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1 2013 course two self-study course The Ohio State University College of Dentistry is a recognized provider for ADA CERP credit. ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit house by boards of dentistry. Concerns or complaints about a CE provider may be directed to the provider or to ADA CERP at The Ohio State University College of Dentistry is approved by the Ohio State Dental Board as a permanent sponsor of continuing dental education contact us p h o n e t o l l f r e e f a x e - m a i l smsosu@osu.edu w e b sterilization ABOUT this COURSE READ the MATERIALS. Read and review the course materials. COMPLETE the TEST. Answer the eight question test. A total of 6/8 questions must be answered correctly for credit. SUBMIT the ANSWER FORM ONLINE. You MUST submit your answers ONLINE at: RECORD or PRINT THE CONFIRMATION ID This unique ID is displayed upon successful submission of your answer form. ABOUT your FREE CE TWO CREDIT HOURS are issued for successful completion of this self-study course for the OSDB biennium totals. CERTIFICATE of COMPLETION is used to document your CE credit and is mailed to your office. ALLOW 2 WEEKS for processing and mailing of your certificate. FREQUENTLY asked QUESTIONS Q: Who can earn FREE CE credits? A: EVERYONE - All dental professionals in your office may earn free CE credits. Each person must read the course materials and submit an online answer form independently. Q: What if I did not receive a confirmation ID? A: Once you have fully completed your answer form and click submit you will be directed to a page with a unique confirmation ID. Q: Where can I find my SMS number? A: Your SMS number can be found in the upper right hand corner of your monthly reports, or, imprinted on the back of your test envelopes. The SMS number is the account number for your office only, and, is the same for everyone in the office. Q: How often are these courses available? A: FOUR TIMES PER YEAR (8 CE credits). Page 1
2 2013 course two HUMAN IMMUNODEFICIENCY VIRUS: The risks and disorders associated with HIV, and the features, prevention, and treatment of those disorders will be discussed. HIV infection can present in the oral cavity in various forms. In some cases, oral manifestations may be the identifiable signs of the disease. Dentists and oral hygienists are the only healthcare professionals that have an advantage due to close association with the oral cavity. For this reason, they should be trained to identify pathological changes in the oral cavity so patients can be guided to seek appropriate medical attention. This self-study aims to familiarize oral health care professionals with some of the more common oral presentations of HIV infection. written by amber kiyani, dds edited by arianne e. saunders, ba mei-ling shotts, bs karen k. daw, mba, cecm carl m. allen, dds, msd INTRODUCTION Human immunodeficiency virus is a retrovirus that may cause Acquired ImmunoDeficiency Syndrome (AIDS), characterized by the progressive failure of the immune system, life threatening opportunistic infections and cancers. AIDS was first clinically recognized in Most of these individuals presented with pneumocystis carinii related pneumonia; a rare disease that only affected an extremely immunocompromised population and Kaposi sarcomas; a non-aggressive malignancy only seen in older individuals of Mediterranean origin at the time. In 1981, the CDC formed a task force to determine the cause of these increasing opportunistic infections and Kaposi sarcomas. In 1983, two separate groups isolated a virus that was associated with this condition; this virus was named HIV-1 in The origins of the virus can be traced to monkeys and chimpanzees in West Africa and transmission to humans is assumed to be due to bush-meat activities. Until the 1990s, AIDS was a universally fatal illness claiming the lives of approximately 500,000 people. Introduction of highly active antiretroviral therapy reduced mortality rates by over 80%. HIV infection is now considered a chronically manageable condition. HIV Virus in Color Background Source: 123RF IN THIS CE, WE WILL DISCUSS: EPIDEMIOLOGY TRANSMISSION PATHOGENESIS CANDIDIASIS HAIRY LEUKOPLAKIA KAPOSI S SARCOMA PERSISTENT GENERALIZED LYMPHADENOPATHY NON-HODGKIN S LYMPHOMA HIV-ASSOCIATED PERIODONTAL DISEASE PREVENTION DIAGNOSIS PROPHYLAXIS TREATMENT THE BERLIN PATIENT Page 2
