INTRODUCTION AIDS is a universal epidemic thatsignificantly affects dental practice, regardless ofgeographic location. The oral cavity is a frequentsite for clinical manifestations of the disease. The ability to recognize and manage the oralmanifestations of this disease is an important partof dental practice. The dentist should be prepared to assisthuman immunodeficiency virus (HIV) – infectedpatients in maintenance of oral health throughoutthe course of their disease.
AIDS is characterized byprofound impairment of theimmune system due to HIVinfection and consists ofmicrobial diseases acquired orreactivated as a result of theimmunosuppression.
CLINICAL DEFINITION OF AIDSAIDS is defined as a severe immunodeficiency disease arising from infection with HIV, accompanied by some of the following symptoms: Life threatening opportunistic infections & persistent fever Unusual cancers Chronically swollen lymph nodes Weight loss and diarrhea Neurological disorders..
ORIGIN OF AIDS Studies comparing the genetics of HIV withvarious African monkey viruses has provided someevidence. HIV-1 & -2 are not closely related to each otheras they are to simian immunodeficiency virus (SIV) HIV-2 ANCESTRAL SIVSM VIRUS SIVSY HIV-1 SIVCPZ SIVAG
The first well-documented case of AIDS occurred in an African man in 1959. Samples of his blood yielded genetic material from an early version ofHIV. It is theorized that it must have first appeared inthe early1950s, after having jumped from original simianhosts. It probably remained in small isolated villages,causing sporadic cases and mutating into more virulentstrains that were readily transmitted from human tohuman.When this pattern was coupled with changing social andsexual mores and increased immigration and travel, apathway was opened up for rapid spread of the virus.
HISTORICAL BACKGROUND AIDS was first recognized in 1981 in USA. Luc Montagnier and colleagues in 1983isolated the causative virus, HIV from bloodlymphocytes. It was recognized to be a Lentivirussubgroup of the family retroviridae and wascalled Lymphadenopathy Associated Virus(LAV).
In 1984 Robert Gallo and colleaguesreported isolation of retrovirus from AIDS patients and called it Human TcellLymphotropic Virus –III (HTLV-III). Other isolates were called as AIDS related virus. The International Committee on virusnomenclature in 1986, decided on the genericname Human Immunodeficiency Virus
STRUCTURE OF HIV HIV is a spherical enveloped virus about 90-120nm in size.
DIAGNOSIS Virus isolation : From T cells in blood and other specimens. Serological tests:Depend upon the demonstration of specific antibodies. ELISA WESTERN BLOTHIV infection can be checked by measuring the viruson the blood using either: 1. A p24 antigen test PCR 2. A viral load assay bDNA
STAGES OF HIV INFECTION1. ACUTE HIV SYNDROME First stage seroconversion• Virus rapidly spreads to organs, especially the lymphoidtissues• HIV virus not very aggressive in causing diseases orsevere symptoms2. ASYMPTOMATIC STATE• Infection is latent• Virus starts to grow and multiply in the lymph nodes
3. SYMPTOMATIC DISEASE/AIDS• Viremia (spread of virus in the blood)• Loss of immune system, mainly due to infection of CD4+ T-Lymphocytes4. END STAGE DISEASE• Immune system collapses• Virus continues to slowly destroy the Immune System forup to 10 yearsUsually an opportunistic infection is the cause of death
Classification of the Most Common Oral Manifestations of AIDSBACTERIAL INFECTIONS Gingivo-Periodontal Disease Linear gingival erythema (LGE) Necrotizing ulcerative gingivitis (NUG) Necrotizing ulcerative periodontitis (NUP) Necrotizing ulcerative stomatitis (NUS)FUNGAL INFECTIONS Candidiasis Pseudomembranous Erythematous Hyperplastic Angular cheilitis
PERIODONTAL TREATMENT PROTOCOL1. HEALTH STATUS2. INFECTION CONTROL MEASURES3. GOALS OF THERAPY4. SUPPORTIVE PERIODONTAL THERAPY5. PSYCHOLOGIC FACTORS
I. HEALTH STATUS - Should be determined from the health history, physical evaluation and consultation with the patient’s physician. - treatment decisions will vary depending on the patient’s state of health - information should be obtained regarding CD4+ T4 lymphocyte level current viral load difference from previous counts and load H/o of drug abuse, multiple infections present medications
2. INFECTION CONTROL MEASURES:Control measures should be based on American Dental Association (ADA) and the Center for Disease Control and Prevention (CDC) or the Organization for Safety and Asepsis Procedure (OSAP).A number of pathogenic microorganisms may be transmitted in the dental setting and these include: Airborne pathogens such as tuberculosis Bloodborne pathogens such as HIV, HBV, HCV Waterborne pathogens such as Legionella and Pseudomonas species Mucosal/ skin borne pathogens such as VZV or HSV
3. GOALS OF THERAPY: Primary goals should be restoration and maintenance of oral health, comfort and function. Treatment should be directed toward control of HIV- associated mucosal diseases such as chronic candidiasis and recurrent oral ulcerations Effective oral hygiene maintenance Conservative, nonsurgical periodontal therapy should be a treatment option for virtually all HIV +ve patients NUP & NUS can be severely destructive to periodontal structures and should be treated appropriately.
