HIV infection and tooth loss Christopher G. Engeland, PhDa, Paul Jang, DMDb, Mario Alves, DDS, DScc, Phillip T. Marucha, PhD, DMDd, and Joseph Califano, PhD, DDSe Chicago, Illinois UNIVERSITY OF ILLINOIS AT CHICAGO

Objectives: The objective of this study was to determine the relationship between HIV infection and tooth loss. Based on periodontal reports, we hypothesize HIV⫹ patients experience greater tooth loss than systemically healthy patients. Study design: This was a retrospective cross-sectional chart study involving 193 HIV⫹ patients and 192 controls matched on age, race, gender, and smoking status. The relationships between tooth loss and age, race, gender, smoking, CD4⫹ cell count, and viral load were determined. This study used a 2-year follow-up/maintenance period and was conducted during the era of highly active antiretroviral therapy (HAART). Results: Tooth loss between groups was not significantly different at any time point: (1) before dental treatment; (2) after initial periodontal and restorative treatment; and (3) following a 2-year maintenance period. Age, race, and smoking were risk factors for tooth loss. Among HIV⫹ individuals, CD4⫹ cell count and viral load did not influence tooth loss. Conclusions: HIV infection, in the era of HAART, does not appear to be a risk factor for tooth loss. We also did not find any association between tooth loss and indices of HIV disease progression. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:321-6)

HIV infection is a serious health problem afflicting more than 33.2 million individuals worldwide, and has resulted in more than 20 million deaths to date.1,2 While the death rate from AIDS has markedly declined in the United States,3 the disease remains 1 of the 5 leading causes of death worldwide,1 with HIV infecting approximately 6800 new individuals daily.2 HIV-associated gingivitis (HIV-G) and HIV-associated periodontitis (HIV-P) do not respond well to conventional therapy and often progress very rapidly.4,5 HIV-P is characterized by rapid destruction of the periodontal supporting apparatus and severe soft tissue necrosis. In some HIV-P lesions, more than 90% of the attachment can be destroyed in as little as 3 to 6 months, resulting in early tooth loss.4 Epidemiological studies have shown considerable variation in the prevalence of both HIV-associated and conventional forms of periodontal diseases in HIV⫹ a

Research Assistant Professor, University of Illinois at Chicago, College of Dentistry, Department of Periodontics. b Postgraduate Resident, University of Illinois at Chicago, College of Dentistry, Department of Periodontics. c Professor of Periodontics, University of Illinois at Chicago, College of Dentistry, Department of Periodontics. d Head, Department of Periodontics, University of Illinois at Chicago, College of Dentistry, Department of Periodontics. e Professor, Director of Postgraduate Periodontics, University of Illinois at Chicago, College of Dentistry, Department of Periodontics. Received for publication Mar 9, 2007; returned for revision Oct 19, 2007; accepted for publication Oct 26, 2007. 1079-2104/$ - see front matter © 2008 Mosby, Inc. All rights reserved. doi:10.1016/j.tripleo.2007.10.012

patients.6-15 Moreover, different diagnostic criteria applied to HIV-associated periodontal diseases render a comparison of these results difficult. Although clinical and epidemiological studies have conflicting results, there is evidence that HIV infection may be a risk factor for progression of periodontal disease and tooth loss. 7,9,16 Highly active anti-retroviral therapy (HAART), introduced in 1995, has reduced the prevalence of a number of HIV-associated oral lesions including periodontal disease.16 However, HAART has increased the prevalence of HIV-related salivary gland disease and xerostomia,17 the latter of which is experienced by approximately 37% of HIV⫹ individuals.18 Xerostomia, alone or in combination with other HAART-induced conditions (i.e., osteoporosis, dyslipidemia, or diabetes), appears to result in greater dental caries in HAART-treated patients.16,19 Thus, HIV⫹ patients, whether receiving HAART or not, may be at an increased risk for tooth loss over time. Previous studies have investigated the relationship between HIV infection and severity of periodontal and dental disease. However, data examining tooth loss in HIV-infected patients have not been reported. Given the relationship between HIV infection and periodontal diseases,7,9 and the increased risk for dental caries caused by HAART,16,19 we hypothesize that HIV⫹ patients experience greater tooth loss compared with systemically healthy patients. To test this hypothesis we determined and compared tooth loss at times of initial presentation (baseline), follow-up, and maintenance between HIV⫹ and control individuals. We then examined the relationship 321

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between measures of HIV disease progression and tooth loss.