3 EPIDEMIOLOGY In the United States alone, about 1.2 million people are estimated to be HIV positive, 20% of which are currently unaware of their infection. With the introduction of highly active antiretroviral therapy (HAART) in 1998, mortality related to HIV has significantly reduced. However, even in 2010, over 17,000 people have died due to the virus. TRANSMISSION The virus is transmitted through blood, intimate contact or from mother to child. Less frequent routes of transmission include organ transplantation, breast feeding and artificial insemination. RISK FACTORS THE RISK OF HIV INFECTION AFTER NEEDLE STICK INJURIES AND EXPOSURE TO BODY FLUIDS IS LESS THAN 1%. IN DENTISTRY THE RISK OF HIV TRANSMISSION IS ALMOST NEGLIGIBLE. THERE ARE 6 DOCUMENTED CASES OF DENTISTRY ACQUIRED HIV INFECTIONS; ALL 6 PATIENTS WERE ALLEGEDLY INTENTIONALLY INFECTED BY THEIR DENTIST WHO DIED OF AIDS IN Source: WSU.edu Source: Davidson College HIV cannot reproduce outside the human body and cannot even survive outside the body for very long. It is not spread by: Air or Water Insects, including mosquitos Saliva, tears, or sweat Casual contact (shaking hands, sharing dishes) Closed-mouth or social kissing PATHOGENESIS CD4 or helper T cells are essential elements in the body s immune response against opportunistic infections. HIV infects and kills these cells. Depleting numbers of CD4 cells predispose the individual to fatal infections. CANDIDIASIS Oral candidiasis is the most common oral fungal infection in the oral cavity, regardless of the immune status, therefore the presence of this organism is not diagnostic of HIV infection. About 90% of HIV patients develop candidiasis at some point of the disease. Candidiasis is caused by a fungal organism called candida albicans that resides as normal flora in the oral cavity in over 60% of the American population. It presents in the oral cavity in four forms: Pseudomembranous candidiasis, Erythematous candidiasis, Hyperplastic candidiasis, and Angular cheilitis. Pseudomembranous Candidiasis Pseudomembranous candidiasis, also known as thrush, is the most commonly recognized form of candidiasis. It presents as white plaques resembling milk curd that can be wiped away by a piece of dry gauze to reveal normal mucosa underneath. This form of candidiasis is mostly asymptomatic and a few patients may complain of a burning sensation or altered taste. Erythematous Candidiasis Erythematous (i.e. redness of the skin) candidiasis is the most common candidal manifestation in the mouth. One of the frequent and least recognized presentations is that of a symmetrical red patch in the center of the tongue, known as central papillary atrophy or median rhomboid glossitis. In rare instances, the candida may be transferred to the palatal mucosa producing a red patch known as a kissing lesion. It may also present as a denuded tongue (loss of lingual papillae) with a burning sensation known as acute atrophic candidiasis following antibiotic therapy. Denture stomatitis or chronic atrophic candidiasis is associated with colonization of the fungal organisms in the acrylic pores of maxillary removable dental appliance. The fungal organisms residing on the denture surface produce erythematous patches on the denture covering area of the palate. Page 3
4 Hyperplastic Candidiasis Chronic hyperplastic (i.e. increase in number of cells) candidiasis or candidal leukoplakia presents as well-defined white plaque most commonly involving anterior buccal mucosa. Since it is difficult to establish whether the organisms are responsible for the changes seen or are superimposed on a previous leukoplakia, clinical diagnosis of this lesion is impossible. The diagnosis can only be rendered if appropriate antifungal therapy completely eliminates the white plaque. Angular Cheilitis Angular cheilitis is the redness, cracking and scaling occurring at the commissure of the lips. Pooling of saliva at the corners of lips creates a favorable environment for the fungal and bacterial organisms to thrive. This occurs more commonly in denture wearing individuals. Lip licking and use of petrolatum products may contribute to the spread of infection to perioral skin. HAIRY LEUKOPLAKIA Hairy leukoplakia is a term designated to Epstein- Barr virus (EBV) related white patches appearing in the oral mucosa following immunosuppression. CLINICAL FEATURES The white patch may be variable in appearance, ranging from faint vertical lines to thick and ragged plaques. Most cases of oral hairy leukoplakia occur on the lateral tongue. Buccal mucosa, soft palate, pharynx and esophagus may be infrequently