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RESEARCH REPORTS |
1 Department of Oral Pathology (Mail Code 9436), New York University, College of Dentistry, 345 East 24th Street, New York, NY 10010, USA;
2 University of Southern California School of Dentistry, Los Angeles, CA, USA;
3 formerly with National Institute of Dental and Craniofacial Research, NIH, Bethesda, MD, USA;
4 University of Illinois at Chicago College of Dentistry, Chicago, IL, USA; and
5 University of California San Francisco, San Francisco, CA, USA;
* corresponding author, joan.phelan{at}nyu.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: dental caries • HIV • women
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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METHODS |
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WIHS medical core sites are located in the Bronx, Brooklyn, Chicago, Washington, DC, San Francisco, and Los Angeles. A separate, centralized site manages data entry and coordinates analyses. HIV+ and HIV- women were recruited from similar sources, resulting in a cohort of subjects with comparable demographic and HIV risk factors (Barkan et al., 1998). Medical core visits are scheduled every 6 mos. From the WIHS core database, HIV status and HIV risk conditions, socio-demographics, smoking status, medications, and primary markers of HIV infection (e.g., CD4, CD8, and HIV RNA) are available for oral health studies. Laboratory testing for HIV-1 RNA and lymphocyte subsets are documented elsewhere (Anastos et al., 2002).
The Oral Substudy
Oral substudy sites are associated with the medical core sites at the Bronx, Chicago, Los Angeles, and San Francisco. Any woman enrolled in the WIHS at these sites was eligible for the oral substudy. Women were enrolled in the oral substudy after providing informed consent to the protocol approved by institutional review boards at each site. The demographics of the oral substudy cohort closely resembled that of the WIHS medical core (Mulligan et al., 2004). Oral substudy examination visits were scheduled every 6 mos, ideally within 2 wks, but no longer than 2 mos after the medical core visit.
The oral substudy protocol was developed jointly by the oral investigators and representatives from the NIDCR. The protocol included an oral health questionnaire, measurement of unstimulated and stimulated salivary flow, evaluation of cervical lymph nodes and major salivary glands, an examination for mucosal lesions, and assessment of the number of teeth, dental plaque, gingival banding, status of the interdental papillae, periodontal attachment loss, restorations, coronal caries, and root caries. Procedures for the assessment of salivary flow, salivary glands, and oral mucosal lesions are documented elsewhere (Greenspan et al.,, 2000; Mulligan et al., 2000; Navazesh et al., 2000). Criteria for caries assessment were developed from those used in recent national surveys (NIDR, 1991). We questioned subjects to identify teeth missing due to disease. Caries assessments were performed on all permanent teeth present, excluding third molars and teeth lost to trauma. Examiners were initially trained and calibrated by NIDCR "gold standard" examiners. Subsequent calibration sessions found less than 5% disagreement in tooth-surface coding between examiners and the "gold standard trainer".
Oral Study Variables
Data collected from coronal and exposed root surfaces were transformed into coronal and root caries indices: DMFS (Decayed, Missing, and Filled Surfaces), DFS (Decayed, Filled Surfaces), and DFSrc (Decayed, Filled Surfaces, Root Caries). The number of permanent teeth present was also recorded. The smoking variable was defined as ‘currently smoking’ or ‘not currently smoking’. Salivary flow variables were ‘unstimulated’ (< 0.1 mL/min vs. 
0.1 mL/min) and stimulated (> 0.4 mL/min < 0.7 mL/min vs. 0.7 mL/min) salivary flow volume.
Age and racial/ethnic groups (non-Hispanic Black, non-Hispanic White, and Latina/Hispanic) used were similar to those of the NHANES II reports (Winn et al., 1996). Remaining racial/ethnic categories were combined into one group. Subject comparisons by age group reflect the baseline age of study subjects. For year 5, the reader should add 5 yrs to each age group.
