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PERIODONTAL MANAGEMENT OF HIV

PATIENTS

ACHI JOSHI SAIMS, INDORE

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Contents 1. Introduction

2. Origin of aids

3. HIV- AIDS in India

4. Structure of HIV

5. Modes of transmission

6. Natural history of HIV

infection

7. Stages of HIV infection

8. CDC surveillance case classification

9. Classification of the most common

oral manifestations of aids

1. Lesions strongly associated

2. Lesions less commonly

associated

3. Lesion less seen in HIV.

10. PERIODONTAL TREATMENT

PROTOCOL

11. Treatment complications

12. Post exposure prophylaxis (PEP)

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INTRODUCTION

AIDS is a lethal viral infection caused by human immunodeficiency

virus (HIV) and is characterized by severe depletion of T4

lymphocytes with associated opportunistic infections.

Oral and perioral lesions are common in patients infected with

human immune deficiency virus (HIV), are often the presenting

feature, and may predict deterioration in general health and a

poor prognosis.

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• Most HIV-infected patients have head and neck

manifestations at some stage of disease and oral lesions are

often early signs.

(Schiodt & Pendborg 1989, Winkler & Robertson 1992)

• Due to multiple oral conditions and periodontal involvement,

periodontists are in a unique position to recognize possible HIV

infection in its early stage and to be involved in the oral care

of these patients.

ORIGIN OF AIDS

Studies comparing the genetics of HIV with various African monkey

viruses has provided some evidence.

HIV-1 & -2 are not closely related to each other as they are to simian

immunodeficiency virus (SIV).

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HIV 1

• HIV-1 is more common

worldwide

• HIV-1 is more pathogenic

• MTCT is relatively common

with HIV-1

HIV 2• HIV-2 is found in West

Africa, Mozambique, and

Angola.

• HIV-2 is less pathogenic

• Duration of HIV-2 infection

is shorter

• MTCT is relatively rare

with HIV-2

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History

• 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 of HIV.

• It probably remained in small isolated villages, causing

sporadic cases and mutating into more virulent strains

that were readily transmitted from human to human.

• AIDS was first recognized in 1981 in USA.

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• The causative virus was isolated in 1983 from blood

lymphocytes and was called Lymphadenopathy Associated

Virus (LAV).

• 1984 - Human T-cell Lymphotropic Virus –III (HTLV-III).

• The International Committee on virus nomenclature in 1986,

decided on the generic name Human Immunodeficiency Virus

(HIV).

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HIV- AIDS in INDIA • India’s first cases of HIV were

diagnosed in Chennai in 1986.

• It is estimated that around 2.5

million people(61% male, 39%

female, 3.5% children) are currently

living with HIV.

• High Prevalence States: Tamil Nadu,

Maharashtra, Karnataka, Andhra

Pradesh, Manipur and Nagaland

STRUCTURE OF HIV

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VIRAL ENEVELOP

VIRAL PROTEIN

CAPSID

RNA

RNA virus.

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MODES OF TRANSMISSION

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STAGES OF HIV INFECTION

1. ACUTE HIV SYNDROME

First stage seroconversion

Virus rapidly spreads to organs, especially the lymphoid tissues

HIV virus not very aggressive in causing diseases or severe symptoms

2. ASYMPTOMATIC STATE

 Infection is latent , No signs of HIV, immune system controls virus

production

 Virus starts to grow and multiply in the lymph nodes

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3. SYMPTOMATIC DISEASE/AIDS

  Viremia (spread of virus in the blood)

Physical signs of HIV infection

 Loss of immune system, mainly due to infection of CD4 T- Lymphocytes

4. END STAGE DISEASE

Immune system collapses

 Virus continues to slowly destroy the Immune System for up to 10 years

Usually an opportunistic infection is the cause of death

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CDC SURVEILLANCE CASE CLASSIFICATION

Category A : includes patients with acute symptoms or

asymptomatic diseases, along with individuals with persistent

generalised lymphadenopathy, with or without malaise , fatigue , or

low grade fever.

Category B : patients have symptomatic conditions such as : Oropharyngeal or vulvo-vaginal candidiasis Herpes zoster Oral hairy leukoplakia Idiopathic thrombocytopenia Constitutional symptoms of fever, diarrhoea and weight loss

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• Category C : patients are those with outright AIDS , as

manifested by life-threatening conditions or identified through

CD4+ T lymphocyte levels of less than 200 cells /mm3 (< 14%

of total lymphocytes)

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Classification of the Most Common Oral Manifestations of AIDS

Pindborg in 1989

• The first classification of the oral manifestations associated

with HIV-infection- based on etiological aspects and

distinguished between lesions caused by fungi, bacteria,

viruses, neo- plastic lesions.

