HIV & PERIODONTIUM

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Presented by

Dr. Dandu Sivasai Prasad

1st yr post graduate

Mamata dental college

CONTENTS Introduction

History

Epidemiology AIDS

CDC definition and classification of AIDS

Virus structure

Mode of transmission

Life cycle of HIV

Clinical features-WHO classification2

Contents…

Classification of oral lesions associated with HIV

Periodontal manifestations of HIV

Periodontal management of HIV infected patients

Diagnostic tests

Occupational exposure and Post-Exposure prophylaxis

Sterilization and precautions to be taken

Conclusion

References3

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INTRODUCTION:

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HISTORY:

1959- Scientists isolated earliest known case of AIDs

1978- Gay men in US, Sweden and Hetrosexuals in Tanzania and Haiti- Showed signs

1981, June 5th- CDC reported confirmed CMV and Candidal infection(LAV)

In 1982 july 27th, the term AIDs first used

In 1984, Robert Gallo discovered the HIV virus- HTLV-III

EPIDEMIOLOGY OF AIDS• As of 2012, approximately 35.3 million people are living with

HIV globally. Of these, approximately 17.2 million are men,

16.8 million are women and 3.4 million are less than 15 years

old. There were about 1.8 million deaths from AIDS in 2010,

down from 2.2 million in 2005

• Sub saharan africa is the region most affected. In 2010, 68%

(22.9 million) of all HIV cases.

• 66% of all deaths (1.2 million).6

EPIDEMIOLOGY OF AIDS…

• The total number of people living with HIV in India is

estimated at 2.4 million.

•  61% male and 39% female.

• The four high prevalence states of South India account for

57% of all HIV infections in the country. Andhra Pradesh-

500,000 cases; Maharashtra- 420,000 cases,  Karnataka -

250,000 cases and Tamil Nadu-150,000 cases

• IDU-12.22% :MSM- 6.82% :FSW at 5.92%. HIV prevalence

amongst IDU, MSM and FSW is 14.92%, 10.31% and 9.48%

respectively

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VIRUS STRUCTURE

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P17

P24

P7

MODE OF TRANSMISSION:

• HIV detected in most body fluids including.

• Blood

• Semen

• Vaginal secretions

• Cerebrospinal fluid

• Breast milk

• Urine

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MODE OF TRANSMISSION…

• Sexual contact

• Blood transfusion

• Needle sharing

• Perinatal transmission

• Intrauterine Postnatal

• Occupational exposure

• Organ transplantation

• Artificial insemination

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LIFE CYCLE OF HIV

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CDC SURVEILLANCE CASE CLASSIFICATION:

• 1982- “presence of oppurtunistic illness or malignancies

secondary to defective immunity in HIV+ individuals”

• 1993-“ inclusion of severe immunodeficiency as

definitive for AIDS”

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AIDS patients have been grouped as follows, according

to the CDC Surveillance Case Classification (1993);

Category A - Acute symptoms or asymptomatic

diseases,.

Category B - Patients have symptomatic

Category C - Life-threatening conditions.

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WHO classification of HIV-associated clinical disease CLINICAL STAGE 1 CLINICAL STAGE 2 CLINICAL STAGE 3 CLINICAL STAGE 4

Asymptomatic Unexplained moderate weight loss (<10)

Unexplained severe weight loss (> 10%), diarrhoea /persistent fever (longer than

one month)

Pneumocystis pneumonia

Persistent generalized lymphadenopathy

Recurrent upper RTI Persistent oral candidiasis Recurrent bacterial pneumonia

Herpes zoster Oral hairy leukoplakia Chronic herpes simplex infection

Angular cheilitis Pulmonary tuberculosis Oesophageal candidiasis

Recurrent oral ulceration Severe bacterial infections Extrapulmonary tuberculosis

Papular pruritic eruptions Acute necrotizing ulcerative stomatitis, gingivitis/periodontitis

Kaposi sarcoma /Lymphoma/Invasive cervical carcinoma

Fungal nail infection Unexplained anaemia (<8 g/dl ), neutropenia (< 0.5 x 109/l) and chronic

thrombocytopenia (< 50)

Cytomegalovirus infection

Central nervous system toxoplasmosis

HIV encephalopathy

Extra pulmonary cryptococcosis including meningitis

Disseminated non-tuberculous mycobacteria infection

Chronic cryptosporidiosis

Chronic isosporiasis

Disseminated mycosis

Atypical disseminated leishmaniasis

Symptomatic HIV-associated nephropathy or HIV-associated

cardiomyopathy

Classification and diagnostic criteria for oral lesions in HIV infection. 1993 revised