involved. Larger lesions may cover multiple oral structures. DIAGNOSIS A biopsy is required for diagnosis. While the histological appearance of the lesional tissue is very characteristic, immunohistochemistry is performed to confirm the presence of EBV. TREATMENT Hairy leukoplakia resolves spontaneously once the immune-competent state is restored. PERSISTENT GENERALIZED LYMPHADENOPATHY Significant lymph node enlargement is usually the first clinical presentation of HIV infection. CLINICAL FEATURES: The nodal enlargement is persistently present over a course of 3 months and involves two or more extrainguinal sites. It serves as an indication that the body is fighting against HIV. Posterior and anterior cervical, submandibular, occipital and axillary lymph nodes are most commonly involved. DIAGNOSIS: Since lymphoma is a constant concern in HIV patients, a biopsy is usually required to establish the diagnosis of persistent generalized lymphadenopathy. Presence of this condition may serve as a warning for the progression of disease to AIDS. KAPOSI S SARCOMA Kaposi s sarcoma (KS) is a human herpes virus 8 (HHV8) related endothelial malignancy that affects about 20% of AIDS patients. However, the malignancy is not exclusive to HIV patients. It is recognized as 4 distinct types: Classic KS, Endemic KS, Immunosuppression-related KS, and HIVrelated KS. CLINICAL FEATURES: KS is primarily a multifocal disease. It commonly involves the trunk, arms, head and neck. Over 20% of KS are seen in the oral cavity, most frequently affecting the hard palate, gingiva and tongue. The lesions begin as non-blanching reddish purple macules that evolve into painful and bleeding nodules. Necrotic tissue may also be identified in some instances. This form of disease is very aggressive and can spread to lymph nodes and various organs without treatment. DIAGNOSIS: A biopsy is required to make definitive diagnosis. Immunohistochemical staining is performed to identify the presence of HHV-8. TREATMENT: HAART limits the progression of these lesions and in most cases causes complete resolution. Page 4
5 NON-HODGKIN LYMPHOMA This is the second most common malignancy seen in about 5% of patients with HIV infection. CLINICAL FEATURES: These lymphomas are usually extra-nodal with CNS being the most frequent site. A small percentage of non-hodgkin s lymphomas are seen in the oral cavity and may involve the gingiva, palate, tongue, tonsil or maxillary sinuses. Bone involvement may resemble periodontitis resulting in extensive bone loss and tooth exfoliation. DIAGNOSIS: A lymph node biopsy or fine needle aspiration biopsy is the initial step in the diagnostic process. Immunophenotyping performs an essential role in the diagnostic process. TREATMENT: Appropriate chemo and radiation therapy is required as soon as possible as non-hodgkin s lymphomas seen in HIV infected individuals are very aggressive and can be fatal very quickly. HAART seems to have very little effect on the prevalence of non-hodgkin s lymphoma. HIV-ASSOCIATED PERIODONTAL DISEASE Linear gingival erythema, necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis are linked to HIV infection. CLINICAL FEATURES: Linear gingival erythema is a 2-3 mm wide erythematous band that appears on the free gingival margin. Scattered erythematous patches may also be seen on the alveolar mucosa and gingiva. Plaque removal has no significant effect on the presentation of disease. Necrotizing Ulcerative Gingivitis (NUG) is ulceration and necrosis of interdental papillae. When NUG is accompanied by rapid bone loss, the disease is termed necrotizing ulcerative periodontitis. The patients complain of bleeding, pain and halitosis. Edema and extensive necrosis are identified on clinical examination. DIAGNOSIS: The diagnosis is primarily clinical. In the absence of a prior diagnosis of HIV, conventional or rapid HIV testing may be recommended. TREATMENT: The condition is treated with debridement and antibiotics (metronidazole). The patients are followed over a period of time to ensure appropriate and timely intervention. Baby with HIV Cured Dr. Deborah Persaud of Johns Hopkins Children s Center stated in a report on March 3, 2013 that an infant from Mississippi is functionally cured. This means that there have been no recurrences of the virus and treatment has been stopped for a year. The baby was treated with antiretrovirals 30 hours after birth and has been on these drugs until the infant was about 18 months old. Although this cure would not likely be successful