1. PERIODONTAL MANAGEMENT OF
HIV PATIENTS

2. INTRODUCTION
AIDS is a universal epidemic that
significantly affects dental practice, regardless of
geographic location. The oral cavity is a frequent
site for clinical manifestations of the disease.
The ability to recognize and manage the oral
manifestations of this disease is an important part
of dental practice.
The dentist should be prepared to assist
human immunodeficiency virus (HIV) – infected
patients in maintenance of oral health throughout
the course of their disease.

3. AIDS is characterized by
profound impairment of the
immune system due to HIV
infection and consists of
microbial diseases acquired or
reactivated as a result of the
immunosuppression.

4. CLINICAL DEFINITION OF AIDS
AIDS 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..

5. 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)
HIV-2
ANCESTRAL
SIVSM
VIRUS
SIVSY
HIV-1
SIVCPZ
SIVAG

6. 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 is theorized that it must have first appeared in
the early1950s, after having jumped from original simian
hosts.
It probably remained in small isolated villages,
causing sporadic cases and mutating into more virulent
strains that were readily transmitted from human to
human.
When this pattern was coupled with changing social and
sexual mores and increased immigration and travel, a
pathway was opened up for rapid spread of the virus.

7. HISTORICAL BACKGROUND
 AIDS was first recognized in 1981 in USA.
 Luc Montagnier and colleagues in 1983
isolated the causative virus, HIV from blood
lymphocytes.
 It was recognized to be a Lentivirus
subgroup of the family retroviridae and was
called Lymphadenopathy Associated Virus
(LAV).

8.  In 1984 Robert Gallo and colleagues
reported isolation of retrovirus from AIDS
patients and called it Human Tcell
Lymphotropic Virus –III (HTLV-III).
 Other isolates were called as AIDS related
virus.
 The International Committee on virus
nomenclature in 1986, decided on the generic
name Human Immunodeficiency Virus

9. STRUCTURE OF HIV
HIV is a spherical enveloped virus about 90-
120nm in size.

10. REVERSE
TRANSCRIPTASE
Outer icosahedral shell
of nucleocapsid
gag p17 env gp120
env gp41
gag p24

11. MODES OF TRANSMISSION

12. 7. BUDDING
1. BINDING
6. VIRAL
ASSEMBLY
2. REVERSE
TRANSCRIPTION
5.TRANSLATION
4. TRANSCRIPTION
3. INTEGRATION

13. P
A
T
H
O
G
E
N
E
S
I
S

14. DIAGNOSIS
Virus isolation : From T cells in blood and other
specimens.
Serological tests:
Depend upon the demonstration of specific antibodies.
ELISA
WESTERN BLOT
HIV infection can be checked by measuring the virus
on the blood using either:
1. A p24 antigen test PCR
2. A viral load assay
bDNA

15. REVISED CDC CLASSIFICATION

16. 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
• Virus starts to grow and multiply in the lymph nodes

17. 3. SYMPTOMATIC DISEASE/AIDS
• Viremia (spread of virus in the blood)
• 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

18. Classification of the Most Common
Oral Manifestations of AIDS
BACTERIAL 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

19. VIRAL INFECTIONS
Epstein-Barr Virus
Oral Hairy Leukoplakia
Herpes Simplex Virus
Primary herpetic gingivo-stomatitis
Recurrent herpetic infection
Variacella-Zoster Virus
Herpes zoster
Human Papilloma Virus
Condyloma accuminatum
Multifocal epithelial hyperplasia
Cytomegalovirus

20. NEOPLASMS
Kaposi's sarcoma
Lymphoma
Other neoplasms
OTHER ORAL LESIONS
Oral ulcers
Salivary gland enlargement

21. PERIODONTAL TREATMENT
PROTOCOL
1. HEALTH STATUS
2. INFECTION CONTROL MEASURES
3. GOALS OF THERAPY
4. SUPPORTIVE PERIODONTAL
THERAPY
5. PSYCHOLOGIC FACTORS

22. 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

23. 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

24. 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.

25. 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

26. 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.

27. MANAGEMENT OF ORAL
AND PERIODONTAL
LESIONS ASSOCIATED
WITH AIDS

28. GENERAL PRECAUTIONS TO BE TAKEN
Infection control measures
1. Gloves should be worn when touching blood, saliva
or mucous membranes.
2. Surgical masks & protective eye wear should be
worn.
3. Disposable or washable gowns.
4. Instruments should be sterilized by autoclaving.
Debris should be removed by scrubbing with soap
and water before sterilization.
5. Surfaces should be decontaminated with sodium
hypochlorite.
6. Needles should be disposed with safety guard.
7. Droplets and aerosol production should be avoided
where possible by use of rubber dam and high
speed evacuation.