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EEC-Clearinghouse on oral problems related to HIV-infection and WHO collaborating center on oral manifestations of the human immunodeficiency

virus.

In 1990, the classification was modified to establish three main groups:

1. Lesions strongly associated with HIV-infection

2. Lesions less commonly associated with HIV-infection, and

3. Lesions seen in HIV-infection

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Lesions strongly associated with HIV/ AIDS

• Oral candidiasis

• Oral hairy leukoplakia

• Kaposi’s sarcoma

• Non-Hodgkin’s lymphoma

• Periodontal diseases -

Linear Gingival Erythema

Necrotizing Ulcerative Gingivitis

Necrotizing Ulcerative Periodontitis

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Lesions less commonly associated

• Bacterial infections-

• Mycobacterium tuberculosis

• Mycobacterium

aviumintracellularae

• Melanotic hyperpigmentation

• Necrotizing ulcerative stomatitis

• Salivary gland diseases- xerostomia

• Thrombocytopenic purpura

• Ulceration (not otherwise

specified)

• Viral infections –

• Herpes simplex virus

• Human papilloma virus

• Condyloma accuminatum

• Multifocal epithelial

hyperplasia

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Lesions seen in HIV infectionBacterial infections:

• Actinomyces israelii

• Escherichia coli

• Klebsiella pneumonia

• Cat-scratch disease

Drug reactions,

• erythema multiforme,

• lichenoid,

• Toxic epidermolysis

Epitheliod (bacillary)angiomatosis

Fungal infection other than

candidiasis

• Cryptococcus neoformans

• Geotrichum candidum

• Histoplasma capsulatum

• Mucoraceae (mucomycosis

zygomycosis)

• Aspergilus flavus

Neurological disturbances

• Facial palsy

• Trigeminal neuralgia

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MOST COMMON ORAL MANIFESTATIONS OF

AIDS

ORAL CANDIDIASIS• Most oral candidal infections are associated with candida albicans

• Candidiasis is the most common oral lesion in HIV diseases and found in 90% AIDS

patients

It has 4 clinical presentations :

1. pseudomembraneous candidiasis

2. erythematous candidiasis

3. hyperplastic candiasis

4. angular cheilitis

Pseudomembraneous candidiasis

Oral Thrush

Multiple superficial, creamy white

plaques that can be easily wiped off

revealing erythematous base.

Yellow white curd-like lesion

Common on hard and soft palate, buccal

and labial mucosa and dorsal surface of

tongue

• Erythematous candidiasis

Appears as red patches

Seen on tongue or palatal mucosa

Associated with depapillation of the tongue

• Hyperplastic candidiasis

Least common form

Lesions appear white and cannot be removed by

scrapping.

Seen in buccal mucosa and tongue

More resistant to removal than other types

• Angular cheilitis

Seen on commissures of lips

Appear as erythematous with surface crusting and fissuring

1. Early oral lesions 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.

MANAGEMENT

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Topical drugs

• CLOTRIMAZOLE (candid® ) 10mg tablets: dissolve in mouth 3-5tablets daily for 7-

14days

• NYSTATIN ( mycostatin® , nystec ® )

a) Oral suspension - (100,000 U/ml : Disp 240ml) Rinse with 1tsp qid.

b) Oral suspension- (extemporaneous) mix 1/8tsp with 4 oz water

c) Tablets(500,000U)- Dissolve 1tablet in mouth 4-5times daily.

d) Pastilles (200,000U)- dissolve 1-2 pastilles in mouth,4-5times daily.

e) Ointment 15g tube- Apply to affected area 3-4times daily

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CLOTRIMAZOLE ( candid) ointment 15g tube: apply to affected area

qid.

MICONAZOLE (oravig)2% ointment 15g tube: qid application.

ITRACONAZOLE ( icoz , sporonox) oral suspension 100-200mg once

daily for 7-28 days.

FLUCONAZOLE oral suspension 200mg of 1st day followed by 100mg

once daily for atleast 2weeks. (3mg/kg)

AMPHOTERICIN B oral suspension 100mg four times daily for 2 weeks.

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Systemic drugs

• Ketoconazole (hyphoral) 200mg tablets: 2 tablets immediately, then 1-2

tablets daily for 5-14days.

• Fluconazole (Diflucan) 100mg tablets: 2 tablets immediately, then 1 tablet

daily for 7-14 days. ( conflu)

• Itraconazole (Sporanox) 100mg capsules: 200mg once daily with meals for

4 weeks.