4. SUPPORTIVE PERIODONTAL THERAPY: Patient should be encouraged to maintain meticulous personal oral hygiene. Recall visits should be conducted at short intervals (2 to 3 months) Systemic antibiotic therapy should be administered with caution Blood and other medical laboratory tests may be required to monitor the patients overall health status and consultation and co-ordination with the patient’s physician are necessary
5. PSYCHOLOGIC FACTORS HIV infection of neuronal cells may affect brain function and lead to outright dementia. Coping with a life-threatening disease may elicit depression, anxiety and anger in such patients and this anger may be directed toward the dentist and the staff (Asher et al 1993). Treatment should be provided a calm, relaxed atmosphere, and stress to the patient must be minimized. Early diagnosis and treatment of HIV infection can have a profound effect on the patient’s life expectancy & quality of life In case of suspected cases, testing for HIV antibody should be advised after patient counseling and information.
MANAGEMENT OF ORAL AND PERIODONTAL LESIONS ASSOCIATED WITH AIDS
GENERAL PRECAUTIONS TO BE TAKEN Infection control measures1. Gloves should be worn when touching blood, saliva or mucous membranes.2. Surgical masks & protective eye wear should beworn.3. Disposable or washable gowns.4. Instruments should be sterilized by autoclaving.Debris should be removed by scrubbing with soapand water before sterilization.5. Surfaces should be decontaminated with sodiumhypochlorite.6. Needles should be disposed with safety guard.7. Droplets and aerosol production should be avoided where possible by use of rubber dam and highspeed evacuation.
ORAL CANDIDIASIS Oral candidiasis is caused by one of thecandida species, usually candida albicans, a normalinhabitant of the oral cavity in many healthyindividuals. Currently at least 11 strains of candida havebeen identified and a major factor associated withovergrowth of candida is diminished host resistance. Candidiasis is the most common oral lesion inHIV diseases and has been found in approximately90% of AIDS patients.
It usually has one of the four clinical presentations:1. Pseudomembranous Candidiasis Painless or slightly sensitive white or yellow spots or plaques that can be scraped and readily separated from the mucosa. Most common in the hard and the soft palate and the buccal or labial mucosa. PSEUDOMEMBRANOUS CANDIDIASIS
2. Erythematous candidiasis Red areas or patches on the buccal orpalatal mucosa, or it may be associated withdepapillation of the tongue. ERYTHEMATOUS CANDIDIASIS
3. Hyperplastic candidiasis Least common form and may beseen in the buccal mucosa & tongueand is more resistant to removal.
4. Angular cheilitis The commissures appearerythematous with surface crusting andfissuring.
Diagnosis of candidiasis is made bymicroscopic examination of tissue sample orsmear, which shows hyphae or yeast forms of theorganisms. Oral candidiasis presents with esophagealcandidiasis in patients at risk for HIV Infection,which is a diagnostic sign of AIDS. Resistant candidiasis is more common inindividuals who have low CD4+ counts.
MANAGEMENT1. Early oral lesions of HIV-related candidiasis are usually responsive to topical antifungal therapy.2. More advanced lesions, including hyperplastic candidiasis may require systemic antifungal drugs.3. Most oral topical antifungal agents contain large quantities of sucrose, which may be cariogenic after long-term use.
