This document discusses periodontal problems in patients with HIV infection. It covers the pathogenesis of HIV and how the virus weakens the immune system over time. As the immune system is damaged, oral infections like oral candidiasis become more common and severe. The document also discusses the various stages of HIV infection and AIDS, as well as highly active antiretroviral therapy (HAART) used to treat HIV. Common oral manifestations seen in patients with HIV infection include oral candidiasis, oral hairy leukoplakia, and Kaposi's sarcoma.

1. PATHOLOGY AND MANAGEMENT OF
PERIODONTAL PROBLEMS IN
PATIENTS WITH HIV INFECTION
Navneet Singh
MDS Student
Dept of Periodontology
and Oral Implantology

2. INTRODUCTION
• Acquired Immunodeficiency Syndrome (AIDS) is
characterized by profound impairment of immune
system.
• First reported in 1981, and a viral pathogen, HIV (Human
immunodeficiency virus) was first identified in 1984.
• The condition was originally believed to be restricted to
homosexual males.
• Currently, sexual activity and drug abuse remain the
primary means of transmission.

3. • HIV has strong affinity for cells of immune system, most
specifically those that carry the CD4 cell surface
receptors.
• Helper T Lymphocytes (T4 cells) are most profoundly
affected, but monocytes, macrophages, Langerhans
cells and some neuronal and glial cells are also involved.
• Viral replication occurs continuously in lymphoreticular
tissues of lymph nodes, spleen, gut associated lymphoid
cells and macrophages.

4. PATHOGENESIS
• In untreated or inadequately treated HIV infection, the
overall effect is gradual impairment of immune system
by interference with T4 (CD4) lymphocytes and other
immune cell functions.
• B cells are not infected, but the altered function of
infected T4 lymphocytes secondarily results in B-cell
dysregulation and altered neutrophil function.
• This may place HIV-positive individuals at increased risk
for malignancy and disseminated infections with
microorganisms such as viruses, mycobacterioses and
mycoses.

5. • HIV has been detected in most body fluids, although it is
found in high quantities only in blood, semen and CSF.
• Transmission occurs almost exclusively by sexual contact,
illicit use of injection drugs or exposure to blood or blood
products.
High risk populations:
• Homosexual and bisexual men
• Use of illegal injection drugs
• Persons with hemophilia or other coagulation therapy
• Recipients of blood transfusions
• Infants of HIV infected mothers

6. • Heterosexual transmission is a common cause of AIDS in
world population.
• It is more likely to occur through contact with HIV-
infected individuals with a high plasma bioload of virus.
• Some short-term studies have suggested that HIV-positive
individuals successfully treated with antiretroviral therapy
cease to be infectious to others.
• Wilson et al. (2008) have developed a mathematical
model that indicates that the potential of HIV transmission
to an uninfected individual by a heterosexual partner with
an undetectable viral load is low but not without risk.

7. CLASSIFICATION AND STAGING
• WHO and CDC have published guidelines regarding the
definition of HIV infection and HIV disease staging.
• Acc to WHO concept, clinical findings may be used to
establish diagnosis and determine eligibility for
antiretroviral therapy.
Clinical Stage 1: Asymptomatic
infection or persistent generalised
lymphadenopathy.
Clinical Stage 2: Mild symptoms
such as mild unexplained weight
loss, angular cheilitis, herpes
zoster or recurrent oral
ulcerations.
Clinical Stage 3: Advanced symptoms
such as severe weight loss, persistent oral
candidiasis, oral hairy leukoplakia, acute
necrotizing stomatitis, gingivitis or
periodontitis.
Clinical Stage 4: Severe symptoms such as
HIV wasting syndrome, Pneumocystis
pneumonia, chronic herpes simplex
infection of more than 1 month duration,
esophageal candidiasis, Kaposi’s sarcome,
CMV infection.

8. • AIDS may present in either Stage 3 or 4 disease.
• CD4 count of less than 350/mm3 is considered
diagnostic for AIDS in adults and children 5 years or
older;
Advanced HIV infection in infants based on
• CD4<30% if younger than 12 months;
• CD4<25% among those ages 12 to 35 months;
• CD4< 20% among those ages 36 to 59 months.