Categories used to assess the effect of anti-retroviral therapy on dental caries indices included: no anti-retroviral therapy, monotherapy, combination therapy, and highly active anti-retroviral treatment (HAART). The anti-retroviral therapy data were derived from subjects’ self-reported use of these medications and were obtained at each core visit. These anti-retroviral categories are used in other WIHS analyses and are described elsewhere (Anastos et al., 2002).
Data Analysis
DMFS, DFS, DFSrc, and number of permanent teeth from the baseline (10/1/95 to 3/31/96) and the tenth (4/1/2000 to 9/30/2000) oral substudy visits were used to make comparisons by HIV status in cross-sectional analyses. Longitudinal regression analysis of DMFS and DFSrc were modeled as continuous dependent variables. Other continuous variables that were included by a stepwise process of elimination were: age, number of permanent teeth, CD4 count, CD8 count, and HIV viral load. HIV status (HIV-seropositive, HIV-seronegative), unstimulated salivary flow volume, anti-retroviral therapy type, and smoking status were entered as categorical data.
SPSS 11.0 and STATA 7.0 statistical software were used for the data analyses. Differences in the dental caries experience between the HIV-seropositive and -seronegative groups were determined by ANOVA, two-tailed statistics by a comparison of means. We used regression models to perform longitudinal analyses of the same data. We used linear regression models to measure whether the independent variable, HIV status, was a predictor of the dependent outcome variables: DMFS, DFS, DFSrc.
Generalized Estimation Equations (GEE) were used for the longitudinal analyses. GEE analysis was used because it is an analysis that takes into account all possible correlations for data with repeated measures. In this manner, the average caries index per subject estimates the development of dental caries during any six-month interval. Throughout all analyses, p-values of < 0.05 were considered to indicate statistically significant findings.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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).
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). HIV-seropositive subjects had statistically significantly fewer permanent teeth (p = 0.03) than HIV- subjects at the initial baseline examination.
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). This trend continued at year 5, with unstimulated salivary volume associated with higher DMFS (p = 0.04) and stimulated salivary volume closely approaching statistical significance (p = 0.06).
At baseline, for the entire cohort, DMFS was significantly higher, and there were significantly fewer permanent teeth in the older age group as compared with the younger age group (p = 0.00) (Table 3). For subjects 18–44 yrs of age, there was a significantly higher DMFS among HIV+ subjects compared with HIV- subjects (p = 0.03) at both baseline and year 5 examinations. None of the other age comparisons showed statistically significant differences. DFS was analyzed because teeth included as missing could have been due to either caries or periodontal disease, and the components of DFS refer strictly to caries (Winn et al., 1996). There were no statistically significant findings for DFS by HIV status (Table 3).
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). Age range comparisons for DFSrc were inconsistent and not statistically significant (Table 3). At baseline, HIV+ subjects in the 18- to 44-year age group had a 1.6-fold higher prevalence of root caries than the HIV- subjects, while the opposite was true for those in the 45-to 64-year age group, in which the HIV- controls had a root caries rate 1.4-fold higher than that in the HIV+ subjects. By year 5, HIV+ subjects in both age groups had a 2.3-fold higher caries prevalence than HIV- subjects. Baseline and year 5 comparisons for DFSrc, with unstimulated and stimulated salivary volume considered, showed no statistically significant findings (Table 2b).
Longitudinal Analysis
The results of the longitudinal analysis are shown for all subjects and then for HIV+ subjects separately (Table 4a). From the baseline measure, for the entire cohort, there was no significant difference associated with HIV status. DMFS increased with increasing age and with decreasing number of teeth, CD4 count, and volume of stimulated saliva. For HIV+ subjects alone, the variables remaining in the final regression model for coronal caries included age, CD4 count, CD8 count, and number of teeth. Since there was a resulting statistical confounding effect with CD4 and CD8 lymphocyte counts, the ratio, e.g., CD4/CD8, of the 2 variables was estimated instead. When the ratio was used, parameter estimates did not significantly change, and this new variable combination remained statistically significant in the final model, i.e., remaining negatively associated with DMFS (p = 0.01), as was the number of teeth. Subjects’ age was positively associated with DMFS. There was no significant association with HIV viral load, anti-retroviral therapy type, or salivary flow volume.
