HIV AND PERIODONTAL DISEASE ...POST GRADUATE SEMINAR

1. HIV AND PERIODONTAL DISEASE

2. CONTENT
 INTRODUCTION AND HISTORY
 HIV AND ITS MODE OF TRANSMISSION
 PATHOGENESIS
 EPIDEMINOLOGY
 HIV CLINICAL STAGING
 DIAGNOSIS
 ANTI RETROVIRAL DRUGS
 PERIODONTAL DISEASE IN HIV PATIENT
 DENTAL TREATMENT COMPLICATION
 PROPHYLAXIS
 CONCLUTION

3. The earliest documented case of HIV infection has been traced to a blood
sample from the Democratic Republic of Congo in 1959.
AIDS is caused by the human immunodeficiency virus (HIV), which progressively
impairs cellular immunity. The origin of HIV is a zoonotic infection with simian
immunodeficiency viruses (SIV) from African primates, probably first infecting local
hunters. But SIVs do not cause disease in their natural primate hosts
.
INTRODUCTION AND HISTORY
Davidson’sPrinciples and Practice ofMedicine 22nd Edition

4. In 1983, human immunodeficiency virus (HIV) was isolated from a patient with
lymphadenopathy, and by 1984 it was demonstrated clearly to be the causative agent of
AIDS.
In 1986 a second type of HIV was isolated in Western Africa, and subsequently the two
were named HIV-1 and HIV-2.
In 1985, a sensitive enzyme-linked immunosorbent assay (ELISA) was developed; this led
to an appreciation of the scope and evolution of the HIV epidemic at first in the United
States and other developed nations and ultimately among developing nations throughout
the world.
Infection with HIV-2 was first reported in the United States in 1987 in an individual who
had migrated from Western Africa
Davidson’s Principles and Practice of Medicine 22nd Edition

5. The two viruses apparently originated in different simian species. HIV-2 is very
similar to HIV-1, but it appears to be less virulent and causes AIDS much more slowly.
Infection with HIV-2 is rarely identified outside of Africa and countries that have been
intimately associated with that area.
HIV-1 was transmitted from chimpanzees and HIV-2 from sooty mangabey monkeys.
HIV-1 is the cause of the global HIV pandemic
Davidson’s Principles and Practice of Medicine 22nd Edition

6. There are three groups of HIV-1 representing three separate transmission events from
chimpanzees: M (‘major’, worldwide distribution), O (‘outlier’) and N (‘non-major
and non-outlier’).
Groups O and N are restricted to West Africa.
Group M consists of nine subtypes: A–D, F–H, J and K
Globally, subtype C (Africa and India) accounts for half of strains and appears to
be more readily transmitted
Subtype B predominates in Western Europe, the Americas and Australia.
In Europe, the prevalence of non-B subtypes is increasing because of migrants
(predominantly from Africa).
Subtypes A and D are associated with slower and faster disease progression respectively

8. HIV is the etiologic agent of AIDS; it belongs to the family of human retroviruses
(Retroviridae) and the subfamily of lentiviruses

9. Robbins and Cotran Pathologic Basis of Disease,9TH EDITION

10. The HIV-1 RNA genome contains the gag( p17, p24), pol(Reverse transcriptase, Integrase)
and env(gp 120, gp 41) genes, which are typical of retroviruses
Products of the gag and pol genes are large precursor proteins that are cleaved by the
viral protease to yield the mature proteins.
HIV contains several other accessory genes, including tat, rev, vif, nef, vpr, and vpu,
which regulate the synthesis and assembly of infectious viral particles and the
pathogenicity of the virus

11. Pathogenesis of HIV Infection and AIDS
The two major targets of HIV infection are the immune system and the central
nervous system
Profound immune deficiency, primarily affecting cellmediated immunity, is the
hallmark of AIDS. This results chiefly from infection and subsequent loss of CD4+ T
cells as well as impairment in the function of surviving helper T cells along with
macrophages and dendritic cells
HIV enters the body through mucosal tissues and blood and first infects T cells
as well as dendritic cells and macrophages
The infection becomes established in lymphoid tissues, where the virus
may remain latent for long periods.
Active viral replication is associated with more infection of cells and progression
to AIDS.

