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    AIDS AND PERIODONTIUM

    SUBMITTED BY

    ANTO ANTONY

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    Acquired immunodeficiency syndrome (AIDS) is character-

    ized by profound impairment of the immune system a viral pathogen, the human immunodeficiency virus

    (HIV), was identified in 1984 HIV has a strong affinity for cells of the immune system,

    (CD4 cell, T4 cells) monocytes, macrophages, Langerhans cells, and some

    neuronal and glial brain. cells may also be involved. Viral replication occurs continuously in the

    lymphoreticular tissues of lymph nodes, spleen, gut-

    associated lymphoid cells, and macrophages. B lymphocytes are not infected, but the altered function ofinfected T4 lymphocytes secondarily results in B-celldysregulation and altered neutrophil function

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    HIV-positive individual are at increased risk formalignancy and disseminated infections

    HIV-positive individuals are also at increased riskfor adverse drug reactions because of altered

    antigenic regulation. HIV has been detected in most body fluids,

    although it is found in high quantities only inblood, semen, and cerebrospinal fluid

    Transmission occurs almost exclusively by sexual

    contact, illicit use of injection drugs, or exposureto blood or blood products

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    HIGH RISK POPULATION

    homosexual and bisexual men

    users of illegal injection drugs

    persons with hemophilia or other coagulation

    disorders recipients of blood transfusions before April

    1985

    infants of HIV-infected mothers (transmission

    occurs by fetal transmission, at delivery,breastfeeding)

    promiscuous heterosexual

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    individuals who engage in unprotected sexwith HIV-positive cohorts.

    HIV-infected individuals with a high plasmabioload of the virus

    organ transplantation and artificialinsemination

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    CDC Surveillance Case Classification AIDS patients have been grouped as follows (1993) Category Aincludes patients with acute symptoms or asymptomatic diseases, along with individuals with

    persistent generalized lymphadenopathy, with or withoutmalaise, fatigue, or low-grade fever Category Bpatients have symptomatic conditions such as

    oropharyngeal or vulvovaginal candidiasis, herpes zoster,oral hairy leukoplakia, idiopathic thrombocytopenia, orconstitutional symptoms of fever, diarrhea, and weight

    loss. Category Cpatients are those with outright AIDS, asmanifested by life-threatening conditions or identifiedthrough CD4+ T lymphocyte levels of less than 200cells/mm3.

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    Oral candidiasis

    Oral hairy leukoplakia

    aposis sarcoma

    Bacillary angiomatosis Oral hyperpigmentation

    Atypical ulcers

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    Linear gingival erythema

    Necrotizing ulcerative gingivitis

    Necrotizing ulcerative periodontitis Necrotizing ulcerative stomatitis

    Chronic periodontitis

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    Candida, a fungus found in normal oral flora A major factor associated with overgrowth of

    Candida is diminished host resistance,immunosuppressive therapy

    Candidiasis is the most common oral lesionin HIV

    It usually has one of four clinical

    presentations: pseudomembranous,erythematous, or hyperplastic candidiasis orangular cheilitis.lsl

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    Pseudomembranous candidiasis("thrush")

    Painless or 'slightly sensitive, yellow-whitecurd like lesions that can be readily scrapedand separated from the surface of the oralmucosa

    Most common on the hard and soft palate

    and the buccal or labial mucosa but can occuranywhere in the oral cavity

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    Erythematous candidiasis

    Present as a component of thepseudomembranous type, appearing as redpatches on the buccal or palatal mucosa

    Associated with depapillation of the tongue

    If gingiva is affected, it may be misdiagnosedas desquamative gingivitis

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    Hyperplastic candidiasis

    Least common form and may be seen in thebuccal mucosa and tongue

    More resistant to removal than the othertypes

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    The commissures of the lips appear

    erythematous with surface crusting and fissuring.

    DIAGNOSIS

    clinical evaluation,

    culture analysis

    microscopic examination of a tissue sample

    smear of material scraped from the lesion, whichshows hyphae and yeast forms of the organisms

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    Topical Drugs Clotrimazole Mycelex) 10-mg tablets Dissolve in mouth

    3-5 tablets daily for 7-14 days.

    Nystatin Mycostatin, Nilstat). Oral suspension.(100,000 U/ml) Tablets (500,000 U) Pastilles (200,000 U Vaginal tablets (100,000 U) Ointment (for angular cheilitis), 15-g tube Amphotericin B oral suspension (Fungizone), 100 mg

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    Systemic Drugs Ketoconazole Nizoral), 200-mg tablets Fluconazole Diflucan), 100-mg tablets

    Itraconazole Sporanox), 100-mg capsules Recent reports indicate that the administration of

    HAART in HIV infections has resulted in a significantdecrease in incidence of oropharyngeal candidiasis

    and oral candidal carriage and has reduced the rateof fluconazole resistance

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    Oral hairy leukoplakia (OHL) primarily occurs in personswith HIV infection