9. • 1982 the CDC developed a surveillance case definition for
AIDS based on the presence of opportunistic illnesses or
malignancies secondary to defective cell mediated immunity
in HIV-positive individuals.
•Candidiasis of bronchi, trachea, or lungs
• Candidiasis, esophageal
• Cervical cancer, invasive
• Coccidioidomycosis, disseminated or extrapulmonary
• Cryptococcosis, extrapulmonary
• Cryptosporidiosis, chronic intestinal (>1 month's duration)
• Cytomegalovirus disease (other than liver, spleen, or nodes)
• Cytomegalovirus retinitis (with loss of vision)
• Herpes simplex: chronic ulcer(s) (>1 month's duration) or bronchitis,
pneumonitis, or esophagitis
• Histoplasmosis, disseminated or extrapulmonary
• Isosporiasis, chronic intestinal (1 month's duration)
• Kaposi's sarcoma

10. Lymphoma, Burkitt's (or equivalent term)
• Lymphoma, immunoblastic (or equivalent term)
• Lymphoma, primary, of brain
• Mycobacterium avium complex or Mycobacterium kansasii,
disseminated or
extrapulmonary
• Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary)
• Mycobacterium, other species or unidentified species, disseminated or
extrapulmonary
• Pneumocystis carinii pneumonia
• Pneumonia, recurrent
• Progressive multifocal leukoencephalopathy
• Salmonella septicemia, recurrent
• Toxoplasmosis of brain
• Wasting syndrome caused by HIV
From Centers for Disease Control: MMWR 41:RR-17, 1993.

11. • The 1993 revision added invasive cervical cancer in
women, bacillary tuberculosis, and recurrent
pneumonia to the AIDS designation.
• Currently, any of 25 specific clinical conditions found
in HIV positive individuals can establish the diagnosis
of AIDS.

12. • The most significant change in the most recent CDC case
definition was the inclusion of severe immunodeficiency :
CD4 cell count<200/mm3 (Normal : 544-1663/mm3)
CD+T lymphocyte percentage <14% of total lymphocytes .
(Normal: 32-60%)
• More recently, HIV plasma bioload has been identified as a
significant factor related to the transmissibility and severity of
disease.
• Range of detection: <50 copies/mL to >750,000 copies/mL.
• Higher peripheral blood viral load is found during first 3
months after initial infection and during late stages of
disease.

13. SIGNS AND SYMPTOMS
• A few weeks to a few months after initial exposure, some HIV
infected individuals may experience acute symptoms, such as
sudden onset of an acute mononucleosis-like illness
characterised by malaise, fatigue, fever, myalgia,
erythematous cutaneous eruption, oral candidiasis, oral
ulcerations and thrombocytopenia.
• This acute phase may last upto 2 weeks with seroconversion
occuring 3 to 8 weeks later.
Transfusion recipients: 7 years
Hemophiliacs: 10 years
Injecting drug users: 10 years
Homosexual/ bisexual men: 8-12 years
MEDIAN INCUBATION PERIOD

14. CDC SURVEILLANCE CASE CLASSIFICATION (1993)
• Category A: include patients with acute symptoms or
asymptomatic disease, along with individuals with persistent
generalised lymphadenopathy, with or without malaise,
fatigue or low grade fever.
• Category B: patients with symptomatic conditions such as
oropharyngeal or vulvovaginal candidiasis, herpes zoster, OHL,
ITP or constitutional symptoms of fever, diarrhea and weight
loss.
• Category C: patients are those with outright AIDS, life
threatening conditions or identified through CD4+T
lymphocyte levels of less than 200 cells/mm3.

15. ANTIRETROVIRAL THERAPY
• To date, 32 drugs or drug combinations of 6 separate classes
have been approved by FDA for treatment of HIV/ AIDS
infection.
• The goals of therapy are to reduce morbidity and mortality
and improve and prolong life.
• Total eradication of HIV does not appear to be currently
possible because reservoirs of latently infected CD4 cells are
established early in the infection and persist even without
treatment.
• Anatomic reservoirs of infection have been located in GIT and
reproductive tracts and in breast, lung and in brain tissue and
recently the oral cavity because a small percentage of HIV-
infected individuals were found to be hyper-excretors of HIV.