12. Harrison’s Principles of Internal medicine , 19th edition

13. Tetherin

14. Robbins and Cotran Pathologic Basis of Disease 9TH EDITION

17. National Aids Control Organization

18. National Aids Control Organization

21. AIDS may be present with either clinical stage 3 or stage 4 disease. A CD4 count of less
than 350/mm3 is considered diagnostic for AIDS in adults and in children who are 5 years
old or older.
Advanced HIV infection in infants is based on a CD4+ cell value of less than 30% ,if the patient
is younger than 12 months old, less than 25% among patients between 12 and 35 months old,
and less than 20% among those between 36 and 59 months old. (These are the WHO case
definitions of HIV for surveillance and the revised clinical staging and immunologic
classifications of HIV-related disease in adults and children.(Centers for Disease Control and
Prevention. 1993 revised classification system for HIV infection and expanded surveillance case
definition for AIDS among adolescents and adults. MMWR. 1993;41:RR–17.))

22. The 1993 revision added invasive cervical cancer in women, bacillary tuberculosis, and
recurrent pneumonia to the AIDS designation.

23. Currently, any of 25 specific clinical conditions found in HIV-positive individuals
can establish a diagnosis of AIDS:----

24. Centers for Disease Control and Prevention Surveillance Case Classification 1993
Patients with AIDS have been grouped as follows, according to the 1993 CDC
Surveillance Case Classification:
Category A includes patients with acute symptoms or asymptomatic diseases as well
as individuals with persistent generalized lymphadenopathy with or without malaise,
fatigue, or low-grade fever
Category B patients have symptomatic conditions such as oropharyngeal or
vulvovaginal candidiasis, herpes zoster, oral hairy leukoplakia, or idiopathic
thrombocytopenia, or constitutional symptoms of fever, diarrhea, or weight loss.
Category C patients are those with outright AIDS as manifested by life-threatening
conditions or as identified by CD4+ T lymphocyte levels of less than 200 cells/mm3.

25. The CDC staging categories reflect progressive immunologic dysfunction, but patients do
not necessarily progress serially through the three stages, and the predictive value of
these categories is not known. However, because HAART drugs may cause severe adverse
side effects, many AIDS treatment centers continue to follow these guidelines to determine
when to initiate or discontinue multidrug therapy

27. CD4 counts and Viral load
CD4 counts
CD4 lymphocyte counts are usually determined by flow cytometry
The CD4 count is the most clinically useful laboratory indicator of the degree of
immune suppression and is used, together with clinical staging, in decisions to start ART
and prophylaxis against opportunistic infections, and in the differential diagnosis of
clinical problems.
The CD4 count varies by up to 20% from day to day and is also transiently reduced by
intercurrent infections. Due to this variability, major therapeutic decisions should not be
taken on the basis of a single count. This is particularly important when ART is
being initiated in patients who do not fulfil the clinical criteria to start ART.

28. The normal CD4 count is > 500 cells/mm3. The rate of decline in CD4 count is highly
variable. People with CD4 counts between 200 and 500 cells/mm3 have a low
risk of developing major opportunistic infections.
Once the count is below 200 cells/mm3, there is severe immune suppression and a high risk
of AIDS defining conditions.(DEC,18th 1992).
The CD4 count should be performed every 3–6 months in patients not yet eligible for ART
and is usually done at similar intervals in patients on ART, together with measurement of the
viral load.

30. Viral load
The level of viraemia is measured by quantitative PCR of HIV-RNA, known as the viral
load. Determining the viral load is important for monitoring responses to ART and also
has some prognostic value before starting ART.
People with high viral loads (e.g. > 100 000 copies/mL) experience more rapid declines
in CD4 count, while those with low viral loads (< 1000 copies/mL) usually have slow
or even no decline in CD4 counts.
There is little point in repeated measurements of viral load before starting ART, as viral
loads remain at a relatively stable plateau after primary infection