on adults, it is still useful for newborns and as a basis for researching further treatment options for HIV. There are, however, 14 adult cases that have also been deemed functionally cured, according to a new study in the journal PLOS Pathogens. Source: Washington Post MYCOBACTERIAL INFECTION The incidence of tuberculosis in the developed world is extremely low. Mycobacterial infections in HIV positive individuals are aggressive and deadly. About 15% of AIDS related deaths are attributed to these infections. Mycobacterium related oral lesions are extremely rare. They appear as chronic painless ulcers most commonly involving the tongue. The buccal mucosa, floor of mouth, palate, lip and gingiva may also be involved. HYPERPIGMENTATION Skin, nails and mucosa of HIV infected individuals show increased melanin pigmentation. These changes are attributed to medication and adrenal gland destruction resulting in addisonian melanosis. In some cases, the changes may be idiopathic. HIV-ASSOCIATED SALIVARY GLAND DISEASE Salivary gland enlargement most commonly involving the parotids is noted in a small percentage of HIV infected patients. The enlargement is bilateral in more than 60% cases. The condition resolves on treatment with antiretrovirals and corticosteroids. Page 5
6 HERPES SIMPLEX VIRUS Recurrent herpetic infections in HIV infected individuals are relatively more widespread and aggressive in nature. Atypical herpetic lesions presenting as large painful ulcers may involve any part of the oral mucosa. Herpes labialis may extend to involve perioral skin. Persistence of lesions beyond one month in HIV patients is diagnostic for the onset of AIDS. VARICELLA ZOSTER VIRUS Recurrent infection by varicella-zoster virus occurs with an increased frequency in HIV infected individuals. While the infection is relatively more aggressive and painful in HIV positive patients, the initial stage involves only a single dermatome. Once AIDS sets in, dermatomal involvement becomes more widespread. In the mouth, the lesions present as painful ulcers that may involve the underlying bone leading to rapid bone degeneration and tooth loss. HUMAN PAPILLOMAVIRUS Human papillomavirus (HPV) is a common organism that may cause verruca vulgaris (common wart) and squamous papilloma in the mouth, regardless of the immune status. HIV individuals acquire unusual forms of the virus and are prone to developing atypical warts. PREVENTION Safer sex practices are the primary way of preventing transmission of HIV. Consistent use of condoms has been reported to reduce the risk of HIV transmission by 80%. Vertical transmission (mother to child) is limited by treating the mother with antivirals and avoiding breastfeeding. Needle exchange programs have also been set up that provide free hypodermic needles to limit infections in intravenous drug users. Scientists have been working for years to perfect an HIV vaccine. Healthcare workers should observe universal (formerly standard) precautions, receive training on Blood-borne Pathogens, and utilize proper PPE. PRE-EXPOSURE PROPHYLAXIS In June 2012, FDA approved the use of a prophylactic drug named Truvada for individuals who are HIV negative but have an increased risk of contracting the virus. The increased risk population was defined as homosexual men, people with infected partners, people with multiple sex partners and intravenous drug users. The drug is only effective in the presence of safe drug practices. According to initial studies, the risk of transmission was reduced about 42-75%. HIV testing for those taking the drug is recommended every 3 months. In case of a positive result, HAART is recommended. RAPID HIV TESTING Exposure incidents in the workplace typically required source patients to obtain laboratory blood draws. In 2012, the only oral fluid rapid HIV test became available for public purchase. The test requires a swab of the outer gums and provides the option of screening for HIV-1 and HIV-2 in the privacy of homes and offices with results available within 20 minutes. However, it can take some time for the immune system to produce enough antibodies for the antibody test to detect. Most people will develop detectable anti-bodies within 2 to 8 weeks (the average being 25 days) of their infection. 97% of persons will develop detectable antibodies in the first 3 months, so additional testing may be required. The CDC states that having a "rapid HIV test could result in decreased use of PEP and spare personnel both undue anxiety and adverse effects of antiretroviral PEP. The CDC also states that "rapid HIV testing of source patients can facilitate making timely decisions regarding use of HIV PEP after occupational exposures to sources of unknown HIV status. Consumers can purchase the OraQuick In-home HIV test from pharmacies and mass retailers around the country for about $40. Kits can also be purchased via dental and medical suppliers, or, from OraSure Technologies at Source: Orasure.com Page 6
