This study demonstrates that both HIV-seropositive and apparently healthy subjects with chronic periodontitis have similar mean PPD, GR, PI, and BI measurements and that HIV infection does not carry with it a greater risk for accelerated periodontal attachment loss [2
]. This conforms with other studies that documented similar clinical manifestations and natural courses of chronic periodontitis in HIV-seropositive and -seronegative subjects [12
The results of this study indicate that the reported general increase in the prevalence of fungal and viral microorganisms observed in periodontal pockets of HIV-seropositive subjects with chronic periodontitis compared to HIV-seronegative subjects with chronic periodontitis [22
] has no influence on the periodontal health status, in spite of the potential of these microorganisms to exacerbate the inflammatory processes and suppress the immune responses in the periodontal tissues [26
]. It is also evident that the reduction in the number of Langerhans cells in the pocket epithelium in HIV-seropositive subjects [27
] and the consequent local immune impairment does not play any particular role in the development and progression of chronic periodontitis.
Therefore, there would appear to be no indication for instituting different treatment modalities for chronic periodontitis in HIV-seropositive subjects and in immunocompetent subjects. If indeed some HIV-seropositive subjects demonstrate increased levels of periodontal tissue destruction, this may be the result of periodontal disease activity that took place before the onset of HIV infection. This could be determined by the study of reliable pre-HIV infection periodontal records [29
The mean GR was similar in HIV-seropositive and healthy subjects, in HIV-seropositive subjects using HAART, and in HIV-seropositive HAART-naïve subjects, and also regardless of lower or higher CD4+ T-cell counts. This does not agree with the findings of McKaig et al. (2000) [10
] and Lamster et al. (1997) [30
] who found a negative correlation between CD4+ T-cell count and increased frequency of recession. McKaig et al., (2000) [10
] reported that recession in HIV-seropositive subjects with chronic periodontitis is more likely to occur in association with low CD4+ T-cell counts (<200
) than with higher CD4+ T-cell counts (200–499
As evident from the results of this study, HIV-seropositive subjects with chronic periodontitis do not have an increase either in the number of sites of gingival marginal recession or in the severity of gingival marginal recession; and a low CD4+ T-cell count is not a risk factor for increased frequency or severity of GR.
Recent studies have shown that the severity of chronic periodontitis is decreased in HIV-seropositive subjects and that there is a positive correlation between clinical attachment levels and the CD4+ T-cell counts; lower CD4+ T-cell counts are associated with reduced periodontal probing depth and with lesser degrees of recession measurements [31
The profound suppression of immunity in HIV disease does not seem to increase the risk of development of chronic periodontitis. The diminution of the CD4+ T-cell count, dysregulation of the cytokine network, and qualitative defects of macrophages, monocytes, polymorphonuclear leukocytes, dendritic cells, and T lymphocytes do not predispose HIV-seropositive subjects to periodontopathic infection [33
]. The profound HIV-associated immune suppression also does not appear to predispose to delayed wound healing of the oral tissues [35
], to increased incidence of wound infection of periodontal or other oral surgery [36
], or to plaque-induced periodontal tissue destruction [12
Since the periodontal tissue destruction in chronic periodontitis is mediated mainly by host-derived cellular immune responses [37
], and since these mechanisms are to a great extent suppressed in HIV infection, HIV-seropositive subjects with chronic periodontitis may be expected to show reduced rather than exaggerated periodontal tissue destruction, compared to immunocompetent subjects with chronic periodontitis. Moreover, active periodontal disease associated with periodontal attachment loss is related mainly to a Th1 cytokine profile [38
]. However, in advanced HIV disease, in the absence of HAART, there is a dysregulation in the cytokine network characterized by a shift from Thl predominant cytokines to a Th2 cytokine profile [40
] that is less associated with periodontal tissue destruction. This reinforces the concept that HIV-related immune dysregulation may not contribute to the development of chronic periodontitis but in fact is associated with reduced periodontal tissue destruction.
Taking into consideration the immune suppression associated with HIV infection one would have expected that HIV-seropositive subjects with low CD4+ T-cell counts would show higher frequencies of infection with periodontopathic bacteria and an increased incidence of wound infection following oral surgery, compared to HIV-seropositive subjects. However, this is not the case. HIV-seropositive and -seronegative subjects show similar types and quanta of periodontopathic bacteria in their subgingival microbiota, similar incidences of infection of surgical wound, and similar wound healing capacity [4
HIV-seropositive subjects, however, demonstrate bacterial species in their subgingival microbiota that are not usually associated with periodontal disease. These opportunistic microorganisms including E. faecalis, A. baumannii,
and Pseudomonas aeruginosa
are probably associated with HIV-related immunosuppression. The fact that HIV-seropositive subjects are frequently treated in a hospital environment might account for the presence of unusual opportunistic microorganisms [31
The process of wound healing is complex, involving interaction between macrophages, dendritic cells, polymorphonuclear leukocytes, epithelial cells, fibroblasts, osteoblasts, cytokines, and growth factors [41
]. While macrophages and growth factors are the driving force behind the process of wound healing [41
], CD4+ T-cells do not play a critical role [42
]. Consequently, in spite of some impairment in the function of macrophages and alteration in the cytokine network, HIV-seropositive subjects do not demonstrate impaired wound healing capacity [43
] or increased incidence of wound infection following oral surgery [35
There is an inverse relation between the CD4+ T-cell count and the frequency of HIV-associated oral lesions, in particular when the CD4+ T-cell count is lower than 200
regardless of the use of HAART [44
]. However, HIV-seropositive subjects using HAART have a significantly lower prevalence of HIV-associated oral lesions compared to HAART-naïve HIV-seropositive subjects [44
Chronic periodontitis is similar to other oral lesions in this respect. The use of HAART in HIV-seropositive subjects has brought about a decrease in the prevalence and severity of chronic periodontitis [11
]. HIV-seropositive subjects with chronic periodontitis using HAART demonstrate reduced counts of periodontopathic bacteria in their subgingival plaque, and their periodontal tissues show reduced inflammation and periodontal attachment loss, compared to HIV-seronegative subjects with chronic periodontitis [34
Even severely immunocompromised HIV-seropositive subjects with chronic periodontitis who are using HAART and with low CD4+ T-cell counts demonstrate similar periodontopathic bacteria in their subgingival microbiota to HIV-seronegative subjects with chronic periodontitis of a comparable degree [33
]. It is possible that HAART-associated reconstitution of components of the immune response is sufficient to control colonization by the periodontopathic pathogens, even though the CD4+ T-cell count remains low [33
]. It is also possible that one or more of the drugs in the cocktail constituting HAART have anti-inflammatory and/or antibacterial properties that act synergistically with the hosts' partially reconstituted immune mechanisms in controlling the periodontopathic bacteria [34
This study has a few limitations. Firstly, the control group comprised subjects of unconfirmed, presumably HIV-seronegative status, and this status could not be confirmed owing to the refusal of the subjects to consent to free HIV testing. Secondly, of the HIV-seropositive cohort of 30 subjects, the CD4+ T-cell count of only 13 subjects were known. The remaining 17 subjects would not consent to free CD4+ T-cell count testing.
