerative colitis is an inflammatory condition with some similarities to Crohn’s disease. Lesions in the colon consist of areas of hemorrhage and ulcerations along with abscesses. Similar lesions may present in the oral cavity as aphthous (small white spots on the mucous membrane) ulcerations or superficial hemorrhagic ulcers. Generally, the oral lesions coincide with exacerbations of the colonic disease. Similar ulcerations may arise on the buttocks, abdomen, thighs, and face. Aphthous ulcers or angular stomatitis (inflammation of the mucous membrane of the mouth) occurs in as many as 5-10% of patients.

Oral ulcerations are not very common (~2-4%) in HIV infected patients. These generally consist of red or white-bordered erosions or ulcerations varying in size from 1 mm to 2 cm on buccal mucosa, oropharynx, tongue, lips, gingiva, hard or soft palate. In general gingival and palate ulcerations represent necrotic or eroded oral mucosa, including tongue. Most such lesions are idiopathic (apthous) or of viral etiology, although they also may be due to fungal, parasitic, or bacteriologic pathogens. Herpetic ulcerations tend to appear on keratinized tissues such as the hard palate or gingiva. Aphthous ulcerations tend to manifest on non-keratinized tissues such as the floor of the mouth, soft palate and lingual (bottom) surface of the tongue. Inquire about other ulcerative gastrointestinal diseases, including HSV, CMV or histoplasmosis; trauma, burn. Inquire about ETOH and smoking history, which can also cause ulcerations.

3.Hemangioma and coagulation defects: The discoloration in the oral cavity may reflect hemangioma and coagulation defects. That would be the rationale for testing it. Hemangiomas are abnormally dense collections of dilated small blood vessels (capillaries) that may occur in the skin or internal organs.

The classically recognized hemangioma is a visible red skin lesion that may be in the top skin layers deeper in the skin (cavernous hemangioma), or a mixture of both. Hemangiomas are usually present at birth, although they may appear within a few months after birth, often beginning at a site that has appeared slightly dusky or differently colored than the surrounding tissue. Hemangiomas, both deep and superficial, undergo a rapid growth phase in which the volume and size increase rapidly. This phase is followed by a rest phase, in which the hemangioma changes very little, and an involutional phase in which the hemangioma begins to disappear.

Treatment: Superficial or "strawberry" hemangiomas often are not treated. When they are allowed to disappear on their own, the result is usuaully normal-appearing skin. In some cases, a laser may be used to eradicate the small vessels. Cavernous hemangiomas that involve the eyelid and obstruct vision are generally treated with injections of steroids or laser treatments that rapidly reduce the size of the lesions, allowing normal vision to develop. Large cavernous hemangiomas or mixed hemangiomas are treated, when appropriate, with oral steroids and injections of steroids directly into the hemangioma. Recently, lasers have been used to reduce the bulk of the hemangiomas. Lasers emitting yellow light selectively damage the vessels in the hemangioma without damaging the overlying skin. Some physicians are using a combination of steroid injection and laser.

Coagulation Defects in Oral Cavity: The Rendu-Osler-Weber disease, also known as hereditary hemorrhagic telangiectasia (HHT), is transmitted as an autosomal dominant disorder characterized by hemorrhages, which can potentially affect any organ and by vascular anomalies (venous and capillary dilatations and arteriovenous malformations) caused by the loss of supporting tissues, which normally surround the vascular walls. Cutaneous (fingertips) and mucosal (lips, oral cavity, conjunctivae, nasal mucosa) telangiectases usually begin around the age of 30 to 50 years. These are small reddish raised lesions, composed of dilated and convoluted capillaries which are extremely fragile and thus easily subject to bleeding with only slight blood loss.