33. Antiretroviral Drugs Approved for Use by the US Food and Drug Administration

34. Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
Abacavir (Ziagen, ABC)
Abacavir plus lamivudine (Epzicom)
Abacavir plus lamivudine plus zidovudine
(Trizivir)
Didanosine (Videx, DDI)
Emtricitabine (Emtriva, FTC, Coviracil)
Emtricitabine plus tenofovir DF (Truvada)
Lamivudine (Epivir, 3TC)
Lamivudine plus zidovudine (Combivir)
Stavudine (Zerit, d4T)
Tenofovir (Viread, TDF)
Zalcitabine (Hivid, ddC)
Zidovudine (Retrovir, AZT, ZDM)

35. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
Delavirdine (Rescriptor, DLV)
Etravirine (Intelence)
Efavirenz (Sustiva, EFV)
Nevirapine (Viramune, NVP)
Protease Inhibitors (PIs)
Amprenavir (Agenerase, APV)
Atazanavir (Reyataz, ATV)
Darunavir (Prezista)
Fosamprenavir (Lexiva, FPV)
Indinavir (Crixivan, IDV)
Lopinavir/ritonavir (Kaletra, LPV/r)
Nelfinavir (Viracept, NFV)
Ritonavir (Norvir, RTV)
Saquinavir (SQV, Invirase)
Tipranavir (Aptivus)

36. Fusion Inhibitor (FI)
Enfuvirtide (Fuzeon, T20)
Entry Inhibitor/Chemokine Receptor Type 5 Co-Receptor
Antagonist
Maraviroc (Selzentry)
Human Immunodeficiency Virus Integrase Strand Transfer Inhibitor
Raltegravir (Isentress)

38. Combination antiviral agents are composed of multiple drugs with various sites of viral
disruption of incorporation into CD4 cells. These combinations represent the
transformation of antiretroviral therapy into HAART
Combinations of three or more antiretroviral drugs are administered simultaneously
for long periods of time in an effort to block HIV replication and plasma viral load and to
restore immune function while minimizing antiretroviral drug resistance and adverse drug
effects. The goals are to improve the patient's quality of life and reduce HIV-related
morbidity and mortality.

39. Three commonly used combinations are one NNRTI plus two NRTIs, one or two
protease inhibitors plus two NRTIs, or three NRTIs. NRTI three-drug combination is
available in a single tablet, but this antiretroviral therapy does not necessarily qualify
as HAART.(Pavlos R, Phillips EJ.,2012)
Some authorities felt that the drugs should not be administered until significant immune
suppression occurred.
Others advocated the initiation of therapy as soon as the diagnosis was established.
Evidence has indicated that early treatment is far more successful than delayed
treatment.(Braithwaite RS, Roberts MS, Goetz MB, et al,2009)
Survival time is shorter despite HAART among individuals who are injected drug abusers,
those with AIDS before the initiation of therapy, those with a very high viral load before
the initiation of therapy (i.e., >100,000 copies/mL), those who are inconsistent in their
adherence to the drug regimen, and those who discontinue the drugs.

40. Studies published in the late 1980s seemed to indicate that both the prevalence and the
severity of periodontitis were exceptionally high in patients with acquired
immunodeficiency syndrome (AIDS) (Winkler & Murray 1987), but a more tempered
picture emerged in subsequent publications.
Cross ‐sectional study of 326 HIV‐infected adults (McKaig et al. 1998) revealed that,
after adjustments for CD4 counts, persons taking HIV antiretroviral medication were five
times less likely to suffer from periodontitis than those not taking such medication,
underscoring the importance of the host’s immunologic competency in this context
PERIODONTAL DISEASE IN HIV PATIENT

41. Although a number of studies (Smith et al. 1995a; Robinson et al. 1996; Ndiaye
et al. 1997; McKaig et al. 1998; Nittayananta et al. 2010; Stojkovic et al. 2011) have
indicated higher prevalence and severity of periodontitis in HIV‐positive subjects
when compared to controls, other studies have either not supported this notion or have
indicated that the differences in periodontal status between HIV‐seropositive
and ‐seronegative subjects are limited (Cross & Smith 1995; Lamster et al. 1997;
Scheutz et al. 1997; Lamster et al. 1998; Vastardis et al. 2003).
Studies investigating the pathobiology of periodontitis in HIV‐infected subjects suggested
that specific IgG subclass responses to periodontopathic bacteria were similar in
HIV‐positive and HIV‐negative subjects (Yeung et al. 2002), while CD4 count levels
were not found to correlate with the severity of periodontitis (Martinez Canut et al.
1996; Vastardis et al. 2003)