Group 1: Lesions strongly associated with HIV infection Candidiasis

Erythematous

Pseudomembranous

Hairy leukoplakia Kaposi’s sarcoma Non-Hodgkin’s lymphoma

Periodontal disease Linear gingival erythema Necrotizing (ulcerative) gingivitis Necrotizing (ulcerative) periodontitis

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Group 2: Lesions less commonly associated with HIV

infection:

Bacterial infections like

Mycobacterium avium - in tracellulare

Mycobacterium tuberculosis

Melanotic hyperpigmentation

Necrotizing (ulcerative) stomatitis

Salivary gland disease

Thrombocytopenic purpura

Ulceration not otherwise specified

Viral infections

Dry mouth due to decreased salivary flow rate

Unilateral or bilateral swelling of major salivary glands

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• Group 3. Lesions seen in HIV infection

Bacterial infections like

Actinomyces israelii

Escherichia coli

Klebsiella pneumoniae

Cat-scratch disease

Drug reactions (ulcerative, erythema multiforme,

lichenoid, toxic epidermolysis)

Epithelioid (bacillary) angiomatosis

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Fungal infection other than candidiasis

-Cryptococcus neoformans

-Geotrichum candidum

-Histoplasma capsulatum

-Mucoraceae (mucormycosis / zygomycosis)

-Aspergillus flavus

Nervous system disturbances

-Facial palsy

-Trigeminal neuralgia

Recurrent aphthous stomatitis

Viral infections

Cytomegalovirus

Molluscum contagiosum

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MEDICAL MANAGEMENT

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ANTI-RETROVIRAL DRUGS

One that blocks binding of HIV to target cells

One that blocks viral RNA clevage

One that inhibits enzyme reverse transcriptase 20

IDEAL REQUIREMENTS

1. Should be as specific as possible.

2. Should reduce viral production from infected cells.

3. Can be administered orally.

4. Should cross blood- brain barrier easily.

5. Should not develop resistance.

6. Shouldn’t be toxic.21

ART…

• Zidovudine (AZT, ZDV)

• Retrovir

• Didanosine

• Videx

• Zalcitabine

• Hivid

• Stavudine

• Zerit

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Nucleoside - stop HIV from replicating within cells by inhibiting the reverse transcriptase protein.

ART…

• Nevirapine

• Viramine

• Delaviradine

• Rescriptor

• Efavirenz

• Sustiva

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Non-nucleoside Reverse transcriptase inhibitors- stop HIV replicating within cells by interfering with HIV's reverse transcriptase protein which it needs to make new

copies of itself

ART…

• .

• Saquinavir

• Invirase

• fortovase

• Ritonavir

• Norvir

• Indinavir

• Crixivan

• Relfiravir

• Viracept

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Protease inhibitors- binds to the protease molecules and interfere with its cleaving function and are more effective viral inhibitors:

“COCKTAIL” OR TRIPLE-THERAPY

• HAART

• Regimens include atleast one protease inhibitor or non-

nucleoside reverse transcriptse inhibitor in addition to one or

more nucleoside reverse transcriptase inhibitors

• SIDE EFFECTS

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• Hemo-Modulator

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works by filtering a patient's blood through the device which blasts

ultraviolet light onto the blood. The ultraviolet light effectively kills

the virus and jump starts the patient's immune system.

PROBIOTICS FOR HIV• Lin Tao (2008) and his colleagues screened

hundreds of bacteria taken from the saliva of volunteers.

Results showed that some lactobacillus strains had

produced proteins capable of binding a sugar found on

HIV envelope, called mannose.

• One strain secreted abundant mannose-binding

protein particles into its surroundings, neutralizing HIV

by binding to its sugar coating.

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WHAT’S THE ROLE OF DENTIST?????

• 1. Provides routine dental care for HIV-infected individuals.

• 2. Understands the significance of oral lesions associated with

HIV disease, and performs evaluations, diagnostics, and

institutes treatment

• 3. Collaborates with other health care workers and social

support systems involved in the overall care of HIV-infected

patients.

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LESIONS COMMONLY ASSOCIATED WITH HIV

INFECTION

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Pseudomembranous Candidiasis Erythematous candidiasis

Hyperplastic candidiasis Angular cheilitis

ORAL CANDIDIASIS

MANAGEMENT• 1. More advanced lesions including hyperplastic candidiasis may require

systemic antifungal drugs.

• 2. Early oral lesions of HIV-related candidiasis are usually responsive to

topical antifungal therapy.

• 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.

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long-term use of ketoconazole may induce liver damage in

individuals with preexistent liver disease.

The increased risk of chronic hepatitis B or hepatitis C

infection in immunosuppressed individuals may put some

patients at risk for ketoconazole induced liver damage.

If ketoconazole is prescribed, patients should receive liver

function tests at baseline and at least monthly during

therapy.

The drug is contraindicated if the patient's aspartate

transaminase (AST) level is greater than 2.5 times normal.