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ORAL HAIRY LEUKOPLAKIA

• Oral hairy leukoplakia most commonly presents as a

white ragged, corrugated or irregular lesion with a hair

like appearance involving the lateral and dorsolateral

tongue.

• Lesions may be unilateral or bilateral.

• Hairy leukoplakia is caused by infection of the lesion

epithelial cells with Epstein-Barr virus (EBV) and is

associated with immune deterioration.

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MANAGEMENT

• Oral hairy leukoplakia generally does not require treatment.

• Resolution has been reported after therapy with acyclovir, zidovudine,

podophyllin and interferon, but usually recurs when treatment is

discontinued.

• In cosmetically objectionable patients, lesions can be removed with laser or

conventional surgery.

• The incidence of OHL has been markedly reduced since the advent of

multidrug antiviral therapy for HIV infection.

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KAPOSI’S SARCOMA

• Kaposi’s sarcoma is a rare, multifocal vascular neoplasm which is the most

common malignant tumor associated with HIV infection.

• Herpes virus (HHV-8)

• This is an aggressive lesions and involves most frequently the palate 95% and

the gingiva 23%

• Kaposi’s sarcoma oral lesions may interfere with function, be cosmetically

objectionable, and proliferate uncontrollably.

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• Early lesions are painless, and appear as reddish purple macules of the

mucosa.

• As lesions progresses it becomes nodular, papular or non-elevated

macules, brown or purple in colour.

• May ulcerate and become painful with difficulty in eating and speech and

may cause cosmetic problems .

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Management • Treatment of oral KS may include use of

• Antiretroviral agents

• Laser excision

• Radiation therapy

• Nichols et al in 1993 described the successful use of intra-lesional injection

of vinblastine at a dosage of 0.1 mg/cm sq.

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• Intra-lesional injections with sodium tetradecyl sulfate (a sclerosing

solution) also have been effective.

• In case of destructive periodontitis in conjunction with gingival KS, scaling

and root planing and other periodontal therapy may be indicated along

with intra-lesional or systemic chemotherapy.

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NON-HODGKIN’S LYMPHOMA

• Second most common neoplasm

• Lesion are large, painful, ulcerated mass.

• Occurrence is more common in the gingiva.

• Has characteristic white verrucous surface or necrosis of the gingiva

resembling ANUG.

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MANAGEMENT

• Surgical excision

• Anti- cancer drugs

• Radiation therapy

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HIV RELATED PERIODONTAL DISEASES• The first report linking periodontal disease and HIV infection was published

in 1985 (Dennison et al)

• Classification on HIV related periodontal disease of the EC Clearing house

on oral problems related to HIV infection 1993.

• Linear gingival erythema.

• Necrotizing ulcerative gingivitis.

• Necrotizing ulcerative periodontitis

• Necrotizing ulcerative stomatitis

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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 treatment

The lesion may be- localised

generalized

• The microflora of LGE may closely mimic that of periodontitis rather than

gingivitis (Clark et al, 1991)

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MANAGEMENT

• LGE is often refractory to treatment but lesions may undergo spontaneous

remission.

• The success of treatment relies on identifying the important causative

factors like plaque, tobacco or substance usage, association with candidal

infection or presence of a number of periopathogenic bacteria consistent

with those seen in conventional periodontitis

• Scaling, CHX mouthwash and proper home care.

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• Step I: Instruct the patient in performance of meticulous oral hygiene

• Step II: Scale and polish affected areas, and perform subgingival irrigation

with chlorhexidine.

• Step III: Prescribe chlorhexidine gluconate mouthrinse for 2 weeks

• Step IV: Reevaluate in 2-3 weeks. If lesions persist evaluate for possible

candidiasis. Consider empiric administration of a systemic antifungal agent

such as fluconazole for 7-10 days

• Step V: Re-treat if necessary and place the patient on 2-3 month recall.

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NECROTIZING ULCERATIVE GINGIVITIS

• NUG has been associated with HIV infection.

• NUG is characteristic of red and swollen gingiva with

yellowish – grey marginal areas of necrosis leading to

destruction of inter-dental papillae usually takes a chronic or

sub acute course.

• Spontaneous hemorrhage and characteristic fetor

accompanied by severe pain.

• NUG rapidly progresses and becomes NUP.

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Management • Basis treatment consists of cleaning and debridement of

affected areas with a cotton pellet soaked in peroxide after

application of topical anesthetic

• The patient should be seen daily or every other day for the

first week; debridement of affected areas is repeated at each

visit and plaque control methods are gradually introduced.