16. 1. Nucleoside reverse transcripatse inhibitors (NRTI’s):
• Act by competing with incorporation into proviral chain,
eliminating chain elongation.
• These are effective against both HIV-1 and HIV-2 .
• Principal drugs in use.
Adverse Effects:
Non-specific GIT syndrome, nausea, vomiting and abdominal pain
but may rapidly progress to hepatic or respiratory failure and
pancreatitis.
Bone marrow suppression, peripheral neuropathy, pancreatitis,
hepatotoxicity and lipodystrophy.

17. Drugs included:
• Abacavir
• Abacavir + Lamivudine
• Abacavir+ Lamivudine+ Zidovudine
• Lamivudine
• Lamivudine+ Zidovudine
• Stavudine
• Didanosine
• Tenofovir

18. 2. Non Nucleoside Reverse Transcriptase Inhibitors
(NNRTI’s)
• Bind to active sites in the developing HIV -1 viral chain
and arrest its development.
• Equally effective but rapidly develop single step mutation
and cross resistance.
Adverse Effects:
• Common with these drugs as they are metabolized by
hepatic p450 system, principally CYP3A4 enzyme.
• Stevens Johnson syndrome may develop and hepatic and
central nervous system manifestations are common.

19. Drugs included:
• Delavirdine
• Etravirine
• Efavirenz
• Nevirapine

20. 3. Protease Inhibitors
• Active against both HIV-1 and HIV-2.
• Bind to HIV protease enzyme and result in formation of
noninfectious HIV virion.
Adverse Effects:
• Also metabolised by hepatic p450 system (CYP3A4
enzyme).
• Gastrointestinal intolerance, hyperlipidemia, insulin
resistance and lipodystrophy common.

21. Drugs:
• Amprenavir
• Atazanavir
• Darunavir
• Indinavir
• Lopinavir
• Nelfinavir
• Ritonavir
• Saquinavir

22. 4. Fusion Inhibitors
• Bind to the gp41 glycoprotein membrane on HIV and
prevent virus fusion into susceptible CD4 cells. These
drugs are administered through subcutaneous injection.
• Injection site reactions are common.
• The only drug available is Enfuvirtide.

23. HIGHLY ACTIVE ANTIRETROVIRAL THERAPY
• Combination of three or more antiretroviral drugs are
administered simultaneously for long periods of time.
• To block HIV replication and plasma viral load and restore
immune function.
• Three commonly used combinations:
1. NNRTI’s + 2 NRTI’s
2. 1 or 2 PI’s + 2 NRTI’s
3. 3 NRTI’s

24. • Some authorities felt that the drugs should not be
administered until significant immune suppression
occurred; as this would decrease the side effects and risk
of developing drug resistance.
• Others advocated initiation of therapy as soon as
diagnosis was established.
• More recently, evidence has indicated that early
treatment is far more successful than delayed
treatment.

25. Survival time is shorter despite HAART in individuals
who:
• Injected drug abusers
• Those with AIDS before initiation of therapy
• Those with high viral load before initiation of therapy
(>100,000 copies/ml).
• Those who are inconsistent in adherence to the drug
regimen
• Those who discontinue the drugs.

26. Other factors that affect the life expectancy in the era
of HAART:
• Smoking
• Excessive alcohol consumption
• Older age at the initiation of therapy
• Comorbidities such as Hepatitis C or other viral, bacterial
or fungal infections.
• Chronic liver, kidney or cardiovascular conditions
conditions and Diabetes mellitus
• Low socioeconomic status

27. Immune Reconstitution Inflammatory Syndrome
(IRIS)
• Associated with the recovery of immunity with HAART.
• In this syndrome, infectious diseases such as
tuberculosis, dissemminated Mycobacterium avium
complex (MAC) disease, hepatitis B and C, Herpes zoster
virus are reactivated.
• There occurs an overwhelming inflammatory response
that makes the symptoms of infection more severe.
• This seems to occur in individuals with low baseline CD4
count who are responsive to HAART.