    Found on the lateral borders of the tongue, OHL frequentlyhas a bilateral distribution and may extend to the ventrum

    This lesion is characterized by an asymptomatic, poorlydemarcated keratotic area ranging in size from a fewmillimeters to several centimeters

    Characteristic vertical striations are present, imparting acorrugated appearance, or the surface may be shaggy andappear "hairy" when dried

    The lesion does not rub off and may resemble otherkeratotic oral lesions

    Associated with EBV

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    DIFFERENTIAL DIAGNOSIS

    White lesions

    dysplasia, carcinoma

    frictional and idiopathic keratosis lichen planus

    tobacco related Leukoplakia

    secondary syphilis

    psoriasiform lesions (e.g., geographic tongue) hyperplastic candidiasis

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    antiviral agents such as acyclovir orvalacyclovir

    Lesions can be successfully removed withlaser or conventional surgery

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    An HIV-positive individual with non-Hodgkin's lymphoma (NHL)

    or Kaposi's sarcoma (KS) is categorized as having AIDS KS is the most common oral malignancy associated with AIDS This angiomatous tumor is a rare, multifocal, vascular neoplasm Caused by HHV-8

    KS is a malignant tumor, in its classic form it is a localized andslowly growing lesion

    In the early stages the oral lesions are painless, reddish purplemacules of the mucosa. As they progress, the lesions frequentlybecome nodular

    Lesions manifest as nodules, papules, or non-elevated macules

    that are usually brown, blue, or purple in color

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    pyogenic granuloma, hemangioma

    atypical Hyperpigmentation

    sarcoidosis bacillary angiomatosis

    angiosarcoma

    pigmented nevi

    cat-scratch disease (skin

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    HAART Therapy antiretroviral agents laser excision cryotherapy radiation therapy intralesional injection with vinblastine interferon-a, sclerosing agents other chemotherapeutic drugs

    injections of 3% sodium tetradecyl sulfate, asclerosing agent

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    Infectious vascular proliferative disease with clinical andhistologic features similar to those of KS

    caused by rickettsia-like organisms (e.g., Bartonellaceae,Rochalimaea quintana).

    Diagnosis of bacillary angiomatosis is based on biopsy, which

    reveals an "epithelioid" proliferation of angiogenic cellsaccompanied by an acute inflammatory cell infiltrate The causative organism in the biopsy specimen may be identified

    using Warthen-Starry silver staining or electron microscopy Bacillary angiomatosis is usually treated using broad-spectrum

    antibiotics such as erythromycin or doxycycline Gingival lesions may be managed using the antibiotic in

    conjunction with conservative periodontal therapy and possiblyexcision of the lesion.

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    Oral pigmented areas often appear as spotsor striations on the buccal mucosa, palate,gingiva, or tongue

    pigmentation may relate to prolonged use ofdrugs such as zidovudine, ketoconazole, orclofazimine. Zidovudine is also associated

    with excessive pigmentation of the skin andnails

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    HIV-associated neutropenia may also feature oralulcerations

    Recurrent herpetic lesions and aphthousstomatitis

    Oral ulcerations have been described in asso-ciation with enterobacterial organisms such asKlebsiella pneumoniae, Enterobacter cloacae, andEscherichia coli

    Herpes simplex virus (HSV), varicella-zoster virus

    (VZV), Epstein-Barr virus (EBV), andcytomegalovirus (CMV) are frequently retrievedfrom nonspecific oral ulcers

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    Management

    Herpes labialis in HIV infected individuals maybe responsive to topical antiviral therapy(e.g., acyclovir, pencyclovir, doconasol)

    Neutropenia can be treated with recombinanthuman granulocyte colony stimulating factor

    Recurrent aphthous stomatitis (RAS): Topicalcorticosteroid therapy (fluocinonide gel

    applied three to six times daily). Systemiccorticosteroids (e.g., prednisone, 40-60 mgdaily). Chlorhexidine mouth wash

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    dverse Drug Effects

    Foscarnet, interferon, and 2'-3'-dideoxycytidine(DDC) occasionally induce oral ulcerations, anderythema multiforme

    Zidovudine and ganciclovir may induce leukopenia,

    resulting in oral ulcers Xerostomia and altered taste sensation have beendescribed in conjunction with diethyldithiocarbamate(Dithiocarb)

    HAART drugs may induce adverse side Nausea Kidney stones Liver cirrhosis

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    Lipodystrophy Insulin resistance

    Gynecomastia

    Toxic epidermal necrolysis

    Blood dyscrasias Oral warts

    Oral lichenoid reactions

    Xerostomia

    Altered taste sensation Perioral paresthesia

    Exfoliative cheilitis

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    LINEAR GINGIVAL ERYTHEMA

    A persistent, linear, easily bleeding, erythematous gingivitis hasbeen described in some HIV-positive patients

    Linear gingival erythema (LGE) may or may not serve as aprecursor to rapidly progressive necrotizing ulcerative

    periodontitis (NUP) Linear gingivitis lesions may be localized or generalized innature

    The erythematous gingivitis (1) may be limited to marginaltissue, (2) may extend into attached gingiva in a punctate or adiffuse erythema, or (3) may extend into the alveolar mucosa.