29. ORAL CANDIDIASIS
Oral candidiasis is caused by one of the
candida species, usually candida albicans, a normal
inhabitant of the oral cavity in many healthy
individuals.
Currently at least 11 strains of candida have
been identified and a major factor associated with
overgrowth of candida is diminished host resistance.
Candidiasis is the most common oral lesion in
HIV diseases and has been found in approximately
90% of AIDS patients.

30. 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

31. 2. Erythematous candidiasis
Red areas or patches on the buccal or
palatal mucosa, or it may be associated with
depapillation of the tongue.
ERYTHEMATOUS CANDIDIASIS

32. 3. Hyperplastic candidiasis
Least common form and may be
seen in the buccal mucosa & tongue
and is more resistant to removal.

33. 4. Angular cheilitis
The commissures appear
erythematous with surface crusting and
fissuring.

34. Diagnosis of candidiasis is made by
microscopic examination of tissue sample or
smear, which shows hyphae or yeast forms of the
organisms.
Oral candidiasis presents with esophageal
candidiasis in patients at risk for HIV Infection,
which is a diagnostic sign of AIDS.
Resistant candidiasis is more common in
individuals who have low CD4+ counts.

35. MANAGEMENT
1. 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.

36. 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.

37. 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.

38. 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.

39. ORAL HAIRY L UK L IA
E OP AK
 Oral hairy leukoplakia most commonly
presents as a white ragged, corrugated or
irregular lesion 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.

40. ORAL HAIRY LEUKOPLAKIA

41. 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 consider
white lesions of the mucosa, which include
dysplasia, carcinoma, frictional and idiopathic
keratosis, lichen planus, tobacco-related
leukoplakia, psorisiform lesions and
hyperplastic candidiasis.

42. 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. 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.

43. 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) has been implicated in the
etiology of Kaposi’s sarcoma.
Kaposi’s sarcoma oral lesions may interfere with
function, be cosmetically objectionable, and
proliferate uncontrollably.
This is an aggressive lesions and involves most
frequently the palate 95% and the gingiva 23%

44. 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 .

45. Diagnosis: Biopsy or identification of distinct clinical
appearance.
Histologic picture:
Endothelial cell proliferation with formation of atypical
vascular channels.
Extravascular hemorrage with hemosiderin deposition
Spindle cell proliferation
Mononuclear inflammatory infilterate, consisting mainly
of plasma cells.
Differential diagnosis: Pyogenic granuloma, hemangioma,
atypical hyperpigmentation, sarcoidosis, pigmented nevi.
Median survival time after onset of KS is 7 to 31 months.

46. KAPOSI’S SARCOMA

47. MANAGEMENT
1. 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.

48. 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.

49. 4. 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.

50. 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.

51. TREATMENT
Broad-spectrum antibiotics such
as erythromycin or doxycycline in
conjunction with conservative
periodontal therapy and possibly
excision of the lesion.

52. NON-HODGKIN’S L P OM
YM H A
 Occurrence is more common in the
gingiva.
 Has characteristic white verrucous
surface or necrosis of the
gingiva resembling ANUG.

53. NON-HODGKIN’S L P OM
YM H A

54. TREATMENT
1. Anti-malignancy drugs
2. Surgical excision
3. Radiation therapy

55. 6.ATYPICAL ULCERATIONS
Most 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.

56. HZV
Herpetic ulcers
Herpetic ulcers Atypical ulcers EBV Ulcers

57. RAS- MAJOR RAS- MAJOR
HPV ULCERS

58. 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) or alternative therapy
(thalidomide, levamisole, pentoxifylline).

59. 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.

60. Oral pigmentation may be caused by,
 Adrenocorticoid insufficiency
caused by prolonged use of
ketoconazole
 Pneumocystitis carinii infection
 Cytomegalovirus infection

61. ORAL PIGMENTATION

62. H RE AT D
IV L E
P RIODONT DISE S
E AL ASE
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

63. 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 treatment
The lesion may be localised or generalized in nature
The microflora of LGE may closely mimic that of
periodontitis rather than gingivitis (Clark et al, 1991)

64. CANDIDIASIS ?
Concomitant oral candidiasis and LGE lesions have
been identified suggesting a possible etiologic role
for candidial species in LGE (Lamster et al, 1994)
Recently, direct microscopic cultures from LGE
lesions suggest that LGE may result from a chronic
infection with C. albicans or other candidial stains
like candida dubliniensis (Velegraki et al 1999)
They also reported complete or partial remission
after systemic antifungal therapy. But it is not yet
known whether candidial infections are etiologic in
all LGE cases.

65. LINEAR GINGIVAL ERYTHEMA

66. MANAGEMENT OF LGE:
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.

67. Step I: Instruct the patient in performance of
meticulous oral hygiene
Step II: Scale and polise 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.

68. 2. 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.