28. • There occurs a rapid increase in CD4 cell numbers and a
hyperinflammatory response that may cause fever and
worsening of an existing bacterial, viral or fungal
infection.
• In oral cavity, IRIS could include CMV infection, VZ
infection, histoplasmosis, cryptococcosis etc.
• IRIS most often occurs within the first 4-8 weeks after
starting antiretroviral therapy in individuals who had
high viral loads and low CD4+T lymphocyte count.
• Difficult to diagnose and manage; may take months to
subside, but it doesn’t appear to affect patient’s
survival.

29. ORAL AND PERIODONTAL MANIFESTATIONS OF
HIV INFECTION
Several reports have identified a strong correlation
between HIV infection and
• Oral candidiasis
• Oral hairy leukoplakia
• Atypical periodontal diseases
• Oral Kaposi’s sarcoma
• Oral Non Hodgkins Lymphoma

30. Less strongly associated lesions include:
• Melanotic hyperpigmentation
• Mycobacterial infections
• Necrotizing ulcerative stomatitis (NUS)
• Miscellaneous oral ulcerations
• Viral infections (HSV, HZV and condyloma acuminatum)

31. ORAL CANDIDIASIS
• Most common oral lesions in HIV patients.
• 90% of AIDS patients.
• Mostly associated with Candida albicans.
• Currently, atleast 11 strains of Candida have been
identified, and non C. albicans infections are more
common among immunocompromised individuals
already receiving antifungal therapy for C. albicans.
• 4 clinical presentations: Pseudomembraneous,
erythematous, hyperplastic candidiasis or angular
cheilitis.

32. • Pseudomembraneous candidiasis (Thrush): painless or
slightly sensitive, yellowish white curd like lesions that
can be readily scraped and separated from the surface of
oral mucosa.
Most common on hard and soft palate and buccal or
labial mucosa.

33. • Erythematous Candidiasis: red patches on the buccal or
palatal mucosa, or it may be associated with
depapillation of the tongue.
• Hyperplastic Candidiasis: least common form and may
be seen in buccal mucosa and tongue. It is more resistant
to removal.

34. • Angular cheilitis: Commissures of the lips appear
erythematous with surface crusting and fissuring.

35. Diagnosis:
• Clinical evaluation
• Culture analysis
• Microscopic examination of tissue sample
• Smear of material scraped from lesion: shows hyphae or
yeast form of organisms.
Many patients at risk for HIV infection who present oral
candidiasis also have esophageal candidiasis, a
diagnostic sign of AIDS.

36. • May respond to antifungal therapy, it is often refractory
or recurrent.
• Relapse can occur due to decreasing
immunocompetence or development of antifungal-
resistant candidal strains.
• Resistant candidiasis is more common in individuals who
have low CD4 counts at baseline.

37. Common Antifungal Therapeutic Agents for Oral
Candidiasis
TOPICAL DRUGS
1. Clotrimazole (Mycelex) 10mg tablets: Dissolve in mouth; 3-5
tabs daily for 7-14 days.
2. Nystatin (Mycostatin)
• Oral Suspension: 100,000/uL; Rinse with 1tsp qid.
• Oral Suspension (extemporaneous): Mix 5,00,000 U in 4 oz
water and rinse qid.
• Tablets (5,00,000 U): Dissolve 1 tablet in mouth, 4-5 times
daily.
• Pastilles (2,00,000 U): Dissolve 1 or 2 in mouth; 4-5 times
daily.

38. • Vaginal tablets (1,00,000 U): Dissolve 1 tablet in mouth tid.
Vaginal troches are sucrose free.
• Ointment for angular cheilitis 15 g tube: Apply to affected area
tid or qid.
3. Clotrimazole Ointment, 15 g tube. Apply to affected area qid.
4. Miconazole 2% ointment 15 g tube. Apply to affected area qid.
5. Itraconazole Oral suspension, 100-200 mg once daily for 7-14
days.
6. Fluconazole Ointment, 3-6mg/kg once daily for 7-14 days.
7. Amphotericin B oral suspension, 100mg qid for 2 weeks.

39. SYSTEMIC DRUGS
1. Ketoconazole (Nizoral), 200mg tablets: Take 2 tablets
immediately, then 1 or 2 tablets daily with food for 5-14
days.
2. Fluconazole (Diflucan), 100 mg tablets: Take 2 tablets
immediately, then 1 tablet daily for 7-14 days.
3. Itraconazole (Sporanox), 100 mg capsules: Take 200mg
once daily with meals for 7-14 days; For AIDS and
neutropenic patients, take for 4 weeks.