4.Kaposi’s sarcoma: A sarcoma is a cancer that develops in connective tissues such as cartilage, bone, fat, muscle, blood vessels, or fibrous tissues (related to tendons or ligaments). Kaposi’s sarcoma (KS) was named for Dr. Moritz Kaposi who first described it in 1872. For decades KS was considered a rare disease that mostly affected elderly men of Mediterranean or Jewish heritage, organ transplant patients, or young adult African men. In the last 30 years, however, the vast majority of KS cases have developed in association with human immunodeficiency virus (HIV) infection and the acquired immunodeficiency syndrome (AIDS), especially among homosexual men. With the use of new treatments for AIDS, this is turning around, and the number of KS cases due to HIV infection is decreasing. Certain diseases occur so often in people with AIDS that they are considered "AIDS-defining conditions" -- that is, their presence in a person infected with HIV is a clear sign that full-blown AIDS has developed. The Centers for Disease Control and Prevention has identified certain cancers as AIDS-defining diseases: Kaposi’s sarcoma, lymphoma (especially non-Hodgkin lymphoma and primary central nervous system lymphoma), anal cancer, and cancer of the cervix that has spread to neighboring tissue (called invasive cervical cancer). Many other kinds of cancer may be more likely to develop in people with HIV infection. Of course, people without HIV or AIDS can also have these types of cancer.

In most cases, epidemic KS causes widespread lesions that erupt at many places on the body soon after AIDS develops. Lesions of epidemic KS may arise on the skin and the mouth and may affect the lymph nodes and other organs, usually the gastrointestinal tract, lung, liver, and spleen. In contrast, classic KS usually involves only one or a few areas of skin, most often the lower legs. At the time of diagnosis, some people with epidemic KS experience no symptoms, especially if their only lesions develop on the skin. However, many -- even those with no skin lesions -- will have swollen lymph nodes, unexplained fever, or weight loss. Eventually, in almost all cases, epidemic KS spreads throughout the body. Extensive lung involvement by KS can be fatal. More often, however, patients die of other AIDS-related complications such as infections. This is rare because modern treatment of the HIV infection usually prevents the development of advanced Kaposi’s sarcoma.

Oral KS in a patient who is not on immunosuppressive therapy correlated with a lowered T4 count and is diagnostic for AIDS. Intraorally, KS appears as brown, bluish, purple, or red patches or papules on the hard palate, mucosa, and gingiva. The initial lesions are flat macules (small spots) or patches on the mucosal surface, but over time, they become nodular, ulcerate, and bleed. KS can also manifest on the skin, as lymph node enlargement, and in the salivary glands. Edema commonly occurs in association with extensive cutaneous involvement. Histologically, KS is characterized by increased vascularity, spindle-shaped cells with little mitotic activity, and hemosiderin deposition. A biopsy may need to be performed to definitively diagnose KS. The course of the disease may be aggressive, and death due to lung involvement may occur.

Patients with about 25 or fewer small skin or mouth lesions may be treated with local therapies such as liquid nitrogen or a cream containing cis-retinoic acid, a drug similar to vitamin A. Because local treatment does not result in a cure, the most important goals are to improve appearance and reduce the suffering and social isolation AIDS can cause.

Local lesions sometimes improve with injections of vinblastine, a chemotherapy drug, directly into the KS lesion. This method, known as intralesional chemotherapy, is an especially good choice for lesions that develop in the mouth. Often treatments are given every 3 weeks for a total of 2 or 3 treatments. Because the drug is injected into the lesion instead of into a vein, it does not spread throughout the body and does not cause side effects in organs and tissues such as the bone marrow or digestive system.

