Clinical Documentation and Occurrence of Putative Periodontopathic Bacteria in Human Immunodeficiency Virus‐Associated Periodontal Disease

Abstract

Human immunodeficiency virus (hiv)‐associated gingivitis (HIV‐G) and HIVassociated periodontitis (HIV‐P) are two intraoral lesions manifested by patients with HIV infection. Periodontal indices were measured for 87 subjects in 5 study groups: HIV‐seropositive patients with healthy periodontium (HIV‐H), with HIV‐G, or with HIVP; and non‐HIV‐infected subjects with healthy periodontium (H) or with adult chronic periodontitis (P). The quantitative clinical parameters were compared and statistically significant intergroup differences were noted. The mean scores on PI and PD do not discriminate between HIV‐seropositive and non‐HIV‐infected seronegative cohorts, but a significant difference in the GI between HIV‐H and H was noted. When categories of PD and AL are examined, some differences become apparent. Generally, the PD and AL of HIV‐P are not as great as those of P. PI correlates well with GI (r = 0.86) in P, but does not (r = 0.33) in HIV‐P. In addition, the occurrence of selected putative periodontopathic bacteria (Porpfiyromonas gingivalis, spirochetes, and motile eubacteria) in these lesions was determined by brightfield (after staining), darkfield and immunofluorescent microscopy. No difference in microbiological profile in the bacterial groups monitored was found between P and HIV‐P. Spirochetes were found to be more abundant than P. gingivalis in the lesions of P and HIV‐P. In marked contrast, P. gingivalis was found to be in highest numbers in samples from the gingival crevice of H as determined by indirect immunofluorescence. J Periodontol 1991; 62:576–585.

A member of the peptidase M48 superfamily ofPorphyromonas gingivalisis associated with virulencein vitroandin vivo

“…Detection of P . gingivalis in similar frequency from periodontally healthy and diseased sites is not uncommon and has been previously observed (26, 27). Therefore, bacteria could be present but not necessarily expressing virulence genes until a triggering event happens and initiation of disease occurs.…”

Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment

“…The only difference between groups was a slight but significantly higher proportion of P. gingivalis in the HIV-positive subjects, which was attributed to a subgroup of HIV-positive subjects with widespread attachment loss. These findings and others (82,231,339) indicate that there is no unique plaque flora which accounts for the aggressive nature of periodontal disease in HIV-positive subjects. Rather, it is the same periodontal flora seen in EOP and AP that causes a more aggressive disease in a compromised host, much as was found in the Down syndrome and Papillon-Lefevre syndrome subjects (16,49,69,174,229).…”

Treponema denticola (ex Brumpt 1925) sp. nov., nom. rev., and Identification of New Spirochete Isolates from Periodontal Pockets

“…The treponemes have been implicated in the etiology of all forms of periodontal disease by virtue of their proliferation to high numbers in diseased sites (6,13,15). Evidence on the quantitative relationship of Treponema denticola to the severity of periodontal disease has been presented previously (22,23).…”