40. ORAL HAIRY LEUKOPLAKIA
• Primarily occurs in persons with HIV infection.
• Found on lateral borders of tongue.
• Has bilateral distribution and may extend to ventrum
• Characterized by asymptomatic, poorly demarcated
keratotic area ranging in size from a few millimeters to
several centimeters.

41. • Vertical striations seen, imparting corrugated
appearance, or the surface may be shaggy and appear
hairy when dried.
• The lesion does not rub off and may resemble other
keratotic lesions.
• Microscopically, shows hyperkeratotic surface with
projections that resemble hairs.
• Beneath parakeratotic surface, acanthosis and some
characteristic ‘balloon cells resembling’ koilocytes are
seen.

42. • It has been demonstrated that these cells contain viral
particles of EBV.
• Epithelial dysplasia is not a feature; little or no
inflammatory infiltrate is present beneath connective
tissue.

43. Differential diagnosis:
Carcinoma, dysplasia, frictional and idiopathic keratosis,
lichen planus, tobacco related leukoplakia, secondary syphilis,
psoriasiform lesions and hyperplastic candidiasis.
Treatment: lesions are responsive to HIV drug therapy or
antiviral agents such as acyclovir, gancyclovir, foscarnet or
valacyclovir.
• Lesions can be successfully removed with laser or
conventional therapy.
• Topical agents like podophylline, retinoids, oral acyclovir or
interferon also used.
OHL lesions tend to recur after the treatment is discontinued.

44. KAPOSI’S SARCOMA AND OTHER MALIGNANCIES
• An HIV positive individual with Non Hodgkin’s Lymphoma
(NHL) or Kaposi’s sarcoma (KS) is categorized as having AIDS.
• KS is most common oral malignancy ; angioproliferative tumor
is a rare, multifocal, vascular neoplasm.
• Originally described in 1872; closely associated with
homosexual and heterosexual transmission.
• Causative agent is HHV-8.
• HHV-8 seroconversion is common, and the virus has been
isolated from 29% American adults and 8% of children in Non-
AIDS general population.

45. • Classic and endemic forms: it is localised and slowly
growing tumor; 71% lesions on gingiva and palate.
• Early stages: painless, reddish purple macules of the
mucosa.
• As they progress, the lesions may manifest as nodules,
papules or non elevated macules that are usually brown,
blue or purple, occasionally normal pigmentation.

46. • Microscopically, it consists of four components:
1. Endothelial cell proliferation with formation of atypical
vascular channels.
2. Extravascular hemmorhage with hemosiderin
deposition.
3. Spindle cell proliferation in association with atypical
vessels
4. Mononuclear inflammatory infiltrate consisting mainly
of plasma cells.

47. • Differential Diagnosis includes pyogenic granuloma,
hemangioma, atypical hyperpigmentation,
angiosarcoma, pigmented nevi and cat scratch disease.
• Treatment includes antiretroviral agents, laser excision,
cryotherapy, radiation therapy and intralesional injection
of vinblastine, IFN-gamma, sclerosing agents or other
chemotherapeutic agents.
• Nichols et al. (1993) described the successful use of
intralesional injection of vinblastine at a dose of
0.1mg/cm2 using a 0.2mg/ml solution of vinblastine
sulfate in saline.

48. NON HODGKIN’S LYMPHOMA (NHL)
• NHL is characterized by malignancy of B or T
lymphocytes, and tumors are typed by WHO classification
system as indolent, aggressive or highly aggressive.
• NHL is treated by chemotherapy.
• HAART does not appear to reduce the incidence or
prognosis of malignancies.

49. • Oral lesions usually appear as erythematous,
painless enlargement that may become ulcerated
because of traumatic injury.
• Bone involvement may occur in some cases.

50. • Diagnosis : physical examination, complete blood count,
imaging studies, lymph node and tissue biopsy.
• AIDS patients with NHL may require management of
HIV-related opportunistic infections, chemotherapy-
induced mucositis and thrombocytopenia, and possibly
Graft-versus-host disease, if hematopoietic cell
transplantation is performed.

