Periodontal Management of HIV-infected Patients : An Overview

Recognition and diagnosis of the general oral manifestations and specific periodontal manifestations of HIV infection will continue to be a major responsibility of the dental practitioner. By combining local and systemic therapy aimed at both preventing and treating oral lesions and periodontal diseases, combined with new systemic antiviral and vaccine therapies, dental and medical practitioners may together help reduce both the dental morbidity and the overall patient morbidity in the HIV infected patient. With the advent of newer pharmacological approaches to the treatment of human immunodeficiency virus (HIV) infection, the incidence and progression of both atypical and conventional periodontal diseases are changing. While the accepted approaches to treating the spectrum of periodontal diseases in HIV patients remain essentially unchanged over the past 15 years, the impact of newer systemic therapies on patient immunocompetence may influence treatment decisions.


INTRODUCTION
HIV infection remains a global health problem of unprecedented dimensions.Unknown 27 years ago, HIV has already caused an estimated 25 million deathsworldwide and has generated profound demographic changes in the most heavily affected countries.While the percentage of people living with HIV has stabilized since 2000, the overall number of people living with HIV has steadily increased, as new infections occur each year, HIV treatments extend life and in addition, new infections still outnumber AIDS deaths.Eradication of HIV infection cannot be achieved withavailable antiretroviral regimens.This is mainly attributed to the fact that the pool of latently infected CD4 + Tcells is established during the earliest stages of acute HIV infection and persists with a long halflife, even with prolonged suppression of plasma viraemia 1 Human immunodeficiency virus (HIV) is a lent virus (a member of the retrovirus family) that causes acquired immunodeficiency syndrome (AIDS), a condition in humans in which the immune system begins to fail, leading to life-threatening opportunistic infections.

Oral lesions associated with hiv infection
The first report linking periodontal disease and HIV infection was published in 1985

Viral infections
Cytomegalovirus, Molluscum contagiosum, Linear gingival erythema Two types of gingival/periodontal disease associated with HIV infectionhave been widely reported in the literature.In the past, these have been called HIV-associated gingivitis (HIV-G) and HIV-associated periodontitis (HIV-P).There is now evidence that these diseases also occur in HIVnegativeimmunocompromised individuals and are not specific to HIV infection, thus making the original terms inappropriate.[6] It is not yet clear where in the spectrum of HIV disease these conditions occur or which patients are at greatest risk for developing them There is some evidence that NUP is associated with a low CD4 count (<200 cells/mm3) 7

Periodontal considerations
Periodontal diseases form an important part of the constellation of oral manifestations of HIV infection 8 as lesions strongly associated with the infection.As a microbial disease affecting the hard and the soft tissues of the oral cavity, periodontal diseases acquire a unique status in the diversity of their manifestations, having implications not only for oral health but also on systemic health.Parra B et al ., 1996, stated that Human viruses have been identified in GCF from periodontal pockets. 9Some investigations done byBarr et al.1996 have assessed HIV viral burden in oral fluids by means of HIV RNA quantification. 10ugars et al., 11 who quantified HIV-1 RNA in saliva and plasma of 40 HIV seropositive adults.Many (42%) of their subjects had detectable salivary HIV-1 RNA, which highly correlated with plasma viral levels, and HIV-associated periodontal disease.Patel et al., 2003 concluded from his research works that, many species of the periodontal microflora found in sites with diseases associated with HIV are also found in non-HIV infected individuals with classic periodontitis in particular, Porphyromonas gingivalis, Prevotellai ntermedia, Fusobacterium nucleatum, A.Actinomycetemcomitans, Eikenellacorrodens, and Campylobacter rectus.A combination of certain periodontal pathogens may be responsible for chronic periodontitis seen in HIV-infected patients .threecombinations of periodontal pathogens (P.nigrescens and C. rectus; P. nigrescensand P. gingivalis; and P. nigrescens and T. denticola) were significantly associated with HIV-positive compared with HIVnegativepatients. 12 In GCF of HIV-positive patients, the levels of IL-1, IL-6, and TNF were higher than thenon-HIV infected individuals.The levels were higher in deeper pockets than in shallow pockets. 13This may explain the increased rate of attachment loss and tissue destruction seen in HIV-positive patientsan in the GCF of HIV-negative patients.

Management
The most important components in the management of HIVassociatedgingival and periodontal disease should be the removal of local irritants from the root surfaces, debridement of necrotic tissues, and appropriate use of antibiotics.

Systemic
antibiotics, such as metronidazole, tetracycline, clindamycin, amoxicillin, and amoxicillin-clavulanate potassium, should be combined with debridement of necrotic tissues.As systemic antibiotics increase the patient's risk of developing candidiasis, concurrent, empiric administration of an antifungal agent should be considered.
Frequent appointments are appropriate and recommended in the acute and healing stages of NUP to perform the necessary periodontal therapies, to assess tissue response, and to monitor the patient's oral hygiene performance.