4. Sucrose-free nystatin, itraconazole and amphotericin-B are available.5. Fluconazole oral suspension, chlorhexidine and cetyl pyridinium chloride oral rinses may also be effective against oral candidal infection.6. Systemic antifungal agents such as ketoconazole, fluconazole, itraconazole and amphotericin-B are effective in treatment of oral candidiasis.
TOPICAL DRUGS1. Clotrimazole 10mg tablets: dissolve in mouth 3-5tablets daily for 7-14days2. Nystatina. Oral suspension (100,000 U/ml : Disp 240ml) Rinse with 1tsp qid.b. Oral suspension (extemporaneous) mix 1/8tsp with 4 oz waterc. Tablets(500,000U): Dissolve 1tablet in mouth 4-5times daily.d. Pastilles (200,000U) disolve 1-2 pastilles in mouth,4-5times daily.e. Ointment 15g tube: Apply to affected area 3-4times daily.3. Clotrimazole ointment 15g tube: apply to affected area qid.4. Miconazole 2% ointment 15g tube: qid application.5. Itraconazole oral suspension 100-200mg once daily for 7-28 days.6. Fluconazole oral suspension 200mg of 1st day followed by 100mg once daily for atleast 2weeks.7. Amphotericin B oral suspension 100mg four times daily for 2 weeks.
SYSTEMIC DRUGS1. Ketoconazole (Nyzoral) 200mg tablets: take 2 tablets immediately, then 1-2 tablets daily for 5-14days.2. Fluconazole (Diflucan) 100mg tablets: take 2 tablets immediately, then 1 tablet daily for 7-14 days.3. Itraconazole (Sporanox) 100mg capsules: 200mg once daily with meals for 4 weeks.
ORAL HAIRY L UK L IA E OP AK Oral hairy leukoplakia most commonlypresents as a white ragged, corrugated orirregular lesion involving the lateral anddorsolateral tongue. Lesions may be unilateral or bilateral. Hairy leukoplakia is caused byinfection of the lesion epithelial cells withEpstein-Barr virus (EBV) and is associatedwith immune deterioration.
Microscopically, the lesion shows a hyperparakeratotic surface with projections that often resemble hairs. beneath parakeratotic surface are acanthosis and some characteristic balloon cells resembling koilocytes.Differential diagnosis of OHL must considerwhite lesions of the mucosa, which includedysplasia, carcinoma, frictional and idiopathickeratosis, lichen planus, tobacco-relatedleukoplakia, psorisiform lesions andhyperplastic candidiasis.
MANAGEMENT1. Oral hairy leukoplakia generally does not require treatment.2. Resolution has been reported after therapy with acyclovir, zidovudine, podophyllin and interferon, but usually recurs when treatment is discontinued.3. In cosmetically objectionable patients, lesions can be removed with laser or conventional surgery.4. The incidence of OHL has been markedly reduced since the advent of multidrug antiviral therapy for HIV infection.
KAPOSI’S SARCOMAKaposi’s sarcoma is a rare, multifocal vascularneoplasm which is the most common malignanttumor associated with HIV infection.Herpes virus (HHV-8) has been implicated in theetiology of Kaposi’s sarcoma.Kaposi’s sarcoma oral lesions may interfere withfunction, be cosmetically objectionable, andproliferate uncontrollably.This is an aggressive lesions and involves mostfrequently the palate 95% and the gingiva 23%
Early lesions are painless, andappear as reddish purple macules of themucosa. As lesions progresses it becomesnodular, papular or non-elevatedmacules, brown or purple in colour. May ulcerate and become painfulwith difficulty in eating and speech andmay cause cosmetic problems .
Diagnosis: Biopsy or identification of distinct clinicalappearance.Histologic picture:Endothelial cell proliferation with formation of atypical vascular channels.Extravascular hemorrage with hemosiderin depositionSpindle cell proliferationMononuclear inflammatory infilterate, consisting mainlyof plasma cells.Differential diagnosis: Pyogenic granuloma, hemangioma,atypical hyperpigmentation, sarcoidosis, pigmented nevi. Median survival time after onset of KS is 7 to 31 months.
MANAGEMENT1. Treatment of oral KS may include use of antiretroviral agents, laser excision, radiation therapy or intralesional injection with vinblastine, interferon α, or other chemotherapeutic drugs.2. Nichols et al in 1993 described the successful use of intralesional injection of vinblastine at a dosage of 0.1 mg/cm2 using a 0.2mg/ml solution of vinblastine sulfate in saline.