Its absorption also may be hampered by the gastropathy

experienced by many HIV-infected individuals

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• TOPICAL DRUGS

• 1.Clotrimazole 10mg tablets: dissolve in mouth 3-5tablets daily for 7-14days

• 2.Nystatin

• 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) 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.

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SYSTEMIC DRUGS

1. 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 LEUKOPLAKIA

• 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.

• Epithelial displasia is not a feature and in

most OHL lesions little or no inflammatory

infiltrate in underlying C.T is seen

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MANAGEMENT:

• 1. 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. Laser or Conventional surgery.

• 4. The incidence of OHL has been markedly reduced

since the advent of multidrug antiviral therapy for HIV

infection.

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NON-HODGKIN’S LYMPHOMA

• Occurrence is more common in the gingiva.

• Has a characteristic white verrucous surface or necrosis of the

gingiva resembling ANUG.

• TREATMENT

• 1. Anti-malignancy drugs

• 2. Surgical excision

• 3. Radiation therapy37

KAPOSI’S SARCOMA• Kaposi’s sarcoma is a rare, multifocal

vascular. • Median survival time after onset of KS

is 7 to 31 months• Histologic picture:• Endothelial cell proliferation with

formation of atypical vascular channels• Extravascular hemorrhage with

hemosiderin deposition• Spindle cell proliferation• Mononuclear inflammatory infiltrate,

consisting mainly of plasma cells38

MANAGEMENT

• 1. Treatment includes use of antiretroviral agents,

laser excision, radiation therapy or intralesional

injection with vinblastine, interferon α, or other

chemotherapeutic drugs.

• 2. Nicholas 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

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• Destructive periodontitis has also been reported in

conjunction with gingival KS. In such instances, scaling and root

planing and other periodontal therapy may be indicated in

addition to intralesional or systemic chemotherapy.

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ATYPICAL ULCERATIONS

• Most reported oral ulcers are to herpes simplex

virus, CMV, EBV, histoplasmosis, herpes zoster

and mainly recurrent apthous ulcers are often

associated.

• Resistant viral strains are treated with foscarnet,

ganciclovir or valacyclovir hydrochloride.

• Topical corticosteroid therapy (fluocinonide gel

applied three to six times daily) is safe

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ORAL HYPERPIGMENTATION:

• 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.

Oral pigmentation may be caused by: Adrenocorticoid insufficiency caused by

prolonged use of ketoconazole Pneumocystitis carinii infection Cytomegalovirus infection

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PERIODONTAL CONSIDERATIONS

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Periodontal considerations…

Dennisn et al- first report linking periodontal disease and

HIV

Parra & slots- HIV in GCF

Barr et al- HIV RNA quantification in oral fluids

Shugers et al- serum viral load corelates with the salivary

viral load

Mononuclear cells present in GCF harbour HIV-1 DNA that

represents as a sourse of HIV in the oral cavity in the

presence or absence of bleeding- Maticic et al. 2000

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LINEAR GINGIVAL ERYTHEMA:

Clinical features:

• A persistent, linear, easily bleeding,

erythematous gingivitis (LGE) has

been described in some HIV-positive

patients.

• May be localised or generalised

• No evidence of pocketing or

attachment loss.

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Causes and pathogenesis

• candidal infection-Robinson

• Velegrakiet et al - Candida dubliniensis

• Winkler et al- CD4+ T cell depletion

• Barr et al46

LGE treatment…

Treatment:

- Does not respond well to plaque removal

- Conventional therapy plus rinsing with 0.12% chlorhexidine

gluconate twice daily has shown significant improvement after 3

months (Grassi M et al).

- Povidone-iodine substantially reduced pain associated with the

lesions (winkler et al).

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LGE treatment…

• Step 1: Instruct the patient in performance of meticulous

oral hygiene.

• Step 2: Oral prophylaxis.

• Step 3: Chlorhexidine gluconate mouthrinse.

• Step 4: Reevaluate the patient in 2 to 3 weeks. If lesions

persist, evaluate for possible candidiasis. Consider empiric

administration of a systemic antifungal agent such as

fluconazole for 7 to 10 days.

• Step 5: Re-treat if necessary.

• Step 6: Place the patient on 2- to 3-month recall.

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NECROTIZING GINGIVITIS: Clinical features:

• HIV-related necrotizing gingivitis is

defined by EC-WHO as destruction of one

or more interdental papillae.

• In the acute stage -ulceration,

necrosis and sloughing may be seen with

ready hemorrhage and characteristic fetor

• The anterior gingiva is most

commonly affected (Greenspan1993).