Linear gingival erythema
There is, on the other hand, little information based on controlled studies of linear gingival erythema.
Conventional therapy plus rinsing with 0.12% chlorhexidine gluconate twice daily has shown significant improvement after 3 months 14 However, HIV-associated free gingival erythema did not respond to removal of plaque by intense scaling and root leavage and improved plaque control measures alone or supplemented with povidoneiodine irrigation 3-5 times daily.
No significant improvement in clinical features or indices was obtained after 1 or 3 months of treatment.However,povidine-iodine substantially reduced pain associated with the lesions. 15

Necrotizing Gingivitis
Necrotizing gingivitis in HIV-infected patients does not always respond to conventional treatment with scaling and improved oral hygiene. 15owever, the adjunctive use of metronidazole in these patients is reported to be extremely effective in reducing acute pain and promoting rapid healing. 16e to the susceptibility of HIV-infected patients to leavaginfections simultaneous treatment with appropriate antimycotic agents may be necessary.Sometimes healing is delayed in HIVinfected patients and pain may be prolonged.
Necrotizing periodontitis in HIV-infected patients does not always respond to conventional treatment with scaling and improved oral hygiene. 15owever, the adjunctive use of metronidazole in these patients is reported to be extremely effective in reducing acute pain and promoting rapid healing. 16Due to the susceptibility of HIV-infected patients to leavag infections simultaneous treatment with appropriate antimycotic agents may be necessary.Sometimes healing is delayed in HIVinfected patients and pain may be prolonged.

Necrotizing Periodontitis
In Initial visit,Prescribe narrow spectrum antibiotics such as metronidazole 500 mg, dispense 14 to 20 tablets, take 1 tablet twice daily for 7 to 10 days.Other antibiotic options include clindamycin and amoxicillin.Pain management is extremely important, Nutritional supplementation or counseling may be necessaryDetailed periodontal care, such as scaling and root planning as afollowup visits. 17

Necrotizing stomatitis
The treatment aspects for necrotizing stomatitis are similar to those mentioned for necrotizing periodontitis.

Anti Fungal medications Dosage
Ketoconazole (an imidazole), fluconazole Common dosage: ketoconazole 200 mg once daily; (a triazole), itraconazole (a triazole) fluconazole 100 mg once daily; and itraconazole 200 mg once daily.Amphotericin B (a polyene antifungal agent) Used as an intravenous medication that may be used for candidiasis resistant to other medications.(Note: Amphotercin B is also available as a topical preparation.)

Anti Fungal medications Dispense Dosage
Clotrimazole troches (an imidazole) 2-to 4-week Slowly dissolve one 10-mg troche supply in mouth 5 times/day for treatment.Slowly dissolve 1 troche in mouth 3 times/day for maintenance therapy.Nystatin oral suspension (a polyene 2-to 4-week Hold 1 teaspoonful (500,000 u) in antifungal agent)* supply mouth for 5 minutes, 4 times/day.Amphotericin B oral suspension (a 2-to 4-week Place 1 mL (100 mg) on tongue polyene antifungal agent) † supply and swish in mouth for as long as possible before swallowing.

Anti-retroviral drugs
Act at different stages of life cycle of HIV 1.
One that blocks binding of HIV to target cells 2.
One that blocks viral RNA leavage.

3.
One that inhibits enzyme reverse transcriptase.

Classification Inhibitors of viral attachment
Recombinant soluble CD4 or immunoglobulins

Integrase Inhibitors
Agents that block virus assembly and budding: Interferons

Antiretroviral Therapy Regimens
Antiretroviral therapy (ART) is the combination of several antiretroviral medicines used to slow the rate at which HIV makes copies of itself (multiplies) in the body.A combination of three or more antiretroviral medicines is more effective than using just one medicine (Monotherapy) to treat HIV.Currently, the national programme provides the following combinations for first-line regimens.
The development of highly active antiretroviral therapy (HAART) especially after 1995, has significantly modified the course of HIV disease, at least in the industrialized world, into a manageable chronic disease.With longer survival and improved quality of life inHIV-infected.HAART generally consists of a dual nucleoside analogue reverse transcriptase inhibitor (NRTI) backbone' and a third or drug, such as a no nucleoside inhibitor (NNRTI) or a protease inhibitor (PI), usually a "boosted' one.The use of a NNRTI as a third drug is less potent and therefore, in most settings not a preferred option and it is recommended that baseline resistance testing should guide the specific regimen design.HAART increases CD4 + cell count, decreases levels of HIV RNA and extends AIDSfree survival, at least in the short-term.Moreover, HIV suppression with antiretroviral therapy may decrease inflammation andImmune activation thought to contribute to higher rates of cardiovascular and other co-morbidities reported in HIV-infected cohorts.Cannot be achieved with available antiretroviral regimens.This is mainly attributed to the fact that the pool of latently infected CD4 + T-cells is established during the earliest stages of acute HIV infection and persists with a long half-life,even with prolonged suppression of plasma viraemia. 19,20(i)Stavudine (30 mg) + Lamivudine (150 mg) (ii)Zidovudine (300 mg) + Lamivudine (150 mg) (iii)Stavudine (30 mg) + Lamivudine (150 mg) + Nevirapine (200 mg)(iv)Zidovudine (300 mg) + Lamivudine (150 mg) + Nevirapine (200 mg)(v)Efavirenz (600 mg)(vi)Nevirapine (200 mg)

CONCLUSION
By combining local and systemic therapy aimed at both preventing and treating oral lesions and periodontal diseases, combined with new systemic antiviral and vaccine therapies, dental and medical practitioners may together help reduce both the dental morbidity and the overall patient morbidity in the HIV infected patient.