42. Two companion publications, from a short term follow‐up study (Smith et al. 1995b;
Cross & Smith 1995) involving a group of 29 HIV‐seropositive subjects who were
examined at baseline and at 3 months, reported a low prevalence and incidence of clinical
attachment loss. The subgingival microbial profiles of the seropositive subjects resembled
those of nonsystemically affected subjects, and did not correlate with their CD4 and CD8
lymphocyte counts.
Similarly, in a small follow‐up study of 12 months’ duration, Robinson et al. (2000) found no
difference in the progression of periodontitis between HIV‐positive and HIV‐negative
subjects
Hofer et al. (2002) demonstrated that compliant HIV‐positive subjects can be successfully
maintained in a manner similar to non‐infected controls.

43. However, a 20‐month follow‐up study of 114 homosexual or bisexual men (Barr et al.
1992) revealed a clear relationship between incidence of clinical attachment loss and
immunosuppression, expressed through CD4 cell counts
According to Papapanou and Lindhe seropositivity in combination with older age confers
an increased risk for attachment loss.
Similar observations were reported by Lamster et al. (1997), who concluded that
periodontitis in the presence of HIV infection is dependent upon the immunologic
competency of the host as well as the local inflammatory response to the subgingival
microbiota.
It appears therefore that there is no consensus in the literature on the association of
HIV/AIDS and periodontitis. Variation in the severity of oral pathologic conditions
due to ongoing advancements in HIV/AIDS therapy will likely further contribute to
the diversity of the findings (Freed et al. 2005).

44. Periodontal diseases in HIV-infected patient
HIV-associated periodontal lesions as listed by EC Clearinghouse (1993)
include:
(i) Linear gingival erythema.
(ii) Necrotizing ulcerative periodontal diseases, including necrotizing ulcerative
gingivitis, necrotizing ulcerative periodontitis, and necrotizing ulcerative
Stomatitis.
(iii) Chronic periodontitis.

45. Linear gingival erythema
Linear gingival erythema (LGE) is regarded as a gingival manifestation of immunosuppression
characterized by a distinct linear erythematous band limited to the free gingiva (Holmstrup
1999 ) .The intensity of the erythema is disproportionate to the amount of plaque present.
There is no ulceration, pocketing, or attachment loss and the condition does not respond
predictably to conventional periodontal therapy.
Linear gingival erythema and necrotizing
ulcerative gingivitis in a patient with acquired
immunodeficiency syndrome.
The diagnosis should be considered if the
lesion persists after removal of plaque at the
initial visit (Umadevi et al. 2006) .
A key feature of LGE is now considered
to be lack of bleeding on probing (Robinson
et al. 1994).

46. There are indications that candidal infection is the background of some cases of gingival
inflammation including LGE (Winkler et al. 1988; Robinson et al. 1994), but studies have
revealed a microflora comprising both C. albicans and a number of periopathogenic
bacteria consistent with those seen in conventional periodontitis, that is Porphyromonas
gingivalis, Prevotella intermedia, Actinobacillus actinomycetemcomitans, Fusobacterium
nucleatum, and Campylobacter rectus (Murray et al. 1988, 1989, 1991).
In one study, direct microscopic cultures from LGE lesions implicated Candida dubliniensis
in four patients, all of whom experienced complete or partial remission after systemic
antifungal therapy. It is not yet known whether candidal infection is an etiologic factor in all
LGE cases(Velegraki A, Nicolatou O, Theodoridou M, et al,1999).

47. A systematic review indicates that LGE is more common among HIV-infected populations
but that most individuals who are HIV positive do not experience LGE. (Patton LL.2003)
Others have reported that LGE is most often found in HIVpositive individuals whose
CD4+ counts are depressed (200 to 500 cells/mm3 or <200 cells/mm3) or whose viral
loads are elevated, suggesting that it may represent an early marker of progressive
immunodeficiency or even the transition to outright AIDS. (Sontakke Sa,et al, 2011)
An interesting histopathologic study of biopsy specimens from the banding zone has
revealed no inflammatory infiltrate but an increased number of blood vessels, which
explains the red color of the lesions (Glick et al. 1990). The incomplete inflammatory
reaction of the host tissue may be the background to the lack of response to conventional
treatment.