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NUG…

• Causes and pathogenesis

• The isolated organisms include Borrelia, gram-positive

cocci, P-hemolytic streptococci and C. albicans (reichert et al)

• Thompson et al

• Barr et al

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Treatment

• Basic treatment may consist of cleaning and

debridement of affected areas with a cotton pellet

soaked in peroxide after application of a topical

anesthetic.

• Escharotic oral rinses such as hydrogen

peroxide should only rarely be used, however, and are

especially contraindicated in immuno-compromised

individuals.

• Patient should be seen daily or every other day

for the first week

• 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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NUG…

• Does not always respond to conventional treatment with

scaling and improved oral hygiene (winkler jr et al).

• Adjunctive use of metronidazole & Antimycotic agents in

these patients is reported to be extremely effective in reducing

acute pain and promoting rapid healing (scully et al)

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NECROTIZING PERIODONTITIS:

• Clinical features:

• According to the description by

EC-WHO necrotizing periodontitis is

periodontitis characterized by soft tissue

loss as a result of ulceration or necrosis.

Exposure, destruction or sequestration of

bone may be seen.

• The distinctive feature- loss

attachment

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NUP…

• NUP is severely painful in onset and immediate therapy

is necessary

• On occasions, however, patients undergo spontaneous

resolution of the lesions, leaving painless, deep interproximal

craters that are difficult to clean and may lead to conventional

periodontitis 54

NUP…

Causes and pathogenesis:

• Higher proportions of C. albicans and C. rectus.

- Debilitating health and progression of disease

- However, some studies have also indicated that the association

between HIV-related immune depletion and periodontal

destruction is less strong (Martinez-Canut P, Guarinos J, jp

1996)

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Treatment

Local debridement

Scaling and Root planing,

Irrigation with an effective antimicrobial agent.

In severe NUP, antibiotic therapy may be necessary

but should be used with caution in HIV-infected patients to

avoid an opportunistic and potentially serious localized

candidiasis or even candidal septicemia.

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NUP…

• Does not always respond to conventional treatment with

scaling and improved oral hygiene (winkler jr et al).

• Prophylactic prescription of a topical or systemic

antifungal agent is prudent if an antibiotic is used.

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INDICATIONS FOR HIV TESTING OF DENTAL PATIENTS

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DIAGNOSTIC TESTS:

DIAGNOSTIC TESTS

ELISA

WESTERN BLOT (WB)

(PCR)P24 ANTIGEN

LAB-ON-A-CHIP

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OCCUPATIONAL EXPOSURES AND POSTEXPOSURE PROPHYLAXIS (PEP):

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GENERAL PRECAUTIONS TO BE TAKEN

• 1. Surgical gloves should be worn when touching

blood, saliva or mucous membranes.

• 2. Surgical masks and protective eyewear should be

worn.

• 3. Disposable or washable gowns should be used.

• 4. Instruments should be sterilized by autoclaving.

• 5. Debris should be removed by scrubbing with soap

and water before sterilization.63

GENERAL PRECAUTIONS TO BE TAKEN…

• 6. Surfaces should be decontaminated with sodium

hypochlorite.

• 7. Needles should be disposed with safety guard.

• 8. Droplets and aerosol production should be avoided where

possible by use of rubber dam and high-speed evacuation.

• 9. Apparent Fumigation of the operating room is required as a

part of disinfection.

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CONCLUSION:

The pathogenesis periodontal diseases in HIV+

subjects may be due to the microflora, the effects of HIV

and other viral agents, and/or alterations in the host

response. These factors should be taken into

consideration in the treatment and prevention of

periodontal diseases in the HIV patient.

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REFERENCES• Textbook of clinical periodontology- Carranza 10th Edition• Textbook of clinical periodontology- Carranza 9th Edition• Textbook of periodontology and implantology- Linde 5th Edition• Textbook of periodontology- Rose & Mealey• Textbook of periodontology- Eley & Manson• Textbook of Microbiology- AnanthNarayana• Textbook of Immunology- Roitt’s• The American Academy of Oral Medicine, Clinician’s guide to

HIV- infected patients. 3rd Edition.• Periodontology 2000,vol 60, 2012: 78-97• Periodontology 2000,Vol 50, 2009: 52–64• Periodontology 2000,vol 44, 2007: 55-81 66

References…• DCNA 2003, 467-492• R.G. Nair et al. Coinfections associated with HIV

infection: Workshop 1A. Adv Dent Res 2011;23(1): 97-105

• Scheutz F et al. Is there an association between periodontal condition and HIV infection. JCP 1997, 24: 580-587

• Murray et al. the Microbiology of HIV- Associated periodontal lesions. JCP 1989; 16: 636-642

• Angelika Langford. Gingival and periodontal alterations associated with infection with HIV. Quintessence Int 1994; 25: 375-387

• http://www.ambha.org/new-hiv-aids-treatment-methods.html

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Thank u…