51. BACILLARY (EPITHELIOID) ANGIOMATOSIS
• Infectious vascular proliferative disease with clinical and
histologic features similar to those of KS.
• Believed to be transmitted by cat scratch and caused by
Rickettsia like organisms (eg. Bartonella henselae and B.
quintana).
• Can occur in immunocompetent persons but commonly
associated with AIDS.

52. • Gingival BA manifests as red, purple or blue edematous
soft tissue lesions that may cause destruction of
periodontal ligament and bone.

53. • More prevalent in HIV-positive individuals with low CD4
levels.
• Diagnosis: Biopsy; epithelioid proliferation of angiogenic
cells accompanied by an acute inflammatory infiltrate.
• Differential diagnosis includes KS, angiosarcoma,
hemangioma, pyogenic granuloma and non specific
vascular proliferation.
• Treatment : using broad spectrum antibiotics such as
erythromycin or doxycycline.
• Gingival lesions are managed using antibiotics in
conjunction with conservative periodontal therapy and
possibly excision of the lesion.

54. ORAL HYPERPIGMENTATION
• Often appear as spots or striations on
the buccal mucosa, palate, gingiva or
tongue.
• May be related to prolonged use of
ketoconazole, zidovudine or
clofazimine.
• May also be the result of
adrenocorticoid insufficiency induced
in an HIV-positive individual by
prolonged use of ketoconazole or by
Pneumocystis jiroveci infection or
CMV or other viral infections.

55. ATYPICAL ULCERS
• Non specific oral ulcerations, may be due to neoplasms
such as lymphoma, KS and squamous cell carcinoma.
• HIV infected patients have a higher incidence of
recurrent herpetic lesions and apthous stomatitis.
• The CDC HIV classification system indicates that
mucocutaneous herpes lasting longer than 1 month is
diagnostic of AIDS in HIV-infected individuals.
• Apthae and apthae like lesions are common.

56. Herpetic lesions in HIV infected patients
• Herpes may involve all mucosal surfaces and extend to skin
and persists for months.
• Atypical, large, persistent, non specific and painful ulcers are
common in immunocompromised individuals.
• If healing is delayed, lesions are secondarily infected and
become indistinguishable from persistent herpetic lesions.
• May require biopsy, microbial cultures, or both to determine
etiology.

57. Recurrent Apthous Stomatitis (RAS)
• Occur as a component of the initial acute illness of HIV
seroconversion.
• Increased incidence of major apthae, and the
oropharynx, esophagus and other areas of GIT may be
involved.
• Treatment include topical or intralesional corticosteroids,
chlorhexidine or other antimicrobial rinses, oral
tetracycline rinses, or topical amlexanox.

58. • Acyclovir (200-800 mg administered 5 times daily for 10 days
has been proven to be effective.
• Subsequent daily maintenance dose therapy (200 mg 2-5
times daily) may be required to prevent recurrence.
• Resistant viral strains are treated with foscarnet, ganciclovir
or valacyclovir.
• In cases with large apthae, administration of systemic
corticosteroids (Predinisolone 40-60 mg daily) or alternative
therapy (thalidomide, levamisole or pentoxifylline) should be
considered.

59. SALIVARY GLAND DISORDERS AND
XEROSTOMIA
• Salivary gland hypofunction and xerostomia may be
most common in HIV infected individuals.
• It worsens as the viral load increases to more than
100,000 copies/mm3.
• Also associated with increased candidal carriage due to
reduced salivary flow.
• Longitudinal studies have indicated that submandibular/
sublingual hypofunction occurs earlier than parotid
hypofunction, but parotid glands progressively become
less functional over time.

60. • Navazesh M (2000) in his study has shown that HIV
positive individuals were nearly three times more likely
to have zero unstimulated salivary flow rate as HIV
negative individuals.
• Zero unstimulated salivary flow rate is associated with
CD4 count< 200, with no differences found relative to
viral load.

61. ADVERSE DRUG EFFECTS
• Foscarnet , interferon and 2,3-dideoxycytidine (DDC)
induce oral ulcerations.
• Erythema multiforme reported with use of didanosine
(DDI)
• Zidovudine and ganciclovir may induce leukopenia,
resulting in oral ulcers.
• Xerostomia and altered taste sensation have been
described with diethyldithiocarbamate (Ditiocarb).
• Patients are more susceptible to drug-induced mucositis
and lichenoid drug reactions than general population.