7 THE BERLIN PATIENT POST-EXPOSURE PROPHYLAXIS Post-exposure prophylaxis is a short term antiviral treatment for individuals who have potentially been exposed to the virus. Single or multiple drug therapies are provided to reduce the likelihood of contracting the infection. The drug administration is initiated within 48 to 72 hours after exposure and continued over a course of four months. TREATMENT The attempts to eradicate AIDS were initiated in 1983 following the discovery of the virus. The first signs of success were seen when two nucleosides were combined with a non-nucleoside reverse transcriptase inhibitor in A protease inhibitor was eventually introduced to the list of drugs to formulate several drug combinations that are recognized today as highly active antiretroviral therapy or HAART. According to federal guidelines, antiretroviral therapy is initiated when the CD4 count falls below 350/mm3. HAART does not eliminate the virus from the body completely; it reduces it to insignificant amounts and allows for strengthening of the immune system. This has led to significant reduction in the morbidity and mortality associated with HIV. The treatment is however very expensive and is linked to serious side effects. One of the highlights of innovative treatment strategies is the case of Timothy Brown, also known as the Berlin patient. Timothy was diagnosed with HIV in Although, the prognosis for HIV individuals was bad at the time, he survived long enough for the arrival of HAART. In 2006, Timothy was diagnosed with leukemia requiring him to have a bone marrow transplant. The stem cells from the donor bone marrow introduced into his system carried a rare mutation called delta 32. This mutation inhibits the pathway of the virus into the cell, thus making Timothy Brown resistant to the disease and he remains virus free to this day. While this treatment strategy shows promising results, the high cost and unpredictability of finding a suitable donor limits its usefulness. Source: Tumblr ABOUT THE AUTHOR AMBER KIYANI, DDS ORIGINATING FROM PAKISTAN, AMBER WENT TO RIPHAH UNIVERSITY FOR THEIR 5-YEAR DENTAL SCHOOL PROGRAM. GRADUATING WITH A 4.0 GPA, SHE CAME TO OHIO STATE UNIVERSITY IN ORDER TO FURTHER HER STUDIES FOCUSING ON ORAL AND MAXILLOFACIAL PATHOLOGY. SHE PLANS TO TAKE THE INFORMATION SHE LEARNS BACK TO PAKISTAN FOR BOTH DIAGNOSTIC AND TEACHING PURPOSES. HER CURRENT RESEARCH STUDIES AS A FELLOW AT OSU INVOLVE EVALUATING THE ORAL CHANGES ASSOCIATED WITH GASTROINTESTINAL DISEASES. Electron microscope image of HIV, seen as small spheres on the surface of white blood cells. Source: CDC.gov REFERENCES ARE AVAILABLE UPON REQUEST DR. AMBER KIYANI CAN BE CONTACTED AT: KIYANI.1@OSU.EDU Page 7
8 post-test instructions - answer each question ONLINE - press submit - record your confirmation id - deadline is May 31, % or fewer of Kaposi s Sarcoma cases are seen in the oral cavity, and may feature necrotic tissue. 1 T F SUBMIT 2 T F Significant lymph node enlargement is usually the first clinical presentation of HIV infection. Mycobacterial infections in HIV+ individuals are aggressive and deadly. About 15% of all AIDS-related deaths are attributed to these infections. 3 ONLINE T F 4 T F If a patient is diagnosed with Persistent Generalized Lymphadenopathy, the patient may have AIDS. SUBMIT 5 T F involving the anterior buccal mucosa. ONLINE 6 T F 7 T F 8 T F HIV can be transmitted through blood, saliva, and organ transplantation. Chronic Hyperplastic Candidiasis presents as well-defined white plaque most commonly The risk of HIV infection after needle-stick injuries and exposure to bodily fluids is less than 1%. T cells are elements in the body s immune response against opportunistic infections. d i r e c t o r carl m. allen, dds, msd allen.12@osu.edu a s s i s t a n t d i r e c t o r karen k. daw, mba, cecm daw.37@osu.edu p r o g r a m a s s i s t a n t arianne e. saunders, ba saunders.268@osu.edu l a b t e c h n i c i a n mei-ling shotts, bs shotts.5@osu.edu Page 8
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