Table I. Subject demographics Gender

MATERIALS AND METHODS This is a retrospective cross-sectional chart study in which the subjects studied were patients of the College of Dentistry, University of Illinois at Chicago (UIC). The enrollment protocols were reviewed and approved by the Institutional Review Boards. Each patient had to meet the following criteria in order to be included in the study sample: 1. Enrolled as a patient prior to 1999 and involved in maintenance program (i.e., scheduled dental visits every 4 to 6 months) for at least 2 years following active treatment. 2. Between the ages of 20 and 70 at the time of enrollment at the College of Dentistry. 3. Full-mouth dental radiographs were taken at the time of enrollment as a patient. Data extracted from each patient record were age, smoking, race, gender, and diabetic status. The progression of disease in the HIV⫹ group was measured by CD4⫹ cell count (⬍200, 200-500, and ⬎500 cells/ mm3) and viral load count (0-1000, 1000-10,000, 10,000-20,000, 20,000-30,000, and ⬎30,000 copies/ mm3), which were determined at the time of the initial visit (baseline) and at follow-up. Only categorical data were available for viral load. The test group consisted of 200 randomly selected HIV⫹ patients from the Ryan White Clinic at the UIC College of Dentistry. The control group consisted of 200 patients from the general undergraduate clinic that did not report a history of being HIV⫹. These control subjects were matched to the test group by age (20-29, 30-39, 40-49, 50-59, and 60-69), smoking (yes or no), gender, and race (white, black, Hispanic, Asian, and other). Of 200 subjects selected in each group, 193 HIV⫹ patients and 192 control patients met the above criteria and were included in the study sample. At the time of baseline, CD4⫹ and viral load counts were available only for a subset of HIV⫹ patients (n ⫽ 143 and n ⫽ 111, respectively). This was also true at the time of follow-up (n ⫽ 78 and n ⫽ 75, respectively). All patients were initially seen (baseline) between January 1999 and December 2001. The number of intact teeth was determined from the full-mouth radiographs and patient record. This was defined as the number of teeth present excluding residual roots, and periodontally or restoratively hopeless teeth, based on clinical judgment by the presenting clinician. Third molars were not included in any counts. Information on the date of, and reason for, tooth loss was not collected. The number of intact teeth was

Age

Smoking Race

Total

Male Female 20-29 30-39 40-49 50-59 60-69 Smoker Nonsmoker White Black Hispanic Asian Other

HIV ⫹

Control

146 (76%) 47 (24%) 20 (10%) 60 (31%) 81 (42%) 28 (15%) 4 (2%) 28% 72% 34% 44% 18% 2% 2% 193

136 (71%) 56 (29%) 29 (15%) 46 (24%) 67 (35%) 35 (18%) 15 (8%) 26% 74% 35% 42% 19% 2% 2% 192

determined before the start of active treatment (baseline), following active treatment (follow-up) and at the end of 2 years of maintenance. Active treatment included any postdiagnostic restorative/reconstructive dental work performed prior to the patient being placed on routine maintenance, which entailed scheduled dental visits every 4 to 6 months for at least 2 years. Thus, the quality of dental care and frequency of periodontal maintenance was approximately equal between groups. Statistical analysis Data were analyzed using analysis of variance (ANOVA), which treated HIV status, age group, gender, race, and smoking as between-subject factors. Analyses of tooth loss between sampling times were performed using repeated measures, with time point as a within-subject factor. For post-hoc comparisons, separate ANOVAs were used. When these analyses did not include Age Group as a variable, an analysis of covariance (ANCOVA) was then used, which treated age (in years) as a covariate. Correlations were determined using Pearson’s product moment correlations (r). All hypothesis tests were 2 tailed and used ␣ ⫽ 0.05 to determine significance. Data were analyzed using SPSS 14.0 for Windows (SPSS Inc., Chicago, IL). RESULTS HIV⫹ and control groups were evenly matched by gender, age group, smoking status, and race (Table I). In both groups, most individuals were male, belonging to age groups 30-39 or 40-49, nonsmokers, and black or white (Table I). Mean tooth loss was examined. Both HIV⫹ and control groups lost teeth during the study period. The mean tooth loss for control patients was 4.01 ⫾ 0.427 at baseline, 4.61 ⫾ 0.471 at follow-up, and 4.78 ⫾

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Controls HIV+

Number of Missing Teeth

Number of Missing Teeth

5.5

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5.0 4.5 4.0 3.5 3.0

Initial

Follow-up

8

4 2 0

Maintenance

20-39

Examination

Fig 1. Mean tooth loss at baseline, follow-up, and following a 2-year maintenance period. Error bars represent standard error of the mean (SEM).