3. Intralesional injections with sodium tetradecyl sulfate, a sclerosing solution, also have been effective.4. In case of destructive periodontitis in conjunction with gingival KS, scaling and root planing and other periodontal therapy may be indicated along with intralesional or systemic chemotherapy.
4. BACILLARY (EPITHELIOD) ANGIOMATOSIS (BA) BA is an infectious vascularproliferative disease with clinical andhistologic features very similar tothose of kaposi’s sarcoma. Caused by Rickettsia likeorganism - Bartonellaciae henselia,quintana, or others.
Gingival manifestations are redpurple or blue edematous soft tissuelesions that cause destruction of theperiodontal ligament and bone.Histological picture Epitheloid proliferation of angiogeniccells Acute inflammatory cell infiltrate.
TREATMENTBroad-spectrum antibiotics suchas erythromycin or doxycycline inconjunction with conservativeperiodontal therapy and possiblyexcision of the lesion.
NON-HODGKIN’S L P OM YM H A Occurrence is more common in the gingiva. Has characteristic white verrucous surface or necrosis of thegingiva resembling ANUG.
6.ATYPICAL ULCERATIONSMost common reported oral ulcers seen in patients with HIV are due to herpes simplex virus, CMV, EBV, histoplasmosis, herpes zoster and mainly recurrent apthous ulcers are often associated.Oral viral infections are often treated with acyclovir (200 to 800 mg administered five times daily for atleast 10 days). Subsequent daily maintenance therapy (200mg two to five times daily) may be required to prevent recurrence.Resistant viral strains are treated with foscarnet, ganciclovir or valacyclovir hydrochloride.
Topical corticosteroid therapy (fluocinonidegel applied three to six times daily) is safe andefficacious for treatment of recurrent aphthousulcer or other mucosal lesions inimmunocompromised individuals. Prophylactic antifungal medications shouldbe prescribed Large aphthae in HIV+ve individuals may betreated with systemic corticosteriods (prednisone40 to 60 mg daily) or alternative therapy(thalidomide, levamisole, pentoxifylline).
ORAL HYPERPIGMENTATION:An increased incidence of oral hyperpigmentationhas been described in HIV-infected individuals.Pigmented areas often appear as spots or striationsin the buccal mucosa, soft palate and the gingiva ortongue.The pigmentation may relate to prolonged use ofdrugs such as zidovudine, ketoconazole orclofazimine.Zidovudine is also associated with excessivepigmentation of the skin and nails.
Oral pigmentation may be caused by, Adrenocorticoid insufficiencycaused by prolonged use ofketoconazole Pneumocystitis carinii infection Cytomegalovirus infection
H RE AT D IV L E P RIODONT DISE S E AL ASE The first report linking periodontal diseaseand HIV infection was published in 1985(Dennison et al) Classification on HIV related periodontaldisease of the EC Clearing house on oral problemsrelated to HIV infection 1993. Linear gingival erythema. Necrotizing ulcerative gingivitis. Necrotizing ulcerative periodontitis Necrotizing ulcerative stomatitis
1. LINEAR GINGIVAL ERYTHEMA:Characterized by a marginal band of intense erythema with more apical focal and/or diffuse areas of erythema that may extend beyond the mucogingival line and is associated with earlier stages of HIV infection and CD4+ suppression.No ulceration, pocketing or attachment loss and strongly resistant to local treatmentThe lesion may be localised or generalized in natureThe microflora of LGE may closely mimic that of periodontitis rather than gingivitis (Clark et al, 1991)
CANDIDIASIS ?Concomitant oral candidiasis and LGE lesions havebeen identified suggesting a possible etiologic rolefor candidial species in LGE (Lamster et al, 1994)Recently, direct microscopic cultures from LGElesions suggest that LGE may result from a chronicinfection with C. albicans or other candidial stainslike candida dubliniensis (Velegraki et al 1999)They also reported complete or partial remissionafter systemic antifungal therapy. But it is not yetknown whether candidial infections are etiologic inall LGE cases.
MANAGEMENT OF LGE:LGE is often refractory to treatment butlesions may undergo spontaneousremission.The success of treatment relies onidentifying the important causativefactors like plaque, tobacco or substanceusage, association with candidal infectionor presence of a number ofperiopathogenic bacteria consistent withthose seen in conventional periodontitis.