48. There is little information about treatment based on controlled studies
Conventional therapy plus rinsing with 0.12% chlorhexidine gluconate twice daily has
been shown to give significant improvement after 3 months (Grassi et al. 1989).
It was mentioned above that LGE in some cases might be related to the presence of
Candida strains. In accordance with this finding, clinical observations suggest that
improvement is frequently dependent on successful eradication of intraoral
Candida strains, which results in disappearance of the characteristic features (Winkler
et al.1988).
The treatment of choice may be the empiric administration of a systemic antifungal
agent, such as fluconazole, for 7 to 10 days.(Hofer D,2002)

49. Necrotizing Ulcerative Gingivitis
Some reports have described an increased incidence of NUG among HIV-infected
individuals, although this has not been substantiated by other studies. (Syrjanen S, et
al., 1989. Drinkard CR, et al, 1991, Horning GM,Cohen ME, 1995)
There is no consensus regarding whether the incidence of NUG increases in HIV-positive
patients.(Patel AS, Glick M. 2003, Patton LL.,2003.)
However, one study evaluated the HIV status of individuals who presented with
necrotizing periodontal diseases, and 69% were found to be HIV seropositive.(Shangase
L,et al 2003)
The treatment of NUG in these patients does not differ from that in HIV-negative
individuals
Hydrogen peroxide should be used only rarely for any patient, and they are especially
contraindicated in immunocompromised individuals.

50. The patient should avoid tobacco, alcohol, and condiments. An antimicrobial oral
rinse 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
The use of prophylactic antifungal medication should be considered if antibiotics are
prescribed

51. Necrotizing periodontal disease
HIV infection attacks T‐helper cells, causing a drastic change in the T‐helper (CD4
positive)/T‐ suppressor (CD8 positive) ratio with severe impairment of the host’s
resistance to infection
Depleted peripheral helper T‐lymphocyte counts correlate closely with the occurrence
of NG, as demonstrated in a study of 390 US HIV‐seropositive soldiers (Thompson et
al. 1992), and an inverse correlation between NPD and CD4‐positive T‐cell counts
was recently found among patients who had not started HAART in intavenous non
drug user than intravenous drug user; (Ranganathan et al. 2012).
According to Glick et al(1994) mentioned that NUP should be considered for
inclusion in AIDS surveillance definition.

52. Other studies depict no correlation was found between CD4‐positive T‐cell count
or neutrophil count and extent and severity of NPD in studies of South African
patients (Phiri et al. 2010; Wood et al. 2011).
A complete absence of T cells in gingival tissue of HIV infected patients with
periodontitis has been reported (Steidley et al. 1992). The lack of local immune
effector and regulatory cells in HIV‐seropositive patients could in fact explain the
characteristic and rapidly progressive nature of periodontitis in these patients

53. Protective effect against NPD has been encountered with HAART of the HIV
infection (Tappuni et al. 2001), as well as against HIV‐associated gingivitis and
periodontitis (Masouredis et al. 1992).
NP has been revealed as a marker for immune deterioration, with a 95% predictive
value that CD4‐ positive cell counts were below 200 cells/mm3, and, if untreated, a
cumulative probability of death within 24 months (Glick et al. 1994).
As a consequence of this finding, a test for HIV infection, if possible, may be
recommended for all NPD patients.
If an antibiotic is necessary, Metronidazole (250 mg, with two tablets taken
immediately and then two tablets taken four times daily for 5 to 7 days) is the drug of
choice. The prophylactic prescription of a topical or systemic antifungal agent is
prudent if an antibiotic is used.