Controls HIV+

6

50-69

Age Range (Yrs)

Fig 2. Effect of age on tooth loss. Error bars represent SEM.

**

Number of Missing Teeth

6

0.479 at the end of 2 years of maintenance. The mean tooth loss for HIV⫹ patients was 3.62 ⫾ 0.402 at follow-up, and 4.50 ⫾ 0.421 at the end of 2 years of maintenance. No significant differences in tooth loss were evident between the HIV⫹ and control groups at baseline, follow-up, or over the 2-year study period (Fig. 1). We also examined the small subset of individuals (n ⫽ 27) within this study who lost teeth during the 2-year maintenance program. There was no difference between groups for the number of teeth lost per individual (not shown). There was a significant main effect of age group, as older individuals exhibited significantly more tooth loss than younger individuals at baseline (F[4,367] ⫽ 12.89, P ⬍ .001) (Fig. 2). Post hoc analyses revealed the incidence of tooth loss was significantly greater in individuals aged 40 to 49 than in younger individuals aged 20 to 39 (P ⬍ .001). In addition, individuals aged 50 to 69 exhibited significantly greater tooth loss than either of these 2 younger groups (P ⬍ .001 for each comparison). There were no deleterious effects of HIV infection on tooth loss overall or in any of these age groups separately (Fig. 2). Gender had no effect by itself, and did not interact with HIV status on tooth loss. An ANCOVA, which treated age as a covariate, revealed a significant main effect of race on tooth loss at baseline (F[2,367] ⫽ 4.12, P ⬍ .05). Post hoc analyses showed that blacks exhibited significantly more tooth loss than whites (P ⬍ .01) (Fig. 3). There was no interaction between race and HIV status on tooth loss. A Smoking ⫻ Age Group interaction was revealed (F[1,362] ⫽ 6.54, P ⬍ .05). Post hoc analyses revealed that smokers exhibited significantly greater tooth loss

40-49

5 4 3 2 1 0 White

Hispanic

Black

Race

Fig 3. Effect of race on tooth loss. Error bars represent SEM. ** P ⬍ .01.

than nonsmokers at baseline, but this difference was only apparent in individuals aged 50 years and older (F[2,74] ⫽ 11.64, P ⫽ .001; not shown). A Smoking ⫻ HIV status interaction approached significance (F[1,361] ⫽ 2.75; P ⫽ .098). An ANCOVA, performed within control subjects, found that smokers exhibited greater tooth loss than nonsmokers (P ⬍ .05). This was not seen in HIV⫹ subjects (Fig. 4). A separate ANCOVA did not indicate a significant effect of diabetes, or interaction between diabetes and HIV status, on tooth loss (nondiabetic individual: 3.72 ⫾ 0.28 missing teeth; diabetic individual: 5.61 ⫾ 1.48; P ⫽ .108). However, with only 19 of 385 subjects reporting a diagnosis of diabetes, there were not enough subjects to definitively assess this relationship.

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Number of Missing Teeth

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Table II. CD4⫹ counts in HIV⫹ patients at baseline

*

Nonsmoker Smoker

5

Gender Age

4 3

Smoking

2

Race

1 0 Controls

HIV+

Total

Male Female 20-39 40-49 50-69 Smoker Non-smoker White Black Hispanic Asian Other

CD4⫹

N

417.1 ⫾ 27.9 349.2 ⫾ 39.0 362.9 ⫾ 34.6 400.6 ⫾ 33.9 516.6 ⫾ 71.1 451.8 ⫾ 62.4 373.0 ⫾ 24.9 474.2 ⫾ 45.6 352.5 ⫾ 32.8 394.1 ⫾ 40.0 316.0 ⫾ 140.0 595.3 ⫾ 302.1

113 30 62 58 23 32 96 46 69 23 2 3 143

Group

Fig 4. Effect of smoking on tooth loss. Error bars represent SEM. * P ⬍ .05.