Step I: Instruct the patient in performance of meticulous oral hygieneStep II: Scale and polise affected areas, and perform subgingival irrigation with chlorhexidine.Step III: Prescribe chlorhexidine gluconate mouthrinse for 2 weeksStep IV: Reevaluate in 2-3 weeks. If lesions persistevaluate for possible candidiasis. Consider empiricadministration of a systemic antifungal agent such asfluconazole for 7-10 daysStep V: Re-treat if necessary and place the patient on 2-3 month recall.
2. NECROTIZING ULCERATIVE GINGIVITIS NUG has been associated with HIV infection. NUG is characteristic of red and swollen gingiva with yellowish – grey marginal areas ofnecrosis leading to destruction of inter-dentalpapillae usually takes a chronic or sub acutecourse. Spontaneous hemorrhage and characteristic fetor accompanied by severe pain. NUG rapidly progresses and becomes NUP.
MANAGEMENTBasis treatment consists of cleaning and debridement ofaffected areas with a cotton pellet soaked in peroxideafter application of topical anestheticEscharotic oral rinses such as hydrogen peroxideshould be avoidedThe patient should be seen daily or every other day forthe first week; debridement of affected areas is repeatedat each visit and plaque control methods are graduallyintroduced.A meticulous plaque control program should be taughtand started as soon as the sensitivity of the area allows it.
Patient should refrain from tobacco, alcohol andcondimentsAn antimicrobial mouthrinse such as chlorhexidinegluconate 0.12% should be prescribedSystemic antibiotics such as metronidazole or amoxicillinmay be prescribed for patients with moderate to severetissue destruction, localized lymphadenopathy or systemicsymptoms or both. The use of prophylactic antifungalmedication should be considered if antibiotics areprescribed.The periodontium should be re-evaluated 1 month afterresolution of acute symptoms to assess the results oftreatment and determine the need for further therapy.
NECROTIZING UL RAT CE IVE P RIODONT IS E IT NUP is necrotizing, ulcerative, rapidlyprogressive form of periodontitis which occurs inHIV – Positive individuals NUP may represent an extension of NUG inwhich bone loss and periodontal attachment lossoccurs. NUP is characterized by soft tissue necrosis,rapid periodontal destruction and interproximalbone loss. Lesions may be localized or generalizedand may be present after marked CD4+ celldepletion.
Bone is often exposed resulting in necrosis andsubsequent sequestration.On treatment, patients undergo spontaneousresolution of the necrotizing lesions, leavingpainless, deep interproximal craters that aredifficult to clean and may lead to conventionalperiodontitis (Glick et al, 2000).Data implicate a similar microbial component inboth NUP and chronic periodontitis (Glick et al1994, Murray etal 1991).
Glick and associates in 1994 reported theincidence of periodontal diseases in 700HIV+ve individuals.They found NUP in only 6.3% andconcluded that NUP is a predictivemarker for severe immune deficiencybecause patients with NUP were 20.8times as likely to have CD4+ lymphocytecounts <200/mm3
MANAGEMENT1. Gradual, gentle, local debridement of affected area.2. Scaling and root planing with oral hygiene instruction3. In office irrigation with an effective antimicrobial agent such as chlorhexidine gluconate or povidine iodine.4. Chlorhexidine gluconate 0.12% - 0. 2% mouth rinse twice daily.5. Metronidazole, 500 mg loading dose and 250 mg four times daily until ulcers are healed, alternatively penicillin or tetracycline.6. Prophylactic topical or systemic antifungal agent and followup visit within next 3 days.
NECROTISING ULCERATIVE STOMATITIS: NUS maybe severely destructive and acutely painful. It is characterized by necrosis of significant areas of oral soft tissue and underlying bone. It may occur separately or as an extension of NUP and is commonly associated with severe depression of CD4+ immune cells and an increased viral load (GRASSI et al 1988)
The condition appears to be identical tocancrum oris (NOMA), a rare destructive processoccasionally reported in nutritionally deprivedindividuals.
TREATMENT1. Prescription of an antibiotic such as Metronidazole and use of an antimicrobial mouthrinse such as Chlorhexidine gluconate.2. If osseous necrosis is present, it is often necessary to remove the affected bone to promote wound healing (Winkler et al, 1989).