In the semirural community of Ga-Rankuwa, South Africa, refusal of any form of testing in relation to HIV disease, even if offered free of charge, is common and is probably related to the perceived stigma associated with HIV disease and to the possibility that HIV-seropositive subjects may be shunned by their communities. Consequently, there is reluctance to learn one's own HIV-serostatus, and when the HIV-serostatus is known, to denial.
In a study investigating necrotizing periodontal diseases (NPD) in HIV-seropositive and—seronegative subjects in the same cohort as in our study [45
], 35% of subjects with NPD and unaware of their HIV-serostatus refused to test their HIV-serostatus in spite of strong recommendation and detailed explanation on the well-established association between NPD and HIV infection in the cohort. Even in research into oral disease not commonly associated with HIV infection, the offer of voluntary serostatus testing for HIV infection is invariably refused.
According to Statistics South Africa, an estimated 16.2% of South Africans between the ages of 15 and 49 years are HIV seropositive [46
]. Therefore, although scientific proof of HIV-seronegativity would obviously be preferable, statistically an estimated 83.8% of control subjects in this study were likely to be HIV-seronegative. There were no statistically significant differences between the periodontal indexes of HIV-seropositive subjects all of whom had chronic periodontitis, and of control subjects all of whom had chronic periodontitis.
CD4+ T-cell counts were available for only 13 HIV-seropositive subjects (eight subjects using HAART and five HAART-naïve subjects). With such a small cohort, the statistical analysis of CD4+ T-cell counts relative to periodontal indexes could have been skewed. In this study, the correlation coefficient of PPD with CD4+ T-cell count in the HIV-seropositive HAART-naïve group of subjects was significantly negative (P
< 0.01). This differs from other studies [32
] that documented a positive correlation between CD4+ T-cell counts and PPD measurements in HIV-seropositive subjects and that HIV-seropositive subjects with healthy periodontium that are using HAART have lower CD4+ T-cell counts, while HIV-seropositive subjects with chronic periodontitis using HAART, have higher CD4+ T-cell counts [31
]. These differences between the results of our study and the results of other studies may be attributed to our small sample of subjects with known CD4+ T-cell counts.
In this study, the mean CD4+ T-cell counts found in HIV-seropositive HAART-naïve subjects (257
) was higher than in HIV-seropositive subjects using HAART (172
) (). This seemingly paradoxical finding could very well be attributed to skewed statistics associated with the small number of subjects with known CD4+ T-cell counts. However, on second consideration, this finding could be real. In South Africa, many people with oral conditions suggestive of HIV disease refuse to undergo serological testing for HIV and often prefer to be treated by traditional healers. As a result, HIV infection is often diagnosed and HAART is often introduced late in the course of the disease when the CD4+ T-cell count has already fallen very low (200
). In addition, in the South African context, HIV-seropositive subjects, who depend on provincial (governmental) services for their medical care, are subject to an official policy ruling that HAART may start only when their CD4+ T-cell count has fallen to 200
or below. Under these circumstances, in practice, HAART is initiated only when the CD4+ T-cell count has fallen substantially below 200
. It is well established that starting HAART when the CD4+ T-cell count is very low will lead to a lower level of reconstitution of CD4+ T-cell numbers compared to the achieved level of reconstitution of CD4+ T-cell numbers when starting HAART at a higher CD4+ T-cell count. Hence, this seemingly paradoxical finding that the HIV-seropositive subjects using HAART in this study had a lower CD4+ T-cell count compared to the CD4+ T-cell count of HIV-seropositive HAART-naïve subjects.
In this study, the mean PPD in the HAART-naïve HIV-seropositive subjects with chronic periodontitis was slightly greater than in HIV-seropositive subjects using HAART (r
= 0.01); the mean CD4+ T-cell count in the group of HIV-seropositive subjects using HAART was lower than in the group of HIV-seropositive HAART-naïve subjects. This conforms to other studies that report a positive correlation between PPD measurements and CD4+ T-cell counts [31