62. GINGIVAL AND PERIODONTAL DISEASES
LINEAR GINGIVAL ERYTHEMA
• Persistent, linear, easily bleeding, erythematous gingiva.
• Microflora closely mimcs that of periodontitis.
• May be localised or generalised.
• Erythematous gingiva may be limited to marginal
gingiva, may extend to attached gingiva in a punctate or
diffuse erythema or may extend into alveolar mucosa.

63. • LGE is sometimes unresponsive to corrective therapy,
but such lesions may undergo spontaneous
remission.
• The affected sites should be scaled and polished.
• Subgingival irrigation with chlorhexidine or 10%
povidone iodine may be beneficial.

64. • Meticulous oral hygiene reinforcement to be done.
• The condition should be re-evaluated after 2 or 3 weeks
after initial therapy.
• Treatment of choice may be systemic antifungal drug,
fluconazole for 7 to 10 days.

65. Necrotizing Ulcerative Gingivitis
• Acute, punched out crater like depressions covered with
grayish pseudomembraneous slough. Spontaneous
gingival hemorrhage or bleeding on slightest stimulation
may occur.
• Gingiva is acutely painful and caution is taken to avoid
undue patient discomfort.
• Basic treatment includes cleaning and debridement of
affected areas with cotton pellet soaked in peroxide
after application of topical anaesthetic.

66. • Escharotic oral rinses , such as hydrogen peroxide should
only be rarely used.
• The patient should be seen daily or every other day for
the first week and debridement of affected area is
repeated at every visit.
• After initial healing, patient is able to tolerate scaling and
root planing if needed.
• Patient should avoid tobacco, alcohol and condiments.
• 0.12% chlorhexidine mouthrinse is also prescribed.

67. • Systemic antimicrobials such as metronidazole or
amoxicillin may be prescribed for patients with moderate
to severe tissue destruction, localised lymphadenopathy
or systemic symptoms, or both.
• The periodontium should be re-evaluated 1 month after
resolution of acute symptoms to assess the results of
treatment and determine if further therapy is needed.

68. NECROTIZING ULCERATIVE PERIODONTITIS
• May represent an extension of NUG in which bone loss
and periodontal attachment loss has occurred.
• NUP is characterised by soft tissue necrosis, rapid
periodontal destruction and interproximal bone loss.
• Generalised NUP is sometimes present after marked CD4
cell depletion.
• Bone is often exposed, resulting in necrosis and
subsequent sequestration.

69. • Therapy includes local debridement, scaling and root planing,
in-office irrigation with antimicrobial agent, establishment of
meticulous oral hygiene.
• If antibiotic is necessary, metronidazole (250mg; 2 tabs
immediately and then 2 tabs 4 times daily for 5-7 days).
• Prophylactic prescription of topical or systemic antifungal
agent is prudent if an antibiotic is used.

70. NECROTIZING ULCERATIVE STOMATITIS
• Occasionally reported in HIV positive individuals.
• Associated with severe suppression of CD4 immune cells and
elevated viral load.
• The condition appears to be identical to cancrum oris (noma), a
rare destructive process reported in nutritionally deprived
individuals.
• Treatment include antibiotic (metronidazole), and use of
antimicrobial rinse such as chlorehexidine gluconate.
• If osseous necrosis is present, it is necessary to remove necrotic
bone.

71. CHRONIC PERIODONTITIS
• Robinson PG (2002) in the study indicated that gingival
recession and early attachment loss are more common in
HIV positive individuals.
• However, several studies have indicated that pro-
inflammatory cytokines are increased in HIV positive
individuals.
• HIV infected individuals are potential candidates for
conventional periodontal treatment including periodontal
surgery and implant placement.
• Treatment decisions should be based on overall health of
patient, motivation and ability of the patient to perform
effective oral hygiene.

72. PERIODONTAL TREATMENT PROTOCOL
HEALTH STATUS
• Complete history, physical evaluation and consultation
with physician.
• Treatment decisions depend on the patients’ state of
health.
• Eg. Delayed wound healing and increased risk of post-
operative infections are possible complicating factors in
AIDS patients.