All of the above effects on tooth loss were similarly apparent when data were examined at either (1) the time of follow-up or (2) after 2 years of maintenance. No other main effects or interactions were found. CD4⫹ cell counts (Table II) and viral load (not shown) in HIV⫹ individuals correlated negatively with each other (e.g., at baseline: r ⫽ – 0.380, P ⬍ .001, n ⫽ 107), as higher viral load related to lower CD4⫹ counts. Importantly, neither variable correlated with tooth loss at any time point. DISCUSSION Periodontal disease has been previously associated with HIV infection, and HIV infection has been considered a risk factor for periodontal disease. Many studies have examined and evaluated the relationship between HIV infection and severity of periodontal disease. The reported prevalence of chronic periodontitis among HIV⫹ patients shows considerable variation.6-15 A number of studies among HIV⫹ individuals report a high prevalence of severe attachment loss,7,9 but others fail to show differences between HIV⫹ and HIV– individuals.10-13 Longitudinal cross-sectional studies, conducted either before or after the advent of HAART therapy, found there was no significant difference in attachment loss between HIV⫹ and HIV– groups.14,15 Our study is in agreement with these latter reports, as we found the prevalence of tooth loss in HIV⫹ individuals was no greater than in matched controls. When examining the small subset of individuals (n ⫽ 27) that exhibited tooth loss during the 2-year maintenance period, there was again no difference in the frequency or extent of tooth loss between HIV⫹ patients and controls. Indices of disease progression

(CD4⫹ cells and viral load) were also unrelated to tooth loss. One possible explanation as to why HIV⫹ patients have been reported to have periodontal health similar to control patients may be advancement and improvement in medications that have significantly prolonged the life of HIV⫹ patients. Better management of HIV infection may have beneficial effects on oral health. Since the introduction of combination drugs and HAART, HIVinfected patients are living healthier and longer lives. Public health data, cohort studies, and randomized clinical trials demonstrate dramatic improvements in HIVrelated morbidity and mortality since the introduction of HAART.20-22 HAART therapy has also reduced the incidence of HIV-associated periodontitis.16 However, evidence suggests that the risk of caries is increased due to HAART-induced xerostomia and this, in turn, could increase tooth loss over time.16,19 The era of HAART is still in its infancy and future longitudinal studies are needed to describe the effects of HAART on intraoral findings. In the present study, information regarding the type of drug therapy that HIV⫹ individuals received was not available. The effect of different HIV drug therapies on periodontal status or tooth loss may be an important area for future study. HIV infection results in depletion of T-helper lymphocytes and impairment of neutrophil function; therefore, changes in the periodontium might be expected as part of this disease. A recent study showed that among HIV-infected women, CD4⫹ count and viral load had no consistent relation with probing depth or attachment level.15 However, the question of whether the progression of HIV disease, as expressed by CD4⫹ cell counts and viral load, affects the course and severity of tooth mortality still remains. In this study, CD4⫹ cell count and viral load was not related to tooth loss in HIV⫹ individuals. One limitation of our study was the limited number of HIV⫹ patients with available information

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on CD4⫹ cell count and viral load. Therefore, the state of immunosuppression was unknown for some HIV⫹ subjects. Studies on periodontal health and tooth loss have established that smoking is a true risk factor for both13,23,24 and smoking cessation is beneficial for tooth retention.25 A strong correlation of tobacco use with probing attachment loss has been presented in HIV⫹ patients.26 However, it has been observed that HIV⫹ smokers did not show more alveolar bone loss than an HIV– smoking control group.27 In our study, an effect of smoking on tooth loss was not apparent in HIV⫹ individuals. Both HIV⫹ and control groups had a smoking prevalence similar to that found in the general population.28 It is not clear why a relationship between smoking and tooth loss, established in other populations29 and in our control group, was not apparent in the HIV⫹ group. Possibly HIV drugs ameliorate the effect of smoking on tooth loss. Future study should evaluate the duration and quantity of tobacco use, since smoking has been associated with tooth loss in an exposure-dependent manner.30 With respect to age, there was significantly greater tooth loss with increasing age in both HIV⫹ and control groups. This concurs with previous findings that have reported an age-related increase in tooth loss.31 The present study also found that blacks exhibited greater tooth loss than whites. Data from several nationwide studies have similarly reported earlier tooth loss in black compared with white Americans.32 Importantly, a deleterious effect of HIV infection on tooth loss was not apparent within any age group, any race, or either gender. There are many reasons why teeth were extracted or lost during the investigation period. It can be assumed that most of the teeth were lost as a result of periodontal disease or caries. In this study, data were not available to specifically address the reasons for tooth loss. We saw no larger incidence of tooth loss during the maintenance period in HIV⫹ patients compared with matched controls, suggesting HIV-P did not play a significant role in tooth loss in this study.4,5 It has been suggested that HIV-infected individuals do not respond well to routine dental care and are difficult to manage because of recurrence of periodontal disease, caries, and manifestation of acute rare oral diseases.5 However, with current advancements in drug therapy, HIV⫹ individuals are able to minimize further immunosuppression and reduce the occurrence of opportunistic infections. At this time, there is not enough information in the literature comparing the effectiveness of regular dental maintenance to the overall oral health of HIV-infected individuals. Several studies have supported the need for regular oral health care for