• A meticulous plaque control program should be taught and

started as soon as the sensitivity of the area allows it.

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• Patient should refrain from tobacco, alcohol and condiments

• An antimicrobial mouthrinse such as chlorhexidine gluconate 0.12%

should be prescribed

• Systemic antibiotics such as metronidazole or amoxicillin may be

prescribed for patients with moderate to severe tissue destruction,

localized lymphadenopathy or systemic symptoms or both. The use of

prophylactic antifungal medication should be considered if antibiotics are

prescribed.

• The periodontium should be re-evaluated 1 month after resolution of

acute symptoms to assess the results of treatment and determine the

need for further therapy.

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NECROTIZING ULCERATIVE PERIODONTITIS

• NUP is necrotizing, ulcerative, rapidly progressive

form of periodontitis which occurs in HIV Positive

individuals

• NUP may represent an extension of NUG in which

bone loss and periodontal attachment loss occurs.

• NUP is characterized by soft tissue necrosis, rapid

periodontal destruction and interproximal bone loss.

Lesions may be localized or generalized and may be

present after marked CD4+ cell depletion.

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• Bone is often exposed resulting in necrosis and subsequent

sequestration.

• On treatment, patients undergo spontaneous resolution of the

necrotizing lesions, leaving painless, deep interproximal craters

that are difficult to clean and may lead to conventional

periodontitis (Glick et al, 2000).

• Data implicate a similar microbial component in both NUP and

chronic periodontitis (Glick et al 1994, Murray et al 1991).

• They found NUP in only 6.3% and concluded that NUP is a

predictive marker for severe immune deficiency because patients

with NUP were 20.8 times as likely to have CD4+ lymphocyte

counts <200/mm3

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MANAGEMENT

• Gradual, gentle, local debridement of affected area.

• Scaling and root planing with oral hygiene instruction

• In office irrigation with an effective antimicrobial agent such as chlorhexidine

gluconate or povidine iodine.

• Chlorhexidine gluconate 0.12% - 0. 2% mouth rinse twice daily.

• Metronidazole, 500 mg loading dose and 250 mg four times daily until ulcers

are healed, alternatively penicillin or tetracycline.

• Prophylactic topical or systemic antifungal agent and follow up visit within

next 3 days.

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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)

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Management

• Metronidazole

• Antimicrobial mouth rinse

• If osseous necrosis is present, its necessary to remove the affected bone to

promote wound healing

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ORAL HYPERPIGMENTATION• An increased incidence of oral hyperpigmentation has been described in

HIV-infected individuals.

• Pigmented areas often appear as spots or striations in the buccal mucosa,

soft palate and the gingiva or tongue.

• The pigmentation may relate to prolonged use of drugs such as zidovudine,

ketoconazole or clofazimine.

• Zidovudine is also associated with excessive pigmentation of the skin and

nails.

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Oral pigmentation may be caused by,

• Adrenocorticoid insufficiency caused by

prolonged use of ketoconazole

• Pneumocystitis carinii infection

• Cytomegalovirus infection

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ATYPICAL ULCERS

• HIV-infected patients have a higher incidence of recurrent herpetic lesion and

aphthous stomatitis

• Atypical large , persistent , non specific, painful ulcers

• Caused by-

• herpes simplex virus (HSV)

• varicella-zoster virus (VZV)

• epstein-barr virus (EBV)

• cytomegalovirus (CMV)

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Herpes labialis

• Seen as vesicles on lip and adjacent facial skin which break down to produce

shallow ulcers.

• HIV infected individuals responsive to topical antiviral therapy

• Acyclovir , pencyclovir , doconasol

• Reduces healing time of lesion

Recurrent aphthous stomatitis

• Sites : oropharynx, oesophagus, or other areas of GIT.

• Treatment:- Topical or intralesional corticosteroids, chlorhexidine,

antimicrobial mouth rinses, oral tetracycline rinses

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• Topical corticosteroid therapy (fluocinonide gel applied three to six times

daily) is safe and efficacious for treatment of recurrent aphthous ulcer or

other mucosal lesions in immunocompromised individuals.

• Prophylactic antifungal medications should be prescribed

• Large aphthae in HIV+ve individuals may be treated with systemic

corticosteriods - prednisone 40 to 60 mg daily

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Xerostomia

• Xerostomia may be associated with HIV disease and may be a complication of

prescribed medication that may be xerostomic.

• The disease is characterized by diffuse enlargement of the major salivary glands

and/ or xerostomia. CMV has been demonstrated in the salivary gland of xerostomic

patients (Greenspan et al. 1992).