73. Information regarding :
• CD4+ T lymphocyte level?
• Current viral load?
• How do current CD4+ T4 cell and viral load counts differ
form previous evaluations?
• How long was the HIV infection identified?
• Is there a history of drug abuse, STDs, multiple infections
or other factors that might alter immune response?
• What medications is the patient taking?
• Any adverse effects from medications?

74. Infection control measures
• Strict adherence to established methods of infection
control, based on guidance from American Dental
Association (ADA) and CDC.
• Compliance with universal precautions will eliminate or
minimize risks to patients and dental staff.
• Immuno compromised patients are potentially at risk for
acquiring as well as transmitting infections in dental
office.

75. Periodontal Therapy
• Scaling , root planning and curettage may cause iatrogenic
bacteremia but have not shown to be associated with higher
incidence of systemic signs and symptoms.
• A daily antibacterial mouthrinse prior to and three days
following therapy may reduce the incidence of local and
systemic side effects.
• Deep block injections should be avoided; local infiltration or
intra ligamentary injections should be used.
• Surgical procedures should be performed in a manner to
minimize invasion of pathogens from oral cavity into deeper
facial planed and spaces.

76. Maintenance Therapy
• Patient should maintain meticulous oral hygiene.
• Recall visits to be conducted at short intervals (2 or 3
months) and any progressive periodontal disease treated
vigorously.
• Systemic antibiotics should be administered with caution.
• Blood and other medical laboratory tests:
Platelet count,
Prothrombin time (PT)/ INR.
Partial Thromboplastin time (PTT)
Hb, WBC count

77. Psychological factors
• Patients may be greatly concerned with the maintenance
of medical confidentiality and it must be upheld.
• Coping with life-threatening diseases may elicit
depression, stress, anxiety and anger towards the
dentist and staff; important to display concern and
understanding for the patient’s situation.
• Treatment should be provided in a calm, relaxed
atmosphere and stress to the patient should be
minimized.

78. Antibiotic Prophylaxis
INDICATIONS:
• Valvular heart disease
• Higher incidence of
previous SBE and
cardiomyopathies.
• Neutrophil count < 500
cells/mm3.
BACTERIOSTATIC DRUGS
given (1 hr before
treatment):
• Amoxicillin
• Ampicillin
• Azithromycin
• Cefadroxil
• Cephalexin
• Clarithromycin (high dose)
• Penicillin

79. Post-Exposure Prophylaxis
• Perform HIV antibody testing for atleast 6 months post
exposure (ie baseline, 6 weeks, 3 months and 6 months).
• Perform HIV antibody testing if illness compatible with acute
retroviral syndrome develops.
• Person advised to use precautions to prevent secondary
transmission during follow up period.
• Evaluate exposed person taking PEP within 72 hours after
exposure to monitor for drug toxicity for atleast 2 weeks.

80. Basic and Expanded Regimen HIV PEP of 28 days
Duration
REGIMEN CATEGORY ANTIRETROVIRAL DRUGS AND DOSE REGIMEN
BASIC Zidovudine (600mg/day in 2-3 divided doses) or
Lamivudine (150mg bd)
ALTERNATIVE BASIC Lamivudine (150 md bd) and
Stavudine (40mg bd)
ALTERNATIVE BASIC Didanosine (400mg qid empty stomach)
Stavudine (40mg bd)
EXPANDED Basic regimen plus Indinavir 800mg qid empty stomach
EXPANDED Basic regimen plus Nelfinavir 750mg tid/ 1250mg bd with meals
EXPANDED Basic regimen plus Efavirenz 600mg qid bedtime
EXPANDED Basic regimen plus Abacavir 300mg bd.

81. CONCLUSION
• Dentists often encounter HIV-infected patients who
are unaware of their disease status.
• Early diagnosis and treatment of an HIV-infected
patient has a profound effect on life expectancy.
• Patient should be informed and questioned
regarding any previous exposure to HIV.
• Written informed consent is desirable before all the
medical tests.

82. • Effective combination drug therapy is necessary for the
lifetime of infected individuals.
• Long term control of the infection may be difficult
because the antiviral agents currently used have many
adverse effects and readily develop drug-resistant variant
strains