69. NECROTIZING UL RAT
CE IVE GINGIVITIS

70. MANAGEMENT
Basis treatment consists of cleaning and debridement of
affected areas with a cotton pellet soaked in peroxide
after application of topical anesthetic
Escharotic oral rinses such as hydrogen peroxide
should be avoided
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.

71. 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.

72. NECROTIZING UL RAT
CE IVE
P RIODONT IS
E IT
 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.

73. 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 etal 1991).

74. Glick and associates in 1994 reported the
incidence of periodontal diseases in 700
HIV+ve individuals.
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

75. NECROTIZING UL RAT
CE IVE
P RIODONT IS
E IT

76. MANAGEMENT
1. Gradual, gentle, local debridement of affected area.
2. Scaling and root planing with oral hygiene instruction
3. 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.

77. 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)

78.  The condition appears to be identical to
cancrum oris (NOMA), a rare destructive process
occasionally reported in nutritionally deprived
individuals.

79. TREATMENT
1. 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).

80. CONCLUSION
ANTIRETROVIRAL THERAPY IN ADULTS
The primary goals of antiretroviral therapy are:
• to prolong life expectancy.
• to improve quality of life.
• to prevent development of opportunistic
infections 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.

81. ANTIRETROVIRAL DRUGS
Drugs currently available attempt to block viral
replication by inhibiting two viral enzymes -
either HIV reverse transcriptase or the HIV
protease.
Other drugs such as fusion Inhibitors, which
block entry of the virus into the cell and HIV
integrase inhibitors which prevent integration of
DNA into the cell nucleolus, are under
investigation.

83. REVERSE TRANSCRIPTASE INHIBITORS
1. 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 building
blocks of DNA so that when the reverse transcriptase tries
to add the drug to a developing strand of DNA, it cannot
be completed. NRTIs need to be activated first by
phosphorylation.
NNRTIs inhibit activity of the reverse
transcriptase directly.

84. 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 bd
Abacavir (Ziagen®) 300mg bd. Unfortunately this drug
is currently very expensive.

85. Non-Nucleoside Reverse Transcriptase
Inhibitors (NNRTIs)
Nevirapine (Viramune®)
Dose: One 200mg tablet daily for two
weeks, then 200mg bd.
Efavirenz (Stocrin®)
Dose: 600mg once daily.

86. PROTEASE INHIBITORS
Protease inhibitors act at a later stage
and interfere with a viral enzyme, HIV
protease, which cleaves viral polyproteins
into functional end products.
This prevents the formation of
mature infectious virus and results in the
release of immature non-infectious viral
particles.

87. PROTEASE INHIBITORS (PIS)
Indinavir (Crixivan®)
Ritonavir (Norvir®)
Saquinavir (Invi-rase®, Forto-vase®)
Nelfinavir (Vira-cept®)
Lopinavir / ritonavir (Kaletra®)

88. ADVERSE DRUG EFFECTS:
Foscarnet, interferon and dideoxycytidine (DDC)
occasionally induce oral ulcerations and erythema
multiforme has been reported with use of
didanosine (DDI)
Zidovudine and ganciclovir may induce
leukopenia, resulting in oral ulcers.
Xerostomia and altered taste sensation may be
seen with diethyl dithiocarbamate (Dithiocarb).
Drug induced mucositis and lichenoid drug
reactions are common in HIV +ve patients.

89. Protease-inhibiting drugs can cause adverse
reactions including nausea, development of kidney
stones, lypodystrophy, an increase in abdominal
fat mass, and development of the classic “buffalo
hump” usually associated with administration of
systemic corticosteroid
Combined drug therapy may also induce more
severe liver cirrhosis in individuals with hepatitis
c/HIV co-infections.
The dentist should remain alert for general signs
and symptoms of adverse drug effects, some of
which can affect oral tissues.

90. AIDS VACCINE ?
Complication is mainly because the virus becomes latent in
cells 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. In
humans the vaccine could expose humans to mutation
and cancer and the virus itself could mutate to its
virulent form and can spread.

91. In the viral vector technique, vaccinia virus or
adenovirus is genetically engineered to carry only
the HIV envelope gene. This hybrid virus replicates
and expresses the HIV genes when it is Injected into
the host stimulating immunity.

92. CONCLUSIO
N

93. The median period between initial HIV
infection and outright AIDS is approximately 12
years and the life expectancy of persons living with
AIDS has been significantly prolonged with current
anti-retroviral drug therapy.
This indicates that HIV-infected patients are potential
candidates for conventional periodontal treatment
and treatment decisions should be based on overall
health status of the patient, the degree of periodontal
involvement and the motivation and ability of the
patient to perform effective oral hygiene procedures.

94. By combining local and
systemic therapy with new
antiviral drugs, dental and medical
practitioners may together help to
reduce morbidity in HIV – infected
patients.

95. TH
AN
KY
OU