In many cases, local KS tumors of the skin, mouth, or anus improve significantly when treated with low-dose external beam radiation therapy (radiation treatments administered using a machine positioned outside the body). Depending on the specific clinical situation, beams of photons or electrons may be used. Another common technique is to give small doses of radiation frequently over a period of several weeks. At some treatment centers, doctors may give 10 to 20 doses over a period of weeks. In general, use of radiation may result in less scarring or skin disfiguration than surgery. Unfortunately, KS lesions are often widespread throughout the body. Even as lesions in the irradiated area are getting smaller, a new lesion often appears elsewhere in the body. For this reason, low-dose radiation therapy of the entire skin surface is sometimes used. As a rule, doctors use radiation therapy to relieve symptoms or treat highly visible lesions, although some patients who also have lesions in their internal organs have improved following this treatment. Patients with more than 25 KS skin or mouth lesions, or a lot of swelling around the lesions or lung or gastrointestinal lesions, may do best with systemic chemotherapy. Response rates (the number of patients whose lesions get smaller) range from about 30% to 85%, depending on various factors, such as the stage of the KS and the presence of other AIDS-related illnesses.

Usually, a single chemotherapy drug is given for KS in the early stages, and combinations are used in more advanced disease. Among the single chemotherapy drugs given to treat KS are bleomycin, etoposide, paclitaxel (Taxol), vinblastine, vincristine, and doxorubicin (Adriamycin). Combination regimens include vinblastine + vincristine; bleomycin + vinblastine or vincristine; or bleomycin + doxorubicin + vinblastine or vincristine. Depending on the results and the onset of certain side effects, doctors may change regimens from time to time.

Recently it was discovered that placing the active molecules of certain drugs into liposomes increases their effectiveness and reduces many side effects. Drugs delivered in this way tend to concentrate in KS lesions and are gradually released. Two liposome-encapsulated forms of the cancer drugs doxorubicin and daunorubicin are now available. Paclitaxel (Taxol) produces partial or complete responses in more than 50% of patients with AIDS-related KS. The drug seems particularly effective in reducing swelling quickly. Also, antiviral therapy with a drug called foscarnet (Foscavir) appears to help in the treatment of KS, perhaps because it works against viruses, including the new herpes virus that has been found in many KS lesions. The Center for Disease Control and Prevention has reported that people with AIDS who were treated with foscarnet for any reason were 70% less likely to develop KS than those not treated with the drug.

Biological treatment has been given using certain kinds of interferons. Interferons work by preventing viruses from reproducing and by activating immune system cells that attack and destroy the virus. Between 25% and 50% of patients improve when given high doses of these drugs. The best success rates occur in patients who do not have opportunistic infections and those who have a relatively healthy immune system. The most common side effects of interferon therapy are flu-like symptoms (fever, pain, and weakness). There is also research underway to determine whether better results occur when interferon is used in combination with chemotherapy drugs.

6.Blood Tests for AIDS Infection: The first type of test is the HIV antibody test. This test shows whether a person has been infected with HIV, the virus that causes AIDS.

The second type of test is P24 antigen testing. It is primarily used to screen the blood supply but in some places it is used for testing for HIV in individuals. P24 antigen is a protein that is part of the HIV. Early in the infection, it is produced in excess and can be detected in the blood serum by a commercial test. The P24 test can detect HIV infection before the HIV antibody test can. Therefore, P24 antigen testing is used in diagnosing HIV early in the course of infection

The main cell HIV attacks are called a T-helper cell or CD4 cell. The T-helper cell plays an important part in the immune system. It helps to co-ordinate all the other cells to fight illnesses. Any damage to T-helper cells can have a serious effect on the immune system. The T-helper cell has a protein CD4 on its surface. HIV needs the CD4 in order to enter the cells it targets to infect. If HIV is able to enter the T-helper cell, it can take over the cell and then use it to duplicate itself. When HIV produces more copies of itself, the amount of CD4 cells decreases. As a result, there are fewer cells available to help the immune system to fight illnesses.The CD4 test measures the number of CD4 or T-helper cells in your blood. The more CD4 cells in your blood you have per ml, the stronger is your immune system. The stronger the immune system, the better the body can fight illnesses. A low CD4 count does not mean that you will certainly become ill, but it makes it more likely. The general recommendation is for treatment to begin when the CD4 count is between 200 and 350 per ml.