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). There was no association with HIV status or CD4 or CD8 lymphocyte counts. The direction of association for age, number of teeth, and salivary flow was not different from that for coronal caries in this group, except that it was unstimulated rather than stimulated salivary volume that was negatively associated with root caries. In this model, there was a positive association between root caries and smoking (p = 0.01). For HIV+ subjects alone, the variables remaining in the final regression model included age, number of teeth, and average stimulated salivary volume. Root caries increased with increasing age (p = 0.02), decreasing number of teeth, and stimulated salivary volume (p = 0.03 and p = 0.03, respectively). There was no association with CD4 or CD8 lymphocyte counts, HIV viral load, or anti-retroviral therapy. |
DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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Interpretation of the DMFS is complicated by the fact that missing teeth included in the index could be due to either caries or periodontal disease. Examination of mean DFS did not help to clarify this problem. Analysis of gingival/periodontal findings among WIHS subjects has not found significant differences between HIV+ and HIV- women (Mulligan et al., 2004), suggesting that the differences in the numbers of teeth, and thus the ‘missing’ component of the DMFS in this cohort, are more likely associated with caries than with periodontal disease. To date, only one HIV study has reported dental caries findings transformed to DMFS (Bretz et al., 2000). In that study, all subjects were HIV+ and were predominantly men. The overall DMFS prevalence was 42.9 ± 28.9, a finding very similar to that of our study, in that, among HIV+ women, the overall DMFS at baseline was 44.0 ± 30.
The results for the root caries index are not as clear as those for coronal caries. Although there appeared to be a trend toward an increased prevalence of root caries in HIV+ women, this did not reach significance. Subsequent longitudinal analyses with data from additional WIHS visits may reveal clearer results. The association between smoking and an increased incidence of root caries was seen across the entire cohort. Smoking has been reported to be a significant risk indicator for dental caries and strongly associated with periodontal disease (Axelsson et al., 1998; Pihlstrom, 2001; Calsina et al., 2002; Jansson and Lavstedt, 2002). Examination of the relationship among smoking, gingival recession, and root caries in WIHS subjects may clarify this finding.
Access to dental care, salivary flow, and medications are areas that require further study. In the overall WIHS cohort at baseline, more HIV+ than HIV- women reported that they had received dental care in the preceding 6 mos (Barkan et al., 1998), and, similarly, in the oral substudy at baseline, HIV+ women were more likely than HIV- women to have seen a dentist in the preceding 6 mos (Mulligan et al., 2004). Differences in DMFS could be related to access to dental care and variations in dental professional practices. The prevalence of salivary gland disease and decreased salivary flow has been reported to be increasing in HIV-infected individuals (Patton et al., 2000). Previously reported studies from the WIHS have also reported increased prevalences of decreased unstimulated salivary flow (Navazesh et al., 2000) and increased salivary gland enlargement (Mulligan et al., 2000) among HIV+ women. In this study, salivary flow was associated, albeit inconsistently, with increased DMFS in both the cross-sectional and longitudinal results. The associations in the longitudinal analysis between DMFS and decreased CD4/CD8 ratio suggest another area to be explored.
After many iterations of estimation equations, there was no significant difference in coronal or root caries by HIV status, nor did the results of this study support a relationship between anti-retroviral therapy and increased dental caries risk. This is consistent with the results of the study reported by Bretz et al.(2000). Anecdotal reports have suggested a relationship between anti-retroviral therapy and dental caries (Glick et al., 1998), and an association between decreased salivary flow and HAART in the WIHS oral cohort has been reported (Navazesh et al., 2003). Combination anti-retroviral therapy emerged during the time of this study. At baseline, more than half of the HIV+ subjects in the oral cohort were not yet taking any anti-retroviral therapy (356/679), and by year 5, less than half of the remaining HIV+ subjects were taking HAART (121/308). This study may not have been long enough for us to see the effect of anti-retroviral therapy on dental caries indices.