54. Chronic periodontitis in HIV-infected subjects
Before and after the widespread use of antiretroviral therapy, there were conflicting reports
as to the relationship of HIV infection with attachment loss and bone loss.
Barr et al. 1992 reported that the risk for periodontal attachment loss may be six times
higher in HIV-infected subjects over 35 years of age with CD4+ T lymphocyte counts
<200 cells/mm3.
After the introduction of HAART there was an increase in life span in this population and
consequently many individuals with pre-existing periodontitis experienced a higher
clinical attachment loss due to increasing age. (Yin et al 2007)

55. Before the introduction of HAART, Robinson et al 1996 reported an increased
attachment loss without pocketing as a condition frequently seen in HIV-infected
individuals, resulting from past episodes of ulceration.
More recently, Goncalves et al 2007 demonstrated that the long-term use of HAART
in Brazilian HIV-infected individuals resulted in a decrease in the severity of CP.
In this study they compare the subgingival microbiota of HIV positive and negative
patient with chronic periodontitis and found periodontal pathogens more prevalent
among HIV negative as compared to HIV positive undergoing HAART therapy.

56. A study conducted by Ndiaye et al. 1997 in HIV-infected Senegalese individuals not
undergoing antiretroviral therapy and with periodontal disease, a significantly higher
prevalence of individuals with clinical attachment levels 6 mm was observed in HIV-
infected individuals than in the non HIV infected control group.
Despite this, it is unclear how antiretroviral therapy can impact the clinical parameters
of CP in HIV-infected individuals and further studies are needed to confirm these
findings

57. Oral candidiasis
In the pre-antiretroviral therapy era, the various forms of oral candidiasis were the most
common HIV-related oral lesion with prevalence ranging from 5% to 92%. (Patton et al
2002)
A study from India reported that oral candidiasis infections are more common among
males than females, although 92% of infected men and 95% of infected women reported
acquiring the infection through heterosexual contact. (Rao UK,2012)
The most common organism involved with the presentation of candidiasis is Candida
albicans.
It has 4 clinical presentations :
1. Pseudomembranous candidiasis.
2. Erythematous candidiasis.
3. Hyperplastic candidiasis.
4. Angular cheilitis.

58. Non–C.albicans candidal species (Candida glabrata, Candida tropicalis, Candida
krusei, Candida parapsilosis, Candida lusitaniae, Candida guilliermondii )appear to
be especially prone to the development of azole resistance, species identification may
become more important for the control of candidiasis.(Kantheti LP,2012)
Smoking and the presence of removable full or partial dentures increased the risk.
(Witzel AL,2012)
Although the incidence of oral candidiasis has been reported to decrease significantly
after HAART treatment, colonization and oral infection remain common among
HIV-positive individuals of all ages, either as evidence of unsuccessful therapy or as
a result of IRIS.( Tami-Maury IM,2011, Patel PK,2012)

59. In the past, 30% of patients with AIDS-related candidiasis relapsed within 4 weeks of
treatment, and 60% to 80% relapsed within 3 months. This relapse may have resulted from
decreasing immunocompetency or the development of antifungal-resistant candidal strains.
(Hood SV, et al 1999.)
10% of candidal organisms become resistant to long-term fluconazole therapy, and
cross-resistance to other azoles (i.e., Ketoconazole, Itraconazole, Miconazole, or
Clotrimazole) and Amphotericin B may develop.
Resistant candidiasis is more common among late-presenting individuals with AIDS
who have low CD4 counts and high viral loads at baseline. (Hood SV, et al 1999.)
Administration of HAART to patients with HIV infection has resulted in a significant
decrease in the incidence of oropharyngeal candidiasis and oral candidal carriage,
and it has also reduced the rate of fluconazole resistance. (Ceballos-Salobrena A et al ,
2004,Cossarizza A et al,2001.)When esophageal candidiasis is present during HAART,
there is an increased incidence of non–C. albicans species and fluconazole-resistant
organisms.

60. Early oral lesions of HIV-related candidiasis are usually responsive to topical antifungal
therapy . More advanced lesions, including hyperplastic candidiasis, may require systemic
antifungal drugs; systemic therapy is mandatory for esophageal candidiasis.
Most oral topical antifungal agents contain large quantities of sucrose, which may be
cariogenic after long-term use. For this reason, some authorities recommend oral use
of vaginal tablets because they do not contain sucrose. However, such tablets are
relatively low in active units (100,000) as compared with usual oral dosages of 200,000
to 600,000 units.( Terry D. Rees, 2018)
Sucrose free oral suspensions of itraconazole and amphotericin B oral rinse have also
been used in oral candidiasis.
Fluconazole oral suspension has been reported to be more effective as an antifungal than
liquid nystatin.
Chlorhexidine and cetylpyridinium chloride oral rinses may also be of some prophylactic
value against oral candidal infection.(Giuliana G,1999. )
Fluconazole may be the agent of choice when systemic therapy is required.

