HIV Modifies the Effect of Tobacco Smoking on Oral Human Papillomavirus Infection.

BACKGROUND: People living with HIV (PLWH) are more likely to smoke and harbor oral human papillomavirus (HPV) infections, putting them at higher risk for head and neck cancer. We investigated effects of HIV and smoking on oral HPV risk. METHODS: Consecutive PLWH (n = 169) and at-risk HIV-negative individuals (n = 126) were recruited from 2 US health centers. Smoking history was collected using questionnaires. Participants provided oral rinse samples for HPV genotyping. We used multivariable logistic regression models with interaction terms for HIV to test for smoking effect on oral HPV. RESULTS: PLWH were more likely to harbor oral HPV than HIV-negative individuals, including α (39% vs 28%), ß (73% vs 63%), and γ-types (33% vs 20%). HIV infection positively modified the association between smoking and high-risk oral HPV: odds ratios for smoking 3.46 (95% confidence interval [CI], 1.01-11.94) and 1.59 (95% CI, .32-8.73) among PLWH and HIV-negative individuals, respectively, and relative excess risk due to interaction (RERI) 3.34 (95% CI, -1.51 to 8.18). RERI for HPV 16 was 1.79 (95% CI, -2.57 to 6.16) and 2.78 for ß1-HPV (95% CI, -.08 to 5.65). CONCLUSION: Results show tobacco smoking as a risk factor for oral HPV among PLWH.

Oral Human Papillomavirus Infection and Oral Lesions in HIV-Positive and HIV-Negative Dental Patients.

We evaluated the risk factors associated with oral human papillomavirus (HPV) infection and oral lesions in 161 human immunodeficiency virus (HIV)-positive patients and 128 HIV-negative patients presenting for oral examination at 2 urban healthcare centers. Patients were interviewed on risk factors and provided oral-rinse samples for HPV DNA typing by polymerase chain reaction. Statistical associations were assessed by logistic regression. Oral HPV was prevalent in 32% and 16% of HIV-positive patients and HIV-negative patients, respectively, including high-risk HPV type 16 (8% and 2%, respectively; P = .049) and uncommon HPV types 32/42 (6% and 5%, respectively; P = .715). Among HIV-negative patients, significant risk factors for oral HPV included multiple sex partners (≥21 vs ≤5; odds ratio [OR], 9.1; 95% confidence interval [CI], 1.7-49.3), heavy tobacco smoking (>20 pack-years vs none; OR, 9.2; 95% CI, 1.4-59.4), and marijuana use (OR, 4.0; 95% CI, 1.3-12.4). Among HIV-positive patients, lower CD4(+) T-cell count only was associated with oral HPV detection (≤200 vs ≥500 cells/mm(3); OR, 4.5; 95% CI, 1.3-15.5). Detection of high-risk HPV was also associated with concurrent detection of potentially cancerous oral lesions among HIV-negative patients but not among HIV-positive patients. The observed risk factor associations with oral HPV in HIV-negative patients are consistent with sexual transmission and local immunity, whereas in HIV-positive patients, oral HPV detection is strongly associated with low CD4(+) T-cell counts.

Outcomes of implants and restorations placed in general dental practices: a retrospective study by the Practitioners Engaged in Applied Research and Learning (PEARL) Network.

OBJECTIVES: The authors conducted a study to determine the types, outcomes, risk factors and esthetic assessment of implants and their restorations placed in the general practices of a practice-based research network. METHODS: All patients who visited network practices three to five years previously and underwent placement of an implant and restoration within the practice were invited to enroll. Practitioner-investigators (P-Is) recorded the status of the implant and restoration, characteristics of the implant site and restoration, presence of peri-implant pathology and an esthetic assessment by the P-I and patient. The P-Is classified implants as failures if the original implant was missing or had been replaced, the implant was mobile or elicited pain on percussion, there was overt clinical or radiographic evidence of pathology or excessive bone loss (> 0.2 millimeter per year after an initial bone loss of 2 mm). They classified restorations as failures if they had been replaced or if there was abutment or restoration fracture. RESULTS: The authors enrolled 922 implants and patients from 87 practices, with a mean (standard deviation) follow-up of 4.2 (0.6) years. Of the 920 implants for which complete data records were available, 64 (7.0 percent) were classified as failures when excessive bone loss was excluded from the analysis. When excessive bone loss was included, 172 implants (18.7 percent) were classified as failures. According to the results of univariate analysis, a history of severe periodontitis, sites with preexisting inflammation or type IV bone, cases of immediate implant placement and placement in the incisor or canine region were associated with implant failure. According to the results of multivariate analysis, sites with preexisting inflammation (odds ratio [OR] = 2.17; 95 percent confidence interval [CI], 1.41-3.34]) or type IV bone (OR = 1.99; 95 percent CI, 1.12-3.55) were associated with a greater risk of implant failure. Of the 908 surviving implants, 20 (2.2 percent) had restorations replaced or judged as needing to be replaced. The majority of P-Is and patients were satisfied with the esthetic outcomes for both the implant and restoration. CONCLUSIONS: These results suggest that implant survival and success rates in general dental practices may be lower than those reported in studies conducted in academic or specialty settings. PRACTICAL IMPLICATIONS: The results of this study, generated in the private general practice setting, add to the evidence base to facilitate implant treatment planning.