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ACKNOWLEDGMENTS |
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Received August 25, 2003; Last revision August 1, 2004; Accepted August 23, 2004
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REFERENCES |
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Axelsson P, Paulander J, Lindhe J (1998). Relationship between smoking and dental status in 35-, 50-, 65- and 75-year-old individuals. J Clin Periodontol 25:297–305.[ISI][Medline]
Barkan SE, Melnick SL, Preston-Martin S, Weber K, Kalish LA, Miotti P, et al. (1998). The Women’s Interagency HIV Study. Epidemiology 9:117–125.[ISI][Medline]
Bretz WA, Flaitz C, Moretti A, Corby P, Schneider LG, Nichols CM (2000). Medication usage and dental caries outcome-related variables in HIV/AIDS patients. AIDS Patient Care STDS 14:549–554.[ISI][Medline]
Brown JB, Rosenstein DD, Mullooly J, O’Keeffe RM, Robinson S, Chiodo G (2002). Impact of intensified dental care on outcomes in human immunodeficiency virus infection. AIDS Patient Care STDS 16:479–486.[ISI][Medline]
Calsina G, Ramón JM, Echeverria JJ (2002). Effects of smoking on periodontal tissues. J Clin Periodontol 29:771–776.[ISI][Medline]
Glick M, Berthold P, Danik J (1998). Severe caries and the use of protease inhibitors (abstract). J Dent Res 77:84.
Greenspan D, Komaroff E, Redford M, Phelan JA, Navazesh M, Alves MEAF, et al. (2000). Oral mucosal lesions and HIV viral load in the Women’s Interagency HIV study (WIHS). J AIDS 25:44–50.
Jacob LS, Flaitz CM, Nichols CM, Hicks MJ (1998). Role of dentinal carious lesions in the pathogenesis of oral candidiasis in HIV infection. J Am Dent Assoc 129:187–194.[Abstract]
Jansson L, Lavstedt S (2002). Influence of smoking on marginal bone loss and tooth loss—a prospective study over 20 years. J Clin Periodontol 29:750–756.[ISI][Medline]
Mulligan R, Navazesh M, Komaroff E, Greenspan D, Redford M, Alves M, et al. (2000). Salivary gland disease in human immunodeficiency virus-positive women from the WIHS study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 89:702–709.[ISI][Medline]
Mulligan R, Phelan JA, Brunelle J, Redford M, Pogoda JM, Nelson E, et al. (2004). Baseline characteristics of participants in the oral component of the Women’s Interagency HIV Study. Community Dent Oral Epidemiol 31:1–13.
National Institute of Dental Research (1991). Oral health surveys of the National Institute of Dental Research—diagnostic criteria and procedures. Washington, DC: US Government Printing Office, NIH Publ. No. 91-2870.
Navazesh M, Mulligan R, Komaroff E, Redford M, Greenspan D, Phelan J (2000). The prevalence of xerostomia and salivary gland hypofunction in a cohort of HIV-positive and at-risk women. J Dent Res 79:1502–1507.
Navazesh M, Mulligan R, Barron Y, Redford M, Greenspan D, Alves M, et al. (2003). A 4-year longitudinal evaluation of xerostomia and salivary gland hypofunction in the Women’s Interagency HIV Study participants. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 95:693–698.[ISI][Medline]
Patton LL, McKaig R, Strauss R, Rogers D, Eron JJ Jr (2000). Changing prevalence of oral manifestations of human immuno-deficiency virus in the era of protease inhibitor therapy. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 89:299–304.[ISI][Medline]
Pihlstrom BL (2001). Periodontal risk assessment, diagnosis and treatment planning. Periodontol 2000 25:37–58.
Winn DM, Brunelle JA, Selwitz RH, Kaste LM, Oldakowski RJ, Kingman A, et al. (1996). Coronal and root caries in the dentition of adults in the United States, 1988–1991. J Dent Res 75:642–651.
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