Pathology and Management of Periodontal Problems in Patients with Human
Immunodeficiency Virus Infection
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Prof(Dr) Vivek kr. Sharma
PART -1
OUTLINE
*Introduction
*Pathogenesis
*HIV
*Oral & Periodontal Manifestation
*Dental treatment Complication
*Gingival/Periodontal Disease
*Periodontal Treatment Protocol
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The earliest documented case of HIV infection has been traced to a blood sample from the Democratic Republic of Congo in 1959.
Human immunodeficiency virus (HIV),
INTRODUCTION
Acquired Immunodeficiency Syndrome3
The origin of HIV is a zoonotic infection with simian
immunodeficiency viruses (SIV) But SIVs do not cause disease in their natural primate hosts
Impairs cellular immunity
1983, Human immunodeficiency virus (HIV) was isolated from a patient with lymphadenopathy.
1984 it was demonstrated clearly to be the causative agent of AIDS.
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1986 a second type of HIV was isolated in Western Africa, and subsequently the two were named
HIV-1 and HIV-2 .
HIV belongs to the family of Human retroviruses (Retroviridae) and the subfamily of l Lentiviruses
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Structure of HIV-1: gp120 Envelop, gp41 Transmembrane components of envelop, Genomic RNA, Enzyme Reverse transcriptase, p18 inner membrane Matrix and p24 core protein(capsid)
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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.
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Stage 4
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HIV clinical categories
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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 above 5 yrs of age
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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 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.
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Category Aincludes patients with acute symptoms or asymptomatic diseases aswell as individuals with persistent generalized
lymphadenopathy with or without malaise, fatigue, or low-grade fever
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Antiretroviral Drugs
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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 later 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
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Some studies have indicated higher prevalence and severity of periodontitis in HIV‐positive subjects when compared to controls
,Smith et al. 1995a; Robinson et al. 1996; Ndiaye et al. 1997; McKaig et al. 1998; Nittayananta et al. 2010; Stojkovic et al. 2011
But 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)
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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.
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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
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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).