• Identification of the dry mouth and reduced saliva production can also lead to further

investigation and diagnosis and requires management in order to control the

conditions associated with a dry mouth including increased risk of candidiasis and

caries risk. In addition, management of xerostomia will improve oral comfort, may

affect the quality of speech, and affect the use of any prosthesis.

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Treatment • Salivary stimulants – sugar free gums

• Systemic sialogouges pilocarpin 5 mg - 3 times daily

• Flouride rinses- decay

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BACILLARY (EPITHELIOD) ANGIOMATOSIS (BA)

• BA is an infectious vascular proliferative disease with clinical and histologic

features very similar to those of kaposi’s sarcoma.

• Caused by Rickettsia like organism - Bartonellaciae henselia, quintana, or

others.

• Gingival manifestations are red purple or blue edematous soft tissue

lesions that cause destruction of the periodontal ligament and bone.

• Histological picture

Epitheloid proliferation of angiogenic cells

Acute inflammatory cell infiltrate.

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TREATMENT

• Broad-spectrum antibiotics such as erythromycin or doxycycline in

conjunction with conservative periodontal therapy and possibly excision

of the lesion.

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PERIODONTAL TREATMENT PROTOCOL

• HEALTH STATUS

• INFECTION CONTROL MEASURES

• GOALS OF THERAPY

• SUPPORTIVE PERIODONTAL THERAPY

• PSYCHOLOGIC FACTORS

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HEALTH STATUS1. Should be determined from the health history, physical evaluation and

consultation with the patient’s physician.

2. Treatment decisions will vary depending on the patient’s state of health

3. 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

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Viral load

Severity of illness is determined by amount of

virus in the body (increasing viral load) and

the degree of immune suppression

(decreasing CD4+ counts)

Higher the viral load, the sooner immune

suppression occurs

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INFECTION CONTROL MEASURES

1. 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).

2. A number of pathogenic microorganisms may be transmitted in

the dental setting and these include:

• Airborne pathogens - tuberculosis

• Blood borne pathogens -HIV, HBV, HCV

• Waterborne pathogens Legionella and Pseudomonas species

• Mucosal/ skin borne pathogens VZV or HSV

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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 + patients

• NUP & NUS can be severely destructive to periodontal structures and

should be treated appropriately.

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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

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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.

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DENTAL TREATMENT COMPLICATIONS1. Adverse Drug Effects

• Foscarnet, Interferon - Oral ulcerations

• Didanosine - Erythema Multiforme

• Zidovudine & Ganciclovir - Leucopenia

• Dithiocarb - Xerostomia & Altered taste sensation

• HIV-positive patients more susceptible to drug-induced Mucositis &

Lichenoid drug reactions

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2. HAART drugs

• Insulin resistance, gynecomastia, blood dyscrasias, nausea, development of kidney

stones, oral warts

• Individuals with Hepatitis C + HIV co- infection are susceptible to liver cirrhosis

Lipodystrophy

• Redistribution of body fat

• Gaunt facial features yet display excessive abdominal fat or even a fat pad on the

rear of the shoulders (buffalo hump)

Severe systemic hyperlipidemia

Oral or perioral adverse effects oral lichenoid reactions, xerostomia, altered taste

sensation, perioral parasthesia, and exfoliative cheilitis

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TO ERR IS HUMAN

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Post exposure prophylaxis (PEP)• The term post-exposure prophylaxis mean the medical response

given to prevent the transmission of blood-borne pathogens

following a potential exposure to HIV.

• PEP should be provided following exposure of non-intact skin

(through percutaneous sharps injury or skin abrasion) or mucous

membranes (through sexual exposure or splashes to the eyes, nose

or oral cavity) to a potentially infected body fluid from a source

that is HIV-positive or has unknown HIV status.

•

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•When exposure occurs, Provide immediate care to the exposure

site.

•Wash needlestick injuries and cuts with soap and water.

• Flush mucous membranes with a sterile solution of water or

saline. If sterile solutions are not available, use clean potable

water.

• No data have demonstrated that using antiseptics or squeezing a

wound reduces the risk of transmission of a bloodborne pathogen.

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Evaluating eligibility for HIV post-exposure prophylaxis involves

assessing the following:

• The timing of the potential exposure

• The person’s HIV status

• The nature and risk of the exposure and

• The HIV status of the source of the potential exposure

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Conclusion

• HIV associated oro-facial lesions have been considered-

• Early clinical picture thus act as Clinical indicators of HIV in

otherwise healthy individual

• Also oral lesions are predictors of disease progression.

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THANK YOU