61. Kaposi Sarcoma
KS is the most common oral malignancy associated with AIDS
This angioproliferative tumor is a rare, multifocal, vascular neoplasm; it was originally
described in 1872 as occurring in the skin of the lower extremities of older men of
Mediterranean origin.
There are at least four distinct epidemiologic forms of KS:
(1) The classic form that occurs in older men of predominantly Mediterranean or eastern
European Jewish backgrounds with no recognized contributing factors
(2) The equatorial African form that occurs in all ages, also without any recognized
precipitating factors
(3) The form associated with organ transplantation and its attendant iatrogenic
immunosuppressed state
(4) The form associated with HIV-1 infection
Harrison’sPrinciples of Internal medicine , 19th edition

62. It is a manifestation of excessive proliferation of spindle cells that are believed to be of
vascular origin and have features in common with endothelial and smooth-muscle cells.
HIV disease the development of KS is dependent on the interplay of a variety of factors
including HIV-1 itself, Human Herpes Virus 8 (HHV-8), immune activation, and
cytokine secretion.
In HIV , KS is a much more aggressive lesion, and the majority of patients (71%) develop
lesions of the oral mucosa, particularly the palate, the gingiva, and the tongue. (Jin Y-T, et
al,1996. Pantanowitz L, et al, 2013.)
Oral lesions may be unifocal or multifocal. The oral cavity may often be the first or only site
of the lesion. (Barrett AP, et al,1988.)

64. Treatment of oral KS includes antiretroviral agents, laser excision, cryotherapy, radiation
therapy, and intralesional injection with vinblastine, interferon-γ, sclerosing agents, or
other chemotherapeutic drugs.
Nichols and colleagues(1993) described the successful use of intralesional vinblastine
injections at a dose of 0.1 mg/cm2 with the use of a 0.2 mg/mL solution of vinblastine
sulfate in saline . In responsive patients, treatment was repeated at 2-week intervals
until resolution or stabilization of the lesions occurred.
Total resolution was achieved in 70% of 82 intraoral KS lesions with one to six
treatments.
Destructive periodontitis has also been reported in conjunction with gingival KS. In
such patients, scaling and root planing as well as other periodontal therapy may be
indicated in addition to intralesional or systemic chemotherapy. Shibosky CH,
Winkler JR, 1993

65. AIDS-related KS is uncommon except in those who are unaware of their HIV-positive
status, those who are not taking HAART, or those who have discontinued HAART for
one reason or another. Campo-Trapero J,2008
Recurrent aphthous stomatitis has been described in HIV-infected individuals, but the
overall incidence may be no greater than that found in the general.( population.EC-
Clearinghouse on Oral Problems Related to HIV Infection,1993)

66. PERIODONTAL TREATMENT PROTOCOL
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+ T lymphocyte level.
- Current viral load.
- Difference from previous counts and load.
- H/o of drug abuse, multiple infections.
-Present medications.

67. II. 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 - tuberculosis
- Blood borne pathogens -HIV, HBV, HCV
- Waterborne pathogens- Legionella and Pseudomonas species
- Mucosal/ skin borne pathogens-- VZV or HSV

68. III. 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.

69. IV. 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)
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

70. V. PSYCHOLOGIC FACTORS
HIV infection of neuronal cells may affect brain function
---outright dementia.
Life-threatening disease may elicit
depression,anxiety and anger in such patients & this anger may be directed
toward the dentist and the staff. (Asher et al 1993).
During treatment calm, relaxed atmosphere, and stress to the patient must be
minimized

71. 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.
When exposure occurs, Provide immediate care to the exposure site. Wash needle stick
injuries and cuts with soap and water. Flush mucous membranes with a sterile solution
of saline.

74. CONCLUSION
The pathogenesis of 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.