    Concomitant oral candidiasis and LGE lesions have beenidentified, suggesting a possible etiologic role for candidialspecies in LGE

    LGE is more common among HIV infected

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    MANAGEMENT The affected sites should be scaled and

    polished

    Subgingival irrigation with chlorhexidine or10% povidone-iodine

    meticulous oral hygiene procedures

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    condition should be reevaluated 2 to 3 weeksafter initial therapy If the patient is compliant with home care

    procedures and the lesions persist, the possibilityof a candidial infection should be considered

    empiric administration of a systemic antifungalagent such as fluconazole for 7 to 10 days the patient should be carefully monitored for

    developing signs of more severe periodontalconditions (e.g., NUG, NUP, NUS). The patient

    should be placed on a 2- to 3-month recallmaintenance interval and re-treated as necessary

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    sudden onset, bleeding on brushing pain and characteristic halitosis the gingiva appears fiery red and swollen and yellow

    to grayish necrosis is observed on the tip of the

    interdental papilla and margins of the gingiva mostly anterior gingiva is affected and normally

    limited to the soft tissue of the periodontium Basic treatment may consist of cleaning and debride-

    ment of affected areas with a cotton pellet soaked inperoxide after application of a topical anesthetic

    oral rinses such as hydrogen peroxide should onlyrarely be used

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    The patient should be seen daily or every other day for thefirst week debridement of affected areas is repeated at each visit,

    and plaque control methods are gradually introduced The patient should avoid tobacco, alcohol, and condiments An antimicrobial oral rinse such as chlorhexidine

    gluconate 0.12% is prescribed Systemic antibiotics such as metronidazole or amoxicillin

    may be prescribed for patients with moderate to severetissue destruction, localized lymphadenopathy or systemicsymptoms, or both

    The use of prophylactic antifungal medication should beconsidered if antibiotics are prescribed.

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    A necrotizing, ulcerative, rapidly progressive form of periodontitisoccurs more frequently among HIV-positive individual

    Necrotizing ulcerative periodontitis (NUP) may represent an extension ofNUG in which bone loss and periodontal attachment loss occur.

    NUP is characterized by soft tissue necrosis, rapid periodontaldestruction, and interproximal bone loss

    Lesions may occur anywhere in the dental arches and are usuallylocalized to a few teeth, although generalized NUP is sometimes presentafter mar.ked CD4+ cell depletion.

    Bone is often exposed, resulting in necrosis and subsequent sequestra-tion.

    NUP is severely painful at onset, and immediate treatment is necessary The lesion may undergo spontaneous resolution leaving painless inter

    proximal craters that are difficult to clean and may lead to periodontitis May be presented with candidial or Herpes infection

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    MANAGEMENT local debridement

    scaling

    root planing,

    in-office irrigation with an effective antimicrobialagent such as chlorhexidine gluconate orpovidone-iodine (Betadine)

    establishment of meticulous oral hygiene,including home use of antimicrobial rinses orirrigation.

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    NUS may be severely destructive and acutely painfuland may affect significant areas of oral soft tissueand underlying bone

    It may occur separately or as an extension of NUP andis often associated with severe suppression of CD4immune cells

    The condition appears to be identical to cancrum oris(noma), a rare destructive process reported innutritionally deprived individuals, especially in Africa

    Treatment for NUS may include an antibiotic such as

    metronidazole and use of an antimicrobial mouthrinse such as chlorhexidine gluconate. If osseousnecrosis is present, it is often necessary to removethe affected bone to promote wound healing

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    Health Status

    CD4+ T4 lymphocyte level viral load, history of drug abuse, sexually transmitted

    diseases, multiple infections, or other factorsthat might alter immune response

    medications taken adverse side effects from medications

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    Infection Control Measures

    universal precautionary methods should be taken

    Goals of Therapy

    The primary goals of dental therapy should be

    the restoration and maintenance of oral health,comfort, and function control of HIV-associated mucosal diseases,

    such as chronic candidiasis and recurrent oralulcerations

    Acute periodontal and dental infections shouldbe managed, and the patient should receivedetailed instructions in performance of effectiveoral hygiene procedures

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    Maintenance Therapy

    Blood and other medical laboratory tests may berequired to monitor the patient's overall healthstatus, and close consultation and coordination withthe patient's physician are necessary.

    Psychological Factors

    HIV infection of neuronal cells may affect brainfunction and lead to outright dementia

    elicit depression, anxiety, and anger in such patients The dentist should be prepared to advise and counsel

    patients on their oral health status

    Early diagnosis and treatment of HIV infection canhave a profound effect on the patient's lifeexpectancy and quality of life, and the dentist shouldbe prepared to assist the patient in obtaining testing

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