Engeland et al. 325

individuals with HIV infection.33,34 Depending on the initial clinical diagnosis, the response to mechanical therapy and the effectiveness of a patients’ oral hygiene efforts, a 2- to 4-month interval for maintenance care has been recommended.33,34 In the present study, periodontal maintenance consisted of regularly scheduled visits every 4 to 6 months with screening of the oral tissues, monitoring of periodontal health, a restorative exam, reinforcement of oral hygiene, and removal of supra- and subgingival plaque and calculus by scaling and root planing as needed. The results of this study suggest HIV⫹ individuals can be treated and maintained as successfully as HIV– individuals. Importantly, dental practitioners should be encouraged by such findings and be more willing to treat and maintain HIV⫹ patients. In conclusion, the results of the present study suggest that HIV⫹ patients do not experience greater tooth loss than matched individuals not diagnosed with HIV. Within HIV⫹ patients, indices of disease progression did not appear related to tooth loss. In order to more fully determine the relationship between HIV infection and tooth loss in the future, carefully designed prospective randomized controlled trials, with large sample sizes and a longer duration of study, are needed. REFERENCES 1. Piot P, Bartos M, Ghys PD, Walker N, Schwartlander B. The global impact of HIV/AIDS. Nature 2001;410:968-973. 2. Global Health Reporting.org. Global HIV/AIDS estimates, end of 2007. Available at: http://www.globalhealthreporting.org/ diseaseinfo.asp. Accessed Dec 5, 2007. 3. Weiss RA. Gulliver’s travels in HIV land. Nature 2001;410: 962-7. 4. Winkler J, Grassi M, Murray P. Clinical description and etiology of HIV-associated periodontal diseases. In: Robertson PB, Greenspan JS, editors. Perspectives on oral manifestations of AIDS. Littleton, MA: PSC-Publishing; 1988. p. 49-70. 5. Holmstrup P, Westergaard J. HIV infection and periodontal diseases. Periodontology 1998;18:37-46. 6. Glick M, Holmstrup P. HIV infection and periodontal diseases. In: Rose LF, Genco RJ, editors. Periodontal Medicine. Hamilton, ON: BC Decker Inc.; 2000. p. 183-91. 7. Yeung SC, Steward GJ, Cooper DA, Sindhusake D. Progression of periodontal disease in HIV seropositive patients. J Periodontol 1993;64:651-7. 8. Lamster IB, Grbic JT, Mitchell-Lewis DA, Begg MD, Mitchell A. New concepts regarding the pathogenesis of periodontal disease in HIV infection. Ann Peridontol 1998;3:62-75. 9. Lucht E, Heimdahl A, Nord CE. Periodontal disease in HIVinfected patients in relation to lymphocyte subsets and specific microorganisms. J Clin Periodontol 1991;18:252-6. 10. Riley C, London JP, Burmeister JA. Periodontal health in 200 HIV-positive patients. J Oral Pathol Med 1992;21:124-7. 11. Drinkard CR, Decher L, Little JW, Rhames FS, Balfour HH Jr, Rhodus NL, et al. Periodontal status of individuals in early stages of human immunodeficiency virus infection. Community Dent Oral Epidemiol 1991;19:281-5. 12. Smith GL, Cross DL, Wray D. Comparison of periodontal dis-

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Reprint requests: Joseph Califano, DDS, PhD Department of Periodontics University of Illinois at Chicago, College of Dentistry 801 S. Paulina Street, Room 331 Chicago, IL 60612 [email protected]