Characterizing traditionally defined periodontal disease in HIV+ adults.

BACKGROUND

Results have varied from previous studies examining the level and extent of periodontal disease (PD) in HIV-1 infected (HIV+) adults. These studies used different methodologies to measure and define PD and examined cohorts with divergent characteristics. Inconsistent methodological approaches may have resulted in the underestimation of traditionally-defined PD in HIV+ individuals.

OBJECTIVES

To characterize the level, extent and predictors (i.e. immunologic, microbiologic, metabolic and behavioral) of PD in an HIV+ cohort during the era of highly active antiretroviral therapy (HAART).

STUDY DESIGN

Cross-sectional study.

SETTING

HIV+ adults receiving outpatient care at three major medical clinics in Cleveland, OH. Subjects were seen from May, 2005 to January, 2008.

MEASUREMENTS

Full-mouth periodontal examinations included periodontal probing depth (PPD), recession (REC) and clinical attachment level (CAL). Subgingival plaque was assessed for DNA levels of Porphyromonas gingivalis (Pg), Tannerella forsythia, and Treponema denticola by real-time DNA PCR assays developed for each pathogen. Rather than using categories, we evaluated PD as three continuous variables based on the percent of teeth with >or=1 site per tooth with PPD >or= 5mm, REC > 0 mm and CAL >or= 4mm.

RESULTS

Participants included 112 HIV+ adults. Each subject had an average 38% (+/-24%) of their teeth with at least one site of PD >or= 5 mm, 55% (+/-31%) of their teeth with at least one site of REC > 0 mm, and 50% (+/-32%) of their teeth with at least one site of CAL >or= 4 mm. CD4+ T-cell count <200 cells/mm(3) was significantly associated with higher levels of REC and CAL, but not PPD. Greater levels of Pg DNA were associated with PPD, REC and CAL.By regression analysis, CD4+ T-cell count <200 cells /mm3 had approximately twice thedeleterious effect on CAL as did smoking (standardized beta coefficient 0.306 versus 0.164) [corrected]. Annual dental visit compliance remained an independent predictor for lower levels of PD.

CONCLUSIONS

The level and extent of PD were high in this cohort even though most patients were being treated with HAART. The definition of periodontal disease used and cohort characteristics examined can influence the level of periodontal disease reported in studies of persons with HIV. Traditional periodontal pathogens are associated with PD in this cohort. Those with CD4+ T-cell counts <200 cells/mm(3) are at greater risk for PD. Therefore, earlier HAART initiation may decrease exposure to immunosuppression and reduce PD morbidity. Continuity of dental care remains important for HIV+ patients even when they are being treated with HAART.