CONCLUSION ANTIRETROVIRAL THERAPY IN ADULTSThe primary goals of antiretroviral therapy are:• to prolong life expectancy.• to improve quality of life.• to prevent development of opportunisticinfections and other AIDS-related conditions.• to encourage immune reconstitution.• to suppress viral replication as far as possible and for as long as possible.• to prevent transmission of the virus.
ANTIRETROVIRAL DRUGSDrugs currently available attempt to block viralreplication by inhibiting two viral enzymes -either HIV reverse transcriptase or the HIVprotease.Other drugs such as fusion Inhibitors, whichblock entry of the virus into the cell and HIVintegrase inhibitors which prevent integration ofDNA into the cell nucleolus, are underinvestigation.
REVERSE TRANSCRIPTASE INHIBITORS1. Nucleoside reverse transcriptase inhibitors (NRTIs)2. Non-nucleoside reverse transcriptase inhibitors(NNRTIs)These drugs forestall genetic integration of the virus. NRTIs resemble the natural nucleotide buildingblocks of DNA so that when the reverse transcriptase triesto add the drug to a developing strand of DNA, it cannotbe completed. NRTIs need to be activated first byphosphorylation. NNRTIs inhibit activity of the reversetranscriptase directly.
Nucleoside Reverse Transcriptase Inhibitors (NRTIs)Zidovudine (AZT, Retrovir®) 250mg - 300mg bd or 200mg tds.Stavudine (d4T, Zerit®) 40mg bd (30mg bd if weight < 60kg).Lamivudine (3TC®) 150mg bd.Didanosine (ddI, Videx®) 200mg bd (125mg bd if weight<60kg).Zalcitabine (ddC, Hivid®) 1.125mg bdAbacavir (Ziagen®) 300mg bd. Unfortunately this drug is currently very expensive.
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)Nevirapine (Viramune®)Dose: One 200mg tablet daily for twoweeks, then 200mg bd.Efavirenz (Stocrin®)Dose: 600mg once daily.
PROTEASE INHIBITORS Protease inhibitors act at a later stageand interfere with a viral enzyme, HIVprotease, which cleaves viral polyproteinsinto functional end products. This prevents the formation ofmature infectious virus and results in therelease of immature non-infectious viralparticles.
ADVERSE DRUG EFFECTS:Foscarnet, interferon and dideoxycytidine (DDC)occasionally induce oral ulcerations and erythemamultiforme has been reported with use ofdidanosine (DDI)Zidovudine and ganciclovir may induceleukopenia, resulting in oral ulcers.Xerostomia and altered taste sensation may beseen with diethyl dithiocarbamate (Dithiocarb).Drug induced mucositis and lichenoid drugreactions are common in HIV +ve patients.
Protease-inhibiting drugs can cause adversereactions including nausea, development of kidneystones, lypodystrophy, an increase in abdominalfat mass, and development of the classic “buffalohump” usually associated with administration ofsystemic corticosteroidCombined drug therapy may also induce moresevere liver cirrhosis in individuals with hepatitisc/HIV co-infections.The dentist should remain alert for general signsand symptoms of adverse drug effects, some ofwhich can affect oral tissues.
AIDS VACCINE ?Complication is mainly because the virus becomes latent incells and its cell surface antigens mutate rapidly. Nearly 25 vaccines are at various development stage based on recombinant viruses and viral envelope or core antigens. Difficulty in human trials lie in determining the safety of the vaccine in volunteers. One live attenuated virus vaccine had shown intact T- cell count after vaccination in SIV model. Inhumans the vaccine could expose humans to mutationand cancer and the virus itself could mutate to itsvirulent form and can spread.
In the viral vector technique, vaccinia virus oradenovirus is genetically engineered to carry onlythe HIV envelope gene. This hybrid virus replicatesand expresses the HIV genes when it is Injected intothe host stimulating immunity.
The median period between initial HIVinfection and outright AIDS is approximately 12years and the life expectancy of persons living withAIDS has been significantly prolonged with currentanti-retroviral drug therapy.This indicates that HIV-infected patients are potentialcandidates for conventional periodontal treatmentand treatment decisions should be based on overallhealth status of the patient, the degree of periodontalinvolvement and the motivation and ability of thepatient to perform effective oral hygiene procedures.
By combining local andsystemic therapy with newantiviral drugs, dental and medicalpractitioners may together help toreduce morbidity in HIV – infectedpatients.