Enhanced interleukin 1 beta, interleukin 6 and tumor necrosis factor alphain gingival crevicular fluid from periodontal pockets of patients infectedwith human immunodeficiency virus 1

Citation
Aama. Baqui et al., Enhanced interleukin 1 beta, interleukin 6 and tumor necrosis factor alphain gingival crevicular fluid from periodontal pockets of patients infectedwith human immunodeficiency virus 1, ORAL MICROB, 15(2), 2000, pp. 67-73
Citations number
50
Categorie Soggetti
Microbiology
Journal title
ORAL MICROBIOLOGY AND IMMUNOLOGY
ISSN journal
09020055 → ACNP
Volume
15
Issue
2
Year of publication
2000
Pages
67 - 73
Database
ISI
SICI code
0902-0055(200004)15:2<67:EI1BI6>2.0.ZU;2-M
Abstract
Loss of periodontal support and eventually tooth loss is a common finding a mong acquired immunodeficiency syndrome (AIDS) patients. The cause of this destruction may be an increase in periodontal disease activity at sites wit hin the same individual and also may be related to an increase in the pro-i nflammatory cytokines, diffused through the gingival crevicular sulcus in A IDS patients. A study was undertaken to determine the relative levels of th e pro-inflammatory cytokines, interleukin 1 beta (IL-1 beta), IL-6, and tum or necrosis factor alpha (TNF-alpha), in gingival crevicular fluid collecte d from the deep (>5 mm periodontal pocket depth) and shallow (less than or equal to 3 mm periodontal pocket depth) periodontal pockets of 39 HIV-1-inf ected patients and 20 age-, race- and sex-matched uninfected controls. Comp lete medical history including risk factors such as intravenous drug abuse was taken. Gingival crevicular fluid samples were collected on periopaper s trips. Cytokines were estimated by solid-phase enzyme-linked immunosorbent assay. To assess the degree of HIV activity, the viral load of these patien ts was determined by an Amplicor HIV-1 monitor kit using reverse transcript ase polymerase chain reaction. Gingival crevicular fluid from HIV-l-infecte d patients showed a two-fold increase in both IL-1 beta and TNF-alpha in de ep periodontal pockets in comparison to shallow pockets, whereas IL-6 incre ased 1.8-fold. There was a significant (P<0.05) increase in IL-I beta, IL-6 and TNF-alpha in gingival crevicular fluid (both shallow and deep pockets) from HIV-1-infected patients in comparison to uninfected controls and also significantly elevated in deep versus shallow pockets in these patients. A lthough IL-1 beta, IL-6 and TNF-alpha levels among HIV-1-infected patients with a high viral load (>10,000 copies/ml) were higher than those from pati ents with a low Viral load (<400 copies/ml), only the increase in IL-1 beta level associated with deep pockets was significant (P<0.05). There was als o a trend of an increase in all the three cytokines among intravenous drug- abusing HIV-1-infected patients in comparison to non-intravenous drug abuse rs, but only the difference in IL-1 beta levels from deep pockets reached s ignificance (P<0.05). These enhanced pro-inflammatory cytokine levels in th e gingival crevicular fluid of HIV-positive patients may be an important fa ctor in causing the advanced periodontal lesions sometimes observed in HIV- positive patients.